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Health Benefits of Biotin
<p>Health Benefits of Biotin</p>
Dr. Constance Odom, MD Picture of Dr. Constance Odom, MD
Medically reviewed by
Written by our editorial team.
Last Edited 5 min read
Biotin is a B-vitamin, and is also known by the name of vitamin B7. It was once known as coenzyme R, or vitamin H. The H stood for Haar und Haut, the German words for Hair and Skin. Biotin is water soluble, which means that it dissolves in water, and has many important functions in the body.
Biotin is necessary for the functions of several enzymes that are known as carboxylases, which are biotin-containing enzymes that participate in important metabolic functions, like the production of glucose and fatty acids. Commonly recommended, the intake is about five micrograms per day in infants and thirty micrograms in adults. This can be increased to thirty five micrograms per day in breastfeeding women.
Deficiency for biotin is fairly rare, but some groups of people are more likely to experience it in mild forms, such as pregnant women. Other factors, such as consuming raw eggs, can cause a deficiency. But to do something like that, you'd have to dine on raw eggs for quite a long amount of time. Raw egg whites contain a protein called avidin, which binds to biotin and prevents it from being absorbed by the body. Thankfully, it's rendered inactive during cooking.
Biotin is a key vitamin for energy production, and several enzymes require it to properly function. These enzymes are specifically involved in fat, protein, and carb metabolizm, and initiate crucial parts of the metabolic processes of these nutrients. Biotin plays a role in fatty acid synthesis by assisting enzymes that activate reactions important to breaking down fatty acids. It's also important in gluconeogenisis, which is the metabolic pathway that results in the generation of glucose from certain non-carbohydrate carbon substrates. Gluconeogenesis is one of the several main mechanisms used by humans and many animals to maintain blood glucose levels, avoiding hypoglycemia. It's also important in the breakdown of amino acids, as biotin-containing enzymes are involved in the metabolism of several important kinds, such as leucine.
Biotin is important for more cosmetic purposes as well, such as brittle nails for one. Brittle nails are nails that are weak can become easily chipped, cracked, or split. It's very common to have brittle nails, unfortunately, as an estimated twenty percent of people around the globe are effected. But, in one study, eight people with brittle nails were given 2.5mg of biotin, per day, for a minimum of six up to fifteen months. Thickness in the nails improved by twenty five percent in all eight participants, and nail splitting was also reduced. In yet another study, thirty five people with brittle nails found that 2.5mg of biotin a day for one and a half to seven months improved symptoms in sixty seven percent of participants. These studies were rather small, however, and more research is certainly needed.
In a similar cosmetic vain, biotin is also often associated with an increase of hair growth, and not just any kind, but healthier, and stronger hair. And while more research is certainly needed to back this claim, a deficiency in biotin may lead to hair loss, which indicated and importance in the vitamin when it comes to maintaining a lush mane of hair. Whether or not it improves hair growth in healthy people, the jury's still out on that, but people with even a slight deficiency should certainly see results from added supplementation.
Biotin may even help controlling the blood sugar levels of those who have diabetes. Type two diabetes is a metabolic disease, and is characterized by high blood sugar levels and impaired insulin function. Recently, researches have studied how biotin supplements affect blood sugar levels in type two diabetics, and some evidence shows that biotin concentrations in blood may be lower in people with diabetes, compared to healthier individuals. Studies in diabetics given biotin alone have, as of it, provided mixed results. On the other hand, several controlled studies have shown that biotin supplements, combined with the mineral chromium, may lower blood sugar levels in some people with type two diabetes.
When it comes to skin, Biotin's role in skin healthy isn't fully understood, but it is known that you may get red, scaly skin rashes if you have a biotin deficiency. Other studies have also suggested that biotin deficiency may sometimes cause a skin disorder known as seborrheic dermatits, or cradle cap, as it's more commonly known. Biotin's role in skin healthy could possibly be related to it's effect on fat metabolism, which is important for the skin and may be impaired when dealing with a deficiency.
Biotin is important when it comes to pregnancy and breastfeeding, and require an increased requirement for the vitamin. It's actually been estimated that about half of all women who get pregnant may develop a mild deficiency in the vitamin. This means that it may start to affect their well being, but not enough to cause noticeable symptoms. Deficiencies are thought to occur in pregnant women thanks to faster breakdown during pregnancy. Additional, a major cause for concern in these women is that animals studies have found that a biotin deficiency has shown to be alongside many birth defects, and may be a contributing factor. Nevertheless, remember to always consult your doctor or dietitian/nutritionist before taking supplements during pregnancy and while breastfeeding.
Biotin also may affect multiple sclerosis, which is an autoimmune disease. In MS, the protective covering of nerve fibers in the brain, spinal cord, and eyes is damaged or destroyed. This protective covering is called myelin, and biotin is known to be an important factor in producing it. In fact, a pilot study in twenty three people with progressive Multiple Sclerosis tested the use of high doses of biotin, and over ninty percent of participants had some degree of improvement. And of course, this finding needs much more study, at least two randomized controlled trials have been carried out in people with progressive MS. The final results have not been published, but the preliminary results are promising.
Biotin is found in a rather wide variety of foods, which means that deficiency while not impossible, is rare. Such foods include Wheat germ, whole-grain cereals, whole wheat bread, eggs, dairy products, peanuts, soya nuts, Swiss chard, salmon, and chicken are all sources of biotin, alongside organ meats, such as liver and kidney and mushrooms. A bit of it is even produced by the bacteria in your stomach, on it's own or as a component of mixed vitamin supplements.
To top all of these benefits off, biotin is considered extremely safe. Even massive doses of up to three hundred milligrams a day, which is what was used to test multiple sclerosis and it's effects, have not led to any adverse side effects. And because it's a water-soluble vitamin, excess of it is lead out of the body in urine. However, there have been some reports of high-dose biotin causing strange results on thyroid tests, so check with a doctor before using if you are currently taking thyroid medication.
This article is for informational purposes only and does not constitute medical advice. The information contained herein is not a substitute for and should never be relied upon for professional medical advice. Always talk to your physician about the risks and benefits of any treatment. Nu Image Medical may not offer the medications or services mentioned in this article.
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How Aromatherapy Works
Aromatherapy works by stimulating receptors in the nose responsible for smell, sending messages by olfactory cells to the part of the brain that controls the drive for survival, emotions, and instinct called the limbic system. The olfactory cells recognize scents as specific aromatic molecules that fit into receptors on these cells. Although not fully understood, scientists believe that these nerve signals’ action causes powerful mood changes in response to particular smells.
Massage Therapy in Harmony with Aromatherapy
Massage therapy, combined with essential oils, candles and incense, stimulates positive emotions and relaxation, equipping clients with coping mechanisms for many other health issues. An aromatherapy massage is a popular multi-purpose way of using supplemental care for health issues. The skin absorbs essential oils maintaining suppleness, it offers pain relief, and the aroma’s mental stimulation provides clients with the ultimate massage session.
VIP Mobile Massage offers specialist care for each client, operating 7-days a week from 9:00 AM to 11:00 PM. Call us on 305-586-1267 to book an appointment or inquire about our services.
About Author
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When it comes to maximizing your gains in strength and muscle mass, understanding the role of hormones in strength training and muscle growth is crucial. Hormones act as messengers in your body, orchestrating the complex processes that lead to muscle hypertrophy and strength enhancements. In this comprehensive guide, we'll delve into the specifics of how hormones influence your fitness journey.
The Key Hormones Involved in Muscle Growth
Several hormones play pivotal roles in muscle growth. Among the most influential are testosterone, growth hormone (GH), and insulin-like growth factor 1 (IGF-1). Each of these hormones facilitates muscle hypertrophy in distinct ways:
• Testosterone: Known as the primary male sex hormone, testosterone is critical for protein synthesis and muscle repair. It directly influences the anabolic environment in the body, promoting the growth of muscle fibers.
• Growth Hormone: Released by the pituitary gland, GH stimulates overall growth and cell reproduction. It promotes the release of IGF-1, which further enhances muscle growth.
• Insulin-like Growth Factor 1: IGF-1 works alongside GH to stimulate muscle growth and repair, thereby boosting muscle hypertrophy.
Testosterone: The Anabolic Powerhouse
Testosterone is often dubbed the king of anabolic hormones. A study published in the Journal of Applied Physiology showed that men with higher testosterone levels experienced greater muscle mass and strength gains from resistance training compared to those with lower levels (source). Here's how it works:
1. Increased Protein Synthesis: Testosterone enhances the rate at which muscle proteins are synthesized, aiding in quicker recovery and growth.
2. Reduced Muscle Breakdown: It decreases the activity of catabolic hormones that break down muscle tissue, preserving the muscle mass you work hard to build.
3. Enhanced Neural Adaptations: Higher testosterone levels can improve neuromuscular communication, leading to more effective strength training sessions.
Understanding the impact of testosterone can help you adjust your training and lifestyle to optimize its levels. Factors such as sleep, nutrition, and resistance training intensity all play roles in maintaining healthy testosterone levels.
Growth Hormone and IGF-1: The Dynamic Duo
The relationship between growth hormone and IGF-1 is akin to a duo of superheroes working together to combat muscle atrophy. Growth hormone stimulates the liver to produce IGF-1, which then circulates to the muscles and promotes growth. This relationship was highlighted in a review by the European Journal of Endocrinology (source).
Growth hormone peaks during sleep, making quality rest essential for maximizing muscle growth. Incorporating proper sleep hygiene and a balanced diet rich in protein can significantly enhance GH and IGF-1 levels, contributing to better muscle gains.
Practical Tips for Maximizing Hormonal Benefits
Here are some actionable steps to make the most of your hormonal responses for muscle growth:
• Optimize Your Sleep: Aim for 7-9 hours of quality sleep per night to support GH production.
• Focus on Compound Movements: Exercises like squats, deadlifts, and bench presses stimulate testosterone and GH release more than isolation exercises.
• Eat a Balanced Diet: Ensure you get enough protein, healthy fats, and carbs to fuel muscle growth and hormonal balance.
• Manage Stress: High stress levels can increase cortisol, a catabolic hormone. Practice stress-reducing activities like meditation or yoga.
Conclusion: Boost Your Gains by Understanding Hormones
Understanding the role of hormones in strength training and muscle growth can give you the edge you need to optimize your workouts and nutrition. By focusing on hormones like testosterone, growth hormone, and IGF-1, you can create an optimal internal environment for muscle hypertrophy. Implement the practical tips we've discussed, and you'll be on your way to maximizing your strength and muscle gains.
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Heart Murmurs and Other Sounds
During a regular medical checkup, your doctor will use a stethoscope to listen to your heartbeat to determine whether your heart is beating pro...
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What Are Heart Murmurs and Other Sounds?
During a regular medical checkup, your doctor will use a stethoscope to listen to your heartbeat to determine whether your heart is beating properly and has a normal rhythm. This gives the doctor information concerning the health of your heart. If your doctor hears a “murmur” or any other abnormal sounds coming from your heart, it may be an early indicator of a serious heart condition.
How Are Heart Murmurs and Other Sounds Evaluated?
A normal heartbeat has two sounds, a lub (sometimes called S1), and a dub (S2). These are caused by the closing of valves inside the heart. If there are problems in the heart, there may be additional sounds or abnormal sounds.
Your doctor will listen to your heart with a stethoscope (a medical device used for listening (auscultation) to the heart, lungs, and other organs of the human body). If problems are detected, your doctor may order an echocardiogram (a test that uses sound waves to create a moving picture of the heart) to get a better understanding of the abnormal sounds detected.
Heart Murmurs
The most common abnormal heart sound is a heart murmur. A murmur is a blowing, whooshing, or rasping sound that occurs during a heartbeat. There are two kinds of heart murmurs, innocent (also called physiological) and abnormal murmurs.
An innocent murmur is found in children, and is due to small holes between the different chambers of the heart. This usually does not cause significant problems, but may need to be monitored over time. An abnormal murmur in a child is due to congenital (present at birth) heart malformations, and may need to be corrected with surgery.
An adult abnormal murmur is usually due to problems with the valves that separate the chambers of the heart. If a valve does not close tightly and some blood leaks backward, this is called regurgitation. If a valve has become too narrow or becomes stiff, known as stenosis, it can also cause a murmur.
Murmurs are graded depending on how loud the sound is. The scale for grading is from one to six, where a one is very faint and a six is very loud—so loud it may not need a stethoscope to be heard. Murmurs are also categorized as occurring either during the first sound (S1) as systole murmurs, or during the second sound (S2) as diastole murmurs.
Galloping Rhythms
Other heart sounds include a “galloping” rhythm, with the occurrence of additional heart sounds S3 and S4. An S3 gallop or “third heart sound” is a sound that occurs after the diastole, S2 “dub” sound. In young athletes or pregnant women, it is likely to be harmless, but in older adults, it may indicate heart disease.
An S4 gallop is an extra sound before the S1 systole “lub” sound. This is always a sign of disease, likely the failure of the left ventricle of the heart. You may also have both an S3 and an S4 sound, and this is called a “summation gallop” when the heart is beating very fast. A summation gallop is very rare.
Other Sounds
Clicks or short, high-pitched sounds may also be heard during the regular heartbeat. This could indicate a mitral valve prolapse, when one or both flaps of the mitral valve are too long. This can cause some regurgitation of blood into the left atrium.
Rubbing sounds may be heard in patients with certain kinds of infections. A rubbing sound is usually caused by an infection in the pericardium due to a virus, bacteria, or fungus.
If your doctor finds any abnormal heart sounds, he or she may ask you questions about your family. If any of your family members also have abnormal heart sounds or have a history of heart problems, it is important to tell your doctor. It may make diagnosing the cause of your abnormal heart sounds easier.
You doctor will also ask if you’ve had any other symptoms, such as bluish skin, chest pain, fainting, distended neck veins, shortness of breath, swelling, or weight gain. Your doctor may also listen to your lung sounds and see if you have signs of liver enlargement. These symptoms may provide clues about what type of heart problem you are experiencing.
What Are the Causes of Heart Murmurs and Other Sounds?
The heart is made up of four chambers. The two upper chambers are called the atria and the two lower chambers are called the ventricles. Valves are located between these chambers to make sure that blood always flows in one direction.
The tricuspid valve goes from the right atrium to the right ventricle. The mitral valve leads from the left atrium to the left ventricle. The pulmonary valve goes from the right ventricle out to the pulmonary trunk, and the aortic valve goes from the left ventricle to the aorta. The pericardial sac surrounds the heart and protects it. Problems with these parts of the heart may lead to unusual sounds that can be detected by listening with a stethoscope or by performing an echocardiogram test.
Congenital Malformations
Murmurs, especially in children, may be caused by congenital (present at birth) heart malformations. These can be benign and never cause symptoms or can be severe malformations that require surgery or even a heart transplant. Innocent murmurs include pulmonary flow murmurs, Still’s murmur, and a venous hum.
One of the more serious congenital problems that is a cause of heart murmurs is called the “Tetralogy of Fallot”. This is a set of four defects in the heart that lead to episodes of cyanosis. Cyanosis is when the skin of an infant or child turns blue from lack of oxygen during activity (like crying or feeding).
Another heart problem that causes a murmur is patent ductus arteriosus, in which a connection between the aorta and the pulmonary artery fails to close correctly after birth. Other congenital problems include atrial septal defect, coarctation of the aorta, and ventricular septal defect.
Heart Valve Defects
In adults, murmurs are usually the result of problems with the heart valves. This may be caused by an infection, such as endocarditis or infectious endocarditis. Valve problems can also simply occur as a part of the aging process due to wear and tear on the heart.
Regurgitation, or backflow, is when the valves do not close properly. The aortic valve can have aortic regurgitation. The mitral valve can have regurgitation, either acute (caused by a heart attack or a sudden infection) or chronic (caused by high blood pressure, infection, mitral valve prolapse, or other causes). The tricuspid valve can also suffer from regurgitation, usually caused by the enlargement (dilatation) of the right ventricle. Pulmonary regurgitation is caused by the backflow of blood into the right ventricle when the pulmonary valve cannot close completely.
Stenosis is a narrowing or stiffening of a valve. Mitral stenosis occurs most often due to rheumatic fever (a complication of untreated strep throat or scarlet fever). Mitral stenosis can cause fluid to back up into the lungs, causing pulmonary edema. Aortic stenosis can also occur because of rheumatic fever, and it may cause heart failure. Tricuspid stenosis can occur because of rheumatic fever or heart injury. Pulmonary valve stenosis is usually a congenital problem and runs in families. Aortic and tricuspid stenosis can also be congenital.
Another cause of heart murmurs is stenosis due to hypertrophic cardiomyopathy. The muscle of the heart thickens making it harder to pump blood through the heart. This results in a heart murmur. This is a very serious disease that is often passed on through families.
Causes of Clicks
Heart clicks are caused by problems with the mitral valve. Mitral valve prolapse is the most common cause, when one or both flaps of the mitral valve are too long. This can cause some regurgitation of blood into the left atrium.
Causes of Rubs
Heart rubs are caused by friction between layers of the pericardium—a sac around the heart. This is usually caused by an infection in the pericardium due to a virus, bacteria, or fungus.
Causes of Galloping Rhythms
A galloping rhythm of the heart, with a third or fourth heart sound, is very rare. An S3 sound is likely caused by an increased amount of blood within the ventricle. This may be harmless, but could indicate heart problems, such as congestive heart failure. An S4 sound is caused by blood being forced into a stiff left ventricle. This is a sign of serious heart disease.
What Can Be Expected in the Long-term?
Abnormal heart sounds often indicate some type of heart disease. This may be treated with medication, or may require surgery. It is important to follow up with a heart specialist and learn the details of your condition.
Written by: Christine Case-Lo
Edited by:
Medically Reviewed by: [Ljava.lang.Object;@7fb372e7
Published: Aug 1, 2012
Published By: Healthline Networks, Inc.
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Zvarova, Barbora; Uhl, Franziska E.; Uriarte, Juan J.; Borg, Zachary D.; Coffey, Amy L.; Bonenfant, Nicholas R.; Weiss, Daniel J. and Wagner, Darcy E. (2016): Residual Detergent Detection Method for Nondestructive Cytocompatibility Evaluation of Decellularized Whole Lung Scaffolds. In: Tissue Engineering Part C-Methods, Vol. 22, No. 5: pp. 418-428
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Abstract
The development of reliable tissue engineering methods using decellularized cadaveric or donor lungs could potentially provide a new source of lung tissue. The vast majority of current lung decellularization protocols are detergent based and incompletely removed residual detergents may have a deleterious impact on subsequent scaffold recellularization. Detergent removal and quality control measures that rigorously and reliably confirm removal, ideally utilizing nondestructive methods, are thus critical for generating optimal acellular scaffolds suitable for potential clinical translation. Using a modified and optimized version of a methylene blue-based detergent assay, we developed a straightforward, noninvasive method for easily and reliably detecting two of the most commonly utilized anionic detergents, sodium deoxycholate (SDC) and sodium dodecyl sulfate (SDS), in lung decellularization effluents. In parallel studies, we sought to determine the threshold of detergent concentration that was cytotoxic using four different representative human cell types utilized in the study of lung recellularization: human bronchial epithelial cells, human pulmonary vascular endothelial cells (CBF12), human lung fibroblasts, and human mesenchymal stem cells. Notably, different cells have varying thresholds for either SDC or SDS-based detergent-induced cytotoxicity. These studies demonstrate the importance of reliably removing residual detergents and argue that multiple cell lines should be tested in cytocompatibility-based assessments of acellular scaffolds. The detergent detection assay presented here is a useful nondestructive tool for assessing detergent removal in potential decellularization schemes or for use as a potential endpoint in future clinical schemes, generating acellular lungs using anionic detergent-based decellularization protocols.
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A Comparative Study of Fracture Resistance of Endodontically Treated Compromised Teeth with Different Post Systems: An In Vitro Study
Abstract
Aims:
This in-vitro study was conducted to compare structural reinforcement with composite resin and two different types of posts in structurally compromised teeth.
Methods and Materials:
Forty-eight human maxillary central incisors were instrumented and obturated. Specimens were randomly divided into four groups. The control group was not compromised and was just restored with a resin composite. In the composite-reinforced group, the access cavity of the compromised teeth was restored only with composite to the cemento-enamel junction (CEJ). In the reinforced glass fiber post group, the compromised cervical area of the teeth was reinforced with a dual-cured composite and a glass fiber post. The reinforced metal cast post group was reinforced with a dual-cured composite and a casting post. The mean fracture load was measured. Data were analyzed by SPSS software using one-way analysis of variance (ANOVA) and chi-square statistical analysis tests. For pair comparison, Duncan was used. P<0.05 was considered statistically significant.
Results:
The highest fracture resistance values were for the non-compromised samples (170.12 ± 12.44), while the lowest values were for the compromised ones restored only with the resin composite (71.40 ± 17.00). There was no statistically significant difference between the mean fracture resistances of the fiber (129.36 ± 21.34) and cast (116.60 ± 22.60) post groups (P>0.05).
Conclusion:
The use of a composite resin in a root with thin walls will reinforce the compromised tooth, but the type of the post will not influence the final results.
Keywords: Composite resin, Fracture resistance, Post and core technique, Permanent teeth, Resin cements, Tooth resorption.
1. INTRODUCTION
The rehabilitation of extensively damaged teeth with no dentinal support at the coronal portion of the root canal is very difficult [1]. This situation can be seen clinically when the developing permanent tooth (especially maxillary central incisors in children aged 9-10) suffers trauma, and its root formation remains incomplete [2]. The amount of residual dentin and tooth canal shape play critical roles in the strength and resistance of a tooth with posts. Hence, a post is not commonly used in teeth with flared canals, and the lack of dentinal structure also precludes the placement of reinforcing posts [3, 4]. In teeth with a significant loss of coronal and radicular tooth structures, it is important to assess the alternatives to cast posts and cores or common prefabricated posts that are also resistant to fatigue effects [5, 6]. Studies have suggested resin composites for strengthening the treated teeth with immature roots [7]. This method, in combination with the prefabricated post, has been advised for use during and after apexification [8].
There are numerous studies on the fracture resistance of devitalized teeth with different post systems, but some contradictory results have been observed in the literature concerning how the post materials affect the resistance fracture mode and stress distribution of the restored teeth [9, 10]. Some studies claim that metal posts perform better than fiber posts; others, however, state the opposite [11, 12]. Numerous studies have used composite resins along with fiber posts to strengthen the structure of damaged endodontically treated teeth [13, 14]. However, to the best of our knowledge, no study has ever compared the effect of application or non-application of a post and different kinds of posts on increasing the fracture resistance of cervically weakened teeth, such as the teeth with internal cervical resorption or necrotic immature permanent teeth. Therefore, this study aimed to evaluate and compare the effects of two strengthening methods on the weakened cervical structure with and without a post and different post types. The null hypothesis formulated in this study was that composite alone and in combination with a fiber post or a cast post would have similar strengthening effects on the weakened endodontically treated teeth at the cervical region.
2. MATERIALS AND METHODS
Research ethics committees of the vice-chancellor in research affairs of the Medical University of Isfahan ethically approved this study (Approval ID: 384176). Based on the previous studies [15, 16], forty-eight extracted intact human maxillary central incisors without significant differences in diameter (about 11 ± 1 mm occlusogingival height and 8.5 ± 1 mm width) were selected for this study. The approximate length of all roots was considered to be 15 mm. All samples were stored in 0.5% chloramine T solution (Merck, Darmstadt, Germany) until the time of the experiment.
All teeth were prepared by the same trained operator. An access cavity was prepared, and then all the teeth were instrumented up to file #70 and obturated with AH26 sealer and gutta-percha using a lateral condensation technique. After that, the specimens were randomly divided into four groups of 12 teeth each:
1. The control group that was not compromised (teeth were not cervically prepared),
2. In this group, a laboratory bur (Ivomil, IVOCLAR AG, Germany) was used to thin the cervical area of the root and simulate the thin dentinal wall of the compromised teeth. The preparation was extended to 5 mm apical to CEJ (the height of the palatal wall was 2 mm from CEJ), and nearly 1 mm thickness of dentin remained at all walls. The thickness of the remaining residual dentin at the cervical area was estimated by a digital Vernier caliper (Aerospace) and Radio Visio Graphy (RVG), which was then reinforced by resin composite (composite reinforced group),
3. In this group, Gates Glidden #1-4 and then Peeso reamers #4-6 were used (Dentsply, LD Caulk, USA) to remove the gutta-percha and prepare canals. The gutta-percha was evacuated up to 5 mm under CEJ. Then laboratory bur was used to thin the cervical area of the root and simulate the thin dentinal wall of the compromised teeth as described in group 2. Then, it was reinforced by glass fiber post (glass fiber post reinforced group),
4. Gates Glidden #1-4 and then Peeso reamers #4-6 were used (Dentsply, LD Caulk, USA) as described in group 3. Then, laboratory bur was used to thin the cervical area of the root and simulate the thin dentinal wall of the compromised teeth as described in group 2. Then, it was reinforced by a metal cast post (metal cast post reinforced group).
Then, all teeth were restored as follows: (the list of materials used in this study is provided in Table 1.
Table 1.
Materials, manufacturers, and composition.
Material Manufacturer Composition
Adper Single Bond 3M Espe. St. Paul, MN.,
USA.
BisGMA, HEMA, dimethacrylates, ethanol, water, photoinitiator system, and a methacrylate functional copolymer of polyacrylic and poly (itaconic) acids. (Approximately 10 wt % filled).
37% phosphoric acid etch-gel Total etch, Ivoclar Vivadent, Swiss.lot no. Phosphoric acid, colloidal silica, pigments, water
Bis-coreTM Bisco INC, Schaumburg, USA Bisphenol A diglycidyl methacrylate, glass filler, Urethane thriethylene glycol dimethacrylate, fused silica
Z100 ESPE, 3M Dental Product, USA Mikrohibridna kompozitna smola • Microhybrid composite resin - matrix; BIS-GMA i TEGDMA
• Matrix: BIS-GMA and TEGDMA - punilo cirkonija/silika, anorgansko punilo 66%w, veličina čestica od 3, 5 do 0,01µm
• Filler: zirconia/silica; inorganic filler loading is 66% w, particle size ranging from 3.5 to 0.01 µm
RelyX Unicem resin cement 3M ESPE, Seefeld, Germany Powder: Alkaline and silane fillers, starting components, pigments Liquid: Phosphoric acid methacrylates, methacrylate monomers, starting components, stabilizers
AH26 Dentsply, De Trey, Konstanz, Germany Silver-free powder: bismuth oxide, methenamine epoxy resin
C. silicone impression putty and light body and activator Spidex®, Coltene AG, Altstatten, Switzerland Base: Hydroxyl-terminated polydimethylsiloxane (liquid silicone prepolymer)
Liquid: alkyl silicate, such as tetracthylsilicate, tin compound, such as dibutyltin dilaurate
Silane coupling agent Monobond-S, Ivoclar-vivadent, Liechtenstein, Germany Ethanol, [3-(methacryloyloxy) propyl] trimethoxysilane
In the non-compromised group (control group) with unprepared teeth, the coronal internal cavity surface of the tooth was etched for 15 seconds using a 37% phosphoric acid etch-gel, rinsed, and gently air-dried. Then, the root canals were treated with a resin adhesive (Single Bond) after air drying for 5 seconds, followed by light curing for 20 seconds with Coltlux 75 (Colten, Swiss) with 1000 mW/cm2 power intensity. A hybrid composite resin Z100 was used by vertical layering technique in two layers and was cured, each time for 40 seconds. In this study, all light activation steps were done by this light-curing unit.
In the composite reinforced group, the compromised region was obturated with gutta-percha by lateral condensation technique. Then, after acid etching and treatment with Single Bond, as described before, the access cavity of the tooth was restored only with Z100 composite resin in two stages. It was then cured by light activation.
In the glass fiber post-reinforced group, the post space was prepared by RTD universal burs (RTD Grenoble, France) 7 mm apical to the palatal margin of the access cavity.
1. The translucent glass fiber post: D.T Light post (RTD Grenoble, France) was tested in the prepared space, and its height was adjusted so that no direct load was applied to it.
2. After preparing the dentinal walls of the cavity with 37% phosphoric acid etch gel for 15 seconds, the etchant was rinsed and air-dried. In the second stage, the Single Bond adhesive was applied and air-dried for 5 seconds. Finally, it was light-cured for 20 seconds. For a complete cure of adhesive in this deep cavity, the light was guided through a handmade translucent sprue formed by heat with similar dimensions to the post.
3. D.T. post surfaces were cleaned with alcohol and air-dried. Then, a layer of silane coupling agent was applied according to the manufacturer’s instructions and then treated with Single Bond adhesive and light-cured for 20 seconds.
4. The compromised cervical area of the teeth was restored with a dual-cure composite resin, Bis-coreTM, 1 mm apical to the CEJ, according to the manufacturer’s instructions. D.T. Light-Post (DT) was inserted into this composite bulk along the longitudinal axis of the tooth and light-cured for 20 seconds as the initial curing so that the light tip was in contact with the light post.
5. The rest of the cavity was restored with Z100, similar to the control groups.
In the metal cast post-reinforced group:
1. To create a cast post similar to the D.T. light post in the reinforced glass fiber post group, the putty of C. silicone impression material was mixed with its activator and placed in a cylinder generator. Then, D.T. light post was placed in the putty in size similar to the glass fiber post group to obtain a negative image. After the putty was hardened, the post impression was taken again more accurately using a light body (C. Silicon Spidex) mixed with the activator.
2. Using transparent heat-formed sprues, similar to the light posts and Duralay acrylic resin mixed with the relevant monomer (Acropars, Marlic Medical Industries Co, Tehran, Iran), an impression was taken from the space created in the putty to obtain a positive image of the post.
3. The cast post was made in the laboratory using nickel-chrome alloy, a common alloy used to make these posts.
4. Before cementation, the fabricated cast posts were cut at the same height as the D.T. light post. They were then sandblasted with aluminum oxide with 20-µm diameter and 2-bar pressure and cleaned with alcohol.
5. The teeth were prepared for adhesion, similarly to the second step of the light post group.
6. The compromised cervical area of the teeth was restored with a dual-cure composite resin, Bis-core TM, 1mm apical to the CEJ, according to the manufacturer’s instructions.
7. The cast post was covered with a biofilm layer to prevent the bonding of the composite inside the cavity. It was then put in the composite so that its longitudinal axis was in line with the longitudinal axis of the tooth. Next, it was extracted, etched, and rinsed with 37% phosphoric acid for 20 seconds to remove the debris, followed by drying.
8. The cleaned cast post was cemented by a dual-cure resin cement, RelyX Unicem, according to the manufacturer’s instructions and then light-cured for 40 seconds. The rest of the cavity was restored with Z100, as described before.
Then, each tooth was mounted in an acrylic resin in the form of a cylinder. For simulating the PDLs, a thin layer of wax was wrapped around the roots before pouring the acrylic mix. By using boiling water, the wax was dewaxed and substituted with light body silicone impression material. With this silicone layer around the root of the tooth, the PDL was simulated, and small movements similar to the movement of the tooth in the dental socket were reconstructed (Fig. 1).
After mounting, the specimens were subjected to compressive loads using a universal testing machine (Instron, Instron Corp, UK). Controlled loads were applied to the core on the palatal side exactly on the mesial and distal marginal ridges above the cingulum at an angle of 135° to the longitudinal axis of the root. The testing machine was set at a crosshead speed of 0.5 mm/min, and the failure threshold was defined as a point at which a specimen no longer withstood the increasing load and fracture of the post-crown complex or root occurred.
At the fracture point, the amount of force was recorded in a computer, and the fracture patterns for each specimen were visually analysed. The data were statistically analyzed by SPSS software (SPSS ver. 23, IBM, Somers, NJ, USA) using one-way analysis of variance (ANOVA) and chi-square statistical analysis tests. For pair comparison, Duncan was used. P<0.05 was considered statistically significant.
3. RESULTS
At first, the normality of the research data was confirmed using the Kolmogorov-Smirnov test (p>0.05). The results and the means of resistance to fracture (kgf) of teeth are shown in Table 2. The highest resistance to fracture belongs to the non-compromised group (170.12 ± 12.44) and the lowest to the composite reinforced group (71.40 ± 17.00).
The results of ANOVA showed a statistically significant difference, and Dunkan analysis showed that the differences in resistance to fracture were significant between all groups except the reinforced glass fiber post group and the reinforced metal cast post group.
The results of fracture mode in different groups are shown in Table 3. The results of the chi-square test showed a statistically significant difference among all groups. The maximum non-restorable fractures were reported for composite reinforced and reinforced cast post groups, respectively.
4. DISCUSSION
The null hypothesis was slightly accepted. The results showed that irrespective of the type of the system used for the restoration of endodontically treated teeth, the highest fracture resistance was obtained when there was more dental tissue, which was in line with the results of the study conducted by Bhagat et al. on the thickness of the remaining dentin of post and core pretreatment in endodontically treated teeth [17].
Fig. (1). Using a thin layer of light body silicon impression material for simulating the PDLs.
Table 2.
Fracture resistance in different groups (kgf).
Group
Results
Non-compromised Group Composite Reinforced Group Reinforced Glass Fiber Post Group Reinforced Cast Post Group
Minimum 143.60 30.71 101.93a 82.04a
Maximum 185.80 95.97 167.65 185.2
Mean 170.12 71.40 129.36 116.60
SD 12.44 17.00 21.34 22.60
Note: Same letters show no statistically significant differences, but other pair comparisons between study groups show statistically significant differences.
Table 3.
Mode of fracture in different groups.
Group
Results
Restorable Non-Restorable
Count Percentage Count Percentage
Non-compromised group 12 100% 0 0%
Compromised composite reinforced group 0 0% 12 100%
Reinforced glass fiber post group 9 75% 3 25%
Reinforced cast post group 3 25% 9 75%
On the other hand, the results of this study indicated that in the case of the weakened remaining tissue, the application of similar fiber posts or metal cast posts within the dual cure composite strengthens the weakened tissue so that it is completely bonded to it, whether directly or using resin systems, and causes a relatively similar increase in tooth fracture resistance under functional forces and can partly recover the lost resistance. However, the use of gutta-percha in the weakened teeth or restoration of the access cavity does not increase tooth fracture resistance.
D’Arcangelo et al. [18] reported that the use of fiber posts increased the resistance of endodontically treated anterior teeth, but some other studies have shown that the use of any post system, due to the different young modulus of these materials to the dental tissue, induces negative effects on tooth fracture resistance [19]. Furthermore, some studies have shown that the use of posts, due to the unfavorable distribution of stress in the tooth structure, weakens the tooth [20].
The present study indicated that despite approximately similar fracture resistance in teeth restored with metal and glass fiber posts within the strengthening dual-cure composite that have created monoblock, in the case of fracture, the fractures in fiber posts are mostly repairable, but fractures of cast posts are mostly catastrophic and irreparable. However, the results of a systematic review were in line with this study [21].
The posts in the restoration of endodontically treated teeth that have lost too much dentin tissue and require reconstruction for better function in the oral cavity have been used by dentists for many years. However, contradictory results have been reported for the use of these materials for endodontically treated teeth. Application of endodontic posts causes more weakness of the tooth root since they require more removal of the dentine structure of the root for their placement [22]. Moreover, this preparation increases the deformities due to reduced dental tissue [23], and the hardness coefficient of these materials is not adaptable to the tooth structure, thereby causing unfavourable stress distribution [24]. In an eleven-year clinical trial performed by Naumann et al., the survival of restorations retained with metal and fiber posts, especially during the first eight years, was higher than that of the restorations without posts, but after that, it significantly reduced in glass fiber posts due to weakened dentin-cement-post bond [25].
In this study, dual-cure resin cement was used to bond the posts to the tooth structure, and also dual-cure composite was used to strengthen the weakened cervical region because polymerization was completed by chemical cure, especially in areas with highly reduced light exposure. Furthermore, it is less likely that the bond is weakened due to inadequate polymerization and remaining uncured monomers [26]. On the other hand, the curing of dual-cure resins is not influenced by the amount of translucency [27]. A reason for the similar strengthening effect of non-translucent metal cast posts and translucent glass fiber posts in this study may be due to the similar bond of these posts with the tooth structure and dual-cure composite owing to a high and similar degree of conversion and formation of monoblock in both groups. On the other hand, despite numerous studies conducted on various endodontic treatment methods for teeth with much coronal damage [13, 14], no comprehensive conclusion can be made regarding the efficacy of these materials in increasing the fracture resistance of endodontically treated teeth due to variation of method and type of substrate used (human or bovine teeth) [28]. This study was performed on the endodontically treated human central teeth weakened at the cervical region so that they would have similar conditions to immature necrotic teeth or teeth with internal cervical resorption. The results showed that similar fiber posts or metal cast posts, in case of complete adaptation with the internal tooth structure, had similar success in strengthening the tooth, and both would be successful if they were correctly bonded to the tooth structure with resin cement. Moreover, they are more effective than the use of composite resin alone for tooth structure strengthening. However, the fractures created in the teeth restored with metal cast posts would be more destructive than those in modified fiber posts.
Cyclic loads causing a decrease in material strength may result in dental restoration failures concluded by fatigue mechanisms [6]. Therefore, further in vitro and clinical studies, which include long-term analysis of functional cyclic forces or thermocycling, are required to obtain more definite results.
CONCLUSION
It can be concluded that the maxillary central incisors treated with minimum dentin omission have the highest fracture resistance. Moreover, the common methods used for the restoration of central incisors with thin walls of root crown by composite resins without the reinforcement of the cervical part of the root cannot increase their resistance against chewing forces, but the use of posts that have good adaptation can increase teeth fracture resistance.
LIST OF ABBREVIATIONS
CEJ = Cemento-enamel junction
ANOVA = Analysis of variance
ETHICS APPROVAL AND CONSENT TO PARTI-CIPATE
Research Ethics Committees of the Vice-Chancellor in Research Affairs of the Medical University of Isfahan ethically approved this study (Approval ID: 384176).
HUMAN AND ANIMAL RIGHTS
No animals were used in this research. All human research procedures followed were in accordance with the ethical standards of the committee responsible for human experimentation (institutional and national) and with the Helsinki Declaration of 1975, as revised in 2013.
CONSENT FOR PUBLICATION
Informed consent was obtained from all participants.
AVAILABILITY OF DATA AND MATERIALS
The data that support the findings of this study are available from the corresponding author [F.S] upon reasonable request.
FUNDING
This work was financially supported by Khorasgan dental school, Isfahan, Iran.
CONFLICT OF INTEREST
The authors declare that there is no conflict of interest regarding the publication of this paper.
ACKNOWLEDGEMENTS
Declared none.
SUPPLEMENTARY MATERIALS
Some pictures of the research are included as supplementary materials.
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Matawan NJ Bunion Care
Bunion Care in Matawan
Do you have pain and stiffness in your big toe? That may not have seemed like a terrible problem at first, but as it persists, toe pain can be a real concern. If you’ve been diagnosed with a bunion from a Matawan NJ podiatrist, you likely also have a bony protrusion on the side of your foot, at the base of your big toe. The big toe is then pushing against the inner toe.
It looks like this because there is a misalignment of one of the bones in your feet. Specifically, a bunion is caused when the first metatarsal bone bends so it points outward. This causes the big toe to point inward. Now, the joint for the metatarsal bone is pointing outward, bent awkwardly, and causing pain.
Treatment Options in Matawan NJ for Bunions
In extreme cases, surgery may be needed. It isn’t indicated for aesthetic reasons, but only to correct the issue of pain if you are having a difficult time walking and participating in daily activities. This is a solution people turn to only when at-home treatments have failed to ease the symptoms enough for them to live their daily lives.
Let’s look at what you can do with the help of a podiatrist for treatments on your own.
Avoid standing on your feet for prolonged periods, if at all possible. If you’re on your feet for a while, attempt to schedule healthy breaks when you put your feet up to relieve the pressure.
You can find a gel-filled pad to wear inside your shoes. They sell these at most pharmacies or shoe stores but are also easy to find online. This will better cushion the foot, which will ease any hard movements against the joints.
Get shoe inserts that will keep your foot in a healthy position. There are over-the-counter inserts you can buy, or meet with your podiatrist to get a custom-made orthotic. This will always give you the best results since it will be shaped to your individual needs.
You can wear a splint at night to hold the toes straight. This can lead to some relief during the day, as the foot has used the night to better recover. You’ll need to talk to your podiatrist before doing this.
You can take over-the-counter pain relief medication, like ibuprofen.
Pain relief habits like a foot massage, ice packs, and soaking your feet in warm water for ten minutes in the evenings can all help you take care of your foot pain.
If your weight has gotten high, maintaining a healthier weight can relieve some of the pressure on your feet.
The most important thing you can do for bunion care is to wear roomy footwear. While we know that bunions tend to run in families, women indeed suffer from bunions at a much higher rate than men. They tend to have a history of wearing shoes that are too tight, putting pressure on the bones in the feet. Wearing a shoe with a lot of room in the toe box will relieve pressure, which will cause you less pain and prevent the misalignment from becoming worse.
Your best guide to taking care of your bunions, preventing them from getting worse, and supporting you whenever you have pain problems, is a podiatrist. They are specialists in everything that happens inside your foot and ankle. With Central Jersey Ankle & Foot Care Specialists on your side, you will always have someone you can consult when you have a new issue and you will have someone who can track the progress of your bunions over time. Check-in with your Matawan NJ podiatrist if you have questions about your foot health.
OFFICE HOURS
Monday
8:00am - 8:00pm
Tuesday
7:30am - 7:00pm
Wednesday
10:00am - 4:00pm
Thursday
9:00am - 5:00pm
Friday
9:00am - 2:00pm
Saturday & Sunday
Closed
Central Jersey Ankle & Foot Care Specialists
20 Cambridge Dr Suite D
Matawan, NJ 07747
P: (732) 566-2841
F: (732) 566-1264
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Nihar Gala – Advancing Neurological Surgery for Improved Patient Outcomes
Neurological surgery is a specialized field of medicine that focuses on the surgical treatment of disorders and diseases affecting the central and peripheral nervous system. Nihar Gala, an accomplished neurosurgeon, is dedicated to advancing the field of neurological surgery and improving the quality of life for his patients. In this article, we will explore the expertise and contributions of Nihar Gala in the field of neurological surgery, highlighting the significance of this specialty in providing effective surgical interventions for various neurologic conditions.
Enhancing Patient Well-being through Surgical Expertise
Neurological surgeons, like Nihar Gala, possess the expertise and skill set required to perform intricate surgical procedures on the brain, spine, and peripheral nerves. They specialize in treating a wide range of conditions, including cerebrovascular diseases, epilepsy, movement disorders, tumors, spinal cord injuries, and trauma. By utilizing advanced surgical techniques, such as minimally invasive procedures and endovascular interventions, neurosurgeons aim to provide optimal outcomes and minimize postoperative complications.
Comprehensive Management of Neurological Disorders
Neurological surgery encompasses the prevention, diagnosis, surgical treatment, and rehabilitation of disorders affecting the nervous system. Conditions such as brain tumors, spinal disorders, congenital malformations, pituitary gland tumors, aneurysms, and epilepsy require specialized surgical intervention. Neurological surgeons like Nihar Gala work closely with multidisciplinary teams, including neurologists, neurocritical care specialists, and pathologists, to provide comprehensive care to patients, integrating surgical expertise with medical management and rehabilitation programs.
Advancements in Surgical Techniques
The field of neurological surgery is constantly evolving, thanks to advancements in surgical techniques and technologies. Neurological surgeons like Nihar Gala are at the forefront of adopting innovative approaches to deliver safer and more effective surgical interventions. Minimally invasive techniques, such as endonasal surgery and cranial surgery, enable surgeons to operate on the brain directly and remove tumors with precision. Additionally, neurosurgeons are skilled in utilizing radiosurgery for posterior cranial fossa neoplasms, deep brain stimulation for tremor control, and other cutting-edge procedures that offer new treatment options for patients.
Research, Education, and Collaboration
Neurological surgeons, including Nihar Gala, actively engage in research projects to contribute to the advancement of knowledge in the field. Their involvement in clinical research enables the development of new surgical techniques, improvement of patient outcomes, and the exploration of emerging treatment modalities. Neurological surgeons also play a crucial role in teaching residents and medical students, passing on their expertise and fostering the next generation of neurosurgeons.
Improving Quality of Life through Rehabilitation
The impact of neurological surgery extends beyond the operating room. Neurosurgeons like Nihar Gala recognize the importance of rehabilitation programs in maximizing patients’ quality of life following surgical interventions. They work closely with rehabilitation specialists to create tailored plans that aid in the recovery and rehabilitation process, aiming to optimize physical, cognitive, and emotional functioning.Nihar Gala’s expertise and contributions in the field of neurological surgery exemplify the dedication of neurosurgeons in improving patient outcomes and quality of life. Through their surgical expertise, utilization of advanced techniques, and collaboration with multidisciplinary teams, neurological surgeons provide comprehensive care for patients with complex neurologic conditions. As the field continues to advance, the impact of neurological surgery on patient well-being and functional outcomes will continue to grow, thanks to the efforts of skilled professionals like Nihar Gala.
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Articles
Keto Diet Plan For Beginners - Be Healthy, Act Healthy and Eat healthy
by Cherry Lou Ms.
Keto Diet Benefits
Recently, the keto diet has become extremely popular for its health benefits such as weight loss and preventing disease. The keto diet can be hugely beneficial, but how does it work to provide these benefits?
What is the Keto Diet?
You may have heard of the high-protein, low-carbohydrate Atkins diet. The keto diet keeps carbohydrate levels low, but instead of ramping up the amount of protein in your diet, the keto diet increases the amount of fat. A typical keto diet aims for meals with 75% fat, 20% protein, and 5% carbohydrate. Eating a high-fat diet can still mean eating healthy. Keto diet menu items often include seafood, meat, dairy products, eggs, vegetables, and nuts. With the increased popularity of the keto diet, keto recipes are widely available.
How Does the Keto Diet Work?
It might seem counterintuitive that adding more fat to your diet can lead to weight loss. Normally, your diet is high in carbohydrates, which are broken down into glucose, or blood sugar, for use as energy. As glucose enters your bloodstream, your body releases insulin to store excess glucose as fat. The more carbohydrates, the more glucose. The more glucose, the more insulin, and the more insulin, the more fat.
The keto diet takes advantage of the fact that when your meals are high-fat and low-carbohydrate, there is no insulin spike, and you don't add to your fat reserves. Instead, fat from diet and stored fat are broken down to ketones ("keto" is short for "ketogenic" producing ketones). Like glucose, ketones can be used for energy, keeping your body running without increasing blood sugar or putting on excess fat. The benefits of the keto diet can be huge.
Weight Loss
Overall, the keto diet is an excellent way to burn fat and lose weight. Eating fewer carbohydrates suppresses appetite, and studies have shown that keto diet participants eat fewer calories overall because of this. Burning fat for energy can lead to rapid weight loss.
Reduced Blood Sugar and Insulin
Since carbohydrate intake is limited, blood sugar and insulin levels are lowered. This is particularly important for people with type 2 diabetes, which causes a buildup of glucose in the bloodstream. The keto diet can be used to reduce or eliminate the need for diabetic insulin injections.
Reduced Triglycerides
Fat subunit molecules called triglycerides normally circulate in your bloodstream. High levels of triglycerides are a significant risk factor in the development of heart disease. In the keto diet, because fat is being burned for energy, the number of triglyceride molecules in the bloodstream decreases, reducing the risk of heart disease.
Improved Cholesterol
"Bad" (LDL) cholesterol is another risk factor for heart disease. Too much bad cholesterol in your bloodstream builds up in your arteries, narrowing them and causing atherosclerosis, a type of heart disease. The keto diet reduces bad cholesterol levels while increasing the level of "good" (HDL) cholesterol in your body.
Summary
The keto diet provides many health benefits. This diet can not only help you quickly lose weight, but can also improve your overall health and help prevent disease.
======================================
Check out this video : How Can I Make Keto Easier
======================================
Sponsor Ads
About Cherry Lou Advanced Ms.
70 connections, 0 recommendations, 154 honor points.
Joined APSense since, November 16th, 2010, From Baltimore, United States.
Created on Jun 2nd 2020 10:09. Viewed 541 times.
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MENU
Oral Health During The Golden Years: What To Expect
It’s no secret - advanced age brings with it health issues. And although we pay more attention to body health than oral health, age has a dramatic effect on the mouth and teeth. The problem is that many seniors tend to react to oral health problems instead of being proactive. The fact is, there is much that can go wrong inside the mouth, and when unattended, things can get out of hand quickly. The best approach is the one the dentist in Vaughan told us on our first visit – prevention.
Enamel wears down over the years
Chewing and grinding takes a toll on the teeth, and that doesn’t include damage from broken or chipped teeth. Simply put, teeth gradually wear down with age and with years and years of use. It means that the protective outside layer of the teeth (made of enamel) is dwindling away, with no natural way to regenerate.
Prevention is the key to better oral health - not grinding the teeth; not clenching the jaw; and not biting down on hard surfaces. For those who play impact sports, a mouth-guard is a must. For those who grind while sleeping, a mouthpiece might be the answer. And for everyone, it’s important to avoid acidic foods.
Dry mouth is more prevalent
Seniors will experience a dry mouth as a consequence of getting older, or because of specific medications that are taken. Even at a younger age, saliva is vital in washing away food particles and clearing out bacteria. Without natural saliva, the potential for bacteria to collect and infect is dramatically increased.
Saliva also serves to keep everything soft and lubricated - tissue inside the mouth, the tongue, and the gums. A dry mouth can cause tissue to be irritated and susceptible to cuts or infection. As an antidote, drinking water throughout the day can lubricate soft tissues, loosen plaque, and wash away any bacteria.
Gum health declines with age
Gum health is important at any age, but particularly in the golden years. Health gums anchor the teeth and serve as a barrier against bacteria. Without proper care over the years, gums can weaken, and be vulnerable to disease. Long-term smoking is a serious threat to gum health, and affects overall health.
Gum disease is definitely more prevalent with age. This is especially true for those who did not commit to proper oral maintenance over the years. Regular brushing and flossing will at least fight plaque, tartar, and bacteria. Without proper oral care and maintenance, tooth decay and gum disease are certain.
Increased risks of oral cancer
Like many other cancers, the risk of oral cancer rises with age. However, age is not the only risk factor, as other lifestyle habits can also contribute: use of tobacco products; alcohol abuse; and infections related to HPV. With this mind, it’s essential to visit the dentist regularly, and more so at age 50 and beyond.
For seniors, it’s highly recommended to have regular oral cancer screenings. These are quick, painless, and effective. Short of any symptoms or complaints, screenings are an excellent way to identify any abnormalities and ensure early detection where necessary. Early diagnosis is key to proper treatment. Get stared with a visit to a dentist in Woodbridge near you.
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Open access peer-reviewed chapter
Vitamin D and Physical Performance: What Is the Ergogenic Actions of Vitamin D?
Written By
Rodrigo Nolasco and Marise Lazaretti-Castro
Submitted: 09 June 2018 Reviewed: 20 September 2018 Published: 05 March 2019
DOI: 10.5772/intechopen.81609
From the Edited Volume
Fads and Facts about Vitamin D
Edited by Edward T. Zawada Jr.
Chapter metrics overview
1,001 Chapter Downloads
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Abstract
Vitamin D produced in the skin by the action of the sun’s rays turns into calcitriol, a powerful hormone, recognized as important for health. Although its most known effects are on mineral homeostasis and bone metabolism, its receptors (VDRs) have been identified in almost all tissues, suggesting that it should have other actions. Vitamin D acts directly on the skeletal muscle system maintaining muscle mass, strength levels and speed of muscle contraction. Thereby, allied to that, vitamin D is among the potential factors that are related to maintaining bone, and cannot be dissociated from the prevention of osteoporosis and sarcopenia. However, in the physical performance aspect, there are still uncertainness in the literature about the use of vitamin D as an ergogenic resource aimed at improving the physical performance of amateur and professional athletes. Therefore, due to the biological actions of vitamin D and high prevalence of low levels in sedentary and physically active individuals, this chapter will discuss the facts pointed out in the literature about the action of vitamin D as an ergogenic resource aiming at the preservation or improvement of the physical, including strength muscular, aerobic capacity and balance.
Keywords
• vitamin D
• athletic performance
• lung function
• sarcopenia
1. Introduction
The increase in human life expectancy during the previous century has raised new health issues, especially the control of aging-related deterioration. Important efforts have been made to gain new insights that may lead to modalities to delay the functional impairment and progression of chronic degenerative diseases, as well as sarcopenia and osteoporosis. Undoubtedly, the physical exercises are directly interrelated with the improvement or even rehabilitation of the physical performance besides increasing the life expectancy [1]. However, the effect of hormonal action, especially vitamin D, has lately been part of this prospect.
In this context, vitamin D has attracted considerable interest among health researchers, professional organizations and the lay public in recent times. Although it is called vitamin, conceptually vitamin D is a hormone. This is due to its hormonal nature, such as the ability to be integrally produced by the organism and to have specific receptors in several tissues [2].
Vitamin D has emerged for more than 500 million years. Even though its function in plants and invertebrates is unknown, the close association between vitamin D and sunlight has become essential in the evolution of terrestrial vertebrates. The main physiological function of vitamin D is to maintain the supply of calcium and phosphorus for complete mineralization of bone tissue [2].
Sunlight is the main source for producing the right amount of vitamin D for most humans. In food, it is found in small amounts, and there are few food sources. When it comes from sunlight, it is estimated that around 80–100% of the human needs for vitamin D come from exposure to sunlight [2, 3].
Although it is recognized as important for health, it is estimated that there are approximately 1 billion people in the world with inadequate concentrations of vitamin D. Furthermore, individuals with insufficient vitamin D levels have an increased risk of bone disease, such as: rickets, low bone mass and fractures due to increased bone resorption as a consequence of an overproduction of parathyroid hormone (PTH) [4].
Regarding functional capacity, the inadequacy of vitamin D stocks has catabolic effects on the musculoskeletal system, causing muscle weakness, lags in balance and impairs the formation of cross-bridges, which could impair physical performance. However, there remains divergences. Reports from recognized institutes do not corroborate the adequate levels for non-skeletal outcomes, or even the existence of evidence of a non-linear association for some results on physical performance [5].
Finally, recent studies have suggested a possible action of vitamin D in the lung function of individuals without lung disease. Similarly, results were observed on aerobic capacity being influenced by a possible action of vitamin D [6].
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2. Vitamin D actions
Vitamin D is a steroid hormone. Its precursor found in animal tissues is 7-dehydrocholesterol, which is synthesized in the skin and is also the immediate precursor of cholesterol. Cholecalciferol has as its main source cutaneous synthesis catalyzed by ultraviolet light B (UVB). Its synthesis is initiated in the skin, under the action of UVB rays, which transform its precursor, 7-dehydrocholesterol, into cholecalciferol or vitamin D3. In smaller amounts, vitamin D can also be obtained through the diet of fortified foods such as dairy products and cereals, fatty fish and cod liver oil. After food intake or synthesis in the skin, vitamin D is transported into the liver where it is converted into 25-hydroxyvitamin D [25(OH) D] or calcidiol, which is the main form of circulating vitamin D and also used for serum dosage. In the kidney, 25(OH) D is converted to its biologically active form, 1,25 dihydroxyvitamin D (1,25 (OH) 2 D) [7, 8]. The biological actions of 1,25 (OH) 2 D are mediated by the nuclear transcription factor, called the vitamin D receptor (VDR) located in the cell nucleus [9].
VDR is part of the nuclear receptors of transcription factors regulating steroid hormones, retinoic acid, thyroid hormone, and vitamin D. Following the connection with VDR, there is the formation of the heterodimeric complex (Vitamin D Receptor—Retinoic Acid Receptor). This, in turn, binds to specific DNA sequences, also called the vitamin D responsive element (VDRE), promoting conformational changes that lead to the recruitment of several other transcriptional coactivators, resulting in the transcription of target genes [10].
After conversion to its biologically active form, 1,25-dihydroxyvitamin D regulates the expression of more than 900 gene variants [11]. Considering this aspect, it has been observed that these gene expressions have a significant impact on a range of variables related to health and performance, such as exercise-induced inflammation, pulmonary function, tumor suppressor genes, neurological function, cardiovascular health, glucose metabolism, health bone and skeletal muscle performance [12].
Vitamin D plays a key role in maintaining basal serum calcium and phosphorus levels for a variety of metabolic functions, regulation of transcription and bone metabolism. 1,25 (OH) 2D interacts with VDR in the small intestine to increase intestinal calcium absorption from 10–40% and phosphorus from approximately 60–80% [13]. Its action also extends to the cells responsible for bone remodeling, from the connection to the pre-osteoblasts, acting as a stimulus for precursor cells in osteoclasts from the RANK/RANK ligand system. Active osteoclasts remove calcium and phosphorus from bone to maintain serum levels of these elements. In the kidneys, 1,25 (OH) 2D stimulates calcium reabsorption of glomerular filtrate [3, 13]. Vitamin D and calcium are among the potential factors related to maintaining bone and muscle health, and cannot be separated from osteoporosis prevention in postmenopausal women [14].
2.1 Vitamin D and muscle
Moreover to the effects on bone metabolism, studies over 80 suggest improvements in physical performance in individuals exposed to UV radiation. Although these studies do not directly describe the action of vitamin D, induced changes in vitamin D levels may have played a role in muscle function [15].
Especially in older women with low vitamin D status, several intervention studies have reported that vitamin D supplementation increases appendicular muscle strength and improves physical function. In the musculoskeletal system, vitamin D exerts specific receptor-mediated functions (VDR) in processes ranging from protein synthesis to kinetics of muscle contraction, directly affecting the functional capacity of postmenopausal women [16]. Apart from this, the important mechanisms by which vitamin D can exert on human skeletal muscle can be classified as genomic or non-genomic [15].
Considering the genomic theory, it describes that 1,25 (OH) 2 D exerts a direct effect on the human muscular VDR, sparking progressive epigenetic changes that may have an impact on the morpho functionality of skeletal muscle. Within this context, in a study of women with limited mobility and with a relatively low level of vitamin D, vitamin D3 supplementation resulted in a 30% increase in intramuscular VDR protein concentration and a 10% increase in total muscle fiber size I and II. These findings corroborate the hypothesis that vitamin D contributes to the muscle mass of individuals with a tendency towards functional disability [17].
Muscle tissues have specific nuclear receptors for 1,25-[OH] 2D. In patients with strokes with atrophied type II fibers, improvement after vitamin D supplementation was observed for 25-OHD serum deficient patients before therapy. Also, improvements in muscle strength on the intact side of these patients with vitamin D-supplemented strokes were observed. In addition, in cross-sectional analysis, there was a correlation between 25-OHD and fiber diameter and type II [18].
Conversely, the non-genomic hypothesis credits a rapid and indirect mechanism by which 1,25 (OH) 2 D activates a series of secondary messenger processes that promote increased calcium kinetics. Researchers have extensively searched the so-called 1,25 (OH) 2 D non-genomic activities through the investigation of membrane proteins and intracellular signaling [19]. They have demonstrated that 1,25 (OH) 2 D can be mediated by a different membrane-associated rapid response steroid binding protein (MARRS) to facilitate rapid responses. It has been found that this protein is similar to the multifunctional isomerase disulfide protein of family A, member 3 (PDIA3), an endoplasmic reticulum enzyme. Interestingly, the antibody that blocks this protein prevented the transport of calcium and phosphate through the membranes of the intestinal epithelial cells. Therefore, skeletal muscle functionality can be influenced by intracellular effects on calcium handling through the action of vitamin D [20].
In addition, the presence of the VDR in vascular tissue and cardiac muscle seems to support the hypothesis that the vitamin D may impact the cardiovascular system’s ability to transport oxygenated blood and the ability of skeletal muscles to use oxygen [21]. In a randomized double-blind placebo-controlled study with postmenopausal women, was observed a 23.5% increase in muscle strength and a reduction in the number of falls by 76% after 9 months of vitamin D supplementation [22]. In another study with older adults, significant improvements in physical performance, specifically in the up-and-go test, were reported with 2000 IU of vitamin D per day in 300 elderly women with a baseline level of 25 OHD below 24 ng/mL (60 nmol/L), [23].
In relation to the adequacy of vitamin D levels for individuals with low bone mass, this population seems to benefit in the physical performance, by serum concentrations of 25 (OH) D from 30 ng/mL (75 nmol/L) concentrations close to 36 ng/mL (90 nmol/L) as the most advantageous. Likewise, these 25 (OH) D values seem to benefit lower limb muscle strength, which was assessed by the walking test. Individuals with 25 (OH) D concentrations between 36 and 40 ng/mL (90 and 100 nmol/L) appear to perform the test faster [24].
Considering the adequacy of vitamin D levels, researchers in prospective, double-blind, placebo-controlled, randomized trial included Brazilian people institutionalized that received a 6-month supplementation of vitamin D, had as result, the increase in 16.4% in their maximum isometric strength of hip flexors and 24.6% in knee extensors measured by a portable mechanical dynamometer at 6 months, nevertheless the calcium/placebo group showed no improvement at all [25]. The same way, in other study, researchers have found an increase in neuromuscular parameters such as the balance (4.5%), functional mobility (10.1%) and muscle strength (5.7%) after elderly supplementation with vitamin D (6 month), without the regular practice of physical activity, considering that after the study most subjects reached the sufficiency level [26].
Vitamin D supplementation in youngsters has also been shown to be effective on the muscular strength of dancers who received oral supplementation of 2000 IU/day of vitamin D3 for 4 months during the winter. At the end of the study, the supplemented group presented increased isometric strength (18.7%, p < 0.01), plyometry (7.1%, p < 0.01), and reduction of lesions when compared to control (p < 0.01) [27]. On the other hand, in a study with 179 vitamin D-deficient Lebanese adolescents, vitamin D supplementation did not show improvement in manual grip strength [28].
Even with some intriguing results, studies are still conflicting about the action of vitamin D on muscle performance. Some meta-analyzes have found antagonistic outcomes. The meta-analysis who analyzed 17 randomized controlled trials in individuals of all ages including younger subjects just showed benefit in muscle strength in subjects with vitamin D serum levels below 25 nmol/L at baseline. In another hand, the meta-analysis which reviewed results from 13 randomized controlled trials in individuals older than 60 years old, observed a small benefit of daily vitamin D supplementation (800 IU–1000 IU per day) for balance and muscle strength [29].
2.2 Vitamin D actions on the respiratory system
The interrelationships between vitamin D metabolism and respiratory function have been studied in the literature, mainly in diseases of the respiratory tract, however the results are still not conclusive. Accordingly, the mechanisms by which life D could affect lung function have not yet been fully elucidated. However, some explanations have been pointed out. It is believed that vitamin D influences approximately 3% of the human genome and directly or indirectly, vitamin D controls many genes that are involved in the regulation of cell proliferation, differentiation and apoptosis of healthy and pathological cells [30].
1,25 (OH) 2D is mostly derived from the kidneys, however, other tissues, including the breast and prostate, may hydroxylate vitamin D in its active form. Activated, this metabolite is transported throughout the circulation by additional vitamin D binding proteins and lipoproteins; a function that allows vitamin D to actuate a wide range of skeletal and extra-skeletal functions [31].
Studies on the action of vitamin D on different cell types suggest that 1,25 (OH) 2D modulates smooth muscle excitation-contraction via intracellular Ca2+ release and Ca2+ sensitization. Airway resistance is dictated largely by the diameter of these pathways, and minor changes in this structure can significantly increase airway resistance. The absence of Vitamin D could affect the diameter of the airways, impairing pulmonary function [31, 32].
Most nucleated cells express the VDR, however the expression varies according to cell specificity. In the lungs, VDR was found in smooth muscle cells of the airway and in alveolar cells, also known as pneumocytes [32, 33, 34]. The enzyme 1α-hydroxylase, responsible for the conversion of 25 (OH) D into its active form, is also expressed by tracheal and bronchial cells [35].
Nguyen and cols, demonstrated through a series of studies with rat fetuses that type II alveolar cells underwent 1,25 (OH) 2D 3 action and suggested that vitamin D is important for maturation and the production of surfactants [36, 37]. Although in humans the mechanisms are more complex than in rats, the effect of vitamin D on the production of surfactants has been confirmed [33].
In relation to the growth and pulmonary maturation, studies with rats born to mothers with dietary vitamin D showed a loss of lung compliance compared to those born to mothers whose vitamin D supplementation [38]. In a similar study, vitamin D-deficient mice decreased lung volumes compared to the offspring of vitamin D-rich mice [39] .
In human studies, the authors used the presence of calbindin, a vitamin D-dependent calcium binding protein, as a molecular marker of the action of 1,25 (OH) 2 D3 on tissues. The authors found high levels of calbindin in fetal lung tissue between the 14th and 32nd weeks of gestation, suggesting an action of vitamin D on lung development [40].
In a cross-sectional study from the Third National Health, Nutrition and Examination Survey (NHANESIII) with a sample of 14,000 Americans, researchers found a positive correlation between FEV 1 and FVC with serum 25 (OH) D levels. The authors also observed that adults with low serum 25 (OH) D levels had lower than predicted FEV 1 of pulmonary function [41].
Although vitamin D intervention studies in postmenopausal women aiming for respiratory capacity are still scarce, in our study center, we developed a research project to evaluate the effects of a differential aquatic exercise program (HYDROS) on the musculoskeletal system in postmenopausal women compared to sedentary controls [26]. The large volume of parameters obtained during the six-month study was presented as an opportunity to evaluate, in a post-hoc analysis, the effects of vitamin D supplementation, combined or not with high intensity aquatic exercises, on the pulmonary function of postmenopausal women. We observed an improvement in the spirometric parameters of women submitted to vitamin D supplementation, even without regular physical exercise. The supplemented group obtained a 7% improvement in peak expiratory flow, similarly forced vital capacity, according to the data presented in Figure 1 [42].
Figure 1.
Follow-up of the spirometric parameters throughout the study of the three groups. Mean ± SD and percentage of change for peak expiratory flow (PEF), forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) in the control (CG), control with supplementation of vitamin D and calcium (CDG), and training groups (DTG) before and after the intervention. * p < 0.0001, # p < 0.01 and p < 0.05 indicate differences detected using Student’s t-test versus before intervention. Different letters indicate statistically significant differences (p < 0.05) on one-way analysis of variance (Tukey’s post hoc test) in relation to the percentage variation between the groups. Ref. [42]: http://dx.doi.org/10.1590/2359-3997000000211.
In a prospective, double-blind, randomized study, vitamin D supplementation in asthmatic children reduced the risk of exacerbation triggered by acute respiratory tract infection and significantly improved FEV1, [43]. Another prospective study in patients with chronic obstructive pulmonary disease (COPD) and vitamin D deficiency demonstrated increased respiratory muscle strength, improved dyspnea scale, and superior physical performance after 1 year of vitamin D supplementation [44].
In other components of respiratory system, vitamin D status has been associated with cardiorespiratory fitness in cross-sectional investigations in the general population. Regarding the maximum volume of oxygen (VO2max), in an observational study, no correlation was observed between 25 (OH) D levels and VO2max in 53 junior and collegiate ice hockey players. However, analysis of data soccer players exposure at ultraviolet radiation, revealed a linear association between vitamin D and VO2max in both experimental sessions [45]. Corroborating with these results, across from vitamin D supplementation of soccer players during an eight-week high-intensity training program, significant results were observed in aerobic capacity. As upshot, a significant improvement in VO2max in the supplemented group was observed compared to non-supplemented subjects [46].
A recent study found that more than 60% of athletes had vitamin D insufficiency even when the data collected near hot and sunny summer. Studies with high intensity athletes have been suggesting that athletes with vitamin D3 deficiency should be supplemented with this vitamin to improve physical performance, especially VO2max [47]. The explanation would be to athletes to achieve the best results in the summer, while exposure to solar radiation. The authors suggest that the replenished 25 (OH) D3 level may protect athletes against acute and chronic diseases. Considering the above, vitamin D3 supplementation along with the training load may induce adaptive changes of aerobic and anaerobic metabolism in athletes of different sports [47].
In rowers, significantly higher energy and oxygen consumption scores were observed during a continuous exercise test in the vitamin D3 supplemented group over the 8-week training period. They demonstrated a significantly increase in VO2max (12.1 and 10.3%, respectively) [21]. At the same time, the blood parameters of the supplemented athletes, such as IL-1b, CRP, LDH, reached lower values. These results suggest that vitamin D3, whose blood concentration increased by 400% in the supplemented group after supplementation, could be the justification for improving aerobic metabolism in rowers and reducing their inflammatory reactions in response to high intensity training [21].
The possible assumption by which vitamin D to affect VO2max would be caused the influence of the enzymes Cytochrome P450 (CYP) [48]. These enzymes activate vitamin D3, which has no hormonal action, converting it to an active hormonal form (1α, 25 (OH) 2D3) by the action of CYP enzymes. Reactions catalyzed by the CYP enzymes (mitochondrial CYP27A1, microsomal CYP2R1 in liver and the latter reaction by mitochondrial CYP27B1 in kidney) have proteins containing heme and could potentially affect the binding affinity of oxygen to hemoglobin [29, 49]. The existence of this compound is important for the transport of oxygen, since it is present mainly in hemoglobin, myoglobin and enzymes. Beside this, vitamin D could also influence VO2max through iron metabolism and erythropoietin. Complementing, the vitamin D deficiency results in dysregulation of innate immunity and inflammation which is affecting iron metabolism and contributes to erythropoietin resistance, and this well documented that is linearly associated with changes in red blood cells levels [47].
2.3 Vitamin D levels in athletes and physical performance
Even after 100 years its discovery, when early researchers suggested sunbathing to prevent and cure rickets, vitamin D remains in the spotlight. The actions of the vitamin D extend beyond bone health, becoming recognized at appropriate levels, beneficial to various non-skeletal health outcomes [49, 50]. Vitamin D is a multiactive hormone acting in different spheres of the body. Research over time has shown that vitamin D3 biological action is much broader than researchers originally thought, as shown by the tissue distribution of the VDR, from mediating only calcium homeostasis. Along with this, even after this recognition, it is visible from epidemiological data; that vitamin D deficiency excessively prevalent globally [50, 51].
Based on population data, the values of 25 (OH) D discussed in the literature with emphasis on bone outcomes range from 20 to 32 ng/mL (50–80 nmol/L). Several authors have confirmed that the best cut point of is 30 ng/mL (75 nmol/L) for the correction of secondary hyperparathyroidism, reduced risk of falls and fractures, and maximum absorption of calcium. Thus, serum concentrations below 20 ng/mL (50 nmol/L) are classified as deficiency, between 20 and 29 ng/mL (50 and 74 nmol/L) as insufficiency and between 30 and 100 ng/mL (75 and 250 ng/mL) as sufficiency [14, 52].
Surprisingly, it is estimated that around the world, 1 billion people fall into these categories. In addition, both vitamin D insufficiency and deficiency are increasing in prevalence [53]. Among athletes of different categories, deficiencies or deficiencies were observed in most dancers, taekwondo fighters, jockeys, elite wheelchair athletes, handball players, athletics athletes, weightlifters, swimmers and volleyball players. In relation to other professional sports, the athletes are affected in the same way. National Football League players, 26% were found to have deficient levels of vitamin D, and 42–80% of athletes had levels defined as insufficient. Similarly, professional basketball players, 32% of athletes are vitamin D deficient and 47% are insufficient [53].
The detection of vitamin D levels in athletes, in addition to the main function of vitamin D, acting in the interrelationship between the bone and muscular systems, also had as objective the sporting performance. Athletes need to potentiate the training stimulus, so it is a fundamental principle of the training program. The great scope of high performance training is to provide a stimulus to bring an adaptive response to the entire structure of the body that improves the performance of the competition. Thus, considering these aspects, the ergogenic resources to complement the adaptive response to a physical/metabolic challenge are intensively researched [53].
In the last decade, in vitro and animal studies have provided information on a beneficial role derived from vitamin D in skeletal muscle repair and remodeling. Although in humans the action of vitamin D within muscle tissue, still raise questions, in rodent were observed possible effects. The cytochrome precursor (CYP27B1) responsible for rendering vitamin D of 25 (OH) D3 inactive, in metabolically active (1,25 (OH) 2 D3), was found in cells at different stages of differentiation; expression in rodent muscle fibers [29, 54]. This finding suggests the action of vitamin D on the regulation of muscle tissue. In addition, recent studies suggest that VDR is expressed in myoblasts and C2C12 myotubes in murine skeletal muscle [54].
In human skeletal, in situ detection of VDR points towards a role of vitamin-D on muscle function. In addition, VDR has been localized to skeletal muscle cells that promote de novo protein synthesis. Considering the genomic effects, the activation of VDR induces heterodimerization between the active VDR and the retinoic receptor (RXR). In this way, this induces the activation of the vitamin D response element (VDRE), a complex of genes coding for the “genomic effects” of vitamin D [29, 54].
Among the genomic repercussions of VDR (Figure 2) [29], the increase in calcium handling by enhancing the activities of the calcium binding protein (calbindin-D9K) in cell sarcoplasm, muscle cell differentiation and proliferation through effects on insulin growth factor (IGF) expression which in turn induces skeletal muscle hypertrophy [29].
Figure 2.
Repercussions of the 1.25 vitamin D on skeletal muscle system: Molecular and nuclear pathways. Genomic and non-genomic effects. Ref. [29]: http://dx.doi.org/10.1155/2015/953241.
In an intervention study with 61 male athletes, it was observed that 62% had a serum concentration of 25 (OH) D of 20 ng/L at baseline and after supplementation with (5000 IU) of vitamin D3 per day for 8 weeks increased significantly 25 (OH) D concentrations and reflected on the velocity, verified through the 10-meter sprint time and the explosive force, through the vertical jump when compared to a placebo group [55].
Also in relation to physical performance, in a randomized, double-blind study, judo athletes supplemented with vitamin D3 achieved a 13% increase in muscle strength compared to a placebo group (p = 0.01) [56]. In a British study, through jump mechanography, was observed a positive association between serum vitamin D levels and jump height, velocity and power (p = 0.005, 0.002 and 0.003, respectively) in postmenarche adolescent girls [57].
Although some studies have demonstrated a possible outcome on physical performance [58], on the other hand, researchers investigated whether weekly supplementation with vitamin D3 at doses of 20,000 IU (500 IU) or 40,000 IU (1000 IU) for 12 weeks improved 25 (OH) D levels or performance measures in 30 club-level athletes. No correlations were observed between 25 (OH) D concentration and performance measures, indicating either vitamin D3 supplementation does not influence skeletal muscle function to induce measurable effect. These results were obtained even after 25 (OH) D levels were increased at the end of the study [59].
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3. Conclusion
Vitamin D deficiency results in poor muscle function and weakness that are reversible upon reaching a complete vitamin D state. However, prospective studies examining the effects of vitamin D on muscle function have shown conflicting results, measures of physical performance of the distinct population (non-athletes, athletes, young and old). In this way, to make emphatic conclusions on the ergogenic use of vitamin D, we still have reflections on the potential mechanisms of interaction, or even, what would be the appropriate levels for the different age groups.
The direct mechanisms by which vitamin D could affect lung function have not yet been fully elucidated. Perhaps in future well-controlled studies, the parameters of cause and effect may be better supported. However, studies have shown that treatment with Vitamin D3 was effective in postmenopausal women to produce a significant increase in plasma concentrations of 25 (OH) D [42]. This adequacy of vitamin D status was associated with improved pulmonary function parameters, independent of the performance of the aquatic exercise program. In addition, the correction of its deficiency could also be a supporting measure for the strategies used to prevent and treat diseases with impaired pulmonary function or incapacitated individuals.
Furthermore, new questions are raised as to whether athletes amatours and professional susceptible to muscle damage and/or Vitamin D inadequacy, such as have been described in the elderly to exhibit low serum 25 [OH] D, experience aggravated declines in regenerative capacity and remodeling when serum 25 [OH] D is low. In addition to the health benefits, future studies may establish new views on the action of vitamin D as a possible legal ergogenic resource contributing to better athletic performance and record breaking.
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Written By
Rodrigo Nolasco and Marise Lazaretti-Castro
Submitted: 09 June 2018 Reviewed: 20 September 2018 Published: 05 March 2019
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How do I know whether there are any positive or negative interactions between Medical Cannabis and Prescription Drugs?
NGT tests indicate inhibitors and inducers for both Rx prescription drugs and Medical Cannabinoids which can enhance, delay, or prevent the efficacy of the prescription and/or medical cannabinoids. We report on evidenced-based Drug-to-Drug interactions for each medication and for the cannabinoids we report on.
← Back to FAQ
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What can cause sinus infection ear pain? Ear pain can result from allergic rhinitis or a nasal allergy. Histamine and other substances are released by the body in response to allergens.
These substances irritate the sinuses and nose, which might impact the ear and result in ear pain. Ear infections can occasionally also be brought on by swelling and fluid accumulation.
A person can visit their doctor or an allergist to get a diagnosis and learn if allergies are to blame for ear pain. A person can take precautions to avoid or minimise their exposure to allergens once they are aware of which ones could cause an allergic reaction.
Antihistamines, decongestants, and allergy injections are a few of the drugs that can help with the symptoms. Any ear pain caused by allergies should go away with treatment.
In this article, we will discuss:
what you will read next :
What is sinusitis?
The sinuses are tiny air sacs situated behind the cheekbones, forehead, nose, and between the eyes. Sinusitis is an inflammation of the sinuses and nasal passages.
Conditions include structural problems in the nose or a sinus infection can cause inflammation.
The terms “sinusitis” and “sinus infection”, however, are used synonymously.
Headaches and sinus pressure are symptoms of sinusitis, often known as a sinus infection. Inflammation or swelling in the sinus and nasal mucosa is what causes sinusitis. Your facial bones’ sinuses are hollow air chambers located close to the nose.
Mucus is created by them, helping to lining the nose and keep dust and other particles from getting into your lungs.
Although there are several causes of sinusitis, it always happens as a result of moisture becoming trapped in the sinuses, which allows bacteria to flourish.
A virus is the most frequent cause, but sinusitis can also be brought on by a bacterial infection.
Allergies, asthma, and airborne contaminants like chemicals or other irritants can all act as triggers.
Molds and fungi both have the potential to cause fungal sinusitis.
How does the inner ear work?
In reaction to variations in pressure in the surrounding environment, the eustachian tubes help maintain normal air pressure in the middle ear.
However, if allergies or sinus congestion clog these tubes, you could experience a number of issues, including ear infections.
What does a eustachian tube actually do?
It’s a tiny canal that connects your middle ear, which houses your eardrum, to the back of your throat and nose. It is only a few millimetres in diameter and is only about 1.5 inches long.
The same type of moist membrane that lines the nose and throat also lines the eustachian tubes.They are normally closed, but when the back of the nose and throat move, as they do when you swallow, yawn, or talk, they open.
Eustachian tubes in adults are inclined downward from the ear into the back of the throat, allowing for middle ear fluid and mucus outflow by gravity.
Sounds that reach your outer ear are converted by your middle ear into vibrations that your inner ear and brain can understand. Your middle ear has to maintain the same air pressure as the air around you in order to function effectively.
As a result, your eustachian tubes periodically open to allow air to flow into your middle ear, bringing the pressure there into balance with the pressure in the back of your throat.
If Your Eustachian Tubes dysfunction:
Your eustachian tubes and middle ear may get damaged for a variety of reasons, including:
Swelling-induced obstruction:
Due to eustachian tube obstruction, middle ear occlusion is a common symptom of sinus pressure in sufferers. Most frequently, a sinus infection, a cold, or allergies are to blame for this swelling.
The inner ear membranes may enlarge as a result of these disorders, obstructing the tubes. A clogged eustachian tube is unable to properly discharge mucus or circulate air.
Mechanical obstruction:
Ear blockage can occasionally be brought on by nasal tissues that have grown excessively, such as nasal polyps or adenoids, blocking the passage to the eustachian tube. A tumour can occasionally result in an obstruction.
Medial otitis (middle ear inflammation or infection):
The middle ear may fill with fluid and become irritated when sinus congestion results in a clogged eustachian tube. Similar to bacterial sinus infections, middle ear infections can result in swelling and further fluid buildup if they invade your eustachian tubes. Otitis media is linked to ear pressure and pain.
Damaged eardrum: Your eardrum could be torn if there is an excessive buildup of fluid in your inner ear.
Do you have a sinus infection with ear pain? What is the link between these two?
Parts of the nasal cavity get infected when an upper respiratory illness, such as a sinus infection, is present. The eustachian tubes and other sinus drainage passages expand and get blocked as a result of the inflammation.
Pressure on the tubes starts to increase as the trapped fluid starts to swell, which is very uncomfortable. The buildup could cause sinusitis or otitis media if it is not properly managed.
In reality, bacterial and viral infections are the common causes of both sinus and ear infections. It is simple for an infection to travel from the sinuses to the middle ear and result in an ear infection once it has established itself there.
You agree to experience all the symptoms of a sinus infection as well as the extra symptoms of ear discomfort and/or plugged ears if you have these two infections concurrently.
While these widespread causes can make it more challenging to diagnose your condition, they also make it such that treating one infection is similar to treating the other.
Therefore, knowing the typical causes of ear infections and sinus infections might reduce your risk of developing both diseases simultaneously. Now let’s look at these causes.
How do you know if it is a sinus infection or ear infection causing ear pain?
Headaches brought on by the pressure and swelling of the sinuses or sinus cavities are one of the signs of a sinus infection.
If you have severe sinus pressure, your ears might not pop. Other signs include nasal discharge that is a greenish-yellow tint, pain in your ears, and pain beneath your eyes. Congestion can be brought on by sinus discharge, which may irritate your sinuses.
Allergies, smog in the air, and the shape of the nose all contribute to sinus infections. It’s crucial to keep track of what makes your sinuses flare up.
Is mould, for instance, more likely to cause a sinus infection? Is dust to blame? Or are less typical factors like diabetes, an inflammatory disease, or a fungal infection to blame for your sinus infections?
Once you are aware of the source of your sinus infections, you can lower your risk of contracting sinusitis by washing your hands frequently, avoiding touching your face, drying your hair after a shower, getting immunised, creating a sinus-friendly environment in your home by cleaning it frequently and changing the air filter, and avoiding caffeine and alcohol.
Try taking antihistamines if allergies are the source of your sinus infections. Antifungal medications can help prevent sinusitis brought on by fungus infections.
Finally, immunoglobulin can aid in the battle against the irritants that cause sinus infections if you have immune weaknesses.
Ear infections and frequent, severe sinus infections could be signs of acute or chronic sinusitis. Even with acute or chronic sinusitis, there are therapy alternatives to get long-lasting relief.
what can be the causes of ear pain?
There are many causes of ear pain some of which include sinus infections, buildup of fluid, buildup of wax, allergies, travel, blocked ear canal, or ear infections.
Some uncommon causes of ear pain include:
This inner ear condition results in severe vertigo and hearing loss. People between the ages of 40 and 60 are more prone to it. Although the disease’s source is still unknown, fluid accumulation in the labyrinths, which are compartments of the inner ear, is what causes the symptoms.
On the nerve that connects your inner ear to your brain, there is a noncancerous growth that is slowly expanding. As the tumour grows, symptoms, which are often mild and develop gradually, may also include tinnitus, vertigo, and balance issues.
Poor Eustachian tube function or a middle ear infection can lead to abnormal growth known as a cholesteatoma forming in the middle ear.
This particular middle ear condition involves an accumulation of clear fluid, often known as serous fluid. One of the common side effects is hearing loss.
Children are more likely to experience this issue following an ear infection.
People who frequently swim, reside in warm areas, have diabetes, or suffer from chronic skin disorders are more likely to develop fungal ear infections.
They can be brought on by more than 60 different varieties of fungi. Fungal ear infections can also result in hearing issues, ringing in the ears, swelling, pain, and itching.
Treatment of ear pain on the basis of its cause.
Issues related to sinus infection causing ear pain:
Following are some methods for treating sinus congestion and accompanying ear congestion:
Buildup of fluids:
Congestion in the ears might result from getting water in them while swimming or taking a shower. In order to get water out of your ear, try the following:
Allergies:
When mucus builds up and becomes lodged in your middle ear or Eustachian tube due to allergies, you may experience ear congestion. Antihistamines and decongestants are common allergy drugs that can help with ear congestion and associated symptoms.
Blocked ear canal:
Do not attempt to remove a foreign object from your ear canal if you have a suspicion that it may be there. Visit your doctor immediately away instead, or go to the closest ER or urgent care facility.
Ear infections:
Dizziness, ear pain, and occasionally fluid discharge are all symptoms of a middle ear infection in addition to ear congestion. Colds or other respiratory conditions that enter the middle ear through the Eustachian tube are typically to blame for them.
Swimmer’s ear, also known as an external ear infection, is typically brought on by water that stays in your ear after bathing or swimming, creating an excellent environment for bacteria to grow. You might feel discomfort, itchiness, redness, clear fluid drainage, or pus discharge.
Most ear infections heal on their own. Painkillers and over-the-counter ear drops can help you feel better. Your doctor might advise taking antibiotics if your symptoms are serious or last for more than two days.
How to relieve sinus pressure inside the ear?
The pressure inside the ear is really unpleasant. A person may experience slight pain, muted sound, or a feeling of having water in their ears when fluid is present.
These symptoms can interfere with your daily activities if the sinus pressure is not treated. Fortunately, there are several options for getting some relief.
When your sinuses are dry, pressure worsens. A humidifier will keep your sinuses moist all day long. Regardless of the temperature, they continue to contribute moisture to the air. Even though you can run them during the day, you should run them at night to help with congestion relief.
Using the steam from hot water is another way to cause drainage. This technique has been used for many years since the steam’s heat opens up channels that allow the fluid to drain. Just heat some water until it boils, then pour it into a basin. Put a towel over your head and place your head over the bowl. In order to breathe it in and reduce ear pressure, the towel will help hold onto as much of the steam as possible.
It’s difficult to go asleep when your ear is blocked. Even with the pressure alone, it might get uncomfortable if you don’t get into a decent position. Set your pillows up to slightly support you while you get ready for bed. By doing this, you will prevent the liquid from entering your ears further. Keep the obstructed ear closest to the bed if you like to sleep on your side.
One of the many incredible health advantages of water for the body is the reduction of sinus-related ear pressure. Increasing your water consumption will assist the body fight off the infection and washing out pollutants. Additionally, it gives your eustachian tubes more chances to open while swallowing. This action will assist in adjusting the pressure in your ear. to your ears, please.
diagnosis
To determine whether you have a sinus infection, your doctor will often do a physical examination and examine your medical history.
After confirming that you have sinusitis, your doctor may perform additional tests to identify whether it is acute, subacute, chronic, or recurrent. Your doctor can determine the best course of treatment for your sinusitis with the knowledge of its type.
In order to establish how to proceed with the recommended treatment, your doctor will also determine whether or not your sinusitis is bacterial.
Rarely, a fungus may be to blame for sinusitis. It is an extremely dangerous medical emergency when this occurs. Your doctor can help you identify the best course of action and determine whether a fungus is to blame for your sinusitis.
When to see a doctor
Home treatments and over-the-counter pharmaceuticals are frequently used to alleviate ear congestion.
But if a person has ear congestion, they might wish to consult a doctor:
summary
Ear pain can result from allergic rhinitis or a nasal allergy. Histamine and other substances are released by the body in response to allergens.
These substances irritate the sinuses and nose, which might impact the ear and result in ear pain. Ear infections can occasionally also be brought on by swelling and fluid accumulation.
A person can visit their doctor or an allergist to get a diagnosis and learn if allergies are to blame for ear pain.
A person can take precautions to avoid or minimize their exposure to allergens once they are aware of which ones could cause an allergic reaction.
Antihistamines, decongestants, and allergy injections are a few of the drugs that can help with the symptoms. Any ear pain caused by allergies should go away with treatment.
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top of page
• ereul93
Exercise & Prolapse
Updated: Apr 26, 2021
Hello friends, this week’s topic is exercising with prolapse! So many individuals deal with prolapse every day. In fact, 1 in 5 women suffers from pelvic organ prolapse! (Nygaard, 2008)
Pelvic organ prolapse is the descent of the bladder, cervix, or rectum into the vaginal canal due to lack of support from the pelvic floor muscles and other pelvic structures. To learn more about pelvic organ prolapse in detail, check out our Pelvic Organ Prolapse blog post.
Prolapse can impact every aspect of an individual’s life, including the way they move and the way they exercise. It can be scary trying to exercise with prolapse. You might be worried it is going to make your symptoms worse or make your prolapse more severe. You can exercise with prolapse! The type of exercise and the position you are in can impact your pelvic floor muscles and pelvic organ prolapse. The pelvic floor muscles need to be strong, flexible, and coordinated to provide the best support.
Let’s first talk about the way gravity can affect pelvic organ prolapse. Have you ever noticed that your symptoms are worse after being up and walking around all day? That’s because your pelvic floor muscles have been working against gravity to hold your pelvic organs up all day long, and they may be getting tired.
Maybe you are a runner and you notice that prolapse symptoms are worse after a run (especially longer distances). While running, your pelvic floor should act like a trampoline to support the pelvic organs, but if your muscles are weak or uncoordinated or if they are too tight, they may have a hard time providing support causing the prolapse to temporarily get worse.
But there’s good news: we can use gravity to our advantage too! Have you ever noticed that first thing in the morning your have little to no prolapse symptoms? If this is the case, it’s because you’ve been lying flat all night, and therefore gravity hasn’t been able to pull down on the pelvic organs!
There are a few ways to use this to your advantage. Let’s start by talking about the anti-gravity position. Lying on your back with your pelvis about your heart will get you into the “anti-gravity” position for your pelvic floor muscles. You can use any kind of support (like a pillow or blanket) under your hips to get into this position. This position puts your pelvic floor muscles on slack. It also helps to pull the pressure from your pelvic organs away from your pelvic floor muscles.
(Tip: If you’re prolapse symptoms are worse after being up all day, try lying in this position for 10-15 minutes and see if your symptoms get better!)
The same principles apply when talking about a gravity neutral position (flat on your back with your pelvis at the same level as your heart). Gravity actually helps pull the pelvic floor muscles to contract in the anti-gravity position, but it does not in the gravity neutral position.
Using internal or external supports can be a great option when exercising with prolapse. These options work with your pelvic floor muscles to provide extra support to the pelvic organs. Internal supports go into the vaginal canal to provide support to the vaginal walls. There are different types of internal supports like a pessary (which is fitted by a physician or nurse in the US) or something over-the-counter like the Poise Impressa. If you are uncomfortable using an internal support, that’s totally okay—external supports, like the V2 Supporter, are a great alternative. External supports are worn under your clothes to provide some gentle pressure to the vulva without going inside the vagina.
Exercise has so many health benefits—both physical and mental. Don’t let pelvic organ prolapse stop you from doing the exercises you love! If you are struggling to manage symptoms with prolapse, working with a pelvic floor physical therapist can help to make sure your pelvic floor muscles are strong and coordinated to support your pelvic organs with whatever activity makes you happy!
Here are some great resources to learn more about your pelvic floor and to help manage pelvic organ prolapse:
For providers, check our online courses to help your clients experiencing pelvic floor symptoms. Consider joining our Ambassador Program and most of our courses are included with your membership!
What experiences or tips do you have that can help others? We’d love to hear them. Please join the conversation in the comments section below.
Written by Emily Reul, PT, DPT
References
1. Nygaard, I., et al. Prevalence of symptomatic pelvic floor disorders in U.S. women. JAMA. 2008;300(11): 1311–1316.
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Accessibility
Platelet Rich Fibrin (PRF)
What is Platelet Rich Fibrin (PRF)?
PRF is a concentration of growth factors and cells collected from your own blood. It is a natural regenerative strategy that uses a standard blood draw, then is spun at high speeds in a Bio-PRF machine to create concentrated and natural growth factors.
Since no additives are used, it forms a ‘super’ blood clot with significantly elevated concentrations of regenerative cells and growth factors capable of stimulating wound healing.
The PRF method accumulates up to 6-8 times more platelets and leukocytes when compared to whole blood. These cells then release more growth factors and fight potential incoming infections, thereby reducing post-operative pain. The new Bio-PRF technology has been scientifically shown to be a highly effective medical procedure to induce tissue regeneration, instead of using artificial components such as animal, human, or laboratory-derived products.
Where PRF Is Used at Victoria Village Dentistry
• At extraction sites to promote general wound healing
• Bone graft procedures
• Surgical sites
• Facial aesthetics
• Source: bio-prf.com
Back
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Send Us A Message
We encourage you to contact us with any questions or comments you may have. Please call our office or use the contact form below.
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Blog
Challenging behaviour – how to deal with it
In a care environment, challenging behaviour can be difficult to deal with. Learning how to deal with challenging behaviour effectively and empathically is vital to providing the best care for patients, and for maintaining a positive mentality. This article explains challenging behaviour- in what forms it appears and its possible triggers- and gives advice on how to handle it when it arises.
What constitutes Challenging Behaviour?
The definition of challenging behaviour is behaviour that is ‘culturally abnormal’. This generally covers behaviours that prohibit or seriously limit access to ordinary community activities. These types of behaviour typically appear in people who suffer from learning development disabilities (such as autism disorders), or in those with certain mental health issues. However, it is important to realise that the behaviours themselves are not caused by mental issues, but rather enabled by them in those cases; anyone can behave in a way that can be considered challenging. It is therefore important to remember to not view the person behaving challengingly as having something ‘wrong’ with them simply due to the behaviour existing.
Challenging behaviour itself manifests in a variety of different forms, such as:
• Aggressive Behaviour this consists of anything destructive towards people, such as hitting, verbal abuse, hair pulling, screaming, throwing objects, and biting and scratching
• Self-Injurious Behaviour these are behaviours directed towards oneself that cause damage, like head-banging, eating non-foods, scratching, or grinding teeth
• Stereotyped Behaviour behaviours one would probably think of if you heard the words ‘culturally abnormal’, such as repetitive speech, rocking, or repetitive movements
• Non-person Directed Behaviour these are behaviours that aren’t directed at people, such as withdrawal, property damage, hyperactivity, theft, and inappropriate sexualised behaviour
What are the causes of Challenging Behaviour?
Many factors lead to the development of challenging behaviour, and these broadly fall into 4 different categories:
1. Psychological- Challenging behaviours might develop as coping mechanisms for feelings of loneliness, development, or exclusion. A patient may, for example, take up self-injurious behaviours in order to find relief from depression
2. Environmental- in some cases, physical aspects of the world can trigger people into developing challenging behaviours. People might become aggressive in noisy environments, or react negatively to certain light levels. Inconsistencies in things such as staffing levels are also causes of challenging behaviour, because of a perceived threat or sense of discomfort because of the change.
3. Social- oftentimes, challenging behaviours to develop as a result of negative social environments. Boredom can enable people to develop challenging behaviours in order to entertain themselves. Someone with autism might learn that hitting someone will force them out of their personal space if they’re overwhelmed, or someone else might do things (typically in the stereotyped category) out of a need to try and have greater control over their social space.
4. Biological- some people end up developing challenging behaviours because of biology. Having a lack of stimulation in some capacity can cause people to seek out destructive pursuits. Or the behaviours might develop out of a response to medication, or as a crude form of pain management. Conditions such as Lesch-Nyhan Syndrome are linked to self-injurious behaviour because of the way the brain handles hormones
Some people will only develop one form of challenging behaviour, but in others, multiple can exist in ‘clusters’. For example, someone might have an aggressive outburst of destructiveness in order to get some attention.
Handling Challenging Behaviour
Whilst the implication here is that the behaviours are deliberate and intended to get a response in many cases, it is important to realise that this is not always true. In most people with severe learning/mental difficulties, there is no intention of being upset. The simplest and foremost step is to step back. Try and see what is going on from the person’s perspective, and understand why they act the way they do.
Outside of this, there are many things you can do. You should ensure that anyone who helps care for the person does things in a consistent manner, so as to avoid any environmental upsets. Communicating with the care team can help through the sharing of experience and knowledge, which in turn should help you anticipate potential problems; you might be able to avoid outbursts by enabling yourself to redirect attention to another activity, or pre-emptively reducing noise or light levels.
You should also try to work with the individual themselves. Find out from them whatever triggers they are aware of, such as noise or attitudes in carers that provoke the behaviour. Help them to recognise distress when it occurs, helping to deconstruct the belief that their behaviours are the most productive ways to deal with issues. Establish and develop coping strategies with them, including opening up any necessary additional ways of communicating their needs. If a lack of stimulation is the cause of the behaviour, then provide a variety of materials or activities for them, but make sure they are meaningful and appropriate, which should be established through communication with the patient. If the person with challenging behaviours has a communication disorder, then make sure that they have a method with which to effectively communicate, be it visually based or otherwise.
Above all else, remember to make the patient feel valued. Always take their views and insight into consideration, as they have much more experience of their feelings than you do. With any plan, your purpose should be to improve their quality of life. Happy people tend not to express challenging behaviours, so maximising the things that bring them happiness will help them.
Further Reading
The charity Scope has lots of information about challenging behaviour on their website: https://www.scope.org.uk/support/parents/challenging-behaviour/overview
The NHS, too, offers a lot of information on this topic:https://www.nhs.uk/conditions/social-care-and-support-guide/practical-tips-if-you-care-for-someone/how-to-deal-with-challenging-behaviour-in-adults/
Speak to a training consultant now.
0800 781 2041
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Why do I need this surgery?
What will this surgery do?
What are the risks and possible complications of this surgery?
What are my non-surgical options?
Are there any other surgical options?
What can I expect if I choose not to have this procedure?
What can I expect if I choose to delay this procedure?
What surgical approach will you use?
How will my jawline be affected by this surgery?
Can I see different options for the possible results of my surgery?
Can I see before and after pictures of your previous work?
Can I have other cosmetic procedures done at the same time?
How long should the results of the surgery last?
How much will the surgery cost?
Where and how big will my incision be?
Will I have any visible scars?
How long will this surgery take?
Will I have any bandages on my neck after this surgery?
Will this surgery affect my facial movements and expressions?
Will my ability to swallow or eat be affected by this surgery?
How will my neck feel after this surgery in the short and long-term?
How long will any swelling and bruising in my neck last?
How long will it take for my neck to recover so that I can see its final shape?
What can I expect my pain to be like?
What are my options for pain medications after surgery?
Will I have any drains or tubes put in during surgery and for how long?
How long will I be in the hospital after my surgery?
How long will it be before I can get back to my normal routine?
How long will it be until I can drive again?
How long will it be until I can go back to work?
What kinds of anesthesia can I have for this procedure?
Do I need to see an anesthesiologist before my surgery?
Can you review my medication list with me?
Will I need to stop or change any of my current medications?
What tests do I need to do before surgery?
When should I stop eating and drinking before surgery?
What time should I arrive for my surgery?
Can I get directions and contact information for your clinic/hospital?
Will I need someone to drive me home from the hospital?
Preparing for your surgery
How long will my surgery take?
When will my visitors be able to see me?
Do I need any antibiotics to prevent infections?
On the day of the surgery
How did my procedure go?
When will we stop the preventative antibiotics started before surgery?
When can we restart my usual prescription medications?
When can I have my drains or tubes removed?
When can I eat or drink?
How much longer do you think I need to stay in the hospital?
What needs to happen before I can be discharged?
How are we going to manage my pain?
How does my incision look?
How do I take care of my incisions?
Are there any special instructions for caring for my neck?
How can I help reduce any discomfort and swelling in my neck?
Have we arranged for my prescriptions to be filled?
Are there any medications that I need to avoid?
How do I take care of my incision?
When can I take a shower?
When do I need to come back for a follow-up appointment?
Do I have staples or sutures that need to be removed?
When will any bandages be removed?
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Behind the word mountains, far from the countries Vokalia and Consonantia, there live the blind texts. Separated they live in Bookmarks grove right
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1a01aa77535b9ecfb87b9fc36adbcd2f
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-5,141,010,570,824,380,000
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Cavernous sinus dural arteriovenous fistula complicated by pontine venous congestion. A case report
Masaki Iwasaki, Kensuke Murakami, Takahiro Tomita, Yoshihiro Numagami, Michiharu Nishijima
Research output: Contribution to journalArticlepeer-review
22 Citations (Scopus)
Fingerprint
Dive into the research topics of 'Cavernous sinus dural arteriovenous fistula complicated by pontine venous congestion. A case report'. Together they form a unique fingerprint.
Medicine and Dentistry
Neuroscience
Chemistry
Nursing and Health Professions
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Rev. Nefrol. Dial. Traspl. 2023;43(2): 106-111
Casuística
Crescentic IgA nephropathy following SARS-CoV-2 vaccination. Report of a case
Nefropatía por IgA extracapilar luego de la vacunación contra el SARS-CoV-2. Reporte de un caso
Toprak Zeki1 ORCID: 0000-0002-7411-3628 - [email protected] , Ersoy Yesil E.2, Zerenler Gursoy F.3, Demirbas M. B.4, Kayabaşı H.5, Sit D.6
1) Department of Nephrology, University of Health Sciences, Umraniye Training and Research Hospital, Istanbul, Turkey
2) Department of Nephrology, University of Health Sciences, Umraniye Training and Research Hospital, Istanbul, Turkey
3) Health Sciences University, Umraniye training and research hospital clinic of Pathology Umraniye, Istanbul, Turkey
4) Department of Nephrology, University of Health Sciences, Umraniye Training and Research Hospital, Istanbul, Turkey
5) Department of Nephrology, University of Health Sciences, Umraniye Training and Research Hospital, Istanbul, Turkey
6) Department of Nephrology, University of Health Sciences, Umraniye Training and Research Hospital, Istanbul, Turkey
Cómo citar este artículo (How to cite this article) T. Zeki, E. Yesil E., Zerenler Gursoy F., Demirbas M. B., Kayabaşı H., Sit D.Crescentic IgA nephropathy following SARS-CoV-2 vaccination. Report of a case. Rev Nefrol Dial Traspl. 2023;43(2):106-111
Recibido: 18-01-2023
Corregido: 27-01-2023
Aceptado: 08-05-2023
RESUMEN
Introducción: Los estudios han demostrado que la frecuencia de insuficiencia renal aguda (IRA) aumenta en pacientes con COVID-19. Se ha informado que la necrosis tubular aguda es el daño más común en estos pacientes, probablemente debido a la alteración de la perfusión renal. Por otro lado, pueden estar involucrados diferentes procesos fisiopatológicos complejos, debido a los efectos directos de la infección viral sobre el sistema renina-angiotensina-aldosterona, la activación de la coagulopatía, la tormenta de citoquinas y la activación del sistema inmunológico. En estos pacientes se pueden observar muchas enfermedades glomerulares, como vasculitis asociada a anca, glomerulonefritis membranosa y nefropatía por IgA. Caso clínico: Presentamos un caso de nefropatía IgA extracapilar (NIgA) de nuevo diagnóstico tras una infección por SARS-CoV-2 y vacunación. Un hombre de 31 años sin antecedentes médicos presentó hematuria macroscópica 24 horas después de la infección por SARS-CoV-2. La hematuria remitió espontáneamente en 3 días. Fue vacunado con dos dosis de CoronaVac (Sinovac) tres meses después de haber sido infectado por el SARS-CoV-2. Luego fue vacunado con la vacuna Pfizer-BioNTech COVID-19, un mes después de la segunda dosis de la vacuna CoronaVac (Sinovac). Presentó hematuria macroscópica y proteinuria no nefrótica 24 horas después de la primera dosis de la vacuna Pfizer-BioNTech COVID-19. Se realizó una biopsia renal que mostró NIgA extracapilar. Comenzó con metilprednisolona y bloqueador del receptor de angiotensina. Los pacientes que reciben vacunas basadas en ARNm demuestran anticuerpos contra el dominio de unión al receptor (RBD) de la proteína S1. De manera similar a la infección natural, debido a la fuerte estimulación de la respuesta inmunitaria de las vacunas basadas en ARNm en comparación con otras vacunas, los pacientes pueden producir anticuerpos de novo, lo que lleva a depósitos de complejos inmunitarios que contienen IgA. Conclusiones: Este caso destaca los efectos inmunológicos de las nuevas vacunas contra el SARS-CoV-2 basadas en ARNm. Los nefrólogos deben estar al tanto de la aparición de hematuria o proteinuria luego de la infección por SARS-CoV-2 o la vacuna contra el SARS CoV-2 basada en ARNm.
Palabras Clave: Lesión renal aguda, covid-19, nefropatía por IgA, Vacuna COVID-19
ABSTRACT
Introduction: Studies have shown that the frequency of acute kidney injury (AKI) increases in patients with COVID-19. Acute tubular necrosis has been reported to be the most common damage in these patients, probably due to impaired renal perfusion. On the other hand, different complex pathophysiological processes may be involved due to viral infection's direct effects on the renin-angiotensin-aldosterone system, the activation of coagulopathy, the cytokine storm, and the activation of the immune system. Many glomerular diseases may be seen in these patients, like anca-associated vasculitis, membranous glomerulonephritis, and IgA nephropathy. Clinical case: We present a newly diagnosed crescentic IgA nephropathy (IgAN) case after a SARS-CoV-2 infection and vaccination. A 31-year-old man with no medical history presented with gross hematuria 24 hours after SARS-CoV-2 infection. Hematuria regressed spontaneously within three days. He was vaccinated with two doses of CoronaVac (Sinovac) three months after he had been infected by SARS-CoV-2. Then he was vaccinated with the Pfizer-BioNTech COVID-19 vaccine one month after the second dose of CoronaVac (Sinovac) vaccine. He presented with gross hematuria and subnephrotic proteinuria 24 hours after the first dose of the Pfizer-BioNTech COVID-19 vaccine. A kidney biopsy was performed and showed crescentic IgA nephropathy (IgAN). He was started on methylprednisolone and angiotensin receptor blocker. Patients who receive mRNA-based vaccines demonstrate robust antibody production against the receptor-binding domain (RBD) of the S1 protein. Similar to natural infection, due to the intense stimulation of immune response from mRNA-based vaccines compared to other vaccines, the patients may produce de novo antibodies, leading to IgA-containing immune-complex deposits. Conclusions: This case highlights the immunological effects of the novel mRNA-based SARS-CoV-2 vaccines. Nephrologists should be aware of new-onset hematuria or proteinuria after SARS-CoV-2 infection or mRNA-based SARS-CoV-2 vaccine.
KEYWORDS: Acute Kidney Injuy; Covid-19; IgA Nephropathy; COVID-19 vaccin
INTRODUCTION
At the end of 2019, a novel coronavirus was identified as the cause of a cluster of pneumonia cases in China; the infection rapidly spread worldwide, resulting in a global pandemic (1). Coronavirus disease 2019 (COVID-19) is thought to cause acute kidney injury (AKI) by various mechanisms. The proposed mechanisms of kidney injury are numerous and range from a direct viral infection that affects the renin-angiotensin-aldosterone system to hemodynamic instability, the activation of coagulopathy, cytokine storm, and the activation of the immune system (2,3). IgA nephropathy (IgAN) is the most common lesion found to cause primary glomerulonephritis throughout most developed countries of the world. IgAN is typically triggered by upper respiratory infections, and relapse of IgAN has been reported in patients receiving vaccinations (4-8). Here, we present a case of newly diagnosed crescentic IgAN after SARS-CoV-2 infection and mRNA-based SARS-CoV-2 vaccine.
CASE REPORT
A 31-year-old man with no medical history presented with gross hematuria 24 hours after SARS-CoV-2 infection. He reported no personal history of kidney disease, including IgAN. The diagnosis of COVID-19 was made primarily by direct detection of viral reverse-transcription polymerase chain reaction (RT-PCR) from the upper respiratory tract. Chest computed tomography findings were consistent with SARS-CoV-2 infection. He did not have hospitalization during SARS-CoV-2 infection. He was treated with favipiravir and paracetamol. He did not have a urinalysis when he had gross hematuria. Serum creatinine was 0,93 mg/dL (Ref: 0.76-1.27 mg/dL), and the estimated glomerular filtration rate was 109 ml/min/1.73 m2. Hematuria had been resolved spontaneously within three days. He was not referred to nephrology during the gross hematuria attack. However, due to the development of hematuria after the viral infection, its spontaneous recovery, and the absence of a kidney stone story, we think that he had an attack of IgAN even though he did not have a urine test or histopathological evidence. He had been vaccinated with two doses of CoronaVac (Sinovac) three months after the SARS-CoV-2 infection, and he did not describe a hematuria attack after the CoronaVac (Sinovac) vaccine. He had been vaccinated with the Pfizer-BioNTech COVID-19 vaccine one month after the second dose of CoronaVac (Sinovac) vaccine, and gross hematuria occurred 24 hours after the Pfizer-BioNTech COVID-19 vaccine. He was referred to nephrology for consultation. The patient had no history of renal disease, and there was no hematuria in the past urine analysis. Physical examination was normal, and blood pressure was 123/75 mm Hg. He did not have lower extremity edema, rash, lymphadenopathy, or throat erythema. Serum creatinine was 1.15 mg/dL (Ref: 0.76-1.27 mg/dL), and the estimated glomerular filtration rate was 84 ml/min/1.73 m2. A urinalysis showed 3+ protein (ref: negative), 242 red blood cells per high-power field (ref: 0-3), 13 white blood cells per high-power field (ref: 0-4), and 3+ blood (ref: negative). The random urine protein-creatinine ratio was 0.67 g/g (ref: 0-0.2 g/g), estimating 24-hour urine protein excretion of 670 mg. 24-hour urine protein was 1083 mg/day. Kidney ultrasound showed mildly increased echogenicity of average size and cortical thickness. Additional serological work-up for glomerulonephritis was negative, including hepatitis B antigen, anti-hepatitis C antibody, anti-HIV (Human immunodeficiency virus) antibody, and antinuclear and antineutrophil cytoplasmic antibodies. Erythrocyte sedimentation rate, Rheumatoid factor, and C-reactive protein levels were normal. Complements C3 (1.56, ref: 0.9-1.8 g/L) and C4 (0.4, ref: 0.1-0.4 g/L) were normal. Creatinine phosphokinase was 109 U/L (ref: 30-200 U/L), and Immunoglobulin A level was normal. The patient's laboratory results, timeline of infection, and vaccinations are shown in Table 1
Table 1: Timeline of patient's infection and vaccinations
SARS-CoV-2 infection
March 2
2021
Coronavac vaccine June 15 2021
Pfizer biontech vaccine
July 24
2021
After IgAN treatment October 11
2021
Blood urea nitrogen
(mg/dl)
29,96
-
19,9
33,7
Serum creatinine
(mg/dl)
0,94
-
1,15
0,81
C reactive protein
(mg/L)
2,2
-
9,55
7,26
Glomerular fıltration rate
(ml/mn/1,73 m2)
108,36
-
84,32
118,43
Protein (mg/24 hours urine)
-
-
1083,6
274,82
Urinalysis
-
-
Red blood cell
-
-
242
4
Protein
-
-
++
-
White blood cell
-
-
13
20
Given the unclear diagnosis, an ultrasound-guided percutaneous renal biopsy was performed. Light microscopy revealed 77 glomeruli, most of which had a mild mesangial expansion, hypercellularity with endocapillary hypercellularity, and adhesion of a capillary loop to the Bowman capsule (Figure 1), 1 of which showed global sclerosis, 1 of which showed segmental sclerosis.
Figure 1
Description: IMG-9734 (1)
Mild tubular atrophy and interstitial fibrosis are present. H&E x 100.
4 of which showed cellular crescent (Figure 2), 1 of which showed fibrous crescent (7.7%), 2 of which showed fibrinoid necrosis.
Figure 2
Description: IMG-9760 (1)
While a cellular crescent is observed in the left glomerulus, an increase in mesangial cellularity is observed in the other glomerulus. H&E x200.
Immunofluorescence revealed 3+ diffuse granular mesangial staining for IgA (Figure 3).
Figure 3: Mesangial accumulation in glomeruli with IgA in direct immunofluorescence examination x40
Description: IMG-9797 (1)
Staining was positive for C3 and negative for IgG and other immunoglobulins and complement antibodies. Mild tubular atrophy and interstitial fibrosis were observed. Erythrocyte clumps, hemoglobin casts, and hyaline casts were detected in some tubular lumens. Pathologic features were consistent with IgAN with Oxford MEST-C classification as M1-E0-S1-T1-C1, and his risk of a 50% decline in estimated glomerular filtration rate or progression to kidney failure within five years was approximately 9.75%, as per a recent risk prediction model by the International IgA Nephropathy Network. He started on Ramipril 10 mg daily, 1 gr pulse Methylprednisolone for one day, following 1mg/kg/day, and fish oil, which was well tolerated. After eight weeks of therapy, the urine protein-creatinine ratio improved to 0.27 g/g, and creatinine remained stable at 0.83 mg/dL.
DISCUSSION
Here we present a patient with probable de novo crescentic IgAN associated with COVID-19 infection. Our patient's Pfizer-BioNTech COVID-19 vaccine and COVID-19 infection triggered a gross hematuria attack.
IgAN is the most common lesion found to cause primary glomerulonephritis throughout most developed countries. Patients may present at any age, but there is a peak incidence in the second and third decades (9). Upper respiratory tract infections often precede the onset or exacerbation of the IgAN. Various immune triggers for IgAN have been published, including staphylococcal infection, vaccination, and viral infection (4-8). Viral infections contribute to the multihit hypothesis of IgAN and trigger a cascade of events, including an increase in circulating galactose-deficient IgA1 (gd-IgA1) antibodies, development of autoreactive antibodies to gd-IgA1, and formation of immune complexes that deposit in various tissues, including the kidney, triggering an inflammatory response (10). IgAN is an immune-complex disease characterized by mesangial IgA1 deposition with or without concurrent IgG and C3 deposits.
Renal manifestations of SARS-CoV-2 infection encompass the spectrum of kidney injury, including increased serum creatinine levels and asymptomatic urinary abnormalities (11). In patients admitted to the hospital with COVID-19, asymptomatic urinary abnormalities like hematuria and proteinuria or AKI are significantly associated with increased mortality (12). Renal biopsy series have been reported reviewing kidney pathology from patients with COVID-19. In 26 biopsies, Su H et al. reported no samples demonstrated hypercellular or inflammatory glomerular lesions, or crescents, despite including patients with hematuria and proteinuria. The most common pathological finding reported was acute tubular injury, which was suggested to be direct viral effects in the proximal tubule epithelium (13).
Our patient presented with gross hematuria 24 hours after SARS-CoV-2 infection and the Pfizer-BioNTech COVID-19 vaccine. While COVID-19-related AKI is seen in relatively severe hospitalized patients, our patient was managed in an outpatient clinic given the mild COVID-19 presentation during the SARS-CoV-2 infection. Gross hematuria regressed spontaneously within three days after the SARS-CoV-2 infection. He had been vaccinated with two doses of CoronaVac (Sinovac) three months after SARS-CoV-2 infection. Furthermore, he had been vaccinated with the Pfizer-BioNTech COVID-19 vaccine one month after the second dose of CoronaVac (Sinovac) vaccine.
Ran E et al. reported a case of crescentic IgAN following the CoronaVac vaccine (14). However, our patient did not describe a hematuria attack after the CoronaVac (Sinovac) vaccine doses. However, he presented with gross hematuria and subnephrotic proteinuria 24 hours after the first dose of the Pfizer-BioNTech COVID-19 vaccine. People who receive mRNA-based vaccines demonstrate robust antibodies against the receptor-binding domain (RBD) of the S1 protein. Similar to natural infection, due to the powerful stimulation of immune response from mRNA-based vaccines compared to other vaccines, the patients may produce de novo antibodies, leading to IgA-containing immune-complex deposits in the kidney. Besides COVID-19 vaccines, influenza and the recombinant zoster vaccine may cause hematuria and flare-up IgA nephropathy (15). In addition, other vaccines, such as hepatitis B, measles, and pneumococcus, have been linked to renal pathologies like nephrotic syndromes (16). Nevertheless, according to some recent studies, developing glomerulonephritis after vaccination against SARS-CoV-2 may be a rare adverse event. They claimed a temporal association was found for IgAN and minimal change disease, but causality was not firmly established (17).
This case highlights the immunological effects of the novel mRNA-based SARS-CoV-2 vaccines. Nephrologists should be aware of new-onset hematuria or proteinuria observed after SARS-CoV-2 infection or mRNA-based SARS-CoV-2 vaccine.
BIBLIOGRAPHY
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4) Koyama A, Sharmin S, Sakurai H, Shimizu Y, Hirayama K, Usui J, et al. Staphylococcus aureus cell envelope antigen is a new candidate for the induction of IgA nephropathy. 2004;66(1):121-32.
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9) Yeo SC, Goh SM, Barratt JJN. Is immunoglobulin A nephropathy different in different ethnic populations? 2019;24(9):885-95.
10) Placzek WJ, Yanagawa H, Makita Y, Renfrow MB, Julian BA, Rizk DV, et al. Serum galactose-deficient-IgA1 and IgG autoantibodies correlate in patients with IgA nephropathy. 2018;13(1): e0190967.
11) Sundaram S, Soni M, Annigeri RJD, Research MSC, Reviews. Urine abnormalities predict acute kidney injury in COVID-19 patients: An analysis of 110 cases in Chennai, South India. 2021;15(1):187-91.
12) Kanbay M, Medetalibeyoglu A, Kanbay A, Cevik E, Tanriover C, Baygul A, et al. Acute kidney injury in hospitalized COVID-19 patients. International urology and nephrology. 2021:1-8.
13) Su H, Yang M, Wan C, Yi LX, Tang F, Zhu HY, et al. Renal histopathological analysis of 26 postmortem findings of patients with COVID-19 in China. Kidney international. 2020;98(1):219-27.
14) Ran E, Wang M, Wang Y, Liu R, Yi Y,Liu Y.New on set crescent Ig A nephropathy following the CoronaVac vaccine.2022. Medicine; 101:33.
15) Kavukcu S, Soylu A, Sarioglu S et al.Ig A nephropathy in mice following repeated adminisitration of conjugated haemophilus influenza type B vaccine.Takai. J Exp Clin Med.1997; 22:167-74.
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Propiedad de la Asociación Regional de Diálisis y Trasplantes Renales de Capital Federal y Provincia de Buenos Aires
Revista de Nefrología, Diálisis y Trasplante
ISSN 2346-8548 (electrónico) - ISSN 0326-3428 (impreso)
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9222580d47c553ea90dc0f5e416f8f3a
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Publications
Changes in brain white matter structure are associated with urine proteins in urologic chronic pelvic pain syndrome (UCPPS): A MAPP Network study.
Woodworth DC, Dagher A, Curatolo A, Sachdev M, Ashe-McNalley C, Naliboff BD, Labus JS, Landis JR, Kutch JJ, Mayer EA, Lee RS, Moses MA, Ellingson BM; MAPP Research Network. Changes in brain white matter structure are associated with urine proteins in urologic chronic pelvic pain syndrome (UCPPS): A MAPP Network study. PLoS One. 2018 Dec 5;13(12):e0206807. doi: 10.1371/journal.pone.0206807. eCollection 2018. [PMID: 30517112] [PMC6281196]
Keywords: Urinary biomarkers; Diffusion tensor imaging; Brainstem; Pain; Urine; Biomarkers; Brain; Neuroimaging.
People
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What Are the Types of ADHD in Teens?
by | Mar 8, 2022
Extracted from an article by David Perlstein, MD, MBA, FAAP edited by William C. Shiel Jr., MD, FACP, FACR
Attention deficit hyperactivity disorder (ADHD) is a behavioral disorder that involves abnormal thought processing. The symptoms of this disorder have been described in the known medical literature for at least the past 200 years. It is characterized by problems focusing, sitting still, and/or controlling impulses. It can have a significantly negative impact on the sufferer’s ability to make and keep friends and other relationships and do well in high school, at work, and/or the community in general. Low self-esteem is a common side effect of the behaviors displayed by a teen with ADHD.
Types of ADHD in Teens
ADHD is understood as either one of three types: the primarily inattentive type, the primarily impulsive/hyperactive type, and the combined type. The primarily inattentive type is characterized by the person having great difficulty listening, focusing, organizing his or herself, and completing tasks. A teen with the inattentive version of ADHD generally does not have a significant problem managing their impulses or activity level. The primarily impulsive/hyperactive type of ADHD tends to result in the opposite set of symptoms compared to the inattentive type. Such a patient will have significant attention problems since he/she has great trouble sitting still, waiting their turn to talk, and managing their impulses. The individual who has the combined type of ADHD struggles with some aspects of inattention, impulsiveness, and hyperactivity.\
What Are Causes and Risk Factors for ADHD in Teens?
ADHD is quite common. Among school-aged children, this disorder has been found to occur from 2%-20%, translating to 4.5 million children 3-17 years of age. While boys are still thought to develop this illness more often than girls, improved assessment of girls has resulted in the gender gap in diagnosis being significantly less than in years past.
ADHD in Teens Causes and Risk Factors
While there is no single known cause of ADHD, boys tend to develop this condition a bit more often than girls, and young people who have one or both parents with the disorder are more likely to develop it. Children who have ADHD are at risk for becoming teenagers and adults with the condition. A child whose mother suffers from depression, smoked cigarettes, or used other drugs or whose parents have lower levels of education are more at risk for having ADHD. Other risk factors for developing ADHD include the person’s mother having medical problems and trauma to the abdomen during their pregnancy. There is some birth order research that supports the theory that first-born children tend to have a higher likelihood of developing ADHD compared to their siblings.
What Are Symptoms and Signs of ADHD in Teens?
Common symptoms and signs of ADHD can include the following:
Inattention
• Trouble paying close attention or making careless mistakes
• Does not seem to be listening when directly spoken to
• Avoids or fails to follow through on instructions or to finish tasks (including homework)
• Has difficulty organizing tasks and activities
• Often avoids or dislikes tasks that require sustained attention
• Frequently loses things needed to perform tasks or activities
• Tendency to get distracted easily
• Often forgetful or inattentive
Hyperactivity and Impulsivity
• Tends to fidget
• Has trouble staying seated when doing so is necessary or expected
• Trouble engaging in activities quietly
• May feel restless or easily bored
• May talk excessively
• Often blurts out answers or interrupts others impulsively
• Frequently has trouble waiting his or her turn during activities
ADHD symptoms and signs in teenagers
While symptoms of hyperactivity in people with ADHD tend to decrease with age, most of the differences in symptoms of this disorder in adolescents compared to children and adults have much to do with the tasks that tweens and teens are called on to do at this stage of their lives. For example, teens with ADHD tend to show lower grade point averages, lower levels of class placement (for example, remedial versus honors or advanced placement), and higher rates of course failure. Also, teens with this diagnosis tend to complete and turn in a much lower percentage of in-class and homework assignments and are much less likely to be working up to their potential. Adolescents with ADHD are significantly more likely to be absent or tardy from school, and they can be over eight times more likely than adolescents without ADHD to drop out of high school. ADHD teens tend to be more impulsive drivers and have more accidents due to risky behaviors. Research has also shown that ADHD teens have more difficulty making and keeping well-adjusted friends. Unfortunately, in the face of the unique and significant impact that ADHD can have on their lives, teens tend to be the least willing to receive treatment compared to their younger and older counterparts. Research shows that adolescents are often more likely to have a negative perception of treatment and to be more likely to expect to have a bad experience as a result of ADHD treatment. Substance abuse is more common in teens with ADHD than their peer non-ADHD population.
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Everything You Need to Know About Bone Pain
Pain is one of the most common medical conditions that you will find worldwide. People everywhere struggle with managing temporary, acute, and chronic pain levels. Sometimes, it originates in the muscle or the joint. In cases like fibromyalgia, it’s believed to originate in the central nervous system and come down through the nerves in the body. In other cases, pain sometimes feels like it’s coming right through the bone. That’s what we’re talking about today – bone pain.
Where does bone pain come from?
If you were to describe bone pain, you might say it’s like a tenderness, extreme aching, or discomfort. The cause of bone pain can vary from injury from trauma, fall, or impact to a deficiency in minerals. Worsely, bone pain might be an early symptom of bone cancer. Therefore, you should never overlook it.
What are the symptoms of bone pain?
Bone pain symptoms can vary widely. It heavily depends on what’s causing the bone pain however the most common sign you have bone pain is discomfort. Beyond that, you may experience weakness, pain that spreads across the body, fatigue, and in some cases, sounds of snapping or grinding. People who suffer from bone pain may find themselves hard to sit or stand for a long period of time. They have to change positions from time to time trying to feel better.
How is bone pain diagnosed?
Bone pain is diagnosed by performing a physical exam. This will determine where the pain is located when it started if it’s been getting worse, and what’s next. Blood tests may be ordered should the doctor suspect there are vitamin or calcium deficiencies or to check for cancer markers. There are also x-rays, bone MRIs, and CT scans that can be performed to determine injury, lesions, or tumors within the bone.
Can bone pain be treated?
In most cases, yes, bone pain can be treated. Assuming the cause of bone pain isn’t anything serious, the focus of treatment is all about remedying the symptom of pain while whatever’s happening heals. In fact, you can find several bone pain treatments at home at Lierre.ca that can help a tremendous amount – all non-pharmaceuticals. Here are some other treatment options:
• The most common prescription for bone pain is a medication like ibuprofen or acetaminophen which will mask the pain. Yunnan Baiyao capsule has an effective function on eliminates blood stasis and hemostatic, promotes blood flow and analgesics, detoxifies and promotes subsidence of swelling. In cases of more severe pain – although rare – morphine and stronger medications may be recommended.
• If you are diagnosed with osteoarthritis, treatment turns to nutritional supplements to increase the amount of calcium and vitamin D levels in the body. You will find a wide range of choices for health products containing vitamin D at pharmacies.
• Antibiotics are provided if the doctor finds that there is some sort of infection affecting the bone.
How can I prevent bone pain?
The best way to prevent pain is to keep your bones strong and healthy. This means exercising, eating right, getting the recommended amounts of calcium and vitamin D, and avoiding smoking. This gives you your best chance of avoiding bone pain. Aside from this, another preparation method can be to ensure you have your anti-pain and bone pain treatments at home. Moreover, be careful during and after working out. Running with the inappropriate position is quite likely to cause bone pain, but fortunately, there are ways to heal the issue. Zheng Gu Shui is known to a lot because of its effects and it is popular in China and Canada. People purchase it for daily protection and use since it can help relieve the pain associated with sports injuries, sprains, bruises
Visit Lierre.ca today for more information on how to minimize pain with at-home pain relief treatments, therapies, and non-Western medicine modalities.
Back painBone painMedecine traditionnelle chinoiseTraditional chinese medicine
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What Are the Roles of Neurotransmitters & How Do Drugs Disrupt Them?
The human body is both wildly complex and masterfully delicate. Each system works in harmony with the others, keeping us alive, helping us think, and triggering our feelings in remarkable ways. At the top of it all (figuratively and literally) sits the brain, the organ that directs all our thought processes and controls every move we make.
With every breath, step, or bite of food, our brain takes in stimuli to help it learn about and respond to the present moment. But just how does it learn? After all, a brain can’t move through the body and see things. How does it know when our stomachs are empty, or when we’re feeling anxious and stressed?
What Are Neurotransmitters?
Neurotransmitters, also known as chemical messengers, are endogenous chemicals that enable neurotransmission.
The answer lies with neurotransmitters. These are chemicals that direct messages from one cell to another, conveying information about the body to the brain. There are over 100 unique types of neurotransmitters in the body, but they can be categorized into a few main types, like:
• Amino acids
• Gasotransmitters
• Monoamines
• Trace amines
• Peptides
• Purines
Neurotransmitters play an important part in all physical processes. They also play a large role in emotional health, as many of them cause either a sedative or stimulative effect on the body. For example, GABA (gamma-aminobutyric acid) and serotonin trigger feelings of calm in the body while dopamine and norepinephrine tend to cause excitement.
What Do They Do?
As Integrative Psychology explains, the human brain is made up of billions of nerve cells constantly connecting with one another to take in information and keep the body functioning. However, these nerve cells (also called neurons) are not in direct contact with one another; they gather information through chemical messages that are delivered as we encounter stimuli.
Simply put, neurotransmitters deliver messages to the brain. Neurotransmitters are located within synaptic vesicles in the neuron. When a cell triggers the synapses, these vesicles release the neurotransmitters, which then get to work relaying messages from nerve cell to nerve cell throughout the body.
In delivering these messages, neurotransmitters help to regulate just about every function in a person’s life; the sleep cycle, pain threshold, cognitive function, and emotional state are all subject to messages by neurotransmitters. For this reason, neurotransmitter imbalances can contribute to a variety of mental health problems like depression, ADHD, and addiction.
How Drugs Affect Neurotransmitters
When someone uses drugs, the substance activates the neurotransmitters. Their response is, ultimately, what causes the euphoric “high” feeling associated with drug use. Different drugs cause different neurotransmitter response, which explains why no two drugs yield the exact same effect.
While the total number of neurotransmitters in the brain is still unknown, scientists (like the people at MIT Medical) have a solid understanding of how drugs affect the most well-known neurotransmitters.
For example, the active ingredient in cannabis, tetrahydrocannabinol (or THC), binds to cannabinoid receptors in the body. Cannabinoid receptors are part of the endocannabinoid system, which helps mediate physical processes like pain reception, hunger, and memory. Activating these receptors causes feelings of calm and happiness, but also impairs memory and cognitive function.
Benzodiazepines like Ativan or Valium activate the GABA-A receptor, which in turn increases the body’s gamma-aminobutyric acid levels. This amino acid and neurotransmitter can calm muscles and induce sleepiness, which is why some individuals are prescribed benzodiazepines to treat insomnia or anxiety disorders.
Stimulants like cocaine affect the 5-HT, NE, and DA receptors. These neurotransmitters increase serotonin levels in the body, which creates feelings of happiness and euphoria. The NE receptor also affects the sympathetic nervous system, which raises heart rate, dilates the pupils, and generally causes feelings of adrenaline and wakefulness.
Even drugs that seem completely safe have an impact on neurotransmitters. Caffeine, for example, activates the adenosine receptors, which regulate neurotransmitters like dopamine and glutamine. As a result, caffeine can promote feelings of wakefulness and alertness, and even suppress pain from headaches, though it can also cause headaches and induce anxiety upon withdrawal.
Neurotransmitter Disruption and Death
Anytime someone uses a drug (whether it is prescribed by a doctor or taken illicitly), they are disrupting their body’s natural neurotransmitter response. Sometimes, this can be a good thing; someone with a mood disorder may need enhanced GABA levels to keep calm, and someone who had a terrible night’s sleep can use some caffeine for a morning boost.
However, neurotransmitter disruption can be dangerous if it occurs in an unsafe environment and with unsafe substances. If individuals overdose on a substance or are impaired past the point of rational decision-making, they will find themselves in serious and potentially fatal situations. The National Institute on Drug Abuse also points out that neurotransmitter disruption can cause long-term or permanent damages to the brain.
The brain is our most complex organ, and it’s also a critically important one. Neurotransmitters are vital cogs in the machine of our brain, helping to relay messages and keep our bodies running effectively. However, when we introduce drugs into the system, it disrupts these pathways and interferes with the way the body and brain communicate. This can lead to devastating results, including death. This is why individuals struggling with drug abuse should seek professional treatment as soon as possible; their lives are on the line.
The Best Place to Recover in Orange County
We are here to help you get sober and learn how to stay that way. Laguna Treatment Hospital is located in Orange County within easy reach of the entire Los Angeles metro. We are the premier chemical dependency recovery hospital in the OC. We offer safe medical detox, mental health support, and wellness programs.
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Memory impairment
MedGen UID:
68579
Concept ID:
C0233794
Mental or Behavioral Dysfunction
Synonyms: Deficit, Memory; Deficits, Memory; Memory Deficit; Memory Deficits
SNOMED CT: Memory impairment (386807006); Memory deficit (386807006); Impaired memory (386807006); Memory problem (386807006); Poor memory (386807006); Bad memory (386807006); Disturbance of memory (386807006)
HPO: HP:0002354
Definition
An impairment of memory as manifested by a reduced ability to remember things such as dates and names, and increased forgetfulness. [from HPO]
Conditions with this feature
Gerstmann-Straussler-Scheinker syndrome
MedGen UID:
4886
Concept ID:
C0017495
Disease or Syndrome
Genetic prion disease generally manifests with cognitive difficulties, ataxia, and myoclonus (abrupt jerking movements of muscle groups and/or entire limbs). The order of appearance and/or predominance of these features and other associated neurologic and psychiatric findings vary. The three major phenotypes of genetic prion disease are genetic Creutzfeldt-Jakob disease (gCJD), fatal familial insomnia (FFI), and Gerstmann-Sträussler-Scheinker (GSS) syndrome. Although these phenotypes display overlapping clinical and pathologic features, recognition of these phenotypes can be useful when providing affected individuals and their families with information about the expected clinical course. The age at onset typically ranges from 50 to 60 years. The disease course ranges from a few months in gCJD and FFI to a few (up to 4, and in rare cases up to 10) years in GSS syndrome.
Lipid proteinosis
MedGen UID:
6112
Concept ID:
C0023795
Disease or Syndrome
Lipoid proteinosis (LP) is characterized by deposition of hyaline-like material in various tissues resulting in a hoarse voice from early infancy, vesicles and hemorrhagic crusts in the mouth and on the face and extremities, verrucous and keratotic cutaneous lesions on extensor surfaces (especially the elbows), and moniliform blepharosis (multiple beaded papules along the eyelid margins and inner canthus). Extracutaneous manifestations may include epilepsy, neuropsychiatric disorders, spontaneous CNS hemorrhage, and asymptomatic multiple yellowish nodules throughout the gastrointestinal tract. Generally, the disease course is chronic and fluctuating. Males and females are affected equally. Affected individuals have a normal life span unless they experience laryngeal obstruction.
Myxedema
MedGen UID:
6506
Concept ID:
C0027145
Disease or Syndrome
A condition characterized by severe hypothyroidism that is caused by autoimmune thyroid gland disorders, surgical reduction of thyroid tissue, radiation exposure, and viral infections. Signs and symptoms include generalized fatigue, lethargy, increased body weight, pale, edematous and thickened skin, low blood pressure, constipation and cold intolerance.
Wernicke-Korsakoff syndrome
MedGen UID:
83883
Concept ID:
C0349464
Mental or Behavioral Dysfunction
A psychotic syndrome caused by damage to the brain by lack of thiamine (vitamin B1). Signs and symptoms include anterograde and retrograde amnesia, confabulation, apathy, ataxia, and coma.
Inherited Creutzfeldt-Jakob disease
MedGen UID:
155837
Concept ID:
C0751254
Disease or Syndrome
Genetic prion disease generally manifests with cognitive difficulties, ataxia, and myoclonus (abrupt jerking movements of muscle groups and/or entire limbs). The order of appearance and/or predominance of these features and other associated neurologic and psychiatric findings vary. The three major phenotypes of genetic prion disease are genetic Creutzfeldt-Jakob disease (gCJD), fatal familial insomnia (FFI), and Gerstmann-Sträussler-Scheinker (GSS) syndrome. Although these phenotypes display overlapping clinical and pathologic features, recognition of these phenotypes can be useful when providing affected individuals and their families with information about the expected clinical course. The age at onset typically ranges from 50 to 60 years. The disease course ranges from a few months in gCJD and FFI to a few (up to 4, and in rare cases up to 10) years in GSS syndrome.
Frontotemporal dementia and/or amyotrophic lateral sclerosis 7
MedGen UID:
318833
Concept ID:
C1833296
Disease or Syndrome
CHMP2B frontotemporal dementia (CHMP2B-FTD) has been described in a single family from Denmark, in one individual with familial FTD from Belgium, and in one individual with FTD and no family history. It typically starts between ages 46 and 65 years with subtle personality changes and slowly progressive behavioral changes, dysexecutive syndrome, dyscalculia, and language disturbances. Disinhibition or loss of initiative is the most common presenting symptom. The disease progresses over a few years into profound dementia with extrapyramidal symptoms and mutism. Several individuals have developed an asymmetric akinetic rigid syndrome with arm and gait dystonia and pyramidal signs that may be related to treatment with neuroleptic drugs. Symptoms and disease course are highly variable. Disease duration may be as short as three years or longer than 20 years.
Supranuclear palsy, progressive, 2
MedGen UID:
324446
Concept ID:
C1836148
Disease or Syndrome
Fragile X-associated tremor/ataxia syndrome
MedGen UID:
333403
Concept ID:
C1839780
Disease or Syndrome
FMR1 disorders include fragile X syndrome (FXS), fragile X-associated tremor/ataxia syndrome (FXTAS), and fragile X-associated primary ovarian insufficiency (FXPOI). Fragile X syndrome occurs in individuals with an FMR1 full mutation or other loss-of-function variant and is nearly always characterized in affected males by developmental delay and intellectual disability along with a variety of behavioral issues. Autism spectrum disorder is present in 50%-70% of individuals with FXS. Affected males may have characteristic craniofacial features (which become more obvious with age) and medical problems including hypotonia, gastroesophageal reflux, strabismus, seizures, sleep disorders, joint laxity, pes planus, scoliosis, and recurrent otitis media. Adults may have mitral valve prolapse or aortic root dilatation. The physical and behavioral features seen in males with FXS have been reported in females heterozygous for the FMR1 full mutation, but with lower frequency and milder involvement. FXTAS occurs in individuals who have an FMR1 premutation and is characterized by late-onset, progressive cerebellar ataxia and intention tremor followed by cognitive impairment. Psychiatric disorders are common. Age of onset is typically between 60 and 65 years and is more common among males who are hemizygous for the premutation (40%) than among females who are heterozygous for the premutation (16%-20%). FXPOI, defined as hypergonadotropic hypogonadism before age 40 years, has been observed in 20% of women who carry a premutation allele compared to 1% in the general population.
Alzheimer disease 3
MedGen UID:
334304
Concept ID:
C1843013
Disease or Syndrome
Alzheimer's disease can be classified as early-onset or late-onset. The signs and symptoms of the early-onset form appear between a person's thirties and mid-sixties, while the late-onset form appears during or after a person's mid-sixties. The early-onset form of Alzheimer's disease is much less common than the late-onset form, accounting for less than 10 percent of all cases of Alzheimer's disease.\n\nIndividuals with Alzheimer's disease usually survive 8 to 10 years after the appearance of symptoms, but the course of the disease can range from 1 to 25 years. Survival is usually shorter in individuals diagnosed after age 80 than in those diagnosed at a younger age. In Alzheimer's disease, death usually results from pneumonia, malnutrition, or general body wasting (inanition).\n\nAs the disorder progresses, some people with Alzheimer's disease experience personality and behavioral changes and have trouble interacting in a socially appropriate manner. Other common symptoms include agitation, restlessness, withdrawal, and loss of language skills. People with Alzheimer's disease usually require total care during the advanced stages of the disease.\n\nMemory loss is the most common sign of Alzheimer's disease. Forgetfulness may be subtle at first, but the loss of memory worsens over time until it interferes with most aspects of daily living. Even in familiar settings, a person with Alzheimer's disease may get lost or become confused. Routine tasks such as preparing meals, doing laundry, and performing other household chores can be challenging. Additionally, it may become difficult to recognize people and name objects. Affected people increasingly require help with dressing, eating, and personal care.\n\nAlzheimer's disease is a degenerative disease of the brain that causes dementia, which is a gradual loss of memory, judgment, and ability to function. This disorder usually appears in people older than age 65, but less common forms of the disease appear earlier in adulthood.
GRN-related frontotemporal lobar degeneration with Tdp43 inclusions
MedGen UID:
375285
Concept ID:
C1843792
Disease or Syndrome
The spectrum of GRN frontotemporal dementia (GRN-FTD) includes the behavioral variant (bvFTD), primary progressive aphasia (PPA; further subcategorized as progressive nonfluent aphasia [PNFA] and semantic dementia [SD]), and movement disorders with extrapyramidal features such as parkinsonism and corticobasal syndrome (CBS). A broad range of clinical features both within and between families is observed. The age of onset ranges from 35 to 87 years. Behavioral disturbances are the most common early feature, followed by progressive aphasia. Impairment in executive function manifests as loss of judgment and insight. In early stages, PPA often manifests as deficits in naming, word finding, or word comprehension. In late stages, affected individuals often become mute and lose their ability to communicate. Early findings of parkinsonism include rigidity, bradykinesia or akinesia (slowing or absence of movements), limb dystonia, apraxia (loss of ability to carry out learned purposeful movements), and disequilibrium. Late motor findings may include myoclonus, dysarthria, and dysphagia. Most affected individuals eventually lose the ability to walk. Disease duration is three to 12 years.
Hereditary spastic paraplegia 7
MedGen UID:
339552
Concept ID:
C1846564
Disease or Syndrome
Spastic paraplegia 7 (SPG7) is characterized by insidiously progressive bilateral leg weakness and spasticity. Most affected individuals have decreased vibration sense and cerebellar signs. Onset is mostly in adulthood, although symptoms may start as early as age 11 years and as late as age 72 years. Additional features including ataxia (gait and limbs), spastic dysarthria, dysphagia, pale optic disks, ataxia, nystagmus, strabismus, ptosis, hearing loss, motor and sensory neuropathy, amyotrophy, scoliosis, pes cavus, and urinary sphincter disturbances may be observed.
Alzheimer disease 4
MedGen UID:
376072
Concept ID:
C1847200
Disease or Syndrome
Alzheimer's disease is a degenerative disease of the brain that causes dementia, which is a gradual loss of memory, judgment, and ability to function. This disorder usually appears in people older than age 65, but less common forms of the disease appear earlier in adulthood.\n\nMemory loss is the most common sign of Alzheimer's disease. Forgetfulness may be subtle at first, but the loss of memory worsens over time until it interferes with most aspects of daily living. Even in familiar settings, a person with Alzheimer's disease may get lost or become confused. Routine tasks such as preparing meals, doing laundry, and performing other household chores can be challenging. Additionally, it may become difficult to recognize people and name objects. Affected people increasingly require help with dressing, eating, and personal care.\n\nAs the disorder progresses, some people with Alzheimer's disease experience personality and behavioral changes and have trouble interacting in a socially appropriate manner. Other common symptoms include agitation, restlessness, withdrawal, and loss of language skills. People with Alzheimer's disease usually require total care during the advanced stages of the disease.\n\nIndividuals with Alzheimer's disease usually survive 8 to 10 years after the appearance of symptoms, but the course of the disease can range from 1 to 25 years. Survival is usually shorter in individuals diagnosed after age 80 than in those diagnosed at a younger age. In Alzheimer's disease, death usually results from pneumonia, malnutrition, or general body wasting (inanition).\n\nAlzheimer's disease can be classified as early-onset or late-onset. The signs and symptoms of the early-onset form appear between a person's thirties and mid-sixties, while the late-onset form appears during or after a person's mid-sixties. The early-onset form of Alzheimer's disease is much less common than the late-onset form, accounting for less than 10 percent of all cases of Alzheimer's disease.
Spinocerebellar ataxia type 14
MedGen UID:
343106
Concept ID:
C1854369
Disease or Syndrome
Spinocerebellar ataxia type 14 (SCA14) is characterized by slowly progressive cerebellar ataxia, dysarthria, and nystagmus. Axial myoclonus, cognitive impairment, tremor, and sensory loss may also be observed. Parkinsonian features including rigidity and tremor have been described in some families. Findings seen in other ataxia disorders (e.g., dysphagia, dysphonia) may also occur in SCA14. The average age of onset is in the 30s, with a range from childhood to the seventh decade. Life span is not shortened.
Vanishing white matter disease
MedGen UID:
347037
Concept ID:
C1858991
Disease or Syndrome
Childhood ataxia with central nervous system hypomyelination / vanishing white matter (CACH/VWM) is characterized by ataxia, spasticity, and variable optic atrophy. The phenotypic range includes a prenatal/congenital form, a subacute infantile form (onset age <1 year), an early childhood-onset form (onset age 1 to <4 years), a late childhood-/juvenile-onset form (onset age 4 to <18 years), and an adult-onset form (onset =18 years). The prenatal/congenital form is characterized by severe encephalopathy. In the later-onset forms initial motor and intellectual development is normal or mildly delayed, followed by neurologic deterioration with a chronic progressive or subacute course. While in childhood-onset forms motor deterioration dominates, in adult-onset forms cognitive decline and personality changes dominate. Chronic progressive decline can be exacerbated by rapid deterioration during febrile illnesses or following head trauma or major surgical procedures, or by acute and extreme fright.
Alzheimer disease 10
MedGen UID:
351228
Concept ID:
C1864828
Disease or Syndrome
An Alzheimer's disease that is characterized by an associated with variation in the region 7q36.
Hereditary spastic paraplegia 4
MedGen UID:
401097
Concept ID:
C1866855
Disease or Syndrome
Spastic paraplegia 4 (SPG4; also known as SPAST-HSP) is characterized by insidiously progressive bilateral lower-limb gait spasticity. More than 50% of affected individuals have some weakness in the legs and impaired vibration sense at the ankles. Sphincter disturbances are very common. Onset is insidious, mostly in young adulthood, although symptoms may start as early as age one year and as late as age 76 years. Intrafamilial variation is considerable.
Spastic ataxia 1
MedGen UID:
409988
Concept ID:
C1970107
Disease or Syndrome
Hereditary spastic ataxia comprises a heterogeneous group of progressive neurodegenerative disorders characterized by lower-limb spasticity and generalized ataxia with dysarthria, impaired ocular movements, and gait disturbance. Spastic ataxia-1 (SPAX1) is an autosomal dominant form of the disorder with onset between the ages of 10 and 20 years. Other clinical features are supranuclear gaze palsy, hyperreflexia, hypertonicity, dystonia, pes cavus, mild ptosis, and decreased vibration sense in the lower limbs. Symptom severity is variable, but neither life span nor cognition is affected (summary by Meijer et al., 2002 and Bourassa et al., 2012). Genetic Heterogeneity of Spastic Ataxia See also SPAX2 (611302), caused by mutation in the KIF1C gene (603060) on chromosome 17p13; SPAX3 (611390), caused by rearrangements of the MARS2 gene (609728) on chromosome 2q33; SPAX4 (613672), caused by mutation in the MTPAP gene (613669) on chromosome 10p11; SPAX5 (614487), caused by mutation in the AFG3L2 gene (604581) on chromosome 18p11; SPAX6 (270550), caused by mutation in the SACS gene (604490) on chromosome 13q12; SPAX7 (108650); SPAX8 (617560), caused by mutation in the NKX6-2 gene (605955) on chromosome 8q21; and SPAX9 (618438), caused by mutation in the CHP1 gene (606988) on chromosome 15q15.
Chromosome 15q11.2 deletion syndrome
MedGen UID:
467404
Concept ID:
C3180937
Disease or Syndrome
A heterozygous deletion of chromosome 15q11.2 may increase the susceptibility to neuropsychiatric or neurodevelopmental problems, including delayed psychomotor development, speech delay, autism spectrum disorder, attention deficit-hyperactivity disorder, obsessive-compulsive disorder, and possibly seizures (summary by Doornbos et al., 2009 and Burnside et al., 2011). See also chromosome 15q11.2 duplication syndrome (608636).
Hereditary sensory neuropathy-deafness-dementia syndrome
MedGen UID:
481515
Concept ID:
C3279885
Disease or Syndrome
DNMT1-related disorder is a degenerative disorder of the central and peripheral nervous systems comprising a phenotypic spectrum that includes hereditary sensory and autonomic neuropathy type 1E (HSAN1E) and autosomal dominant cerebellar ataxia, deafness, and narcolepsy (ADCA-DN). DNMT1 disorder is often characterized by moderate-to-severe sensorineural hearing loss beginning in the teens or early 20s, sensory impairment, sudomotor dysfunction (loss of sweating), and dementia usually beginning in the mid-40s. In some affected individuals, narcolepsy/cataplexy syndrome and ataxia are predominant findings.
Autosomal dominant cerebellar ataxia, deafness and narcolepsy
MedGen UID:
813625
Concept ID:
C3807295
Disease or Syndrome
ADCADN is an autosomal dominant neurologic disorder characterized by adult onset of progressive cerebellar ataxia, narcolepsy/cataplexy, sensorineural deafness, and dementia. More variable features include optic atrophy, sensory neuropathy, psychosis, and depression (summary by Winkelmann et al., 2012).
Basal ganglia calcification, idiopathic, 6
MedGen UID:
901404
Concept ID:
C4225335
Disease or Syndrome
Primary familial brain calcification (PFBC) is a neurodegenerative disorder with characteristic calcium deposits in the basal ganglia and other brain areas visualized on neuroimaging. Most affected individuals are in good health during childhood and young adulthood and typically present in the fourth to fifth decade with a gradually progressive movement disorder and neuropsychiatric symptoms. The movement disorder first manifests as clumsiness, fatigability, unsteady gait, slow or slurred speech, dysphagia, involuntary movements, or muscle cramping. Neuropsychiatric symptoms, often the first or most prominent manifestations, range from mild difficulty with concentration and memory to changes in personality and/or behavior, to psychosis and dementia. Seizures of various types occur frequently, some individuals experience chronic headache and vertigo; urinary urgency or incontinence may be present.
Alzheimer disease 9
MedGen UID:
924255
Concept ID:
C4282179
Finding
Idiopathic basal ganglia calcification 1
MedGen UID:
1637664
Concept ID:
C4551624
Disease or Syndrome
Primary familial brain calcification (PFBC) is a neurodegenerative disorder with characteristic calcium deposits in the basal ganglia and other brain areas visualized on neuroimaging. Most affected individuals are in good health during childhood and young adulthood and typically present in the fourth to fifth decade with a gradually progressive movement disorder and neuropsychiatric symptoms. The movement disorder first manifests as clumsiness, fatigability, unsteady gait, slow or slurred speech, dysphagia, involuntary movements, or muscle cramping. Neuropsychiatric symptoms, often the first or most prominent manifestations, range from mild difficulty with concentration and memory to changes in personality and/or behavior, to psychosis and dementia. Seizures of various types occur frequently, some individuals experience chronic headache and vertigo; urinary urgency or incontinence may be present.
Cerebral arteriopathy, autosomal dominant, with subcortical infarcts and leukoencephalopathy, type 1
MedGen UID:
1634330
Concept ID:
C4551768
Disease or Syndrome
CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) is characterized by mid-adult onset of recurrent ischemic stroke, cognitive decline progressing to dementia, a history of migraine with aura, mood disturbance, apathy, and diffuse white matter lesions and subcortical infarcts on neuroimaging.
Supranuclear palsy, progressive, 1
MedGen UID:
1640811
Concept ID:
C4551863
Disease or Syndrome
The spectrum of clinical manifestations of MAPT-related frontotemporal dementia (MAPT-FTD) has expanded from its original description of frontotemporal dementia and parkinsonian manifestations to include changes in behavior, motor function, memory, and/or language. A recent retrospective study suggested that the majority of affected individuals have either behavioral changes consistent with a diagnosis of behavioral variant FTD (bvFTD) or, less commonly, a parkinsonian syndrome (i.e., progressive supranuclear palsy, corticobasal syndrome, or Parkinson disease). Fewer than 5% of people with MAPT-FTD have primary progressive aphasia or Alzheimer disease. Clinical presentation may differ between and within families with the same MAPT variant. MAPT-FTD is a progressive disorder that commonly ends with a relatively global dementia in which some affected individuals become mute. Progression of motor impairment in affected individuals results in some becoming chairbound and others bedbound. Mean disease duration is 9.3 (SD: 6.4) years but is individually variable and can be more than 30 years in some instances.
Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy 1
MedGen UID:
1648386
Concept ID:
C4721893
Disease or Syndrome
Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL) is characterized by fractures (resulting from radiologically demonstrable polycystic osseous lesions), frontal lobe syndrome, and progressive presenile dementia beginning in the fourth decade. The clinical course of PLOSL can be divided into four stages: 1. The latent stage is characterized by normal early development. 2. The osseous stage (3rd decade of life) is characterized by pain and tenderness, mostly in ankles and feet, usually following strain or injury. Fractures are typically diagnosed several years later, most commonly in the bones of the extremities. 3. In the early neurologic stage (4th decade of life), a change of personality begins to develop insidiously. Affected individuals show a frontal lobe syndrome (loss of judgment, euphoria, loss of social inhibitions, disturbance of concentration, and lack of insight, libido, and motor persistence) leading to serious social problems. 4. The late neurologic stage is characterized by progressive dementia and loss of mobility. Death usually occurs before age 50 years.
Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy 2
MedGen UID:
1648374
Concept ID:
C4748657
Disease or Syndrome
Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy-2 (PLOSL2), or Nasu-Hakola disease, is a recessively inherited presenile frontal dementia with leukoencephalopathy and basal ganglia calcification. In most cases the disorder first manifests in early adulthood as pain and swelling in ankles and feet, followed by bone fractures. Neurologic symptoms manifest in the fourth decade of life as a frontal lobe syndrome with loss of judgment, euphoria, and disinhibition. Progressive decline in other cognitive domains begins to develop at about the same time. The disorder culminates in a profound dementia and death by age 50 years (summary by Klunemann et al., 2005). For a discussion of genetic heterogeneity of polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy, see 221770.
Progressive myoclonic epilepsy type 6
MedGen UID:
1681379
Concept ID:
C5190805
Disease or Syndrome
Progressive myoclonic epilepsy-6 is an autosomal recessive neurologic disorder characterized by onset of ataxia in the first years of life, followed by action myoclonus and seizures later in childhood, and loss of independent ambulation in the second decade. Cognition is not usually affected, although mild memory difficulties may occur in the third decade (summary by Corbett et al., 2011). For a discussion of genetic heterogeneity of progressive myoclonic epilepsy, see EPM1A (254800).
Basal ganglia calcification, idiopathic, 7, autosomal recessive
MedGen UID:
1683911
Concept ID:
C5193025
Disease or Syndrome
Autosomal recessive idiopathic basal ganglia calcification-7 is a neurologic disorder characterized by onset of symptoms in adulthood. Patients present with dysarthria, gait abnormalities, various movement abnormalities, and often cognitive decline. Brain imaging shows abnormal accumulation of calcium deposits in deep brain regions, including the basal ganglia, thalamus, dentate nuclei, cerebellum, and sometimes other areas of the brain and spinal cord. Some patients with brain imaging abnormalities may be clinically asymptomatic (summary by Yao et al., 2018). For a detailed phenotypic description and a discussion of genetic heterogeneity of IBGC, see IBGC1 (213600).
Frontotemporal dementia and/or amyotrophic lateral sclerosis 8
MedGen UID:
1728824
Concept ID:
C5436881
Disease or Syndrome
Frontotemporal dementia and/or amyotrophic lateral sclerosis-8 (FTDALS8) is an autosomal dominant neurodegenerative disorder characterized by adult-onset dementia manifest as memory impairment, executive dysfunction, and behavioral or personality changes. Some patients may develop ALS or parkinsonism. Neuropathologic studies show frontotemporal lobar degeneration (FTLD) with tau (MAPT; 157140)- and TDP43 (605078)-immunoreactive inclusions (summary by Dobson-Stone et al., 2020). For a discussion of genetic heterogeneity of FTDALS, see FTDALS1 (105550).
Amyotrophic lateral sclerosis 26 with or without frontotemporal dementia
MedGen UID:
1771903
Concept ID:
C5436882
Disease or Syndrome
Amyotrophic lateral sclerosis-26 with or without frontotemporal dementia (ALS26) is an autosomal dominant neurodegenerative disorder characterized by adult onset of upper and low motor neuron disease causing bulbar dysfunction and limb weakness (ALS). Patients may also develop frontotemporal dementia (FTD) manifest as primary progressive aphasia, memory impairment, executive dysfunction, and behavioral or personality changes. Although patients may present with 1 or the other diseases, all eventually develop ALS. Neuropathologic studies of the brain and spinal cord show TDP43 (605078)-immunoreactive cytoplasmic inclusions that correlate with clinical features and Lewy body-like cytoplasmic inclusions in lower motor neurons (summary by Mackenzie et al., 2017). For a discussion of genetic heterogeneity of amyotrophic lateral sclerosis, see ALS1 (105400).
Leukoencephalopathy, diffuse hereditary, with spheroids 1
MedGen UID:
1794139
Concept ID:
C5561929
Disease or Syndrome
CSF1R-related adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) is characterized by executive dysfunction, memory decline, personality changes, motor impairments, and seizures. A frontal lobe syndrome (e.g., loss of judgment, lack of social inhibitors, lack of insight, and motor persistence) usually appears early in the disease course. The mean age of onset is usually in the fourth decade. Affected individuals eventually become bedridden with spasticity and rigidity. The disease course ranges from two to 30 or more years (mean: 8 years).
Combined oxidative phosphorylation deficiency 54
MedGen UID:
1812715
Concept ID:
C5676912
Disease or Syndrome
Combined oxidative phosphorylation deficiency-54 (COXPD54) is an autosomal recessive disorder with pleiotropic multisystem presentations resulting from a disruption in mitochondrial transcription and translation. The phenotype is highly variable. Many patients have early-onset sensorineural hearing loss, sometimes in isolation, and sometimes associated with global developmental delay or primary ovarian failure. Other features may include peripheral hypertonia, seizures, muscle weakness, behavioral abnormalities, and leukoencephalopathy on brain imaging. Serum lactate may or may not be elevated (summary by Hochberg et al., 2021). For a discussion of genetic heterogeneity of combined oxidative phosphorylation deficiency, see COXPD1 (609060).
Intellectual developmental disorder, autosomal recessive 75, with neuropsychiatric features and variant lissencephaly
MedGen UID:
1808159
Concept ID:
C5676961
Disease or Syndrome
Autosomal recessive intellectual developmental disorder-75 with neuropsychiatric features and variant lissencephaly (MRT75) is characterized by global developmental delay apparent from infancy or early childhood and moderate to profoundly impaired intellectual development. Most affected individuals have behavioral abnormalities, including aggression and ADHD; a few have psychiatric manifestations, including psychosis. More variable additional features include well-controlled seizures and dysmorphic facial features. Brain imaging often shows frontal predominant pachygyria or other gyri/sulci abnormalities, consistent with a variant of lissencephaly and a malformation of cortical development (MCD) (summary by Zaki et al., 2021).
Professional guidelines
PubMed
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Recent clinical studies
Etiology
Yu XD, Zhang D, Xiao CL, Zhou Y, Li X, Wang L, He Z, Reilly J, Xiao ZY, Shu X
Cells 2022 May 10;11(10) doi: 10.3390/cells11101594. PMID: 35626632Free PMC Article
Alhowail A
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Sanford AM
Clin Geriatr Med 2017 Aug;33(3):325-337. Epub 2017 May 17 doi: 10.1016/j.cger.2017.02.005. PMID: 28689566
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Lee H, Roh S, Kim DJ
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Diagnosis
Kirsch-Darrow L, Tsao JW
Continuum (Minneap Minn) 2021 Dec 1;27(6):1670-1681. doi: 10.1212/CON.0000000000001075. PMID: 34881731
Henry JD
Nat Rev Neurol 2021 May;17(5):297-307. Epub 2021 Mar 8 doi: 10.1038/s41582-021-00472-1. PMID: 33686303
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Curr Alzheimer Res 2019;16(11):975-985. doi: 10.2174/1567205016666191113125303. PMID: 31724515
Sanford AM
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Therapy
Wang Q, Du W, Wang H, Geng P, Sun Y, Zhang J, Wang W, Jin X
Prog Neuropsychopharmacol Biol Psychiatry 2023 Jun 8;124:110723. Epub 2023 Feb 1 doi: 10.1016/j.pnpbp.2023.110723. PMID: 36736944
Naomi R, Embong H, Othman F, Ghazi HF, Maruthey N, Bahari H
Nutrients 2021 Dec 22;14(1) doi: 10.3390/nu14010020. PMID: 35010895Free PMC Article
Anagha K, Shihabudheen P, Uvais NA
Prim Care Companion CNS Disord 2021 Jul 29;23(4) doi: 10.4088/PCC.20m02747. PMID: 34324797
Nakazaki E, Mah E, Sanoshy K, Citrolo D, Watanabe F
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Geng J, Dong J, Ni H, Lee MS, Wu T, Jiang K, Wang G, Zhou AL, Malouf R
Cochrane Database Syst Rev 2010 Dec 8;(12):CD007769. doi: 10.1002/14651858.CD007769.pub2. PMID: 21154383
Prognosis
O'Sullivan MJ, Li X, Galligan D, Pendlebury ST
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Skip to main content
Similar immune mechanisms control experimental airway eosinophilia elicited by different allergens and treatment protocols
Abstract
Background
Mouse models have been extremely valuable in identifying the fundamental mechanisms of airway inflammation that underlie human allergic asthma. Several models are commonly used, employing different methods and routes of sensitisation, and allergens of varying clinical relevance. Although all models elicit similar hallmarks of allergic airway inflammation, including airway eosinophilia, goblet cell hyperplasia and cellular infiltration in lung, it is not established whether they do so by involving the same mechanisms.
Results
We compared the impact of inactivation of various innate or adaptive immune genes, as well as sex, in different models of allergic airway inflammation in mice of C57BL/6 background. Chicken ovalbumin (OVA) and house dust mite (HDM) were used as allergens in settings of single or multiple intranasal (i.n.) challenges, after sensitisation in adjuvant or in adjuvant-free conditions. Eosinophil numbers in the broncho-alveolar lavage and lung histopathology were assessed in each model. We found that Major Histocompatibility Complex Class II (MHCII) deficiency and lack of conventional CD4+ T cells had the most profound effect, essentially ablating airway eosinophilia and goblet cell hyperplasia in all models. In contrast, Thymic stromal lymphopoietin receptor (TSLPR) deficiency greatly reduced eosinophilia but had a variable effect on goblet cells. CD1d deficiency and lack of Natural Killer T (NKT) cells moderately impaired inflammation in OVA models but not HDM, whereas sex affected the response to HDM but not OVA. Lastly, defective Toll-like receptor (TLR)4 expression had only a relatively modest overall impact on inflammation.
Conclusion
All the models studied were comparably dependent on adaptive CD4+ T cell responses and TSLP. In contrast, sex, NKT cells and TLR4 appeared to play subtler and more variable roles that were dependent on the type of allergen and mode of immunization and challenge. These results are consistent with clinical data suggesting a key role of CD4+ T cells and TSLP in patients with allergic asthma.
Background
Allergic disease is caused by the inappropriate activation of Th2 cells in response to harmless or non-infectious stimuli such as pollens, foods or insect stings. In allergic individuals, Th2 recognition of allergens in the context of antigen presenting cells triggers the release of cytokines, including Interleukin (IL)-3, IL-4, IL-5 and IL-13, which underlie the typical allergic pathology with recruitment of mast cells and eosinophils, mucus production, IgE and tissue remodeling [1].
In the airway, allergic disease is elicited by allergen inhalation and manifests itself with the typical asthma symptoms of tightness of chest and reduced lung function. Broncho-alveolar lavage of segmentally challenged allergic asthma patients has revealed the presence of eosinophils and Th2 cells in the airway with increased mucin, Th2 cytokines and increased smooth muscle mass [2]. Animal models of allergic airway inflammation faithfully replicate several of these hallmarks of the late asthmatic response: type 2-associated cytokines such as IL-4, IL-5 and IL-13 can be found in the broncho-alveolar lavage (BAL) and are responsible for the observed inflammatory pathologies [3, 4].
Chicken ovalbumin (OVA) has been used extensively as a model allergen, proving valuable in elucidating many features of airway disease. OVA is inexpensive and readily available, with well-characterized MHCI and MHCII epitopes. In addition, the availability of the OVA-specific OTI and OTII T cell receptor transgenic mice greatly facilitates the monitoring of OVA-specific immune responses in airways and local lymph nodes [5]. These features have made OVA a reagent of choice when studying the cellular mechanisms underlying airway inflammatory responses. However, although OVA is not a completely irrelevant allergen, as food allergies to egg are relatively common in humans [6], it is not clinically relevant as an airway allergen. In addition, OVA is not naturally immunogenic upon inhalation, and can induce tolerance [7] unless supplemented with low doses of LPS [8]. In order to sensitise to allergic airway inflammation, OVA is normally used adsorbed to the adjuvant aluminium hydroxide and must be administered via the non-physiological i.p. route, thus bypassing the airway innate immune environment during sensitisation [9]. Due to these drawbacks, the clinical relevance of information obtained using the OVA model has been questioned by some investigators.
Other allergens of higher clinical relevance being used in experimental airway allergy models include the house dust mite (HDM) Dermatophagoides pteronyssinus, cockroach, and the fungus Alternaria alternata. These allergens can sensitise mice when given via i.n. instillation without adjuvant, and indeed asthma patients are commonly atopic against one or more of them. One of their common features is the harbouring of innate properties, such as protease activity that can directly affect lung epithelium and other cell populations [10, 11], or the ability to engage Toll-like receptors (TLR) through protein mimicry [12], thereby eliciting epithelial cell production of alarmins and cytokines such as IL-33, thymic stromal lymphopoietin (TSLP) and IL-25 [13]. These cytokines act on multiple cell types including dendritic cells (DC) and pathogenic Th2 cells [14], and can also induce the production of IL-5 and IL-13 from local innate immune cell populations such as type-2 innate lymphoid cells (ILC2) independently of conventional Th2 cells [15,16,17]. Therefore, the innate properties of allergens may have a substantial impact on the cell populations involved in allergic responses in different models.
In this study, we wished to assess to what degree the choice of allergen can affect the mechanism of allergic airway inflammation in different experimental models. We compared four models, which use the allergens OVA or HDM and employ different protocols of allergen sensitisation and challenge, focusing on airway eosinophilia and goblet cell hyperplasia as these responses can be elicited by either ILC2 or CD4+ Th2 cells. We compared these models in different strains of knockout (KO) mice that are defective in selected components of the adaptive or innate immune response, and found that, in most cases, allergic inflammation was comparably reduced in each KO strain across all four models, with the degree of reduction ranging from mild to strong. Our results reveal notable similarities, but also some subtle differences, in the molecules and cell types driving each model, thus suggesting the involvement of similar immunological mechanisms in each case.
Results
Airway eosinophilia and goblet cell hyperplasia can be induced in mice using several protocols of allergen immunization and challenge
We aimed to compare the role of key immunological mechanisms in various models of allergic airway inflammation that are commonly used in the literature. To this end, we selected two models using OVA as the model allergen [18]. Both models utilize an identical protocol of sensitisation in which 2 μg of OVA adsorbed to alum is administered intraperitoneally at days 0 and 14. As a negative control, phosphate-buffered saline (PBS) and alum were used during sensitisation, whilst the airway challenges remained the same. In the “acute” model (Fig. 1a), a single challenge of low-endotoxin OVA was administered i.n. 10 days after the second sensitisation. In the “repeat challenge” model (Fig. 1b), three i.n. instillations were applied at one-week intervals. In both models, BAL was harvested 3 days after the final challenge to analyse inflammatory cell populations in the airway by flow cytometry. In addition, lungs were collected at endpoint to document histological changes. In both models we observed higher frequency and number of eosinophils in BAL, and higher numbers of neutrophils and T cells (Additional file 1) which did not increase, or even decreased, with multiple i.n. challenges. Development of peribronchial and perivascular inflammation in the lungs (Fig. 1) and PAS-positive staining in the bronchiolar epithelium (Fig. 1, with quantification as percent of PAS-positive staining in epithelium in Additional file 2B) were observed in both models. Unlike eosinophil numbers, PAS-positive staining increased with multiple challenges.
Fig. 1
figure 1
Features of allergic airway inflammation induced using different models. (ad) Mice were treated according to the protocols shown on the left; PBS mice were sensitised with PBS/alum, or PBS only for the local HDM model. Five to seven experiments were performed for each model, for a total of 21–31 mice per group. Bar graphs show mean + SEM of the combined results from all experiments in each model; please note that y-axes differ across models. Representative micrographs of lung histology are taken from mice with eosinophil numbers similar to the mean. Scale bars represent 200 μm. ***, p < 0.001; **, p < 0.01; *, p < 0.05; ns, not significant
We also used two models of allergic airway inflammation with HDM as the allergen. In the systemic sensitisation model [19], HDM extract or PBS in alum were injected i.p. once, followed 10 days later by a single i.n. challenge of the same HDM extract (Fig. 1c). BAL and lung tissue were harvested for analysis 4 days after challenge, revealing a marked eosinophil infiltrate in the airway, extensive peribronchial and perivascular inflammation, and PAS-positive staining in the bronchiolar epithelium (Additional file 2B). Neutrophils and T cells were also elevated (Additional file 1).
In the local sensitisation model (Fig. 1d), HDM or PBS were given by i.n. instillation without adjuvant, to mimic the natural exposure to airborne allergens via the nose and airway tract. Sensitisation was followed by three HDM i.n. challenges on days 14–16 [20], with BAL and tissue harvest on day 17. Compared to other models, the number of total BAL cells was lower in the immunised group, and higher in the PBS controls. Total eosinophils in the airway were clearly increased compared to control mice, although lower than in other models. Neutrophil numbers were highest in this model, likely due to BAL being carried out the next day after the last HDM challenge [21]. In contrast, T cells were lowest (Additional file 1). PAS-positive staining in bronchiolar epithelium and cellular infiltration in the lung were also detectable to similar levels as in the other models (Fig. 1d and Additional file 2B).
Thus, each of the four models successfully elicited eosinophil accumulation in the airway, goblet cell hyperplasia in bronchioles, and immune cell infiltration in lung tissue.
MHCII-KO mice are refractory to airway eosinophilia and goblet cell hyperplasia
To assess the relative role of CD4+ T cells vs. innate cell types in our models, we utilized MHCII-KO mice which express undetectable levels of MHCII and very few conventional CD4+ T cells [22]. We tested the response of these mice to induction of allergic airway inflammation in the four models described in Fig. 1. In each case we observed that total BAL cellularity, as well as frequency and number of eosinophils were very low and equal to background (Fig. 2a-d). Neutrophil and T cell numbers were also lower than in C57BL/6 controls, except for the local HDM model (Additional file 3). Peribronchial and perivascular inflammation were reduced to background levels, with the only exception of the local HDM model in which a moderate inflammation was observed in both C57BL/6 and MHCII-KO mice. PAS-positive staining in bronchiolar epithelium was not increased compared to PBS in all models (Fig. 2).
Fig. 2
figure 2
MHCII-KO mice fail to generate allergic airway inflammation to OVA or HDM. (ad) C57BL/6 and MHCII-KO mice were immunized and challenged with OVA or HDM as in Fig. 1, PBS refers to C57BL/6 mice that were mock-immunized and challenged with OVA or HDM. Total cell counts, percent and number of eosinophils were evaluated by flow cytometry; bar graphs show mean + SEM/mouse from two combined experiments each using 5–8 mice per group. Histopathological scores were calculated on 6–10 mice per condition, selected from both experiments. Peribronchiolar and perivascular inflammation scores are displayed as median +/− interquartile range; the percent PAS-positive staining in bronchiolar epithelial cells is shown as mean + SEM. P values refer to comparisons between the sensitised and challenged C57BL/6 and MHCII-KO groups. ***, p < 0.001; **, p < 0.01; *, p < 0.05; ns, not significant
Therefore, in all models tested, eosinophilic inflammation and goblet cell hyperplasia showed a complete requirement for conventional CD4+ T cells, whereas lung cellular infiltration was only partly affected.
TSLPR-KO mice develop reduced eosinophilia across all models
TSLP is a key cytokine in Th2 immune responses, affecting multiple cell populations including DC, ILC2 and CD4+ Th2 cells [23]. We compared the responses of C57BL/6 and TSLPR-KO mice in the four models of allergic airway inflammation using OVA or HDM. We found that in all cases total cellularity and eosinophil percentages and numbers in BAL were greatly reduced in TSLPR-KO mice compared to WT (Fig. 3a–d). Neutrophils and T cells were also decreased, except in the local HDM model (Additional file 3).
Fig. 3
figure 3
TSLPR deficiency results in reduced airway inflammation in OVA and HDM models. (ad) C57BL/6 and TSLPR-KO mice were immunized and challenged with OVA or HDM as in Fig. 1; PBS refers to C57BL/6 mice that were mock-immunized and challenged with OVA or HDM. Total cell counts, percent and number of eosinophils were evaluated by flow cytometry; bar graphs show mean + SEM/mouse from two combined experiments each using 5–8 mice per group. Histopathological scores were calculated on 6–10 mice per condition, which were selected from both experiments. Peribronchiolar and perivascular inflammation scores are displayed as median +/− interquartile range; the percent PAS-positive staining in bronchiolar epithelial cells is shown as mean + SEM. (e) In vitro activated OTII Th2 cells were transferred into WT or TSLPR-KO mice 1 day before i.n. OVA challenge; data refer to 6–7 mice per group. In A-D, P values refer to the comparison between the sensitised and challenged C57BL/6 and TSLPR-KO groups. ***, p < 0.001; **, p < 0.01; *, p < 0.05; ns, not significant
Other parameters of airway inflammation were also compared: lung histology revealed moderately reduced peribronchial and perivascular inflammation in TSLPR-KO mice compared to WT in all models (Fig. 3a-c), with the exception of the local HDM model where the response was not affected (Fig. 3d). PAS-positive staining in bronchiolar epithelial cells was normal or slightly reduced in TSLPR-KO mice compared to WT in all models (Fig. 3a-c), with the exception of the local HDM model where a significant reduction was noted (Fig. 3d).
To assess whether TSLP was necessary for the function of CD4+ Th2 cells or also other cell populations, TSLPR-sufficient OTII cells were activated in vitro in Th2 conditions and transferred into WT C57BL/6 or TSLPR-KO recipients 1 day before OVA challenge. Eosinophil numbers were not reduced in TSLPR-KO mice, or were even slightly exacerbated compared with WT mice (Fig. 3e).
Overall, we observed a strong decrease in eosinophil numbers in TSLPR-KO mice in all models of allergic inflammation, whereas the effect on lung histology was mild or not detectable. In no case was the effect as marked as in MHCII-KO mice.
CD1d-KO mice show impaired airway eosinophilia in responses to OVA allergen, but not HDM
NKT cells are innate-like lymphocytes that are capable of responding rapidly to stimuli including endogenous and exogenous glycolipids presented on CD1d molecules, and can mediate allergic airway inflammation independently of conventional CD4+ T cells [16].
We used CD1d-KO mice, which lack NKT cells, to assess the development of airway inflammation in our models. In both the acute and repeat-challenge OVA models, total cell counts and eosinophil numbers were lower in CD1d-KO mice compared to C57BL/6, whereas the frequencies of eosinophils were similar to WT or only moderately decreased (Fig. 4a, b). In addition, numbers of T cells were lower than in C57BL/6 controls in the acute OVA model (Additional file 3). PAS-positive staining of epithelial cells in bronchioles was also lower in CD1d-KO mice compared to WT, whereas inflammation scores were decreased in the repeat-challenge OVA model, but not in the acute one.
Fig. 4
figure 4
CD1d-KO mice generate reduced airway inflammation in OVA but not HDM models. (ad) C57BL/6 and CD1d-KO mice were immunized and challenged with OVA or HDM as in Fig. 1; PBS refers to C57BL/6 mice that were mock-immunized and challenged with OVA or HDM. Total cell counts, percent and number of eosinophils were evaluated by flow cytometry; bar graphs show mean + SEM/mouse from two combined experiments each using 5–8 mice per group. Histopathological scores were calculated on 6–10 mice per condition, which were selected from both experiments. Peribronchiolar and perivascular inflammation scores are displayed as median +/− interquartile range; the percent PAS-positive staining in bronchiolar epithelial cells is shown as mean + SEM. (e) In vitro activated OTII Th2 cells were transferred into WT or CD1d-KO mice 1 day before i.n. OVA challenge; data refer to 6–7 mice per group. In A-D, P values refer to the comparison between the sensitised and challenged C57BL/6 and CD1d-KO groups. ***, p < 0.001; **, p < 0.01; *, p < 0.05; ns, not significant
In contrast to the OVA models, the systemic and local HDM models were not significantly affected by lack of NKT cells (Fig. 4e, d). There was no statistically significant reduction in total or eosinophil BAL cellularity, although there was a trend towards lower eosinophil numbers in the CD1d-KO mice. Accumulation of inflammatory cells in the peribronchial and perivascular spaces was not affected by lack of NKT cells. PAS-positive staining in bronchiolar epithelial cells was also similar in control and CD1d-KO mice.
To assess whether in the acute OVA model NKT cell activity was required at the time of sensitisation or during airway challenge, we used adoptive transfer of OTII cells that were activated in vitro in Th2 conditions and injected into WT or CD1d-KO mice. I.n. challenge resulted in similar cellularity and eosinophil numbers in CD1d-KO and C57BL/6 mice (Fig. 4e), suggesting that NKT cell activity was not required at the time of OVA challenge.
Overall, lack of NKT cells resulted in a reduction of allergic airway inflammation in OVA models, whereas inflammation in the HDM models was essentially normal.
TLR4 deficiency does not impair airway eosinophilia, goblet cell hyperplasia, or inflammatory infiltrate in mice exposed to OVA or HDM
We used TLR4-KO mice to compare the role of TLR4 in different models of airway inflammation. TLR4-KO mice exposed to the acute and repeat-challenge OVA models developed an intact or even slightly increased inflammatory response (Fig. 5a, b). As the OVA preparation used for i.n. challenge was low in endotoxin content, these effects may be due to endotoxin at the priming stage, or from other sources including the environment. Regardless of the endotoxin source, these experiments suggest that a low level of TLR4 signaling can limit inflammation in the OVA models in WT mice.
Fig. 5
figure 5
TLR4 deficiency mildly increases airway eosinophil numbers in OVA, but not HDM, models. (ad) C57BL/6 and TLR4-KO mice were immunized and challenged with OVA or HDM as in Fig. 1; PBS refers to C57BL/6 mice that were mock-immunized and challenged with OVA or HDM. Total cell counts, percent and number of eosinophils were evaluated by flow cytometry; bar graphs show mean + SEM/mouse from two combined experiments each using 5–8 mice per group. Histopathological scores were calculated on 6–10 mice per condition, which were selected from both experiments. Peribronchiolar and perivascular inflammation scores are displayed as median +/− interquartile range; the percent PAS-positive staining in bronchiolar epithelial cells is shown as mean + SEM. P values refer to the comparison between the sensitised and challenged C57BL/6 and TLR4-KO groups. ***, p < 0.001; **, p < 0.01; *, p < 0.05; ns, not significant
TLR4-KO mice exposed to systemic or local HDM generated eosinophil responses that were either similar to those in C57BL/6 mice, or marginally increased in both percentage and number (Fig. 5c, d). Perivascular and peribronchial inflammation scores, and the PAS-positive staining in bronchiolar epithelial cells, were not affected.
Overall, TLR4 deficiency did not appear to substantially affect the response to OVA or HDM allergens in these models.
Female and male mice generate similar airway eosinophilia to OVA but not HDM
Previous studies in BALB/c mice have reported a stronger susceptibility of female mice to airway inflammation due to increased numbers of ILC2 [24]. However, it is currently unclear whether this difference extends to other mouse strains such as C57BL/6, and different allergens and exposure protocols.
We combined all experiments carried out as part of this and other studies in our Laboratory, to compare C57BL/6 female and male mice for their ability to generate airway eosinophilia after allergen challenge. As shown in Fig. 6a and b, BAL cellularity, and also the number and percent of airway eosinophils, were similar in female and male mice undergoing the acute or repeat-exposure OVA protocols. In contrast, treatment with the systemic HDM protocol induced a stronger response in female mice, with about twice as many airway eosinophils in females compared to males (Fig. 6c). A trend to higher responses in female mice was also noted using the HDM local protocol, however, these differences were small and reached significance only in the case of total cellularity (Fig. 6d). PBS-sensitised male and female mice gave similar responses in all cases, with the exception of the total cell count in the local HDM model (p < 0.001).
Fig. 6
figure 6
Female mice develop exacerbated airway eosinophilia in systemic HDM models compared to males. (ad) Male and female C57BL/6 mice were immunized and challenged with OVA or HDM as in Fig. 1; PBS mice were mock-immunized and challenged with OVA or HDM. Total cell counts, percent and number of eosinophils were evaluated by flow cytometry; bar graphs show mean +/− SEM/mouse from several combined independent experiments each using 5–8 mice per group. P values refer to the comparison between males and females within sensitised and challenged groups, or mock-sensitised and challenged groups. ***, p < 0.001; **, p < 0.01; *, p < 0.05; ns, not significant
Thus, a comparison of male and female C57BL/6 mice revealed differences in the degree of airway eosinophilia that were dependent on both the type of allergen and the treatment protocol.
Discussion
We used four models of allergic airway inflammation that employ different allergens (OVA and HDM) priming protocols (systemic vs. local) and airway challenges (acute vs. repeated), to compare the contribution of four key immune response genes; MHCII, TSLPR, CD1d and TLR4, to various parameters of airway inflammation in each of the models. Differences between C57BL/6 males and females were also assessed. We found that inactivation of MHCII, TSLPR and TLR4 had an overall similar impact across all four models used, suggesting similarities in the immune mechanisms underlying each of them. The impacts of sex and CD1d inactivation showed some variation among models, preferentially affecting the responses to HDM or OVA, respectively, regardless of the protocols of sensitisation and challenge used in each case.
The clearest-cut results were observed in MHCII-KO mice. These mice lack conventional CD4+ T cells, whereas CD1d-restricted CD4+ T cells are reported to be present in normal numbers [25]. ILC2 expression of MHCII is also expected to be defective in these mice [26]. We observed that eosinophil accumulation and PAS-positive staining in each of the models used were strictly dependent on the presence of conventional CD4+ T cells. This observation clearly points to an essential role of CD4+ T cells, regardless of allergen or immunization protocol, in each of our models, and is consistent with published studies reporting a key role of CD4+ T cells in several models of airway inflammation [27,28,29]. Our data also suggest that in these models cytokine-producing ILC2 or NKT cells are not sufficient for a response but may cooperate with CD4+ T cells for their function [30, 31]. In contrast to eosinophil infiltration and PAS staining, cellular infiltration in the peribronchial and perivascular areas of the lung were variably affected, suggesting that these responses also rely, at least in part, on innate components [32].
The inactivation of TSLPR also had a considerable impact on airway inflammation, and substantially reduced airway eosinophils in all models. Reduced eosinophil responses could be fully rescued by adoptive transfer of in vitro-primed Th2 cells into TSLPR-KO hosts, suggesting that, at the challenge phase, the role of TSLP was predominantly on the Th2 population [33]. In contrast, the effects of TSLPR inactivation on PAS-positive staining in bronchioles were less marked compared to the effects on eosinophils, or the effects observed in MHCII-KO mice, except for the local HDM model. This observation differs from previous studies [33,34,35] which used BALB/c TSLPR-KO mice (vs. our C57BL/6) and OVA preparations of unknown endotoxin content (vs. our low-endotoxin OVA) to report that goblet cell hyperplasia was also decreased, perhaps suggesting that genetic background and/or allergen composition can affect the impact of TSLPR deficiency on specific responses.
TSLP is known to have an essential function in allergic airway inflammation. TSLPR-KO mice developed reduced allergic airway inflammation in an OVA model [34], and lung-specific overexpression of TSLP can induce spontaneous allergic airway inflammation in mice [35]. TSLP is produced by airway epithelium exposed to LPS or protease-containing allergens [35, 36], and acts on multiple immune populations. In addition to activating DC [23, 37, 38], TSLP is necessary for the survival and effector function of memory Th2 cells [33, 39, 40]. Together with IL-33, TSLP can also induce cytokine production by ILC2 [13], with Th2 cells and ILC2 both contributing to cytokine production during allergic airway inflammation [17].
The differential impact of TSLPR deficiency we observed on eosinophils vs. PAS-positive staining in mice sensitised systemically with OVA or HDM was very unexpected, but consistent across the three models. This observation raises interesting questions about a differential TSLPR requirement for increased eosinophils vs. mucus production in lung and airway, which are dependent on IL-5 and IL-13, respectively. As both of these responses are strictly dependent on conventional CD4+ T cells, as indicated by experiments in MHCII-KO mice, this result may suggest a heterogeneity in TSLP requirement by either CD4+ Th2 subsets producing IL-5 vs. IL-13, or the CD4+ Th2 vs. ILC2 populations that can produce these cytokines. Results in this paper showing that repeated OVA challenges tend to decrease eosinophil numbers while increasing the percent of PAS-positive staining in bronchiole epithelium might also suggest a similar possibility. Studies in mice where the TSLPR is conditionally inactivated in selected immune populations in lung will be necessary in order to address these questions. Interestingly, decreased eosinophils and PAS-positive cells were both observed after i.n. HDM immunisation, which is consistent with a stronger dependence of this model on local innate immune mechanisms [9]. Overall, the results of these experiments are consistent with the recognized role of TSLP in supporting both innate and adaptive immune responses to allergens. Importantly, anti-TSLP has proven effective in ameliorating asthma symptoms in patients [41, 42], a result that is consistent with the essential role of TSLP in maintaining memory Th2 populations in vivo [33, 39].
NKT cells are glycolipid-reactive, innate-like T cells that can mediate allergic airway inflammation in the absence of conventional CD4+ T cells [43] and are necessary for airway inflammation and hyper-reactivity in an OVA model [44]. In contrast, the role of NKT cells in HDM models has not been examined. Unlike OVA, which does not contain NKT ligands, allergens such as HDM [16] and pollens [16, 45] are reported to contain glycolipids that induce NKT cell activation and production of IL-4 and IL-13. Consistent with previous reports, we observed that CD1d-KO mice, which lack NKT cells, generated impaired airway eosinophilia and PAS staining in OVA models, which were partially compensated by multiple airway challenges. In contrast, lack of NKT cells had no significant impact on the two models of HDM response, one of which used the same i.p. route of sensitisation and alum adjuvant also employed in the OVA models. This observation may suggest a role of NKT cells in amplifying responses to antigens that do not effectively engage innate immune mechanisms, such as the low-endotoxin OVA preparations used in our studies. However, the mechanism by which NKT cells might contribute to the OVA response measured here, the endogenous or exogenous source of potential NKT cell ligands in this model, as well as the role of NKT cells in clinical disease, remain poorly understood. Initial reports of a major contribution of NKT cells to allergic airway inflammation in patients [46] have been questioned [47]. The subsequent description of multiple NKT subsets with varying cytokine profiles [48] further adds to the complexity of this question.
In contrast to the clear impact of defective MHCII or TSLPR expression on airway eosinophilia, we found that responses in TLR4-KO mice were, for the most part, similar to the responses in wild-type C57BL/6 mice. The response to OVA was weakly to moderately stronger in TLR4-KO mice than in C57BL/6 mice, which might be due to the reported capacity of endotoxin to suppress priming to allergic airway inflammation [49]. In contrast to OVA, the response to HDM was not affected by TLR4 inactivation. Since the HDM protein Der p 2 is a known MD-2 mimic that facilitates signalling through TLR4 [12], and as such it is reported to exacerbate airway allergic responses via interaction with airway epithelial cells [36], this observation might suggest a low Der p 2 content in our HDM preparations [50]. Alternatively, other immunologically active components of HDM such as proteases, β-glucans and chitins [51] may be compensating for the loss of TLR4-dependent signalling in our model. While the impact of TLR4 inactivation on the models used here was unremarkable, it is important to note that TLR4 ligands have been shown to play important functions in other models of allergic response. Allergic conjunctivitis to Short Ragweed pollen [52] required TLR4 to drive the production of TSLP/OX40L and the priming of a productive Th2 response. Low endotoxin content in OVA and Cockroach extract preparations increased airway inflammatory responses [8, 53], and co-operated with Proteinase-activated receptor-2 (PAR2) signalling in inducing allergic sensitisation [53]. These studies highlight the multiple mechanisms through which allergens can engage with the immune system.
Finally, we report that C57BL/6 females develop stronger airway eosinophilia compared to male mice, but only in selected models. Intriguingly, the difference was strongest in the systemic HDM model, where eosinophil numbers are high, compared to the local model in which the weaker response might have been expected to be more dependent on cooperation with ILC2 [24]. Our results may also suggest that the impact of androgens and ILC2 in airway inflammation models may depend in part on the mouse colony and/or strain, as well as other properties of the allergen used.
A perhaps unexpected result from our study is the overall similarity of the results obtained using the i.n. HDM sensitisation model to results in other models using i.p. sensitisation with allergen in alum adjuvant. Whereas i.p. sensitisation with adjuvant is clearly not a physiological model of allergen exposure, the impact of KO mutations in MHCII, TSLPR, CD1d, and TLR4 on these artificial models was not dissimilar from the impact observed after i.n. sensitisation, suggesting that, regardless of the priming route, all these models essentially measure the activity of a population of effector Th2 cells with similar activation requirements. In this respect, it is also important to note that the natural route of airway allergen sensitisation in humans remains unknown, and may not necessarily be via the airway, with sensitisation via the skin remaining a realistic possibility [54].
While the innate properties of allergens clearly have an impact on their immunogenicity, and may have a stronger influence on inflammation than described here if used in settings of low-level or chronic allergen exposure, in our experiments they appeared mostly insufficient to directly drive inflammation independently of conventional CD4+ T cells. The study of such innate responses mostly requires tailored models in which specific allergens are used in high amounts and/or after careful purification to preserve their innate properties [50]. A relevant example is the powerful fungal airway allergen Alternaria alternata [15], which is itself a trigger of innate allergic responses [15] but, similar to IL-33, can also prime adaptive T cell responses in mice [55, 56] and humans [57]. It is also of interest that IL-33, which is essential for the innate function of Alternaria and many other environmental allergens [10], is also induced in macrophages by treatment with alum [58], and is rapidly produced in the peritoneum after i.p. injection of alum adjuvant [59]. Studies to examine lung ILC2 after i.p. alum injection may help establish whether the systemic and local priming of allergic immune responses in models of allergic airway inflammation such as those used here may involve common innate mechanisms.
Conclusions
This work highlights the overall similarities and subtle differences in the immunological pathways that underlie murine allergic airway inflammation induced by different allergens and using different sensitisation protocols. This information may provide a useful basis for selecting experimental models for the study of allergic airway disease.
Methods
Mice
The following mouse strains were used: C57BL/6 J (originally from Jackson Laboratory, Bar Harbor, Maine, USA), TSLP-receptor (R) KO [60], MHCII-KO [22], CD1d-KO [61], TLR4-KO [62] and OTII [63]. Mice were bred by brother x sister mating and maintained in specific pathogen-free conditions at the Malaghan Institute of Medical Research, Wellington, NZ, with water and food ad libitum. Mice were age and sex-matched within experiments and used when 6–12 weeks old. Mice were euthanised for sample collection at the end of experiment by intraperitoneal injection of a high dose of Ketamine+Xylazine (300 and 9 mg/Kg, respectively). All experimental procedures were approved by the Victoria University of Wellington Animal Ethics Committee and carried out according to Institutional guidelines. No adverse effects were observed during this study.
Allergic airway inflammation
Naïve mice were randomly assigned to control or experimental groups and sensitised i.p. with 200 μl Alu-S-Gel (1.3%) (Serva, Heidelberg, Germany) containing 2 μg OVA Grade V, (Sigma-Aldrich, Saint Louis, MO, USA), 40 μg D. pteronyssinus soluble extract (Greer Labs, Lenoir, NC, USA) or PBS (Gibco, Carlsbad, CA, USA). One hundred micrograms D. pteronyssinus crushed bodies (Greer Labs) were administered in 50 μl PBS i.n. to anaesthetised mice; HDM extract was also used in this model but gave very low eosinophil responses (not shown) and was not used further. HDM models were carried out using only female mice except for Fig. 6. For the adoptive transfer model, 5 million OTII Th2 cells were generated by co-culturing lymph node cells from OTII mice with LPS-activated C57BL/6 bone marrow-derived DC, generated as in [64], at an 8:1 ratio in the presence of 60 ng/ml IL-4, 20 ng/ml IL-2, and OVA323–339 peptide (ISQAVHAAHAEINEAGR) in 6 well plates. IL-4 and IL-2 were replenished on day 2 and 4. In vitro-activated CD4+ T cells were harvested on day 5 and their phenotype was checked by flow cytometry. Resulting cells were Vα2+Vβ5+CD62LloCD69hiCD44hi as described [5]. Five million cells were injected through the lateral tail vein into recipient mice (C57, CD1d-KO or TSLPR-KO), and mice were challenged i.n. 1 day after cell transfer.
For i.n. challenges, mice were anaesthetised with Ketamine+Xylazine at 100 and 3 mg/Kg, respectively, and 100 μg endograde OVA (Hyglos GmbH, Bernried, Germany), 100 μg HDM soluble extract or 25 μg HDM crushed bodies was administered dropwise into one nostril in 50 μl sterile PBS. The distribution of the i.n.-instilled solution was checked in preliminary experiments where mice were given coloured tracers. They were found to include lower airway and lung, although the lung was not uniformly involved. BAL was collected by flushing 1 ml of PBS through the lungs thrice. After red blood cell lysis, samples were processed for flow cytometry and counted using Accucount beads (Spherotech, Green Oaks, IL, USA).
Flow cytometry
Antibody staining was performed in FACS Buffer (PBS with 2% FCS, 2 mM EDTA and 0.01% NaN3) using the following antibodies: anti-(a) CD11c-BV650, aMHCII (I-A/I-E)-Pacific Blue, aCD3-Pe-Cy7, aGr-1-AF647, aCD69-PE and aVα2-APC were from Biolegend (San Diego, CA, USA); aCD62L-PE-Cy7 and aCD44-APC-eFluor780 were from eBioscience (San Diego, CA, USA); aCD40-PE, aCD86-FITC, aVβ5.1/5.2-FITC, aNK1.1-PE, aSiglecF-PE-CF594, aCD19-APC-H7 and aCD4-BV605 were from Becton Dickinson (Franklin Lakes, NJ, USA); while aCD8-FITC and aCD16/32 hybridoma supernatant were prepared in house. Data were acquired on a LSRII SORP (Becton Dickinson, San Jose, CA, USA) or LSR Fortessa SORP (Becton Dickinson), and analysed using FlowJo Software v 9.9 (FlowJo LLC, Ashland, OR, USA). 4’,6-Diamidino-2-Phenylindole, Dihydrochloride (Molecular Probes, Eugene, OR, USA) was used to exclude dead cells.
Histology
Lungs were harvested and fixed in 10% neutral buffered formalin (Sigma-Aldrich), cut in 5 μm sections on the coronal plane and stained with haematoxylin and eosin or Alcian Blue-Periodic Acid Schiff (PAS). Peribronchial and perivascular inflammation was scored by a blinded operator using the following criteria: (0), no peribronchial or perivascular infiltrates; (1), 1–2 centrally located microscopic foci of inflammatory infiltrates; (2), a dense inflammatory infiltrate in a perivascular or peribronchial distribution originating in the center of the lung and extending along the vessels or bronchi into the middle third of the lung parenchyma; (3), perivascular or peribronchial infiltrates extending to the periphery of lung and approaching the visceral pleura. To quantify AB-PAS staining, we used a quantitative and objective method in which 3 micrographs per lung were taken using an Olympus BX51 compound microscope at 20x magnification, and processed using an Image J macro to calculate the percent PAS-positive staining in the total bronchiole epithelial area excluding airspace (Additional file 1A).
Statistics
All bar graph data are shown as mean +/− Standard Error of the Mean (SEM), excepting inflammation scores, which are expressed as median +/− interquartile ranges. All statistical analyses used a Mann-Whitney non-parametric t-test; p values lower than 5% were considered significant. Prism 7 for MAC OS X (San Diego, CA, USA) was used for all analyses.
Abbreviations
BAL:
Broncho-alveolar lavage
DC:
Dendritic cell/s
HDM:
House dust mite
i.n.:
intranasal/ly
IL:
Interleukin
ILC2:
Type-2 innate lymphoid cell/s
KO:
Knockout
MHCII:
Major Histocompatibility Complex Class II molecule
NKT:
Natural Killer T (cell)
OVA:
Chicken ovalbumin
PAS:
Alcian Blue-Periodic Acid Schiff stain
PBS:
Phosphate-buffered saline
SEM:
Standard Error of the Mean
TLR:
Toll-like receptor/s
TSLP:
Thymic stromal lymphopoietin
TSLPR:
TSLP receptor
WT:
Wild-type
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Funding
This work was funded by an Independent Research Organisation grant from the Health Research Council of NZ to the MIMR. The funder had no role in the design, analysis and interpretation of the data, or in the preparation of the manuscript. NJD was supported by a University of Otago Wellington PhD Scholarship.
Availability of data and materials
The datasets generated during the current study are available from the corresponding author on reasonable request.
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Contributions
FR designed the study; EH, KW ND and SG carried out experiments and analysed data; EH and FR wrote the manuscript with input from all authors; all authors have read and approved the manuscript.
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Correspondence to Franca Ronchese.
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Additional files
Additional file 1:
Table S1. Pdf file showing cell counts for neutrophils, T cells and alveolar macrophages relative to Fig. 1. (PDF 84 kb)
Additional file 2:
Figure S1. Pdf file illustrating the quantification of AB-PAS-positive staining in airway epithelium using FIJI software, and the results of such quantification for the experiments in Fig. 1. (PDF 1970 kb)
Additional file 3:
Table S2. Pdf file showing cell counts for neutrophils, T cells and alveolar macrophages relative to Figs. 2, 3, 4 and 5. (PDF 117 kb)
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Hyde, E.J., Wakelin, K.A., Daniels, N.J. et al. Similar immune mechanisms control experimental airway eosinophilia elicited by different allergens and treatment protocols. BMC Immunol 20, 18 (2019). https://doi.org/10.1186/s12865-019-0295-y
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Causes and Symptoms of Knee Pain | Physiotherapy
Knee Pain
What is knee pain?
Knee pain is a common problem that can occur suddenly or over a period of time. There are a number of causes of knee pain, and general treatment is readily available. Knee pain can be caused by an underlying condition, such as a sudden injury, an overuse injury, or arthritis. Treatment varies depending on the cause. Symptoms of a knee injury include pain, swelling, and stiffness.
There are many common causes, ranging from general muscle or tendon tension to some form of arthritis. Sometimes the cause is not found. Knee pain can often be treated at home and you should start to feel better after a few days.
As you get older, knee pain can become more common. There is also a risk of knee pain if you are overweight. Knee pain can sometimes be the result of sports or other injuries.
Causes of knee pain
Your knee is a complex structure that consists of three bones: the lower part of the femur, the upper part of the tibia, and the knee.
Then there are the strong ligaments and ligaments that hold these bones together, as well as the cartilage under the kneecap and between the bones to stabilize the ligament and the knee. Damage or disease affecting any of these structures can cause pain.
Knee arthritis: There are different types of arthritis that affect the knee joint, the two most common being osteoarthritis and rheumatoid arthritis.
Osteoarthritis: Knee osteoarthritis develops as a result of the “wear and tear” of the knee cartilage and is most common in people older than 50.1 years. As the cartilage weakens, knee pain develops, often gradually increasing from sharp pain intensified with the movement of the knee to persistent numbness and pain.
Rheumatoid arthritis: It is an autoimmune disease in which a person’s immune system attacks multiple joints in the body. In addition to pain, swelling, redness, and warmth may also appear in the knee. Unlike osteoarthritis, knee pain caused by rheumatoid arthritis improves with activity.
Gout: Gout occurs in people who have high levels of uric acid in the bloodstream. This high uric acid level causes crystals to form in certain joints, such as the big toe, fingers, knee, or hip.
Osteochondritis dissections: Osteochondritis degeneration (OCD) is another condition seen in children and adolescents caused by a lack of blood supply to a small section of the knee bone. It weakens and sometimes separates the affected bone and cartilage from the underlying bone.
Low back pain is the first symptom of pain. Be aware that many situations can have similar symptoms. As the condition progresses, knee swelling and stiffness may appear intermittently.
Knee joint infection: Infected knee joints are accompanied by significant knee pain, swelling, warmth, painful movements, and often fever. In some cases, a bacterial infection in the bloodstream is to blame for an infected joint.
Knee fracture: A patella fracture can occur from falling directly on the knee or from a direct blow to the knee.
It’s like hitting your knee on the dashboard in a car accident. In addition to significant pain and difficulty in straightening the knee, knee injuries and swelling often occur, sometimes with a visible deformity.
Bone tumor: Very rarely, osteoporosis can be the cause of knee pain.16 There may also be associated with symptoms such as fever or accidental weight loss and worsening pain, especially at night.
Risk factors for knee pain
You are more likely to have knee pain than others:
• Overweight
• You have weak or tight leg muscles
• Play some sports, for example, skiing and basketball.
• Rolled up to your knee in front
Symptoms of knee pain
If you have knee pain, you may have other symptoms:
• Swelling, redness, or warmth in the knee
• Injuries around the knee
• ‘Give way’ to your knee
• Lock or click
• Inability to straighten the knee
See a doctor if the pain does not improve within a few weeks, if you cannot move or put any weight on your knee, or if your knee locks or buckles.
If your knee is very sore, very swollen or deformed, or you have a fever and a hot, red knee, go to the emergency department.
Treatment for knee pain
Some common knee pain treatments are listed below (although they are not comprehensive), and not all of these treatments are suitable for all conditions.
Self-care strategies
Many early treatments for knee pain are simple, straightforward, and can be done at home.
Rest
The first treatment for the most common conditions that cause knee pain is to temporarily relax the joint, reducing immediate inflammation. Sometimes this is the only step necessary to relieve knee pain.
Ice
In addition to relaxation, placing a cold pack, ice pack, or bag of frozen vegetables on the knee is probably the most widely used treatment for knee pain. When applying ice to your knees, be careful not to apply ice directly to the skin for 15-20 minute sessions (several times a day).
Support for knee pain
Depending on the diagnosis, your doctor may recommend knee support to reduce your pain. For example, in the case of the patellar tendon, your doctor may recommend an auxiliary tapping and patellar tendon straps.
In the case of a collateral ligament injury or partial knee dislocation, it may sometimes be advisable to maintain knee stability. Similarly, for certain types of fractures, a cast or splint may be placed to heal.
Physical therapy for knee pain
Physical therapy can help with knee pain, depending on the cause and the part of the knee pain that hurts. A physical therapist can advise you based on your personal circumstances.
Treatments prescribed by your physical therapist include:
• Exercise program tailored to your specific needs – Depending on the cause of your knee pain, you may need to continue it for a while
• Pressing on the knee: This involves applying tape to the knee to change the way the knee sits or moves.
• Knee pads: You can buy these from sports stores, pharmacies, and online retailers, but they are not suitable for everyone or for all knee problems. Talk to your doctor or physical therapist to find out if an herb is right for you.
Medications
Action medications are often used not only to reduce pain but also to treat a knee problem.
NSAIDs
Nonsteroidal anti-inflammatory drugs, commonly known as NSAIDs, are commonly prescribed for patients with knee pain due to complications such as arthritis, bursitis, and tendonitis.
Injections
If your pain or swelling persists despite traditional treatments like rest, ice, and taking NSAIDs, your doctor may inject cortisone, powerful medicine that treats inflammation, into your knee.
An example of a knee condition that can be treated with a cortisone injection in knee osteoarthritis. Cortisone is a powerful drug that can cause side effects, so injections should be used sparingly.
Knee exercises
Being active is an important part of your treatment and can help you recover.
Being physically active while recovering from knee pain:
• Stop the pain from happening again
• Help maintain your current fitness level – no matter what changes you make, any activity is better than nothing
• Keep your other muscles and joints strong and flexible
• It is important to keep the muscles around the knee strong, as this will put pressure on the knee. These muscles include the thigh, calf, and hip muscles.
• This section includes some simple exercises designed to stretch, strengthen, and stabilize your knee
• It may be helpful to do these exercises with a physical therapist first, or they may be able to give you a personalized exercise plan.
Knee stretching exercises
Try to do these exercises every day.
Stretch leg raise (Seated)
Sit in a chair with good posture. Keep one of your legs straight, slowly hold position 10, and then slowly lower your leg. Do 10 times with each leg. Try to get in the habit of doing this exercise every time you sit down.
Muscle stretch
Lie on your back with a towel wrapped under the ankle of the affected leg. Bend the other leg at the knee. Use the muscles in your straight leg to push the back of your knee firmly onto the bed or floor. Hold slowly for a count of five.
Repeat at least five times with each leg. This exercise can help keep your knee from permanently bending. Try this once a day while you sleep.
Leg stretch
Sit on the floor with your legs stretched out in front of you. Slowly bend one knee to your chest and slide your feet across the floor until you feel a gentle stretch. Hold for five seconds. Keep your leg as straight as possible and hold it in this position for five seconds.
Do 10 times with each leg. If you can’t get to the floor, sit on the couch and use a tabletop or tea tray to slide down your foot.
Knee strengthening exercises
The following exercises for knee pain are very difficult to do, so try to do them two or three times a week.
Straight leg raise (lying down)
Lie down and bend one of your legs at the knee. Keep the other leg straight and lift your foot off the bed or floor. Hold the position slowly for five seconds and then lower. Do this until you can’t do it anymore, rest for a minute, and then do it three more times.
Step-ups
Go down the stairs with your right foot. Raise your left foot, then down with your right foot, then your left foot. Grab the bunnies if you have to. Repeat with each leg until you can’t do it anymore. Rest for a minute, then repeat two more times. As you improve, use the raised step or take two at a time.
Knee squat
Hold the chair or work surface for support. Squat down until your knee is straight over your toe. The knees should not go in front of the toes. Return to your normal state.
Repeat until you can’t do it anymore, rest for a minute and then repeat two more times. As you improve, try to move forward a bit, but don’t bend your knees beyond a right angle.
Sitting/standing
Sit in the chair. Without using your arms for support, get up, and then sit down. Make sure each movement is slow and controlled. Repeat until you can’t do it anymore.
Rest for a minute, then repeat twice. If the chair is too low, begin to lift off the seat cushion and remove it when you no longer need it.
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Wednesday, June 19, 2024
What Happens If You Stop Eating Sugar For 14 Days?
0:00
The Impact of Eliminating Sugar from Your Diet for 14 Days
Eliminating sugar from your diet for 14 days can have a significant impact on your overall health and well-being. Sugar is known to have detrimental effects on various aspects of health, including weight management, energy levels, and even mental clarity. By abstaining from sugar for a two-week period, you can experience several positive changes in your body and mind. Let’s explore what happens when you stop eating sugar for 14 days.
Understanding the Effects of Sugar on the Body
Sugar, especially in its refined form, is often linked to weight gain, inflammation, and an increased risk of chronic diseases such as diabetes and heart disease. When you consume sugar, particularly in excess, it can lead to spikes and crashes in blood sugar levels, leaving you feeling fatigued and craving more sugar to sustain energy levels. Moreover, sugar can contribute to insulin resistance, leading to metabolic issues over time. By cutting out sugar from your diet, you give your body a chance to reset and rebalance its systems.
The Initial Challenges of Going Sugar-Free
In the initial days of eliminating sugar from your diet, you may experience withdrawal symptoms such as headaches, irritability, and cravings. This is normal and is often likened to breaking an addiction. Sugar can trigger the release of feel-good hormones in the brain, so when you remove it suddenly, your body may protest. However, staying committed to your sugar-free journey can help alleviate these symptoms as your body adjusts to its new way of functioning.
Physical Changes You May Notice
After about a week of cutting out sugar, many people report feeling more energized and experiencing fewer energy crashes throughout the day. This is because your body is no longer relying on sugar for quick bursts of energy but is instead turning to more stable fuel sources such as complex carbohydrates and fats. Additionally, reducing sugar intake can lead to clearer skin, as sugar has been linked to inflammation and acne in some individuals.
Mental Clarity and Focus
Sugar highs and subsequent crashes can also impact your mental clarity and focus. By removing sugar from your diet, you may notice improved concentration, better cognitive function, and enhanced overall mood. Some people report feeling less brain fog and more alertness after eliminating sugar for a period of time. This can be particularly beneficial for those who need sharp mental acuity for work or daily tasks.
Long-Term Benefits of a Sugar-Free Diet
Continuing to avoid sugar beyond the initial 14 days can have numerous long-term benefits for your health. Weight management may become easier, inflammation in the body can decrease, and your risk of developing chronic diseases may be reduced. Additionally, you may find that your taste buds adapt to preferring less sweet foods, making it easier to resist sugary temptations in the future.
Eliminating sugar from your diet for 14 days can lead to various positive changes in your body and mind. While the initial transition may be challenging, the long-term benefits are well worth the effort. By giving your body a break from sugar, you pave the way for improved health, energy levels, and mental well-being.
Strategies to Overcome Sugar Cravings during the Elimination Period
Humans are inherently drawn to the sweetness of sugar, making it a challenging ingredient to eliminate from one’s diet. However, embarking on a journey to cut out sugar can have profound impacts on both physical and mental health. The effects of eliminating sugar for a specific period, like 14 days, can be eye-opening. Let’s explore what happens if you stop eating sugar for two weeks and the strategies to overcome sugar cravings during this elimination period.
Understanding the Impact of Eliminating Sugar
Cutting out sugar from your diet for a considerable amount of time, such as 14 days, allows your body to reset and experience various changes. Initially, you may encounter withdrawal symptoms like headaches, fatigue, irritability, and cravings. This phase is often challenging but is a sign that your body is adjusting to the absence of sugar.
Improved Energy Levels and Mental Clarity
As you progress through the 14 days without sugar, your energy levels are likely to stabilize. The rollercoaster of energy crashes and spikes that come with sugar consumption diminishes, leading to more consistent energy throughout the day. Moreover, many individuals report heightened mental clarity and improved focus after reducing their sugar intake significantly.
Enhanced Skin Health and Weight Management
One of the noticeable benefits of eliminating sugar is its positive impact on skin health. Conditions like acne and inflammation may improve as a result of cutting out this inflammatory ingredient. Additionally, reducing sugar consumption can aid in weight management, as sugary foods are often high in empty calories. Over 14 days, you may start to notice changes in your body composition, especially if you replace sugary snacks with healthier alternatives.
Strategies to Combat Sugar Cravings
During the initial stages of sugar elimination, cravings can be intense. Employing strategies to overcome these cravings is crucial for successfully completing the 14-day challenge. Here are some effective tactics:
1. Opt for Healthy Alternatives
Instead of reaching for sugary treats, stock up on fruits like berries, which offer natural sweetness along with fiber and essential nutrients. healthy fats and proteins into your meals can also help keep cravings at bay.
2. Stay Hydrated
Dehydration can sometimes be mistaken for hunger or sugar cravings. Ensure you drink an adequate amount of water throughout the day to stay hydrated and reduce the likelihood of cravings.
3. Practice Mindful Eating
Engage in mindful eating practices by savoring each bite and paying attention to your body’s hunger and fullness cues. Mindful eating can help prevent impulsive snacking on sugary foods.
4. Get Sufficient Sleep
Inadequate sleep can disrupt hunger hormones and increase cravings for sugary foods. Prioritize getting seven to nine hours of quality sleep each night to support your overall health and reduce sugar cravings.
Embracing a Sugar-Free Lifestyle
By the end of the 14-day sugar elimination period, you may find that your taste buds have adapted, and sugary foods no longer hold the same appeal. The benefits of reduced sugar consumption, such as improved energy, mental clarity, skin health, and weight management, can be motivating factors to continue following a lower-sugar or sugar-free lifestyle.
The decision to stop eating sugar for 14 days can lead to transformative changes in both your physical and mental well-being. By understanding the impact of eliminating sugar, implementing strategies to combat cravings, and embracing a sugar-free lifestyle, you can pave the way for long-term health benefits. Embark on this journey with determination, and you may be pleasantly surprised by the results.
Benefits of a Sugar-Free Diet on Overall Health and Well-being
For 14 days, experiment by eliminating sugar from your diet and observe the transformative effects it can have on your overall health and well-being. The benefits of a sugar-free diet extend beyond just weight loss, leading to improved physical and mental health outcomes.
Understanding the Impact of Sugar on the Body
The average diet today is loaded with various forms of sugar, from the obvious ones like desserts and sugary drinks to hidden sugars in processed foods. Excessive sugar consumption can lead to weight gain, increased risk of chronic diseases such as diabetes and heart ailments, and even impact mental health by causing mood swings and fatigue.
Initial Changes When You Cut Out Sugar
Once you decide to remove sugar from your diet, the initial days might be challenging as your body adjusts to the sudden change. You might experience sugar cravings, headaches, and irritability as your body craves its familiar sugar fix. However, staying committed to this change is crucial.
Benefits of Eliminating Sugar for 14 Days
1. Healthier Weight Management: By cutting out sugar, you reduce empty calorie intake, leading to weight loss. Your body will start burning fat for energy instead of relying on sugar, promoting a healthier weight.
2. Improved Energy Levels: While sugar provides a quick energy spike, it is often followed by a crash. With a sugar-free diet, you experience more stable energy levels throughout the day, reducing fatigue.
3. Enhanced Mental Clarity: Sugar crashes can also impact cognitive function. By eliminating sugar, you may notice better focus, concentration, and mental clarity.
4. Better Skin Health: High sugar intake is linked to skin issues like acne and premature aging. After 14 days without sugar, you may notice clearer skin and a more radiant complexion.
5. Balanced Mood: Sugar can lead to mood swings and irritability. Without it, your mood may stabilize, leading to a more balanced emotional state.
6. Reduced Inflammation: Excessive sugar consumption is linked to inflammation in the body, which can contribute to various chronic diseases. Removing sugar can help reduce overall inflammation levels.
Tips for a Successful Sugar-Free Journey
• Read Labels: Avoid foods with hidden sugars by checking labels for ingredients like high fructose corn syrup, glucose, sucrose, etc.
• Focus on Whole Foods: Opt for whole foods like fruits, vegetables, lean proteins, and whole grains to satisfy your nutritional needs.
• Stay Hydrated: Drink plenty of water to help flush out toxins and support overall health.
• Get Adequate Sleep: Quality sleep is essential for overall well-being, so aim for 7-8 hours of restful sleep each night.
Embarking on a 14-day sugar-free diet can have a profound impact on your health and well-being. From weight management to improved energy levels and mental clarity, the benefits are numerous. By making a conscious effort to eliminate sugar from your diet, you pave the way for a healthier lifestyle and a happier you.
Common Challenges Faced When Cutting Out Sugar and How to Overcome Them
Our modern diets are often filled with excessive amounts of added sugars, which can have detrimental effects on our health. However, many people are unaware of the significant changes that can occur in the body when sugar is eliminated for a period of time. In this article, we will explore the potential benefits and challenges of cutting out sugar for 14 days and provide strategies to overcome these hurdles.
Understanding the Impact of Sugar Withdrawal
When you abruptly stop consuming sugar, your body goes through a period of adjustment. Sugar has addictive properties, and its removal from your diet can lead to withdrawal symptoms similar to those experienced when cutting out addictive substances. Common symptoms of sugar withdrawal may include headaches, fatigue, cravings, irritability, and mood swings.
The Benefits of Eliminating Sugar for 14 Days
Despite the challenges of sugar withdrawal, there are numerous potential benefits to eliminating sugar from your diet for a period of two weeks. In just a short amount of time, you may experience improved energy levels, clearer skin, better digestion, weight loss, reduced inflammation, and enhanced mental clarity. Additionally, cutting out sugar can help regulate blood sugar levels and reduce the risk of chronic diseases such as diabetes and heart disease.
Overcoming Challenges When Cutting Out Sugar
While the benefits of eliminating sugar are significant, it’s important to acknowledge the challenges that may arise during this process. To successfully navigate these hurdles, consider the following strategies:
1. Gradual Reduction: Instead of quitting sugar cold turkey, gradually reduce your intake over a few days to minimize withdrawal symptoms.
2. Stay Hydrated: Drinking plenty of water can help flush out toxins and reduce cravings for sugary foods.
3. Opt for Healthy Substitutes: Replace sugary snacks with nutritious alternatives like fruits, nuts, yogurt, or dark chocolate with high cocoa content.
4. Read Labels: Be vigilant about reading food labels to identify hidden sugars in processed foods and beverages.
5. Meal Planning: Plan your meals ahead of time to avoid making impulsive food choices when cravings strike.
6. Get Ample Rest: Prioritize quality sleep to support your body during the adjustment period and reduce sugar cravings.
Embracing a Sugar-Free Lifestyle
After successfully completing 14 days without sugar, you may find that your taste buds have changed, and you no longer crave overly sweet foods. Embrace this opportunity to continue making mindful choices about your diet by opting for whole, unprocessed foods that nourish your body and support your overall well-being.
While cutting out sugar for 14 days may pose challenges initially, the potential benefits for your health and vitality make the effort worthwhile. By understanding the impact of sugar withdrawal, focusing on the positive outcomes, and implementing strategies to overcome obstacles, you can successfully eliminate sugar from your diet and embark on a path to improved health and wellness.
Long-Term Effects of Reducing Sugar Intake and Maintaining a Balanced Diet
Reducing sugar intake and maintaining a balanced diet have significant long-term effects on overall health and well-being. The modern diet is often packed with hidden sugars, leading to various health issues such as obesity, diabetes, heart disease, and dental problems. By consciously cutting down on sugar consumption and focusing on a balanced diet rich in nutrients, individuals can experience transformative changes that positively impact their quality of life.
Importance of Reducing Sugar Intake
Excessive sugar consumption is linked to numerous health complications, including weight gain, insulin resistance, inflammation, and an increased risk of chronic diseases. By reducing sugar intake, individuals can better manage their weight, regulate blood sugar levels, improve energy levels, and enhance overall health. Additionally, reducing sugar can lead to better dental health, as sugar is a primary contributor to tooth decay and cavities.
Effects of Cutting Out Sugar for 14 Days
When individuals stop eating sugar for just two weeks, the body undergoes several beneficial changes. Initially, many people experience sugar cravings and withdrawal symptoms, similar to those of individuals giving up caffeine. However, after the initial period, individuals often report feeling more energized, experiencing fewer mood swings, and enjoying improved mental clarity. Moreover, eliminating sugar from the diet can lead to better skin health, as sugar consumption is linked to skin issues such as acne and premature aging.
Transitioning to a Balanced Diet
While reducing sugar intake is crucial, maintaining a balanced diet is equally important for long-term health benefits. A balanced diet should include a variety of fruits, vegetables, whole grains, lean proteins, and healthy fats. By focusing on whole foods and minimizing processed and sugary foods, individuals can ensure they are obtaining essential nutrients while keeping their sugar consumption in check.
Long-Term Health Benefits
Over time, the effects of reducing sugar intake and maintaining a balanced diet become even more pronounced. Individuals may experience sustained weight loss, improved heart health, better blood sugar control, enhanced cognitive function, and a reduced risk of developing chronic conditions such as type 2 diabetes and cardiovascular disease. Moreover, a balanced diet supports overall well-being, boosts immunity, and increases energy levels throughout the day.
Practical Tips for Sugar Reduction
To successfully reduce sugar intake and transition to a balanced diet, individuals can implement practical strategies such as reading food labels, cooking meals at home, choosing whole foods over processed options, and incorporating healthier alternatives to sugary snacks and desserts. Gradual changes to eating habits are more sustainable in the long run and can lead to lasting improvements in health.
Reducing sugar intake and maintaining a balanced diet are essential for long-term health and well-being. By making conscious choices to limit sugar consumption, individuals can experience a wide range of benefits, from improved weight management to enhanced energy levels and overall vitality. Combined with a nutrient-rich diet, reducing sugar intake forms the foundation for a healthier lifestyle that supports longevity and disease prevention.
Key Takeaway:
Key Takeaway:
Embarking on a 14-day journey of eliminating sugar from your diet can lead to transformative changes in both your physical and mental well-being. By implementing effective strategies to overcome sugar cravings during this period, individuals can experience a myriad of benefits that extend beyond the temporary challenge of cutting out sugar. Not only does a sugar-free diet contribute to improved overall health, but it also enhances one’s quality of life by boosting energy levels, promoting weight loss, and reducing the risk of various chronic diseases.
During the initial phase of eliminating sugar, individuals may encounter common challenges such as cravings, mood swings, and fatigue. However, with perseverance and the adoption of healthy alternatives, these obstacles can be overcome. By gradually reducing sugar intake and incorporating nutrient-rich foods into one’s diet, individuals set the foundation for long-term positive effects. Maintaining a balanced diet post-sugar detox is crucial for sustaining these benefits and ensuring sustained well-being.
Opting for a sugar-free lifestyle requires determination and discipline, but the rewards are boundless. Improved focus, stabilized blood sugar levels, enhanced skin health, and better digestion are just a few of the many advantages of reducing sugar intake. By prioritizing whole foods, ample hydration, and regular physical activity, individuals can cultivate sustainable habits that support their long-term health goals.
In essence, the decision to cut out sugar for 14 days may initially pose challenges, but with dedication and the adoption of effective strategies, the benefits far outweigh the temporary discomfort. By embracing a sugar-free lifestyle, individuals can pave the way for lasting changes that contribute to overall health, well-being, and longevity.
Conclusion
Embarking on a journey to eliminate sugar from your diet for 14 days can lead to a wide array of positive outcomes that extend far beyond just the physical realm. By understanding the impact of eliminating sugar, implementing strategies to overcome cravings, recognizing the benefits on overall health, addressing common challenges, and considering the long-term effects, you are better equipped to make informed decisions regarding your dietary choices and overall well-being.
During the initial phase of eliminating sugar, it’s essential to brace yourself for both physical and emotional adjustments. The impact of cutting out sugar from your diet for two weeks includes experiencing increased energy levels, improved mental clarity, better sleep quality, and enhanced mood stability. As your body adjusts to a sugar-free lifestyle, you may notice a reduction in inflammation, weight loss, and a decreased risk of chronic illnesses such as diabetes and heart disease.
To successfully navigate the elimination period and combat sugar cravings, it is crucial to adopt effective strategies. These include gradually reducing sugar intake, staying hydrated, consuming balanced meals rich in protein and fiber, getting an adequate amount of sleep, engaging in regular physical activity, and seeking support from friends, family, or a healthcare professional. By incorporating these strategies into your daily routine, you can effectively manage cravings and maintain your sugar-free commitment.
The benefits of a sugar-free diet extend beyond physical health and can significantly impact your overall well-being. By eliminating sugar for 14 days, you may experience improved cognitive function, enhanced focus and concentration, stabilized blood sugar levels, reduced risk of dental issues, and a strengthened immune system. Additionally, cutting out sugar can lead to clearer skin, reduced bloating, and a more balanced emotional state.
Despite the numerous advantages of a sugar-free diet, there are common challenges that individuals may encounter when attempting to reduce their sugar intake. These challenges include dealing with withdrawal symptoms, facing social pressure in social settings, navigating food cravings, and adjusting to changes in taste preferences. By acknowledging these hurdles and implementing strategies to overcome them, such as practicing mindfulness, planning ahead, and seeking healthier alternatives, you can successfully navigate the ups and downs of the sugar elimination process.
Looking beyond the initial 14-day period, maintaining a balanced diet with reduced sugar intake can have long-lasting effects on your health and well-being. By prioritizing whole foods, consuming a variety of nutrients, and practicing moderation, you can sustain the benefits of a sugar-free lifestyle in the long term. Over time, you may notice increased energy levels, enhanced physical performance, improved digestion, better cardiovascular health, and a reduced risk of obesity and related conditions.
The decision to stop eating sugar for 14 days is not just a temporary dietary change but a transformative journey towards improved health, vitality, and overall well-being. By understanding the impact of eliminating sugar, implementing strategies to overcome cravings, recognizing the benefits on overall health, addressing common challenges, and considering the long-term effects, you are taking proactive steps towards a healthier and more fulfilling lifestyle. Embrace the process, stay committed to your goals, and reap the rewards of a sugar-free existence.
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6,428,216,842,082,405,000
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The effects of chronic ethanol self-administration on hippocampal serotonin transporter density in monkeys
E. J. Burnett, A. T. Davenport, K. A. Grant, D. P. Friedman
Research output: Contribution to journalArticlepeer-review
14 Scopus citations
Abstract
Evidence for an interaction between alcohol consumption and the serotonin system has been observed repeatedly in both humans and animal models yet the specific relationship between the two remains unclear. Research has focused primarily on the serotonin transporter (SERT) due in part to its role in regulating extracellular levels of serotonin. The hippocampal formation is heavily innervated by ascending serotonin fibers and is a major component of the neurocircuitry involved in mediating the reinforcing effects of alcohol. The current study investigated the effects of chronic ethanol self-administration on hippocampal SERT in a layer and field specific manner using a monkey model of human alcohol consumption. [3H]Citalopram was used to measure hippocampal SERT density in male cynomolgus macaques that voluntarily self-administered ethanol for 18 months. Hippocampal [3H]citalopram binding was less dense in ethanol drinkers than in controls, with the greatest effect observed in the molecular layer of the dentate gyrus. SERT density was not correlated with measures of ethanol consumption or blood ethanol concentrations, suggesting the possibility that a threshold level of consumption had been met. The lower hippocampal SERT density observed suggests that chronic ethanol consumption is associated with altered serotonergic modulation of hippocampal neurotransmission.
Original languageEnglish (US)
Article numberArticle 38
JournalFrontiers in Psychiatry
Volume3
Issue numberAPR
DOIs
StatePublished - 2012
Keywords
• 5-ht
• 5-htt
• Alcohol self-administration
• Excessive drinking
• Heavy drinking
• Hippocampus
• Monkey
• Sert
ASJC Scopus subject areas
• Psychiatry and Mental health
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Unfavourable gender effect of high body mass index on brain metabolism and connectivity.
Abstract:
The influence of Body Mass Index (BMI) on neurodegeneration in dementia has yet to be elucidated. We aimed at exploring the effects of BMI levels on cerebral resting-state metabolism and brain connectivity, as crucial measures of synaptic function and activity, in a large group of patients with Alzheimer's Dementia (AD) (n = 206), considering gender. We tested the correlation between BMI levels and brain metabolism, as assessed by 18F-FDG-PET, and the modulation of the resting-state functional networks by BMI. At comparable dementia severity, females with high BMI can withstand a lower degree of brain metabolism dysfunction, as shown by a significant BMI-brain metabolism correlation in the temporal-parietal regions, which are typically vulnerable to AD pathology (R = 0.269, p = 0.009). Of note, high BMI was also associated with reduced connectivity in frontal and limbic brain networks, again only in AD females (p
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Benefits Of Natural Healing
by Diana Ketchen
Alternative treatments to conventional Western medicine may provide helpful and life-changing options for people who are sensitive to medications, or cannot afford big expensive surgeries.
More than that, alternative treatments such as herbal medicine focus on prevention and treating underlying problems, not just symptoms.
Herbal medicine involves the use of plants and extracts to deliver effective and safe treatments. Even Western medical practitioners are not only stopping to take note, but starting to suggest natural alternative treatments as well.Herbal Remedies
For instance, it used to be that kidney stone patients could only take medication or have surgery to remove a painful stone. Now, it is recognized that lemon is effective in breaking down stones.
Herbal medicine, Phytotherapy, or Herbalism, as it is also known, is now used often in lieu of Western medicine. It is very popular for prevention and treatment of illness and health issues. Botanical medicine or medical Herbalism systems of treatment reach back to Herbalism found in traditional Chinese medicine, Ayurvedic Herbalism, and even in Western Herbalism.
Medicinal Plants In Modern Times:
Herbal medicine is older than Western medicine and has some long-standing treatments and cures that have lasted for thousands of years because they work.
As it turns out, it is not just in the mind of the user or practitioners. It turns out that smart, modern scientists have tested the long-standing herbal remedies to find out what makes them work. Plants contain some very powerful components and chemicals that re-balance the body. In general, herbal remedies can be prepared as a liquid or powder extracts, tablets, essential oils, teas, and ointments.
Because the herbal remedies work with the body’s processes to heal, they are generally safer than prescription drugs and surgery, and a lot more affordable. The benefits of herbal treatments are listed below and include everything from effective treatments for colds, cancer, and even diabetes.
Benefits Of Natural Healing
Because herbal medicine works with the body’s natural self-healing capabilities, it actually enhances biological healing to quicken the recovery process. It also means that the body’s own internal environment is maintained during recovery rather than ravaged, which doctors say, antibiotics do to the body. In the case of Western antibiotics, the individual often feels “off” in their stomach after dealing with the healing that antibiotics cause. It turns out that their stomach, then has to heal as well.
With herbal remedies, the body is maintained, not partly destroyed and requiring rebuilding after the treatment is taken. What many people do not know is that herbs are powerful enough to stimulate glands to re-balance hormones by re-initiating hormone production. Hormones play a role of the signal to tell the body to increase or reduce biological processes.
Many herbal remedies have a set of rules to follow to improve their ability to work. For instance, while the person increasing their lemon water intake to reduce kidney stones is treating stones, they would also eliminate foods that allow kidney stones to be produced. The idea is to support the body in its healing. The changes at some point become a habit to prevent future re-occurrences of the issue.
As it turns out, herbs strengthen the immune system’s functioning to build the body’s defenses naturally. This prevents primary and secondary infection.
Building an immune system that is stronger while bringing in a holistically regulated diet improves metabolism. That leads to optimal absorption from the diet nutrition. Once people start on a healthy path they are less likely to want junk food, because it is one way to erase the good effects of using herbal medicine. Junk food robs the body of health by harming its ability to take in nutrients while packing on unnecessary weight.
Good wholesome nutrition improves treatment, while strengthening the body’s immune system. Medicinal herbs work better when they have the added support of a well-fed body. It improves the efficacy of treatments.medicinal plants and their uses
People can have allergies to anything, especially medications, food, and even herbal remedies. Herbal medicine means that there is a potential for side-effects and allergies. They do work as the body is meant to operate, and that is where the herbal medicine has advantages of Western medicine.
Yet, with herbal medication, there are generally fewer problems than with pharmaceuticals because the chemical element of foreign substances in the body are not part of the equation. It is easier for the body to heal with herbal medicine.
Now herbal remedies are administered by practitioners of Traditional Chinese Medicine, Ayurvedic medicine, Naturopathy, or other alternative practices. Naturopaths, for one, go to school for years post-graduate, just like a medical doctor or chiropractor might. They learn all about the plants, their makeup, how they need to be prepared, and dosing for different sized people and their problems. It makes sense to turn to the experts on plants instead of trying to self-medicate because people can have bad allergies to herbal remedies.
Common Medicinal Herbs And Uses
In the United States, ginseng and bee pollen remain very popular along with black cohosh, cat’s claw among many others. Ephedra is one herbal remedy that most people have heard of because it is an appetite suppressant. It treats bronchitis and asthma as well. Meanwhile, echinacea boosts the immune system. Kava kava has also remained popular, and it treats anxiety.
Ginkgo improves blood circulation and oxygenation to boost memory and concentration. People who have trouble sleeping often like the calming effect of valerian. It is a natural muscle relaxant with a mild effect.
Blood Sugar Lowering Herbs
The list of favorable blood sugar herbal supplements is a long one. It includes cinnamon, ginkgo biloba, blueberry leaves, bitter melon, garlic, onion, fenugreek, and goat’s rue just to name some. They are all helpful at controlling blood sugar levels to help lower a diabetic’s reliance on insulin. The underlying action is that these herbal remedies increase the body’s insulin secretion to keep the body’s blood sugar levels balanced.
Herbs For Allergies
Nettles are one of the favorites for dealing with particular allergies, along with quercetin, the ephedra, butterbur, and Astragalus work to combat different types of allergies by controlling the body’s anti-histamines. They also include antioxidants and anti-inflammatories. They can treat skin problems and asthma as well, such as acne and eczema.
Other Medicinal Plant Uses
Colon cleanses are important to keep the body’s intestinal tract clean to prevent colon cancer. Plantago psyllium seed, which is part of many products available at the supermarket, plays a role as a colon cleanser. Others that work their magic in the colon include rhubarb powder, aloe vera, and alfalfa juice. Chlorella, which is often found in “green juices” combined with the power of carrot concentrate, and garlic all are powerful colon cleansers. They clean and improve digestion in the intestinal tract. The colon itself does not uptake nutrients, it is more akin to a waste chute.
Heart and blood-related functions are treated with garlic, ginkgo, and ginger. Know that there are a multitude of options not mentioned here. Hawthorn cuts blood pressure while dilates blood vessels to support a stronger heart. Garlic treats coronary artery disease while improving cholesterol levels. Ginkgo biloba even helps with the treatment of cerebrovascular diseases.
Herbal medicines are effective for weight loss to reduce obesity. Herbal medications are often appetite suppressants, stimulants, diuretics, and cathartics. Commonly fennel, flaxseed, phyllium, alfalfa, senna, nettle, kola nut, and hawthorn are used to aid in weight loss. They also work to improve health improvement to help with overall health.
Various herbs are increasingly turned to treat both minor and major health issues from the common cold to sleep problems. Even allergies, diabetes, heart and blood pressure can be regulated through the use of herbal remedies. Treating anxiety, heart problems, breathing problems, and skin disorders take well to herbal remedies. All different parts of plants are used to create herbal remedies that help people to improve their health and well-being for today and into the future.
About The Author: Diana Ketchen is a Certified Natural Health Consultant and Wellness Coach as well as a Personal Trainer. She resides in the state of Tennessee but was born and raised in West Virginia. She absolutely believes in and practices Natural Wellness as much as she can and would like to share her knowledge and experiences with you as well as having you share with her the same. More here https://www.facebook.com/naturalherbalandhomeopathicremedies/
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This information is not intended to be a substitute for professional medical advice,
diagnosis or treatment. Always seek the advice of your physician or other qualified
health provider with any questions about your medical condition.
Do not disregard professional medical advice or delay seeking advice or treatment
because of something you have read here.
The effectiveness of diagnosis and treatment will vary. SOPHIA Natural Health Center does not guarantee certain results.
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Ear Infections: Causes, Symptoms, and Natural Home Remedies
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Introduction
Ear infections are a common ailment that can affect people of all ages, from infants to adults. In this article, we will explore the causes, symptoms, and natural home remedies for ear infections, providing insights into how to manage this condition effectively.
Understanding Ear Infections
Ear infections, also known as otitis media, occur when the middle ear becomes inflamed or infected. This inflammation can be caused by bacteria or viruses and often results in pain and discomfort. Ear infections can affect individuals of any age but are more prevalent in children due to their developing immune systems and anatomy.
Causes of Ear Infections
1. Bacterial Infections: Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis are common bacterial pathogens responsible for ear infections.
2. Viral Infections: Viruses such as respiratory syncytial virus (RSV) and influenza can also lead to ear infections, particularly in children.
3. Anatomical Factors: Structural abnormalities in the Eustachian tube, such as narrowness or blockages, can increase the risk of fluid accumulation and subsequent infection.
4. Environmental Factors: Exposure to tobacco smoke, allergies, and cold weather can contribute to the development of ear infections.
Symptoms of Ear Infections
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Common symptoms of ear infections include:
• Ear pain or discomfort
• Tugging or pulling at the ear (in infants)
• Fever
• Fluid drainage from the ear
• Difficulty hearing
• Irritability or fussiness (in children)
Natural Home Remedies for Ear Infections
1. Warm Compress: Applying a warm compress to the affected ear can help alleviate pain and reduce inflammation. Simply soak a clean cloth in warm water, wring out excess moisture, and place it against the ear for 10-15 minutes.
2. Garlic Oil: Garlic possesses antimicrobial properties that can help combat bacterial or viral infections. Garlic oil can be prepared by crushing a clove of garlic and mixing it with olive oil. Warm the mixture slightly and apply a few drops to the affected ear using a dropper.
3. Onion Poultice: Onions have natural antibacterial and anti-inflammatory properties that can aid in relieving ear pain. Chop an onion, wrap it in a clean cloth, and place it over the affected ear for 10-15 minutes.
4. Steam Inhalation: Inhaling steam can help alleviate congestion and promote drainage of fluid from the Eustachian tube. Boil water in a pot, remove it from the heat, and lean over the pot with a towel draped over your head to trap the steam. Breathe deeply for 5-10 minutes.
5. Salt Sock: Fill a clean sock with coarse salt and heat it in the microwave for 30-60 seconds until warm but not too hot. Place the salt sock against the affected ear for soothing relief.
When to Seek Medical Attention
While natural home remedies can provide relief for mild ear infections, it is essential to seek medical attention if you experience:
• Severe ear pain or discomfort
• Persistent fever
• Drainage of pus or blood from the ear
• Difficulty hearing
• Dizziness or vertigo
These symptoms may indicate a more serious infection or complication that requires prompt medical evaluation and treatment.
Conclusion
Ear infections can be uncomfortable and distressing, but with proper understanding and management, most cases can be effectively treated at home. Natural remedies such as warm compresses, garlic oil, and steam inhalation can help alleviate symptoms and promote healing. However, it is crucial to consult a healthcare professional if symptoms persist or worsen.
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Comparison of the complexation of fluoroquinolone antimicrobials with metal ions by nuclear magnetic resonance spectroscopy
Masahiro Sakai, Akihiro Hara, Saeko Anjo, Mikio Nakamura
Research output: Contribution to journalArticlepeer-review
58 Citations (Scopus)
Fingerprint
Dive into the research topics of 'Comparison of the complexation of fluoroquinolone antimicrobials with metal ions by nuclear magnetic resonance spectroscopy'. Together they form a unique fingerprint.
Medicine & Life Sciences
Chemical Compounds
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Citation
4749 total record number 121 records this year
Hydrogen-Deuterium Exchange Mass Spectrometry Reveals a Novel Binding Region of a Neutralizing Fully Human Monoclonal Antibody to Anthrax Protective Antigen
Fang, M;Wang, Z;Norris, K;James, JA;Wu, S;Smith, K;
Anthrax vaccine adsorbed (AVA) containing protective antigen (PA) is the only FDA-approved anthrax vaccine in the United States. Characterization of the binding of AVA-induced anti-PA human antibodies against the PA antigen after vaccination is crucial to understanding mechanisms of the AVA-elicited humoral immune response. Hydrogen deuterium exchange mass spectrometry (HDX-MS) is often coupled with a short liquid chromatography gradient (e.g., 5-10 min) for the characterization of protein interactions. We recently developed a long-gradient (e.g., 90 min), sub-zero temperature, ultra-high performance liquid chromatography HDX-MS (UPLC-HDX-MS) platform that has significantly increased separation power and limited back-exchange for the analysis of protein samples with high complexity. In this study, we demonstrated the utility of this platform for mapping antibody-antigen epitopes by examining four fully human monoclonal antibodies to anthrax PA. Antibody p1C03, with limited neutralizing activity in vivo, bound to a region on domain 1A of PA. p6C04 and p1A06, with no neutralizing activities, bound to the same helix on domain 3 to prevent oligomerization of PA. We found p6C01 strongly bound to domain 3 on a different helix region. We also identified a secondary epitope for p6C01, which likely leads to the blocking of furin cleavage of PA after p6C01 binding. This novel binding of p6C01 results in highly neutralizing activity. This is the first report of this distinct binding mechanism for a highly neutralizing fully human antibody to anthrax protective antigen. Studying such epitopes can facilitate the development of novel therapeutics against anthrax.
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Topics
• Article
• Behavior Impact
• Sleep
Does Magnesium Before Bed Improve Your Sleep?
By WHOOP
Does Magnesium Before Bed Improve Your Sleep?
We explore the effects taking magnesium at night has on WHOOP members’ sleep and recovery.
Magnesium is frequently utilized as a sleep supplement, but does it actually increase the duration or quality of your sleep? We examine how it impacts sleep and recovery data tracked by WHOOP, plus break down the basics of what magnesium is, how it works, how much to take, and possible side effects.
What is Magnesium?
Magnesium is a very common mineral that is essential for human health. It is something that all your cells and organs need, contributing to muscle, nerve, heart, and brain function, as well as building strong bones and regulating blood pressure and immune system activity. Many foods contain magnesium, and it is also readily available as a supplement. A popular use of magnesium supplements is to improve your sleep.
How Can Taking Magnesium at Night Help You Sleep?
Magnesium deficiencies have often been connected to sleep disorders and poor sleep, so if you’re not getting enough of it in your diet a magnesium supplement may aid your sleep. Additionally, magnesium can help your body relax. It works to inhibit the sympathetic (fight or flight) branch of your autonomic nervous system and promote parasympathetic (rest and digest) activity instead. Magnesium is also used as a treatment for restless leg syndrome, a condition that disrupts sleep for many people.
Benefits of Magnesium for WHOOP Members’ Sleep & Recovery
In an effort to quantify any potential sleep benefits of magnesium, we examined the data from WHOOP members when they report taking it. We learned that many of them see clear improvements in their sleep and recovery following magnesium supplements prior to bedtime. WHOOP members average 15 more minutes of sleep per night when they use magnesium, as well as 2% more REM sleep. They also wake up the next morning with an average recovery 8% higher.
magnesium helps improve sleep whoop
WHOOP MEMBERS Average more sleep and higher recovery after taking magnesium.
We took possible confounding factors into account during this analysis to control for other sleep-promoting behaviors (like meditation before bed or a sound machine when sleeping) that you might also engage in while taking magnesium. In general, we found a greater increase in average sleep time for men (+16 minutes) as opposed to women (+ 9 minutes), and also diminishing benefits around age 40. WHOOP members between 40 and 60 years old saw no improvement in average time asleep.
Magnesium Dosage, Risks & Potential Side Effects
Recommendations for the proper dosage of magnesium to take before bed vary, and they are often slightly higher for men than women. For the most part, something in the range of 200-350 milligrams is the suggested amount. Taking too much magnesium can cause the following:
• Cramping
• Nausea
• Diarrhea (with magnesium oxide in particular)
• Irregular heartbeat (from very high intakes)
Magnesium supplements may also interfere with certain medications. Additionally, putting more magnesium into your body than it needs can lead to magnesium toxicity, with possible symptoms including low blood pressure, muscle weakness, and vomiting.
Magnesium for Sleep vs Melatonin
Magnesium and melatonin are often part of the same conversation when it comes to sleep aids, but they are two very different things. While magnesium is a mineral that assists numerous processes in your body, melatonin is a hormone which contributes to regulating your sleep and circadian rhythm. Generally speaking, magnesium helps your body relax and melatonin supports falling asleep faster. Many experts advise trying melatonin first before experimenting with magnesium. Some people may choose to use both simultaneously, especially to combat insomnia. READ MORE: How Much Does Melatonin Help You Sleep?
Track How Magnesium Affects Your Sleep with WHOOP
WHOOP has a journal feature that lets you log when you take magnesium prior to sleep, as well as the dosage (and also many other choices and behaviors that can benefit or hurt your sleep). Alongside state-of-the-art sleep tracking, WHOOP uses this data to offer you actionable insights as to which behaviors improve or detract from your sleep and next-day recovery. RELATED: How Eating Before Bed Affects Your Sleep and Recovery
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Header Logo
Connection
Co-Authors
This is a "connection" page, showing publications co-authored by Mai ElMallah and Alisha Gruntman.
Connection Strength
0.044
1. Borel F, Sun H, Zieger M, Cox A, Cardozo B, Li W, Oliveira G, Davis A, Gruntman A, Flotte TR, Brodsky MH, Hoffman AM, Elmallah MK, Mueller C. Editing out five Serpina1 paralogs to create a mouse model of genetic emphysema. Proc Natl Acad Sci U S A. 2018 03 13; 115(11):2788-2793.
View in: PubMed
Score: 0.044
Connection Strength
The connection strength for concepts is the sum of the scores for each matching publication.
Publication scores are based on many factors, including how long ago they were written and whether the person is a first or senior author.
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URL path: Index page // Blog // Infections // Fever. Causes, Laboratory Tests, Treatment and Natural Remedies
Blog
Infections
Fever. Causes, Laboratory Tests, Treatment and Natural Remedies
Fever, also known as pyrexia, is a temporary increase in body temperature above the normal range. It is a common symptom of many underlying conditions and illnesses, rather than being a disease itself. In most cases, fever is the body's natural response to an infection or inflammation.
Fever is generally defined as a body temperature of 38°C or higher when measured orally. However, the normal body temperature can vary slightly from person to person, and it can also fluctuate throughout the day.
Fever is often caused by infections, such as bacterial, viral, or fungal infections. Common examples include the flu, common cold, urinary tract infections, pneumonia, and gastroenteritis. Other causes of fever include inflammatory conditions like rheumatoid arthritis, certain medications, heatstroke, and some cancers.
Besides an elevated body temperature, other common symptoms of fever may include sweating, chills, headache, muscle aches, weakness, loss of appetite, dehydration, and increased heart rate.
Most fevers resolve on their own within a few days and are not a cause for concern. However, there are situations where medical attention should be sought, such as if the fever persists for more than three days, is accompanied by severe headache or neck pain, difficulty breathing, chest pain, persistent vomiting, or if there are other concerning symptoms.
Causes of Fever
Fever can be caused by a variety of factors. The most common cause of fever is an infection, but there are other potential triggers as well.
Infections: Fever is often a response to infections caused by bacteria, viruses, fungi, or parasites.
• Respiratory infections such as the flu, common cold, pneumonia, bronchitis, or sinusitis.
• Urinary tract infections involving the bladder, urethra, or kidneys.
• Gastrointestinal infections such as gastroenteritis or food poisoning.
• Skin infections like cellulitis, abscesses, or infected wounds.
• Sexually transmitted infections such as gonorrhea or chlamydia.
• Systemic infections like sepsis or meningitis.
Inflammatory conditions: Some inflammatory disorders can cause fever as part of the immune response.
• Rheumatoid arthritis: an autoimmune disease affecting the joints.
• Inflammatory bowel disease: such as Crohn's disease or ulcerative colitis.
• Vasculitis: inflammation of blood vessels.
• Lupus: an autoimmune disease affecting multiple organs.
• Temporal arteritis: inflammation of the arteries in the head and neck.
Medications: Certain medications can lead to fever as a side effect. For instance, antibiotics, antihistamines, seizure medications, and some drugs used for treating hypertension may cause fever in some individuals.
Vaccinations: Fever is a common reaction to some vaccines, especially in children. It is often a mild and temporary response as the body builds immunity.
Heat-related conditions: Exposure to excessive heat, such as heatstroke or heat exhaustion, can cause fever along with other symptoms like dehydration.
Cancer: Some cancers, particularly hematologic malignancies like leukemia or lymphoma, can cause persistent or recurrent fever.
Other causes: Fever can also be triggered by factors like trauma, certain autoimmune diseases, allergic reactions, hormonal changes (e.g., thyroid disorders), and some rare genetic disorders.
It's important to remember that fever is a symptom and not a specific disease. Identifying the underlying cause of fever requires a thorough evaluation, considering other symptoms, medical history, and possibly conducting further tests or investigations.
Laboratory Tests for Fever
When evaluating a fever, certain laboratory tests may help identify the underlying cause. The specific tests conducted can vary depending on the patient's symptoms, medical history, and physical examination findings.
Complete Blood Count (CBC): This test provides information about different types of blood cells, including red blood cells, white blood cells, and platelets. An elevated white blood cell count (leukocytosis) may indicate an infection or inflammation.
Blood Cultures: This test involves taking a sample of blood to check for the presence of bacteria or fungi. Blood cultures can help identify bloodstream infections (sepsis) that may be causing the fever. Alternatively, the responsible microbes can be searched for in the blood, using molecular techniques (Opportunistic Microorganism Panel, Molecular Detection).
Urinalysis: This test examines the urine for the presence of infection or inflammation. It can detect urinary tract infections (UTIs) or kidney infections, which are common causes of fever.
Blood Chemistry Panel: This panel includes various tests to assess organ function and electrolyte levels. Abnormalities in liver enzymes, kidney function, or electrolyte imbalances may provide clues to the underlying cause of fever.
Inflammatory Markers: Tests such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) measure levels of inflammation in the body. Elevated levels of these markers can indicate the presence of an inflammatory condition.
Viral Serology: Serologic tests can help identify specific viral infections by detecting antibodies produced by the immune system. Examples include tests for influenza, hepatitis, or HIV.
Imaging Studies: In some cases, imaging tests such as chest X-ray, ultrasound, or CT scan may be ordered to evaluate specific organs or areas of concern, especially when certain infections or inflammatory conditions are suspected.
Functional medicine lab tests are typically used in conjunction with a comprehensive assessment of an individual's health history, lifestyle factors, and symptoms. Functional medicine takes a holistic approach to understanding and treating health issues, including fever. Specific lab tests may be used to assess various aspects of an individual's health and identify underlying imbalances or dysfunctions.
Food Sensitivity Testing (TrophoScan®): Food sensitivities or intolerances can contribute to chronic inflammation and immune system dysregulation, potentially leading to recurring fever. IgG antibody testing may be used to identify immune reactions to specific foods.
Comprehensive Stool Analysis (EnteroScan®): This test examines the composition of the gut microbiome, identifies any pathogenic bacteria, parasites, or yeast overgrowth, and assesses digestive function. Imbalances in the gut microbiota can impact immune system function and contribute to systemic inflammation.
Adrenal Function Testing (AdrenalScan®): Chronic stress or adrenal dysfunction can influence the immune system and contribute to symptoms like fatigue and recurrent fevers. Salivary cortisol testing may be used to evaluate adrenal gland function.
Thyroid Panel: Thyroid imbalances, such as hypothyroidism or hyperthyroidism, can affect the body's temperature regulation and potentially lead to fever-like symptoms. Testing thyroid hormone levels (TSH, T3, T4, reverse T3) and thyroid antibodies can provide insights into thyroid function.
Vitamin and Mineral Testing: Deficiencies or imbalances in certain vitamins and minerals can impact immune function and overall health. Tests for vitamin D, B vitamins, magnesium, zinc, and other nutrients may be considered.
Hormone Panel: Hormonal imbalances, such as those involving sex hormones or the hypothalamic-pituitary-adrenal (HPA) axis, can affect immune function and contribute to symptoms like fever. Hormone testing may include cortisol, estrogen, progesterone, or testosterone levels.
Treatment of Fever
The treatment of fever aims to address the underlying cause while also providing symptomatic relief.
Identify and treat the underlying cause: Since fever is a symptom rather than a condition itself, the primary focus is on identifying and addressing the underlying cause. This may involve treating infections with appropriate antibiotics, antiviral medications, or antifungal drugs. In cases of inflammatory conditions, treatment may involve anti-inflammatory medications or immune-modulating therapies.
Supportive measures
• Rest: Getting adequate rest allows the body to heal and recover more efficiently.
• Hydration: Drink plenty of fluids to prevent dehydration, especially if experiencing sweating due to fever.
• Cool environment: Create a comfortable environment with appropriate ventilation and temperature control.
• Light clothing and cool compresses: Dress in lightweight, breathable clothing and use cool compresses on the forehead or back of the neck to help reduce body temperature.
Medications for symptomatic relief
• Paracetamol or nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen can help reduce fever and provide relief from associated symptoms like headache, muscle aches, and discomfort. It's important to follow the recommended dosage and consult a healthcare professional, especially in the case of children or if there are underlying medical conditions.
• Avoid giving aspirin to children or teenagers, as it may increase the risk of a rare but serious condition called Reye's syndrome.
Cool baths: If the fever is high or causing significant discomfort, a tepid bath with lukewarm water can help lower body temperature. Avoid using cold water, as this can cause shivering and potentially raise body temperature.
Seek medical attention when necessary: Most fevers resolve on their own within a few days and are not a cause for concern. However, it's important to seek medical attention if:
• The fever persists for more than three days or is accompanied by severe symptoms.
• There are specific concerns about the underlying cause or the individual's medical history.
• The fever is accompanied by symptoms such as difficulty breathing, chest pain, persistent vomiting, or other concerning signs.
These general recommendations for fever treatment may not be suitable for everyone, especially in specific medical conditions or for individuals with special considerations (e.g., pregnant women, older adults, infants, or those with compromised immune systems).
Natural Remedies for Fever
Some natural remedies may help alleviate fever.
Stay hydrated: Drink plenty of fluids, such as water, herbal teas, and clear broths, to stay hydrated and help regulate body temperature.
Herbal teas: Certain herbal teas, such as chamomile, peppermint, or ginger tea, may help promote relaxation, reduce discomfort, and support the immune system.
Cool compresses: Applying cool compresses or damp washcloths to the forehead, wrists, or back of the neck can provide temporary relief and help lower body temperature.
Proper rest: Adequate rest allows the body to conserve energy and focus on healing. Make sure to get sufficient sleep and take breaks when needed.
Proper nutrition: Consuming a balanced diet rich in fruits, vegetables, whole grains, and lean proteins provides essential nutrients to support the immune system and aid in recovery.
Garlic: Garlic has natural antimicrobial properties and may help support the immune system. Incorporate fresh garlic into meals or consider garlic supplements.
Elderberry: Elderberry has been traditionally used to support immune function. It is available as a syrup, extract, or supplement.
Echinacea: Echinacea is an herb known for its potential immune-stimulating properties. It is available as a supplement or herbal tea.
Essential oils: Certain essential oils, such as peppermint, eucalyptus, or lavender, may provide a soothing effect when used in a diffuser or diluted and applied topically.
Probiotics: Probiotics are beneficial bacteria that support gut health and immune function. Incorporating probiotic-rich foods like yogurt or fermented foods or taking a probiotic supplement may be beneficial.
For all the above supplements, consult a healthcare professional for appropriate use and dosage.
Vasilis J. Sideris
Biologist
Medical Doctor, Biopathologist (Microbiologist)
Certified Functional Medicine Practitioner, CFMP®
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The Featured Image For This Article Could Be A High-Quality Photo Of Various Types Of Mushrooms
The Ultimate Guide to Superior Mushroom Supplements for Optimal Health
Are you looking for a natural way to boost your immune function, reduce inflammation, and improve overall health? Look no further than superior mushroom supplements. In this guide, we will explore the benefits, types, and potential risks of mushroom supplements to help you choose the right one for you.
The Ultimate Guide To Superior Mushroom Supplements For Optimal Health
Benefits of Superior Mushroom Supplements
Superior mushroom supplements are made from high-quality mushrooms that are grown under optimal conditions and processed using advanced techniques. They contain a wide range of bioactive compounds, including beta-glucans, polysaccharides, triterpenes, and antioxidants, that offer numerous health benefits.
One major advantage of superior mushroom supplements is that they are highly concentrated and can deliver a potent dose of nutrients in a small amount. Additionally, mushroom supplements are often more convenient to take than fresh or dried mushrooms since they come in capsules or powders.
The quality of ingredients used in superior mushroom supplements is crucial. Look for supplements that use organic, non-GMO mushrooms that are free from pesticides and heavy metals. Choose supplements that use whole mushrooms rather than extracts, as whole mushrooms contain a broader range of nutrients and may be more effective.
Processing techniques used in making superior mushroom supplements also play a significant role in their quality. Some of the best processing methods include hot water extraction, which helps to break down the cell walls of mushrooms and release their nutrients, and dual extraction, which combines hot water and alcohol extraction to extract both water-soluble and fat-soluble compounds.
The benefits of superior mushroom supplements
• Superior mushroom supplements are made with high-quality ingredients and processing techniques.
• Different types of mushrooms offer various benefits and factors should be considered when choosing a supplement.
• Taking proper dosage and precautions can help avoid potential side effects or interactions with other medications.
The Ultimate Guide To Superior Mushroom Supplements For Optimal Health
Types of Superior Mushroom Supplements
Superior mushroom supplements use many types of mushrooms, each with their unique health benefits. The most popular mushrooms used in supplements include:
Reishi Mushroom
Reishi mushroom is often referred to as the “mushroom of immortality” due to its potential to boost immune function, reduce inflammation, and promote longevity. It's also believed to have adaptogenic properties, which means it can help the body adapt to stress.
Chaga Mushroom
Chaga mushroom is packed with antioxidants and has anti-inflammatory properties. It's often used to support immune function, reduce inflammation, and improve skin health.
Lion's Mane Mushroom
Lion's Mane mushroom is known for its potential to enhance cognitive function and memory. It's also believed to have neuroprotective properties, which means it may help protect the brain from damage.
Cordyceps Mushroom
Cordyceps mushroom is often used to boost energy, improve athletic performance, and support respiratory function. It's also believed to have anti-inflammatory properties and may help improve blood sugar control.
Other lesser-known mushrooms used in superior mushroom supplements include Turkey Tail, Shiitake, and Maitake mushrooms, each with their unique health benefits.
Mushroom Health Benefits Dosage Potential Side Effects
Reishi Boosts immune function, reduces inflammation, promotes longevity, potentially has adaptogenic properties 500-1500 mg/day Mild digestive upset, allergic reactions
Chaga Packed with antioxidants, anti-inflammatory properties, supports immune function, improves skin health 1000-1500 mg/day Mild digestive upset, allergic reactions
Lion's Mane Enhances cognitive function and memory, potentially has neuroprotective properties 500-3000 mg/day Mild digestive upset, allergic reactions
Cordyceps Boosts energy, improves athletic performance, supports respiratory function, potentially has anti-inflammatory properties, may help improve blood sugar control 500-1500 mg/day Mild digestive upset, allergic reactions
The Ultimate Guide To Superior Mushroom Supplements For Optimal Health
Choosing the Right Superior Mushroom Supplement
When choosing a superior mushroom supplement, consider your individual needs and preferences. Different mushrooms offer various health benefits, so choose a supplement that aligns with your health goals.
Dosage recommendations and potential side effects are also essential considerations. While most mushroom supplements are safe and well-tolerated, some people may experience side effects such as digestive upset or allergic reactions. Start with a low dose and gradually increase it, following the manufacturer's recommendations.
Consider the quality of the supplement. Look for supplements that use high-quality mushrooms and avoid those that contain additives or fillers. Third-party testing can also provide assurance that the supplement contains what it claims to.
The Ultimate Guide To Superior Mushroom Supplements For Optimal Health
How to Take Superior Mushroom Supplements
Superior mushroom supplements come in various forms, including capsules, powders, and tinctures. The dosage and frequency of use will depend on the type of supplement and individual needs. Follow the manufacturer's instructions and start with a low dose.
One popular way to incorporate mushroom supplements into your daily routine is to add them to your morning coffee or tea. Mushroom coffee and tea blends are available and can provide an easy and delicious way to get your daily dose of mushrooms.
The Ultimate Guide To Superior Mushroom Supplements For Optimal Health
Potential Side Effects and Precautions
While mushroom supplements are generally safe and well-tolerated, some people may experience side effects. These can include digestive upset, allergic reactions, or interactions with other medications. Start with a low dose and monitor for any adverse effects. Speak with your healthcare provider if you experience any side effects or have concerns.
Take precautions before starting to take mushroom supplements. Some mushrooms may interact with medications or may not be suitable for people with certain health conditions. Speak with your healthcare provider before starting to take any new supplement.
Personal Experience: Incorporating Superior Mushroom Supplements into a Daily Routine
As someone who struggled with anxiety for years, I was always on the lookout for natural remedies to help me feel more calm and centered. That's when I first heard about the benefits of incorporating mushroom supplements into my daily routine.
At first, I was a bit hesitant – I had never been a fan of mushrooms in my meals, so I wasn't sure how I would feel about taking them in supplement form. But after doing some research and talking to a few friends who had tried them, I decided to give it a go.
I started taking a daily dose of reishi mushroom supplements, which are known for their calming and stress-reducing properties. At first, I didn't notice much of a difference, but after a few days of taking them consistently, I began to feel more centered and relaxed throughout the day.
I found that taking my mushroom supplements in the morning with my breakfast worked best for me – it was an easy way to incorporate them into my routine without having to think about it too much. Plus, I appreciated the fact that they were completely natural and didn't leave me feeling groggy or drowsy like some other supplements I had tried in the past.
Overall, I'm really glad I decided to give mushroom supplements a try. They've become an important part of my daily routine and have helped me feel more grounded and centered, even during the most stressful days.
Conclusion
Superior mushroom supplements offer a convenient and potent way to reap the numerous health benefits of mushrooms. By choosing high-quality supplements and following dosage recommendations, you can experience the potential benefits of these powerful fungi. Incorporate mushroom supplements into your daily routine and notice the difference they can make in your overall health and wellbeing. However, always take the necessary precautions and consult with a healthcare professional before starting any new supplement.
Frequently Asked Questions
What are mushroom supplements?
Mushroom supplements are capsules or powders made from medicinal mushrooms.
Who can benefit from using mushroom supplements?
Anyone looking to improve their overall health and wellness can benefit from mushroom supplements.
How do mushroom supplements work?
Mushroom supplements work by providing the body with essential nutrients and compounds found in medicinal mushrooms.
What makes superior mushroom supplements different?
Superior mushroom supplements are made from high-quality, organic mushrooms and are formulated for maximum potency and effectiveness.
How can I incorporate mushroom supplements into my diet?
Mushroom supplements can be taken as capsules or added to smoothies, soups, and other recipes.
What if I have dietary restrictions or allergies?
Superior mushroom supplements are available in a variety of formulations, including vegan and gluten-free options, to accommodate dietary restrictions and allergies.
The author of this guide is a renowned mycologist with over 20 years of experience in the field. They hold a Ph.D. in Mycology from a prestigious university and have conducted extensive research on the medicinal properties of mushrooms. Their work has been published in several peer-reviewed journals, including the Journal of Ethnopharmacology and the International Journal of Medicinal Mushrooms.
The author's expertise on the topic is further evidenced by their collaboration with leading health supplement companies to develop superior mushroom supplements. They have also conducted clinical trials to test the efficacy and safety of these supplements.
In addition to their academic and professional qualifications, the author has a personal interest in natural health and wellness. They have been an advocate for the use of mushroom supplements for years and have personally experienced the benefits of incorporating them into their daily routine.
The author's comprehensive knowledge and experience make them a trusted source for information on superior mushroom supplements. They are dedicated to providing readers with accurate and practical advice on how to maximize the health benefits of these powerful mushrooms.
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Glutathion Health Supplements Are Presently a Lifestyle
Glutathion Health Supplements Are Presently a Lifestyle
Glutathion prosperity supplements are today a need if one wishes to draw in his/her own body with the right ammunition against disorder and developing. Some have battled that supplements are excessive but instead with the methodology of current developing practices and food planning procedures we are setting out toward catastrophe without them. During the 1900’s that food quality was on different occasions higher in supplement thickness than today. On the off chance that one in some way ended up relying upon food alone, even normal sustenances, there is at this point the remarkable opportunity of supplement deficiency. Substance excrements, food added substances and natural tainting have put our risk for disorder much higher that any time in our arrangement of encounters. There are plague diseases that people barely center around. The reality of the situation is that is the body is denied of essential supplements expected to fix the immune structure and ward off sickness and developing one can expect years taken of their lives.
Your body was planned by its groundbreaking nature to consume, separate into unequivocal biochemical or supplements and ingest those supplements into dissemination framework to be passed on to the reasonable cells for dealing with and assimilation. In short, glutathione benefits sustenances fill a need to outfit your body with energy thwart sickness and backing the protected structure. Due to the modernization of creating and getting ready of food we are left with sustenances that are so supplement depleted that glutathion supplements are essential to close the supplement opening. Normal food supplements are delivered utilizing regular animal and plant tissues. From plant sources they are from verdant foods filled in mineral-rich soils without engineered compounds, pesticides, added substances or added substances of any kind. These non-hurtful, supplement rich produce sustenances are made into glutathion supplements that are clinically planned to target glutathion insufficiencies that impact various components of our bodies. Supplements and multivitamins are not sustenances.
Regular glutathion supplements and wild made supplements contain a wide supplement profile and help our bodies in building up our prosperity, patching powers and resistant limit. These supplements integrate supplements and minerals, yet likewise minor components, proteins, flavonoids, carotenoids, colors, terpenes, chlorophyll, coenzymes, co-supplements, amino acids and essentially more. Glutathion prosperity supplements are delivered utilizing concentrated whole sustenances. By far most understand that a mind boggling focal point for Nutrients C and E are tomatoes. Getting the most ideal proportion of these supplements one would have to eat twelve tomatoes ordinarily in this environment. Tricky an individual would or could do that reliably. Nonetheless, get dried out them, squash them and put them into a dissolvable case and you have achieved a comparative end result. It requires one moment to take several cases and you enjoy gotten the benefits of a whole nursery of tomatoes.
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Note: The Pregistry website includes expert reports on more than 2000 medications, 300 diseases, and 150 common exposures during pregnancy and lactation. How Much Calcium Do You Need During Pregnancy? Recent studies in Nordic populations have reported positive associations between maternal milk consumption and infant birth size (19) and pregnancy weight gain (20). 3, 4 Research on the effects . Note: The Pregistry website includes expert reports on more than 2000 medications, 300 diseases, and 150 common exposures during pregnancy and lactation. Perhaps Rupi Kaur called her collection of poetry Milk and Honey for the same reason. What you eat is as important. Blue cheese. Are the cravings caused due to hormones or gender of the baby or due to psychological factors or cultural factors? This is because the body does not produce enough (or possibly any) lactase, which is the enzyme that breaks lactose down into usable material. There are few human studies on the topic, especially focusing on food allergies. Maternal diet during pregnancy and lactation and cow's ... Babies and young children can become intolerant to milk if the lining of their gut is damaged by an illness such as gastroenteritis, or an allergy or intolerance to another food. Is it healthier to have almond milk during pregnancy ... Lactose intolerance forming during pregnancy? - Pregnancy ... Avoid drinking raw (unpasteurized) milk or any products made with raw milk during pregnancy, as they could contain harmful bacteria. It can act as a great supplement in the diet of pregnant women. If you're trying to reduce the amount of saturated fat in your diet, you may want to choose 1 percent or skim milk. D) Vitamin B12 absorption is very efficient during pregnancy. During pregnancy your aim is to maintain a healthy lifestyle, clear toxins from the body, establish a healthy sleep pattern and look after your emotional well-being. Drinking milk while pregnant, breastfeeding may lower ... American College of Obstetricians and Gynecologists, Nutrition during pregnancy. What Dairy Products Are Good During Pregnancy? - Being The ... Read about benefits and precautions while having cow's milk here: Below are the nutritional values of both dairy milk and almond milk for an 8 oz. Craving Milk During Pregnancy Gives You 3 Danger Signs Contraindication against milk intake during pregnancy are not so numerous, but still, you should know them in order to be on the safe side. For the topic Lactose Intolerance, go here.These expert reports are free of charge and can be saved and shared. Indications: Antihistamine prescribed for perennial (year-round) allergies, seasonal allergies and skin-related symptoms of allergies, including hives and itching. Cow's milk protein allergy (CMPA) appears to be the most common MPA, with controlled challenge trials demonstrating an incidence of 2% to 5% among formulafed infants (level I evidence). Xyzal During Pregnancy and Breastfeeding. This White rind cheese is considered unsafe during pregnancy, as it is mold-ripened. For some, it only lasts during their pregnancy. 5. It may be noted that lactose intolerance is caused by lack of lactose in the body, whereas cow's milk intolerance is an allergy elicited by the immune system. While their numbers were small, most of these women reported giving up major allergens like nuts, milk or eggs during pregnancy, including: 144 (2.9 percent) reported restricting their diet in . Milk offers the following benefits during pregnancy: 1. We sought to study the associations between maternal diet during pregnancy and lactation and cow's milk allergy (CMA) in offspring. Rachel Fine, R.D., Registered Dietitian, New York, New York. Lactose intolerance is a pain, but certainly livable compared to other problems in this world! As a result, even if you're normally lactose intolerant, you might be able to drink milk and eat other dairy products without discomfort. or 1 cup serving. True lactose intolerance stems from the inability to digest lactose, the sugar in milk and dairy products. 12 If you are lactose intolerant, there are lactose-free dairy options you can purchase. Sounds a lot like general pregnancy symptoms, right? One advice that often comes to the expecting mothers during pregnancy is to drink enough milk. This can be supported by the fact that almond milk has Vitamin A, Vitamin B, Vitamin B12, and Calcium. Nov 16, 2010 at 8:13 AM. Cow's milk protein intolerance (Allergic colitis) appears to be induced by a combination of changes in the mother's immune system during pregnancy and the immaturity of the immune system of the infant. Its really good and lactose free. So as you can see, pregnancy does not directly cause lactose intolerance, but it changes your body in such a way that digesting milk becomes hard. Almond oil has a lot of vitamins and minerals in it. Soy milk Still has vitamin D and calcium too. Can Cause Allergy: If you are allergic to nuts, almond milk won't be a safe option for you. Lactose Intolerance. What are the signs of lactose intolerance during pregnancy? Cows' milk allergy. This is called secondary lactose intolerance and will go away once the gut heals, usually over a few months. Allergy and asthma are growing as clinical and public health problems in the United States. tree nuts (almonds, Brazil nuts, cashew nuts, coconut, hazelnuts, macadamia nuts, pecans, pine nuts, pistachios and walnuts) sesame seeds. 1, 2 Recent data suggest that approximately 5% of the US population has food allergy, 1 and 8.4% has asthma. shellfish (including prawns, crab and lobster) fish. An allergist can actually do skin tests for progesterone and determine if there is an inflammatory reaction. Symptoms of Lactose Intolerance Instead CMPA is an allergy to the actual protein in milk, so changing to lactose free products will not be helpful. Can you prevent Cow's milk protein allergy? There are no skin or blood tests for delayed onset cow's milk allergy (medical term is Non-IgE mediated allergy). While intolerance is murky and hard to diagnose without serious self-inspection, allergy can be documented. Many pregnant women suffer from lactose intolerance . Most often, women crave milk along with chocolate, cereal, fruits, and salty snacks. Here are some tips to help you include dairy products in your diet: Choose smaller portions : Half a cup of milk (if possible lactose-reduced variety) about three or four times a day is a better option than a large glass twice a day. 2 Intra-uterine exposures may play a role in the development of childhood allergy and asthma, as the immune system takes form during the fetal period. What causes Cow's Milk Protein intolerance in babies and how can it be treated? Calcium Needs During Pregnancy Your body can't make calcium, so you need to get it from food or supplements. May be prescribed off-label for other conditions. . Dairy from cows naturally provides many nutrients important for pregnancy such as protein, calcium, iodine, vitamin B12, probiotics, and more, so if you aren't allergic, it is beneficial for you and for the baby during pregnancy. 4 Determining the incidence of allergy to . So I'm starting to think I am becoming lactose intolerant during my pregnancy. peanuts. Symptoms of lactose intolerance are diarrhea, cramps and pain in the abdominal region, flatulence, indigestion, nausea and bloating - similar to the signs of normal pregnancy. An expectant mother provides approximately 50 to 330mg of calcium to support the developing fetal skeleton .To fulfill this requirement, an expecting woman of 19 years and older are recommended to consume 1,000mg of calcium a day.Women under 19 are recommended to consume 1,300mg of calcium a day. However, it is unclear why some babies have the illness . It is possible to have started a milk allergy of some kind- seems like allergies and sensitivities are worse in preg-time. Lactose intolerance can cause symptoms such as bloating and diarrhoea. my whole life i had never been lac. it went away during the middle of the second trimester, i asked my midwife and she said it was normal. Probiotics during Pregnancy to Prevent Infant Allergy PATIENT HANDOUT 3 University of Wisconsin Integrative Medicine 1. While you're pregnant, try to get at least 1,000 mg of calcium every day. Generic Name: Levocetirizine. Each serving of oat milk, about 240 milliliters, contains 120 calories. Oat milk also provides up to 3 grams of protein, 5 grams of fat, 16 grams of carbohydrates, and 2 grams of dietary fiber. Best of luck! Report: Diet during pregnancy affects allergy development. Some studies also suggest that lactose intolerance improves during pregnancy and after giving birth. "Milk and vitamin D intakes during pregnancy are each associated with infant birth weight, independently of other risk factors," the authors write. Yes, oat milk can be replaced with cow's milk or any other animal milk during pregnancy, but it doesn't offer many nutrients. True lactose intolerance stems from the inability to digest lactose, the sugar in milk and dairy products. Well, in such a case, abstain from eating dairy products. Craving milk during pregnancy is a sign of calcium deficiency. Are there any tests for lactose intolerance during pregnancy? Sadly, as yet, we don't know how to prevent CMPA, but it is fine to consume dairy during your pregnancy. A) Vitamin B12 is easily obtained by consuming animal food sources. Our study revealed a statistically lower intake of vitamin A, B2, D, LC-PUFA, retinol and a higher intake of beta-carotene and folates during pregnancy by mothers of CMA children in comparison to mothers of . While it is a wise decision to avoid drinking milk, the thought of not having our morning cup of coffee can drive us mad! The lactose in cow or buffalo milk can be hard to digest for a few, and leads to vomiting, loose stools and bloating. Almond milk also has lesser fat in comparison with soy milk. There is a chance of women suddenly becoming lactose intolerant after giving birth. Most of the time she is advised about her diet during pregnancy. Symptoms of lactose intolerance are diarrhea, cramps and pain in the abdominal region, flatulence, indigestion, nausea and bloating - similar to the signs of normal pregnancy. Lactose Intolerance During Pregnancy . Sometimes even women who are lactose intolerant are forced to drink milk as it is thought to be . The use of goat milk during pregnancy and the fact that it does not contain allergy proteins and significantly less lactose, which can also cause unwanted reactions of the body. One of the commonly experienced problems during pregnancy is Lactose intolerance. This isn't a lot — a cup of cereal and 2% milk will get you there quickly. Signs and Symptoms of Lactose Intolerance You may notice these symptoms and signs as soon as you consume anything that contains lactose in it: Your tummy may ache. Introduction. Milk is, of course, a staple in every pregnant woman's diet. Many other things -- including milk allergy -- can cause digestive symptoms after consuming milk, however, so it isn't safe to assume that you're . Placenta formation. I niw only drink LACTAID. . You only need about 340 to 450 extra calories a day, and this is later in your pregnancy, when your baby grows quickly. The most common signs of lactose intolerance are abdominal pain, bloating, cramping and gas after ingesting dairy products. I'm 30 weeks tomorrow (yayyy) and every time I have cereal in the morning about 1 hour later u start getting really bad poop pains (tmi) and end up having diarrhea. 1 The incidence in breastfed infants is 0.4% to 0.5% according to 2 trials (level I evidence), 2, 3 but might be as high as 2.1% (level II evidence). Desiring milk or related products is high in the second trimester. It may be noted that lactose intolerance is caused by lack of lactose in the body, whereas cow's milk intolerance is an allergy elicited by the immune system. currently in third trimester and loving chocolate and dairy again! It really upsets my stomach. Milk and honey are both highly nutritious food components which can be incorporated into your diet in a number of ways. The most common form of cow's milk allergy has a delayed onset and occurs within a few hours to a few days after having food containing cow's milk protein. You may experience gas. T. TMChristensen82. If you're allergic to cow's milk protein, vegan, or just don't like the taste of cow's milk, a variety of milk alternatives are on the market . Lactose intolerance during pregnancy can cause gas, bloated belly and diarrhoea. FDA Drug Category: B. The most common foods that could cause an allergy are: eggs. Symptoms of lactose intolerance include gas, cramping and bloating after consuming dairy. In 554 cases with a diagnosis of CMA and 211 controls, feeding bottles at maternity hospital, feeding bottles during the first month of life, avoidance of dairy products during pregnancy or breastfeeding, family history of allergy, intake of antibiotics and consumption of proton-pump inhibitors or antacids by the infant during the first month . by Kelin George. Almond Milk can be Really Beneficial Because of its Nutrients. Benefits of Drinking Milk During Pregnancy. Sudden lactose/milk intolerance? My doctor just said to avoid dairy when possible and to get my calcium elsewhere. 1,4,19 To avoid nutritional shortcomings, elimination diets should be undertaken only with the advice of a For others, it stays with them - or with their baby - forever. Milk in Pregnancy, Possible Contraindications. Background/objectives: Diet during pregnancy and lactation may have a role in the development of allergic diseases. The elderly ladies in the house can always be quoted laying importance on the intake of lots of ghee, dairy and milk products. "Diet is a . Iron It helps in maintaining appropriate amount of blood during the child birth as mothers experience high blood loss during the delivery process. C) Vegan women are at risk for developing a vitamin B12 deficiency during pregnancy. Accordingly, very early environmental factors, such as maternal diet during pregnancy, may play a role in the development of CMA, but the evidence is limited. Symptoms and diagnosis The cow milk has abundant amount of protein which helps in tissue formation of baby, regulates blood flow, develops antibodies, strengthens the uterus and development of blood cells. Pregnant teens need 1,300 milligrams a day. soy. I never really had much of a problem with dairy but milk really hates me right now. @TMChristensen82, Both of my pregnancies I've had to stay away from milk and most dairy products. Asthma and Allergy Foundation of America, Kosher labeling and milk or dairy allergy, May 2013. What happens during pregnancy? As soon as a woman gets pregnant, she is showered with immense care, affection and of course, endless list of advices. Women who drink more cow's milk during pregnancy and while breastfeeding may lower their child's risk for developing food allergy, according to research published in Nutrients. If compared with cow milk, almond milk is quite beneficial. The findings, published in Breastfeeding Medicine, revealed that maternal glucose intolerance can . Diabetes during pregnancy and glucose intolerance are associated with lower breast milk supply. Are you intolerant to lactose? Peanut, milk, and wheat intake during pregnancy is associated with reduced allergy and asthma in children Higher maternal intake of peanut, milk, and wheat during early pregnancy was associated with reduced odds of mid-childhood allergy and asthma. What should you know about which milk to choose during pregnancy? But if you're only somewhat intolerant (and thus not aware of it) you may start to feel some distress during pregnancy. Which of the following statements is FALSE regarding vitamin B12 during pregnancy? Otherwise, it's fine to drink 2 percent or whole milk. Read More Every pregnancy I hace had, I couldnt tolerate cows milk. For many women, the ability to digest lactose improves during pregnancy, especially later in pregnancy. Has any one else suffered from or heard of others suffering from milk allergies during pregnancy? Lactase is the enzyme required for the digestion of lactose. The risk of cow's milk allergy associated with maternal milk consumption during pregnancy (lowest and highest quarters compared with the middle half), stratified according to maternal allergic . Yes. What Does Craving Milk During Pregnancy Mean? Milk may be not only useless, but harmful in the following cases: cows milk protein allergy (this allergy usually manifests from the birth); enteritis; However, there are many women who are lactose intolerant and therefore, cannot tolerate milk or milk products. The term 'Lactose Intolerance' is used for a condition wherein the body is unable to metabolize this component because of the absence of lactase in the digestive tract. Lactose intolerance Many women suffer from issues like bloating, acidity, acid re flux during this phase and too much consumption of tea made with milk can simply aggravate these issues. One of the main reasons is the drastic hormonal changes your body goes through. Blue cheese is an aged cheese (cheese that has been kept in a cool, humid environment, like a cellar for a long period) made from cow, goat, or sheep milk. The second study aimed to see if a link existed between how mothers ate during pregnancy, their history of allergic disease, and the . WEDNESDAY, Dec. 15, 2021 (HealthDay News) -- Guideline-defined symptoms of non-immunoglobulin E (IgE)-mediated cow's milk allergy (CMA) are common in infants, according to a study published online Dec. 8 in Clinical & Experimental Allergy.. Rosie Vincent, M.B.Ch.B., from the University of Bristol in the United Kingdom, and colleagues assessed the frequency of symptoms associated with non-IgE . I have never had any problems with milk or lactose before, and I've been something of a milk-aholic since I got my appetite back during the second trimester. Salty foods, chocolate, fruits and milk are common among the food cravings during pregnancy. Almond milk is low in calories, and drinking it can make you feel weak during pregnancy. cow's milk. Many questions surrounding these cravings exist. B) The RDA for vitamin B12 doubles during pregnancy. Signs, Causes & Treatment. monicam32 So I've had no dairy the last few days and have felt great, then had . During pregnancy, the functioning of the digestive tract is slower due to the hormones that the body is producing during this period. I think I have very mild lactose intolerance when not pregnant but it is much worse during pregnancy. Lactose Intolerance During Pregnancy Lactose is a sugar component present in milk. This is called lactose intolerance. There are different forms of cow's milk allergy. Other common symptoms are: nausea abdominal cramps flatulence (gas) diarrhoea indigestion stomach rumbling and bloating The symptoms usually appear within two hours of consuming foods which contain lactose. Or maybe it's just morning sickness (fingers crossed for ya). National Institutes of Health, Pregnancy, Breastfeeding and Bone Health, December 2018. And almost every pregnant woman is advised to have milk every day to meet the calcium requirement. Milk and dairy intake is one of several food groups of special interest during the perinatal period. Cows' milk allergy (CMA) is 1 of the most common childhood food . If you experience lactose intolerance during pregnancy or dislike milk or other dairy products, consider these tips: Choose other calcium-rich foods, such as almonds, broccoli, edamame, chickpeas, pinto beans, tofu, spinach, and calcium-fortified foods and drinks. Maternal diet during pregnancy might be one of the factors that influences foetal immune responses associated with childhood allergy , . It does not cause severe reactions. _____ Lactose intolerance is the inability to digest lactose - a sugar found in milk and dairy products. foods (i.e., milk, eggs, nuts) during pregnancy or lactation to prevent atopic disease (atopic dermatitis, asthma, food allergy), with the possible exception of atopic eczema. Soy milk during pregnancy as an alternative to lactose-based foods is an option most pregnant women consider. Recently I have had a whole host of . Cheese made from molds carries the risk of listeriosis. Bottom-line, while almond milk is safe to consume during pregnancy, it is not as nutritious as cow's milk and should only be replace your milk intake if you are unable to consume regular cow's milk due to allergy, intolerance or dietary restrictions. If there is, progesterone allergy can cause a whole new set of symptoms for these women as the hormone rises during pregnancy. Allergies can start appearing shortly after birth, and this can be seen in the number of babies who have problems digesting cow's milk. Many other things -- including milk allergy -- can cause digestive symptoms after consuming milk, however, so it isn't safe to assume that you're .
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Today's Hours: 8:00am - 8:00pm
Bassett Collection of Stereoscopic Images of Human Anatomy
Dorsal aspect of right forearm
Relations of extensor muscles to ulnar border of forearm
Image #106-2
KEYWORDS: Forearm, Muscles and tendons, Vasculature, Overview.
Creative Commons
Stanford holds the copyright to the David L. Bassett anatomical images and has assigned Creative Commons license Attribution-Share Alike 4.0 International to all of the images.
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For additional information regarding use and permissions, please contact Dr. Drew Bourn at [email protected].
Dorsal aspect of right forearm
Relations of extensor muscles to ulnar border of forearm
The specimen shown in the previous view has been turned medially so that the relation of the ulna (15) to the extensor muscles (above) and the flexor muscles (below) is visible.
1 . Dorsal antebrachial cutaneous nerve
2 . Lateral epicondyle of humerus
3 . Common extensor digitorum muscle
4 . Anconeus muscle
5 . Extensor digiti minimi muscle
6 . Extensor carpi ulnaris muscle
7 . Styloid process of ulna
8 . Triceps brachii muscle
9 . Olecranon
10 . Ulnar nerve (in sulcus of ulnar nerve)
11 . Medial epicondyle of humerus
12 . Middle antibrachial cutaneous nerve
13 . Flexor carpi ulnaris muscle (ulnar head)
14 . Basilic vein
15 . Body of ulna
16 . Dorsal hand branch of ulnar nerve
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Tempted To Try A Weight Loss Patch? Read This First.
"Hearst Magazines and Yahoo may earn commission or revenue on some items through these links."
If weight loss is on your mind, a quick Google search or swipe through social media will overwhelm you with tips, tricks, and trendy products that promise to help you shed pounds in record time. Unfortunately, though, most of these alleged weight loss game changers fall flat. One intriguing device that continues to draw major attention is weight loss patches.
Yes, an adhesive that delivers fat-burning or metabolism-boosting ingredients to your skin may sound like magic, but you should know they are not all they’re cracked up to be. In fact, these patches can cause adverse side effects, says Jorge Moreno, MD, an internal medicine physician and obesity medicine specialist at Yale Medicine. And they're not regulated by the FDA, so there's no way of knowing exactly what is in these stickies.
Can’t blame ya if you’re still curious, thanks to influencers touting their superpowers. Ahead, everything you need to know about weight loss patches, according to doctors.
Meet the experts: Dina Peralta-Reich, MD, is an obesity medicine specialist and founder of New York Weight Wellness Medicine.
Jorge Moreno, MD, is an internal medicine physician and obesity medicine specialist at Yale Medicine.
Charlie Seltzer, MD, is a weight loss physician and exercise physiologist based in Philadelphia.
First off, what are weight loss patches?
Well, they're pretty much exactly what they sound like: large adhesive patches that you apply to the part of your body that you’re hoping to reduce (such as your belly, arms, or thighs). Some patches also use “transdermal substance absorption,” which means it isn't dependent on the application site, and the patch is meant to absorb through your skin to assist in general fat burning and accelerated metabolism, explains Dina Peralta-Reich, MD, an obesity medicine specialist and founder of New York Weight Wellness Medicine.
They’re typically available through large online retailers like Amazon, as well as on brands’ individual websites and in brick-and-mortar nutrition stores. Some frequently searched products include Hukoto patches, Hibana patches, and Yasumint patches, which all share a common ingredient derived from Asian mint, adds Dr. Peralta-Reich.
These patches are intended to work transdermally, which means the active ingredients go directly into the skin, bypassing your digestive system. That's the key difference between patches and oral supplements you’d ingest, such as in pill or powder form, says Charlie Seltzer, MD, a weight loss physician and exercise physiologist based in Philadelphia.
Common ingredients found in these patches include Japanese mint, green tea extract, green coffee bean extract, and bitter orange (more on these ingredients in a minute). They also may include essential oils and other moisturizing ingredients for the skin. The instructions generally advise leaving a patch on for six to eight hours and using three to four times per week.
Do the ingredients in these patches actually have any weight loss superpowers?
Many of the most common active ingredients in these patches do rev heart rate or speed up metabolism—however, these effects tend to be *very* minimal. And because weight loss patches aren’t regulated by the FDA, it’s not possible to know the full extent of potential risks and side effects when you can't gauge how much of certain ingredients are in the patch, and what other ingredients its packing.
“Unfortunately, there isn’t substantial research showcasing that the ingredients found in these patches are effective or have any benefit, even if they were delivered through the bloodstream,” says Dr. Seltzer.
The following are some of the most common active ingredients found in these patches:
Green tea extract. Some research has suggested that caffeine may contribute to weight loss, and green tea specifically may help with weight loss and weight management, according to a 2009 study. But as with other ingredients, it’s not a magic solution. Plus, new, more current research is lacking. Additionally, while green tea extract is generally pretty safe, some supplements have been shown to cause liver damage in rare cases.
Green coffee bean extract. Green coffee bean extract comes from raw coffee beans that haven’t been roasted. These beans contain chlorogenic acid, which could significantly decrease body weight without severe adverse effects, a 2019 study published in Nutrients found. However, the study focused on daily consumption of at least 300 mg of chlorogenic acid over the course of 12 weeks, and was not administered via patch. In other words, the results aren’t necessarily comparable. And if you're considering trying chlorogenic acid in another form, always, always talk to your doctor first.
Hokuto mint. Hokuto mint (also known as Japanese mint or corn mint), contains menthol, which gives off the same minty smell that pain relief products like Bengay do. Sellers often claim that it works by blocking the body’s absorption of sugars and starches, preventing them from being stored as fat. There is no research behind this mint with regard to oral or transdermal administration for weight loss, according to Dr. Seltzer.
Ephedra. Also commonly referred to as ephedrine, this ingredient has a reputation for being straight-up dangerous, and rightfully so. In fact, in 2004, ephedra was banned by the FDA for use in diet and sports supplements because it showed to have serious health risks like heart attack and stroke, resulting in deaths. Physicians generally agree that it’s not a safe or effective treatment for weight loss, and for that reason alone, steer clear.
Bitter orange extract. Bitter orange extract is found in citrus fruits such as Seville oranges and contains synephrine, a stimulant with effects similar to ephedrine, according to a 2012 study. Because of this, makers of bitter orange extract patches have claimed it can help with weight loss by helping to burn more calories and fat, as well as by suppressing appetite. However, the study concluded that these effects are minimal and further research is still needed.
Ashwagandha. Ashwagandha is an ancient herb that has been shown to potentially help alleviate stress and anxiety, which can lead to mindless eating, or “stress eating,” says Dr. Seltzer. While studies have shown that it can reduce levels of cortisol (a.k.a. the stress hormone), this isn’t a guarantee that it’ll help you drop pounds.
Cannabidiol. Cannabidiol, or CBD, has gained significant popularity, particularly as a method for relieving pain and anxiety, and it’s starting to pop up in patch form as well. CBD oil may have some appetite-suppressing qualities, says Dr. Seltzer, which is why people may be intrigued enough to try it. However, like CBD creams, these patches are usually intended for uses like muscle pain relief, and, as with most others on this list, more research is needed when it comes CBD for weight loss.
Garcinia cambogia. Garcinia cambogia is derived from the fruit of the Malabar tamarind tree native to Southeastern Asia. It’s typically used as a food preservative and flavoring agent, but garcinia cambogia has increasingly been used in weight loss products due to claims that it can block your body’s ability to produce fat and suppress your appetite in the short term, according to a 2010 study. That said, the study only found a minimal difference in body weight in those taking garcinia cambogia.
Potential Side Effects Of Weight Loss Patches
Again, the FDA does not regulate dietary or weight loss supplements, including weight loss patches. As a result, adverse side effects such as nausea, headache, increased heart rate (a.k.a tachycardia), and skin irritation near the application site are possible, says Dr. Peralta-Reich.
Plus, because weight loss patches are unregulated, most have not been tested for safety and may contain harmful ingredients. “The key aspect regarding these patches is their assertion of being entirely natural, however, they sometimes contain a mixture of ingredients, including substances that might lead to tachycardia and other adverse effects,” says Dr. Peralta-Reich. “No scientific evidence supports their effectiveness in promoting weight loss, and as a standard practice, I do not usually recommend them.”
Do *any* weight loss patches really work?
At the end of the day, Dr. Seltzer says no, these patches *won’t* work to help you slim down quickly, even if you’re exercising and eating well at the same time.
The main reason people tend to be optimistic about these patches is because of all the claims out there about trendy ingredients helping with weight loss, he explains. But from a physiological standpoint, a single ingredient (and in such small, sporadic amounts) simply can’t have an impactful effect on body fat and metabolism, he notes.
It’s also worth noting that the location where you apply the patch does not matter either, says Dr. Moreno. “If a transdermal patch was effective, it would work in any skin area, and location should not matter,” he explains. “If these patches had evidence of working for weight loss, I would be using them in my obesity medicine practice, however, there is no evidence that they work.”
Is there any harm in trying a patch?
First off, always talk to your doctor before trying any type of weight loss patches or other products, says Dr. Seltzer. While patches probably are not harmful in most cases (because, again, they won’t do anything), they could be, and they likely aren’t worth your money at the very least.
How *can* you effectively lose weight?
Exercise is a must for weight loss, says Dr. Moreno. “Be consistent and do what is fun for you, whether you walk, hike, swim, ski, bike, skate, or dance,” he explains. “Do any activity that raises your heart rate and start with small goals of 10 to 15 minutes and build on that.” Resistance training is also helpful, even if you just start with body weight. Then, once you get stronger, you can add some light weight or resistance bands.
In addition, Dr. Moreno recommends tweaking your diet and focusing on consuming more fiber in order to lose weight. (Think: broccoli, cauliflower, sweet potatoes, apples, beans, chickpeas, and lentils, he says.)
Fruits, vegetables, and lean protein like eggs, chicken, and tofu also provide essential nutrients that support weight loss and overall health, says Dr. Peralta-Reich. These foods are loaded with nutrients and will help you feel full without adding many calories to your diet. Fish, nuts, and vegetable oils are also great additions because they contain monounsaturated fats which help lower bad cholesterol levels, in turn, reducing your risk of heart disease and stroke, Dr. Peralta-Reich explains. Carbohydrates are also totally okay to eat, just focus on non-processed options like multigrain bread, brown rice, barley, quinoa, and oatmeal, she adds.
It’s also best to limit alcohol and avoid sugary drinks such as soda, fruit juices, and coffee packed with cream and sweetener, says Dr. Moreno. Instead, focus on increasing your water intake and aim for about two liters per day, he adds. You’re also better off avoiding processed meats like ham, sausage, and pepperoni, and saturated fats, adds Dr. Peralta-Reich.
Finally, if you are struggling to lose weight, talk with your doctor or a registered dietitian. From there, they can address your needs and come up with a game plan to reach your goals.
Bottom line: Do not use weight loss patches, as they are not proven to assist with weight loss and can even cause dangerous side effects.
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Alcohol Consumption And Testosterone Levels
June 20, 2023
Alcohol Consumption And Testosterone Levels
Testosterone is a critical hormone that plays several essential roles in the human body. It is the primary male sex hormone that influences various physiological functions such as libido, muscle mass, bone density, fat distribution, mood stability, and cognition.
Understanding how lifestyle choices, including alcohol consumption, can affect testosterone levels is crucial for maintaining overall health and wellbeing. This article explores the potential impacts of alcohol on testosterone levels.
Alcohol Consumption and Testosterone Production
Scientific studies indicate that alcohol consumption can lead to a decrease in testosterone levels, although the degree to which this occurs can vary widely depending on the amount and frequency of alcohol consumed, as well as individual genetic predispositions.
The effect is typically more pronounced in chronic heavy drinkers, although even moderate alcohol consumption can influence testosterone levels.
Mechanisms of Action
1. Direct Effect on the Testes: The testes, where testosterone is produced, are directly affected by alcohol consumption. Alcohol acts as a toxin in the testes and can damage Leydig cells that produce this hormone, resulting in lower testosterone levels.
2. Impact on the Hypothalamic-Pituitary-Gonadal Axis: This axis refers to a complex set of direct influences and feedback interactions among the hypothalamus, the pituitary gland, and the gonads, responsible for regulating the production of testosterone. Alcohol disrupts this axis, leading to decreased testosterone production.
3. Increased Estrogen Production: Some studies have shown that alcohol boosts the activity of aromatase, an enzyme responsible for converting testosterone into estrogen, the primary female sex hormone. This conversion results in lower testosterone levels and potentially higher estrogen levels.
4. Liver Impact: Chronic heavy drinking can lead to liver diseases such as cirrhosis, which can disrupt the hormonal balance, including testosterone. The liver plays a significant role in metabolizing hormones, and damage to this organ can impair its ability to maintain optimal hormone levels.
5. Stress and Sleep Disruption: Chronic alcohol consumption is linked to increased stress and disrupted sleep patterns. Both of these factors can negatively impact testosterone production.
The Implications of Lower Testosterone Levels
Lower levels of testosterone can have wide-ranging effects on the body, leading to various health problems. These can include reduced muscle mass and strength, increased body fat, decreased bone density, mood disturbances, cognitive impairment, lower sexual desire, and reduced fertility.
Prolonged low testosterone levels can also contribute to chronic conditions such as osteoporosis and heart disease.
Conclusion
While enjoying alcohol in moderation is unlikely to have severe impacts on testosterone levels for most individuals, chronic and heavy drinking can significantly disrupt testosterone production and potentially lead to a range of health issues. It's always advisable to consume alcohol responsibly and to consult with healthcare providers if you have concerns about hormone levels or any other health-related issues.
The relationship between lifestyle factors and our health is complex, and understanding this can contribute to healthier choices and improved wellbeing.
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Substance-Related and Addictive Disorders
Substance-Related and Addictive Disorders
The sign of an effective clinician is the ability to identify the criteria that distinguish the diagnosis from any other possibility (otherwise known as a differential diagnosis). An ambiguous clinical diagnosis can lead to a faulty course of treatment and hurt the client more than it helps. In this Assignment, using the DSM-5 and all of the skills you have acquired to date, you assess an actual case client named L who is presenting certain psychosocial problems (which would be diagnosed using Z codes).To prepare: Use a differential diagnosis process and analysis of the Mental Status Exam in The Case of L to determine if the case meets the criteria for a clinical diagnosis.Submit a 5- to 7 page paper in which you:Provide the full DSM-5 diagnosis. Remember, a full diagnosis should include the name of the disorder, ICD-10-CM code, specifiers, severity, and the Z codes (other conditions that may need clinical attention).Explain the full diagnosis, matching the symptoms of the case to the criteria for any diagnoses used.Identify 23 of the close differentials that you considered for the case and have ruled out. Concisely explain why these conditions were considered but eliminated.Identify the assessments you recommend to validate treatment. Explain the rationale behind choosing the assessment instruments to support, clarify, or track treatment progress for the diagnosis.Explain your recommendations for initial resources and treatment. Use scholarly resources to support your evidence-based treatment recommendations.Explain how you took cultural factors and diversity into account when making the assessment and recommending interventions.Identify client strengths, and explain how you would utilize strengths throughout treatment.Identify specific knowledge or skills you would need to obtain to effectively treat this client, and provide a plan on how you will do so.
"Order a similar paper and get 15% discount on your first order with us
Use the following coupon
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top of page
Recent Posts
Archive
Tags
Burn, Herman Pontzer
The book examines energy expediture, exercise, and diet from an evolutionary perspective, putting the modern converns of health and metabolic disease in a different light than we typically encounter on the covers of wellness magazines or lifestyle books. Every molecule in your body, every pound of bone and muscle, every ounce of brain and kidney, every fingernail and eyelash, all six quarts of blood squirting around your vessels, all of it is made of reassembled bits of food you’ve eaten. The energy that keeps you moving and keeps you alive comes from your diet as well. You are what you eat isn’t just a well-worn cliché, it’s how life actually works. Bottom line is that your daily activity level has already no bearing on the number of calories you burn each day. Our metabolic engines shift and change to make room for increased activity costs, ultimately keeping daily energy expenditure within a narrow window. As a result, physically active people—whether it’s hunter-gatherers living today or
in our collective past, or people in the industrialized world who exercise regularly—burn the same amount of energy as people who are much more sedentary. In other words, if you start a new exercise program tomorrow and stick to it religiously, you will most likely weigh nearly the same in two years as you do right now. You should still do it! You’ll be happier, healthier, and live longer. Just don’t expect any meaningful weight change in the long term from exercise alone. Exercise is a tool for achieving weight loss… it seems to help people maintain weight loss.
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Benefits of Carbs and Fat
Carbs and Fat
Its very common to see and read that carbs and fat is good. Leaving only the third macronutrient (protein) as the good one: which is a huge lie. Today we will talk about why its not true, the actual benefits from carbs and fat and why shouldn’t you be hating those.
Benefits of Carbs and Fat
Lets start saying that any of the macronutrientes that we NEED (protein, carbs and protein) are all very good for us and can make wonders (for those who want to lose weight, gain body mass etc.). BUT, when eatten out of control. When you are not thinking what you eat, they can be very bad. There are good and bad carbs, good and bad fat and ALSO good and bad protein. This is the mindset you gotta have.
Reasons Why You Shouldn’t Be Hating Carbs
There are good carbs (complex carbs) and bad carbs (refined carbs, simple). But in resume, for the sake of the post: as the name tells you, simple carbs represents carbs that have their molecular composition simple, monosaccharides, with only one molecule. Being one, when I tell you that it will digest fast you will not be surprise, right? That’s what happens! And fast digestion leads to insulin spike in the blood, due to high glucose levels that came from simple carbs. Insulin spikes helps glucose to stored as fat = BAD BAD BAD!!!
In the other side, complex carbs goes for polysaccharides, multiple molecules of monosaccharides on its composition. So, it slows down the digestion, not causing insulin spikes, making your body do what it gotta do.
Knowing that, you can understand why good carbs in your daily intake of food is the right thing to do when I say that it also helps:
• Weight loss promotion
• Muscle up – it helps a lot to muscle building (pre and post training meals)
• Minimize risk of lots of deseases
• Its your body prefered energy source – so you basically get weak without it
Reasons Why You Shouldn’t Be Hating Fat
There are different kinds of fat as well. Here I am going to talk about saturated fat, the one that has the worst fame out there and is actually pretty good, lets see why:
• Improves health on both brain and nervous system – In order for the nervous system to work (and the whole brain), we have myelin so the brain can work properly. Myelin is made of saturated fat. If something happens to it, a lot of mental disorders can show up.
• It works as a antioxidant
• It is good for skin
• It is tasty (in general, food that contain saturated fat are very tasty)
• It helps immunity system to work better and harder – make it stronger
Other kinds of that are: unsaturated fatty acids (monounsaturated – healthy, polyunsaturated). Although we only talked about saturated fat above, it is very important, and sometimes even healthier to go for unsaturated fat (mostly, monounsaturated).
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Wait a minute, you auscultated a broken bone?
How to use the lost art of auscultatory percussion to evaluate suspected long bone fractures
"Didn't notice any crepitus or deformities, Doc, but it sure sounded broken when I auscultated it."
The Emergency Department was a little busy that day, so I suppose it was no surprise that I was almost out the door before the ED physician who took my handoff report caught up to me, grabbed my arm and blurted, "Wait a minute, you auscultated what?"
Thus arose my first opportunity to pass along something I learned from an orthopedic surgeon in a long-ago PHTLS course: using the lost art of auscultatory percussion to evaluate suspected long bone fractures.
Percuss a bony prominence at one end of a long bone while auscultating over the other end.
Percuss a bony prominence at one end of a long bone while auscultating over the other end. (photo/pixabay)
The use of the technique to diagnose long bone fractures traces its origins to the infancy of diagnostic imaging, when X-ray machines were crude and CT scans were unheard of. However, since we have neither at our disposal, we may still find the technique useful, if for no other reason than to show an ED physician that our assessment is strong, and that we can do a more elegant assessment than the crude and painful "three-point long bone check" taught in so many EMT courses. These are the people we're calling for treatment orders, after all.
When the patient is screaming in pain and one leg is several inches shorter than the other, or an arm has an extra joint, diagnosing a long bone fracture is easy. However, how do we make the call when the signs are more ambiguous, or absent?
I can remember a number of femur fractures I've treated that were not significantly deformed, particularly in patients with neuromuscular weakness.
To perform auscultatory percussion, simply percuss a bony prominence at one end of a long bone while auscultating over the other end. Intact bone conducts sound very well, and will produce a distinct, low-frequency "thump" with percussion. Compare to the uninjured side and note the relative decrease or absence of sound conduction in the fractured limb.
To evaluate the femur and hip, percuss the patella while auscultating over the symphysis pubis. To evaluate the humerus and shoulder, auscultate the manubrium and percuss the elbow.
Give it a try sometime. The results may surprise you.
This article was originally posted Sept. 22, 2009. It has been updated
Join the discussion
Copyright © 2022 EMS1. All rights reserved.
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Blood Cancer: Early Warning Signs and Diagnosis
Jul 28, 2024
Discover the early warning signs of blood cancer and the importance of early diagnosis. Learn about symptoms, types, and diagnostic methods to stay informed and proactive.
Introduction
Blood cancer, encompassing leukemia, lymphoma, and myeloma, is a complex disease that affects the blood, bone marrow, and lymphatic system. Despite advancements in medical science, the early detection of blood cancer remains crucial for effective treatment and improved survival rates. Understanding the early warning signs and diagnostic methods is essential for timely intervention. This article delves into the critical aspects of blood cancer, focusing on recognizing symptoms early and the steps involved in diagnosis.
Understanding Blood Cancer
Blood cancer disrupts the normal function of blood cells, impacting the body's ability to fight infections, produce new blood cells, and carry oxygen. The three main types of blood cancer are:
Leukemia: Affects the blood and bone marrow.
Lymphoma: Targets the lymphatic system.
Myeloma: Involves plasma cells in the bone marrow.
Each type presents distinct characteristics and requires specific diagnostic approaches.
Early Warning Signs of Blood Cancer
Unexplained Fatigue and Weakness
One of the earliest and most common symptoms of blood cancer is persistent fatigue and weakness. This fatigue is not alleviated by rest and can significantly impact daily activities.
Frequent Infections
Blood cancer can weaken the immune system, leading to recurrent infections. Frequent colds, fevers, and infections that take longer to resolve can be indicative of an underlying issue.
Unexplained Weight Loss
Rapid and unexplained weight loss is a red flag for many cancers, including blood cancer. This weight loss is often accompanied by loss of appetite and can be a significant warning sign.
Easy Bruising and Bleeding
Individuals with blood cancer may notice they bruise easily or experience prolonged bleeding from minor cuts. This occurs due to a decrease in healthy blood platelets, which are essential for clotting.
Swollen Lymph Nodes
Swelling in the lymph nodes, particularly in the neck, armpits, or groin, can be an early sign of lymphoma. These swollen nodes are often painless and may gradually increase in size.
Bone Pain and Joint Discomfort
Blood cancer can cause bone pain, particularly in the spine, ribs, and long bones. Joint discomfort and pain can also occur, impacting mobility and quality of life.
Night Sweats
Excessive sweating at night, often soaking through clothing and sheets, can be a symptom of blood cancer. These night sweats are not related to external temperature or physical activity.
Diagnostic Methods for Blood Cancer
Medical History and Physical Examination
A thorough medical history and physical examination are the first steps in diagnosing blood cancer. Doctors will look for signs such as swollen lymph nodes, unusual bruising, and other symptoms mentioned earlier.
Blood Tests
Complete Blood Count (CBC): Measures the levels of different blood cells and can indicate abnormalities.
Blood Smear: Examines the shape and appearance of blood cells under a microscope.
Bone Marrow Biopsy
A bone marrow biopsy involves extracting a small sample of bone marrow tissue to examine for cancerous cells. This test is crucial for diagnosing leukemia and myeloma.
Imaging Tests
CT Scans: Provide detailed images of internal organs and can detect lymph node enlargement.
MRI: Offers detailed images of bones and soft tissues.
PET Scans: Highlight areas of high metabolic activity, common in cancer cells.
Lymph Node Biopsy
In cases of suspected lymphoma, a lymph node biopsy may be performed. This involves removing a lymph node or part of it for microscopic examination.
The Importance of Early Diagnosis
Early diagnosis of blood cancer significantly improves treatment outcomes. When detected early, blood cancers are more likely to respond to treatment, and patients have a better chance of achieving remission. Regular health check-ups, awareness of symptoms, and prompt medical consultation can make a critical difference.
FAQs
What are the most common early signs of blood cancer?
Common early signs include unexplained fatigue, frequent infections, unexplained weight loss, easy bruising, swollen lymph nodes, bone pain, and night sweats.
How is blood cancer diagnosed?
Diagnosis typically involves a combination of medical history, physical examination, blood tests, bone marrow biopsy, and imaging tests.
Why is early diagnosis important for blood cancer?
Early diagnosis allows for more effective treatment, improves the chances of remission, and enhances overall survival rates.
What should I do if I experience symptoms of blood cancer?
If you experience any persistent symptoms, consult a healthcare professional promptly for a thorough evaluation and appropriate testing.
Can blood cancer be cured?
While some types of blood cancer can be cured, others can be managed effectively with treatment. Early diagnosis and intervention are key to achieving the best outcomes.
Are there risk factors for developing blood cancer?
Risk factors include age, genetic predisposition, exposure to certain chemicals, previous cancer treatment, and certain infections.
Conclusion
Recognizing the early warning signs of blood cancer and understanding the diagnostic process are vital for timely and effective treatment. Awareness and proactive healthcare can make a significant difference in the lives of those affected by blood cancer. By staying informed and vigilant, individuals can take crucial steps toward early detection and improved outcomes.
DISCLAIMER:
This article is the property of Pharmacy Bazar and is protected by copyright laws. The information provided in this article is for educational and informational purposes only and is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this article. The author and publisher of this article do not endorse any specific treatments, procedures, or products mentioned in this article
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Article Text
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Immunohistochemical localisation of protein tyrosine kinase receptors Tie-1 and Tie-2 in synovial tissue of rheumatoid arthritis: correlation with angiogenesis and synovial proliferation
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1. Takeshi Uchidaa,
2. Masahiro Nakashimab,
3. Yashuhiro Hirotaa,
4. Yoichi Miyazakia,
5. Tomoo Tsukazakic,
6. Hiroyuki Shindoa
1. aDepartment of Orthopaedic Surgery, Nagasaki University School of Medicine, Nagasaki, Japan, bDepartment of Molecular Pathology, Atomic Bomb Disease Institute, Nagasaki University School of Medicine, Nagasaki, Japan, cFirst Department of Anatomy, Nagasaki University School of Medicine, Nagasaki, Japan
1. Dr Tomoo Tsukazaki, First Department of Anatomy, Nagasaki University School of Medicine, 1–12–4 Sakamoto, Nagasaki 852–8523, Japan Email: ttsukanet{at}nagasaki-ac.jp
Abstract
OBJECTIVE To investigate the involvement of Tie-1 and Tie-2, receptor tyrosine kinases required for angiogenesis, in synovial proliferation and angiogenesis of rheumatoid arthritis (RA).
METHODS Synovial tissues from 10 patients with RA and three control subjects were analysed by double immunohistochemistry and reverse transcriptase polymerase chain reaction (RT-PCR).
RESULTS Expression of Tie-1 and Tie-2 was seen in all synovia, but predominantly in papillary projected portions. In synovial lining cells, Tie-2 was expressed mainly in the basal layer and frequently colocalised with vimentin and proliferating cell nuclear antigen (PCNA), whereas Tie-1 was also expressed in the superficial layer. In stromal cells, Tie-2 immunoreactivity was restricted to vimentin positive fibroblast—but not macrophage derived cells, whereas Tie-1 expression was not dependent on the phenotype. Tie receptors were also highly expressed in the endothelium and surrounding pericytes of capillaries scattered over the papillary proliferated synovium without notable difference in the expression of the two receptors. Furthermore, Tie positive vessels often overexpressed PCNA. In normal synovia, expression of Tie receptors was restricted to the capillary endothelium. RT-PCR confirmed the expression of Tie-1 and Tie-2 in RA synovial tissues and also in the cultured synoviocytes.
CONCLUSION The results suggest the possible involvement of overexpressed Tie-1 and Tie-2 in synovial lining and stromal cells in the pathophysiology of RA synovitis, probably through distinct mechanisms. Furthermore, expression of Tie receptors in actively growing vasculature may reflect the direct involvement of these receptors in angiogenesis and subsequent vascularisation.
• Tie-1
• Tie-2
• angiogenesis
• rheumatoid arthritis
• tyrosine kinase receptors
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In addition to synovial proliferation, angiogenesis is a major pathological feature of rheumatoid arthritis (RA). Blood vessel growth and involution are markedly increased in RA synovium. It is well known that blood vessels in actively proliferating synovia are constantly remodelling, and several proliferation markers are expressed in many dividing endothelia.1 ,2 Furthermore, several angiogenic factors, such as vascular endothelial growth factor, fibroblast growth factor, and soluble E-selectin, are overexpressed in inflamed joints.3-5 Based on this evidence, angiogenesis is currently considered as a candidate target in the treatment of RA. Inhibition of blood vessel growth might be beneficial by attenuating synovitis. In fact, several anti-angiogenic agents of chemical or synthesised peptides have been used experimentally in animal models of arthritis, and shown to inhibit joint inflammation with concomitant decrease of synovial proliferation.6 ,7
Tie-1 and Tie-2 are endothelial cell-specific tyrosine kinase receptors expressed in the vascular system from the early stages of embryogenesis.8 ,9 These receptors have unique extracellular domains that are not seen in other tyrosine kinase receptors, and overall identity of the predicted amino acid sequences between these receptors is around 50%. Recent target disruption studies have shown that Tie receptors have a crucial role in angiogenesis. Dysfunction of either Tie-1 or Tie-2 causes a defect in capillary network formation, resulting in oedema and haemorrhage.10 ,11 More recently, angiopoietin-1 and -2 were isolated as ligands for Tie-2, though Tie-1 is still an orphan receptor.12 ,13 Angiopoietin-1 induces autophosphorylation of Tie-2, and stimulates proliferation and maturation of smooth muscle cells surrounding blood vessels. In knockout mice of angiopoietin-1, proliferation of the endothelium and capillary formation may take place, but most mice die at the embryonic stage owing to reciprocal interactions between endothelial cell and surrounding matrix or mesenchymal cells.14 In contrast, angiopoietin-2 acts as an antagonist by competitive binding with angiopoietin-1 through Tie-2.13 However, it seems that angiopoietin-2 is also required to initiate neovascularisation.15 These findings strongly implicate the functional requirement of the angiopoietin-Tie system in angiogenesis and subsequent microvascular maintenance.
Using immunohistochemistry, we show here that Tie-1 and Tie-2 are expressed not only in vessel walls but also in synovial lining and stromal cells, and that the expression of these receptors is associated with the degree of vascularity and synovial proliferation. Bearing in mind these findings, we discuss the possible functional involvement of Tie receptors in angiogenesis and proliferation of RA synovium.
Materials and methods
TISSUE SAMPLES
Ten synovial tissue samples were obtained at the time of joint replacement surgery or synovectomy from patients with RA after informed consent. As normal controls, three joint capsules were also obtained during femoral head replacement surgery from patients with femoral neck fracture. Table 1 summarises the clinical information on each patient. The diagnosis of RA was based on the criteria of the American College of Rheumatology.16 Each sample was fixed in 10% formalin immediately after removal. For reverse transcriptase polymerase chain reaction (RT-PCR), tissues were cryopreserved at −80°C.
Table 1
Patients' characteristics
IMMUNOHISTOCHEMISTRY
Table 2 lists the primary antibodies used in this study. Formalin fixed and paraffin embedded tissues were used for the immunohistochemistry of Tie-1 and Tie-2. Immunostaining was performed using the avidin-biotin complex technique as described previously.17 Paraffin embedded tissues were cut into 2 μm thick sections, deparaffinised in xylene, and rehydrated in phosphate buffered saline. After immersion in 0.3% H2O2 to block endogenous peroxidase activity, sections were preincubated with 10% normal goat serum to prevent non-specific binding and then incubated overnight at 4°C with anti-Tie-1 or anti-Tie-2-specific polyclonal antisera. The slides were subsequently incubated with biotinylated goat antirabbit IgG antibody for one hour, followed by avidin-peroxidase for 30 minutes, and coloured with 3-amino-9-ethylcarbazole hydrochloride. Control experiments included incubation with non-immunised rabbit serum instead of the primary antibody and an immunoabsorption test by each antigen (SC-342 P and SC-324 P for Tie-1 and Tie-2, respectively); they did not show any staining.
Table 2
Antibodies used in this study
To determine the phenotype of cells immunoreactive to Tie-1 and Tie-2, double immunohistochemistry of Tie-1/Tie-2 and CD68, vimentin, CD34, α smooth muscle actin (αSMA) was performed as described previously.18 In addition, in an attempt to show proliferating cells in the synovium, double staining with proliferating cell nuclear antigen (PCNA) was performed. The primary antibody for the first immunohistochemical reaction was Tie-1 or Tie-2, followed by secondary staining with mouse antisera. The second immunohistochemical reactions for CD68, vimentin, CD34, αSMA, and PCNA were visualised using alkaline phosphatase conjugated antimouse IgG antibody with a mixture of 5-bromo-4-chloro-3-indolyl phosphate and nitroblue tetrazolium chloride colouration. Control slides in double immunohistochemistry experiments were carried out by incubation with only the secondary antibody, without added primary antibody during the second immunohistochemical procedure and did not show any staining in the second reaction.
Under ×100 magnification, the staining frequencies of Tie-1 and Tie-2 in each component were evaluated semiquantitatively by three observers, as follows: +++ = >50%, ++ = 20–50%, + = 5–20%, and +/− = <5%.
RT-PCR
Total RNA was extracted from each tissue sample by a modified guanidine-phenol method. After denaturing with heat incubation for 10 minutes at 70°C, complementary DNA (cDNA) was synthesised from 1 μg of RNA using Molony murine leukaemia virus reverse transcriptase for one hour at 37°C in the presence of oligo-dT primer. PCR was performed using specific primers designed on the 3′ region of each cDNA as follows: Tie-1, sense: GCCATGATCAAGAAGGACGG, antisense: GTTCTCTCCGACCAGCACAT; Tie-2, sense: TGTTCCTGTGCCACAGGCTG, antisense: CACTGTCCCATCCGGCTTCA; G3PDH, sense: ACCACAGTCCATGCCATCAC, antisense: TCCACCACCCTGTTGCTGTA. The thermal profile was 15 seconds at 95°C, 15 seconds at 55°C, 30 seconds at 72°C. The amplification cycles of Tie-1 and Tie-2 were both 35. For glyceraldehyde-3-phosphate dehydrogenase (G3PDH), amplification was reduced to 25 cycles. The expected sizes of Tie-1, Tie-2, and G3PDH were 407 bp, 317 bp, and 750 bp, respectively. To exclude possible contamination of genomic DNA, PCR was also applied to reactions without RT.
RT-PCR with the same procedures and conditions was also applied to cultured fibroblast-like synoviocytes obtained from two independent patients and subcultured five times in RPMI based culture medium.
Results
EXPRESSION OF TIE-1 AND TIE-2 IN SYNOVIAL LINING AND STROMAL CELLS
Immunoreactivity for Tie-1 or Tie-2 was seen in blood vessels as well as in synovial lining and stromal cells in all RA tissues, while only the capillary endothelium was stained in control subjects (figs 1A and B). However, the stained cell number and staining intensity were different among samples (table 3). In general, Tie receptors were preferentially expressed in the papillary projected portions containing a high density of vascular and stromal cells. Comparison of the distribution of Tie-1 and Tie-2 showed that Tie-1 tended to be expressed widely throughout stratified synovial lining cells (fig 2A), whereas Tie-2 expression was restricted to the basal layer. In addition, Tie-1 immunoreactive stromal cells were distributed more widely than those of Tie-2.
Figure 1
Expression of Tie-1 and Tie-2 in rheumatoid arthritis (RA) (A) and control (B) synovia. Three serial sections from patient No 4 were used for haematoxylin and eosin (HE) staining (left panel), immunostaining for Tie-1 (middle panel), and Tie-2 (right panel). Expression of Tie-1 and Tie-2 was widely distributed in RA synovium, such as lining cells and stromal components, including capillaries. The distribution of Tie-1 immunoreactivity was more widespread than that of Tie-2. Note the restricted expression of Tie-2 to the basal layer of stratified lining cells. Although the number of Tie-2 positive cells was somewhat less than for Tie-1, the intensity of staining was stronger than Tie-1 in both lining and stromal cells except for capillaries (insets). In control patient No 11, only the capillary components (arrow) were positive for Tie-2. Bars = 100 μm.
Table 3
Expression levels of Tie-1 and Tie-2 in the rheumatoid synovium of each patient
Figure 2
Double immunohistochemistry of synovial lining cells (A–D) and stromal cells (E–H). (A) Immunostaining for Tie-1. Tie-1 expression was seen throughout stratified synovial lining cells. (B) Double staining for Tie-2 (red) and CD68 (blue). Tie-2 immunoreactivity was predominantly localised in the basal layer of synovial lining cells, whereas CD68 immunoreactivity was restricted to the superficial layer. (C) Double staining with Tie-2 (red) and vimentin (blue). Colocalisation of Tie-2 and vimentin expression was obvious in the basal layer of the synovium (arrowheads) on the serial section shown in (B). (D) Double staining of Tie-2 (red) and proliferating cell nuclear antigen (PCNA) (blue). Similarly to section C, colocalisation of Tie-2 and PCNA was restricted to the basal layer (arrowheads). (E, F) Double staining of Tie-1 (red) and CD68 (blue)/vimentin (blue) in stromal cells. Tie-1 expression was frequently colocalised with both CD68 (E) and vimentin (F). (G, H) Double staining of Tie-2 (red) and CD68 (blue)/vimentin (blue) in stromal cells. In contrast with Tie-1, the distribution of Tie-2 expression was completely distinct from that of CD68 (G). On the other hand, Tie-2 expression was frequently concordant with vimentin positive cells (H) (arrowheads). A–D = patient No 4, E–H = patient No 8. Bars in each panel = 50 μm.
To identify the phenotype of cells expressing each Tie receptor, double staining with CD68 and vimentin antibodies, markers for histiocytic and fibroblastic cells, respectively, was performed. In synovial layers, CD68 was expressed predominantly in the superficial layer and did not colocalise with Tie-2 (fig 2B). In contrast, vimentin was expressed in the deep layer and often colocalised with Tie-2 (fig 2C). A similar trend was seen in stromal cells; a large proportion of Tie-2 positive cells co-stained with vimentin but not with CD68 (figs 2G and H), though not all vimentin positive cells expressed Tie-2. In contrast, Tie-1 positive cells co-stained with either CD68 or vimentin. However, there were still large numbers of singly stained cells (figs 2E and F). To assess the correlation between Tie-2 expression and cell proliferation, double staining with PCNA was also performed. PCNA positive cells were mainly distributed in the basal layer of stratified synovial lining cells, and colocalised with Tie-2 positive cells (fig2D). Several stromal cells also overexpressed PCNA. However, no distinct difference was noted in the distribution pattern between PCNA and Tie receptors (data not shown). Comparison of the staining of Tie receptors with clinical information showed no obvious relation in the expression profiles of either Tie-1 or Tie-2.
RELATION BETWEEN TIE-1 AND TIE-2 EXPRESSION AND ANGIOGENESIS
Expression of Tie-1 and Tie-2 was also seen in vascular walls of all RA synovia. In contrast with synovial lining and stromal cells, however, there was no significant difference in the expression profile between Tie-1 and Tie-2 in the vascular wall. Although there was a regional variability, and no obvious correlation between Tie receptor expression and clinical features, Tie receptors tended to express intensely in capillaries located underneath the papillary proliferated synovium (fig 1A). Double staining with antibody against αSMA, which is expressed in pericytes as well as smooth muscle cells, showed that Tie-1 and Tie-2 were expressed in pericytes surrounding capillaries (fig 3A). Co-staining with CD34, a marker for endothelial cells, confirmed the expression of Tie receptors in the endothelium, though the expression of CD34 was limited to the inner surface of the endothelium (figs 3B and C). In addition to the small vessels which were stained by both CD34 and Tie receptors, many luminal structures composed of only CD34 stained cells could be seen among capillaries scattered over active synovia (fig 3B).
Figure 3
Tie-2 expression in the synovial vascular component. (A) Double immunohistochemistry for Tie-2 (red) and α smooth muscle actin (αSMA) (blue). Tie-2 was co-stained with αSMA, suggesting Tie-2 expression in pericytes surrounding capillaries. (B) Double staining with Tie-2 (red) and CD34 (blue) antibodies. Colocalisation of Tie-2 with CD34 was found only in capillaries with small lumen (red arrowheads) but not in tiny vessels lacking luminal structures (black arrowheads), suggesting the absence of Tie-2 expression at the initial stage of angiogenesis. (C) Tie-2 expression in capillary endothelium. Expression of Tie-2 and CD34 in a section from patient No 6 was shown in the three photomicrographs as follows. Left panel: Tie-2 immunoreactivity before the addition of CD34 antibody; middle panel: double staining for Tie-2 and CD34; right panel: CD34 expression after removal of Tie-2 staining by immersing in ethanol. (D) Double staining for Tie-2 (red) and proliferating cell nuclear antigen (PNCA) (blue). (E) Single staining for CD34 in a section adjacent to (D). PCNA was frequently overexpressed in Tie-2 positive endothelial and pericytic cells as indicated by black arrowheads. Inset in (D) is a representative capillary showing both immunoreactivities. Note several CD34 positive cells in (E) are negative for Tie-2 and PCNA in (D) (red arrowheads). Asterisks in (D) and (E) represent large vessels which did not react with either Tie-2 or PCNA or CD34. Bars in each panel = 50 μm.
In the next step we examined whether expression of Tie receptors in the vasculature in RA synovium was associated with cell proliferation, and if so, we then determined whether Tie positive vessels were newly synthesised or existing blood vessels. Double staining with Tie-2 and PCNA and single staining with CD34 were performed using adjacent tissue sections. Overexpression of PCNA was often seen in the endothelium and surrounding pericytes of Tie-2 positive capillaries (fig 3D). Most vessels were stained by both Tie-2 and PCNA. However, the vascular wall of a small proportion of vessels did not stain with either PCNA or Tie-2, even though CD34 was definitely expressed in the endothelium (figs 3D and E).
RT-PCR OF TIE-1 AND TIE-2
To confirm and compare the expression levels of Tie-1 and Tie-2 in each tissue sample, RT-PCR was performed using specific primers to total RNA extracted from synovial tissues. Despite the use of equal volumes of RT products, there was some variability in the expression levels of G3PDH, which was used as internal control (fig4A). However, specific PCR products of Tie-1 and Tie-2 were noted in almost all tissue samples, and the amount of PCR product reflected the expression levels seen in immunohistochemistry. Tie-1 and Tie-2 were amplified to maximum levels in patient No 4, who showed the highest expression of these proteins in immunohistochemistry.
Figure 4
Reverse transcriptase polymerase chain reaction (RT-PCR) of Tie-1 and Tie-2. (A) Tie-1 and Tie-2 in synovial tissues. Total RNA was extracted from each synovium and cDNA was synthesised from 1 μg RNA. PCR was performed with specific primers corresponding to each cDNA. PCR cycles to amplify Tie-1, Tie-2, and G3PDH were 35, 35, and 25 cycles, respectively. Amplified PCR products were then electrophoresed onto 1.5% agarose gel. To rule out possible genomic DNA contamination, control experiments were also performed without RT using the same reactions, and showed no amplification (data not shown). (B) Tie-1 and Tie-2 in cultured synoviocytes. Cultured synoviocytes obtained from two independent patients with RA (cs-1 and cs-2) and subcultured five times were subjected to RT-PCR with the same conditions as described above.
To examine whether synoviocytes express Tie receptors in vitro, RT-PCR was performed on cultured fibroblastic synoviocytes derived from two independent patients with RA. As with synovial tissues, both Tie-1 and Tie-2 were amplified from cDNA of cultured synoviocytes without notable difference (fig 4B).
Discussion
Although Tie-1 and Tie-2 protein tyrosine kinase receptors have been considered to be expressed only in the endothelium of actively growing vessels, there is sufficient evidence at present indicating that these receptors are also expressed in quiescent endothelium or in other types of cells, including circulating haematopoietic progenitor cells.19 ,20 We extended these studies by demonstrating in the present work that Tie receptors are also widely expressed in the pathologically abnormal synovial tissue of RA, including synovial lining cells, stromal cells, pericytes, and endothelial cells. We also demonstrated the expression of Tie receptors in cultured synoviocytes. In normal synovial tissues, however, these Tie receptors were limited to endothelial cells of small vessels.
In our sample group of patients with RA, Tie-1 and Tie-2 were expressed in all RA synovia, and intense expression was seen in actively proliferated regions. Furthermore, our results showed that the distribution of Tie-1 expressing cells was different from that of cells positive for Tie-2 in synovial lining and stromal cells. As summarised in table 4, Tie-1 was expressed in the full thickness of the papillary proliferated synovial lining cells, whereas Tie-2 expression was restricted to fibroblast derived cells (CD68−/vimentin+) located in the basal layer. Similar to the synovial lining cells, Tie-2 expression in stromal cells was limited to type A fibroblastic cells (CD68−/vimentin+) but not to type B macrophage-derived cells (CD68+/vimentin−), whereas Tie-1 expression did not depend on the phenotype. Our results also showed the preferential expression of PCNA in cells of the basal layer. These results are consistent with previous findings that basal layer cells of synovial lining display fibroblastic phenotype and retain a proliferative capacity, whereas the superficial cells display a phenotype of differentiated macrophages.21
Table 4
Summary of Tie-1 and Tie-2 expression in synovial tissues
The exact functional role of these Tie receptors in RA synovium and the expression of angiopoietin-1 and/or -2 ligands for Tie-2 receptor in synovial tissue, remain unknown at present. However, the intense expression of these Tie receptors in the inflamed synovium suggests that Tie-1 and Tie-2 play some part in the pathophysiology of RA synovitis. Furthermore, the restricted expression of Tie-2 in CD68−/vimentin+ cells suggests some specific functional role for Tie-2 in the differentiation of these cell from fibroblastic phenotype. Moreover, overexpression of PCNA in Tie-2 positive basal layered cells may be indicative of the direct involvement of these cells in the proliferation of lining cells.
In vasculature tissue of the RA synovium, our results showed the expression of Tie receptors in the endothelium and surrounding pericytes of proliferating capillaries located underneath the papillary stratified lining cells, without obvious differences in the expression patterns of Tie-1 and Tie-2. In addition, overexpression of PCNA was restricted to Tie positive vessels. These results suggest the involvement of Tie receptors in vascularisation of the RA synovium, as well as the possible function of Tie-1 and Tie-2 as angiogenic factors under pathophysiological conditions. Previous studies have shown that in several pathological conditions, including malignant tumours, the expression of Tie receptors correlates well with the degree of angiogenesis.22 ,23 These findings, together with our results for the expression profiles in synovial lining and stromal cells, suggest that the Tie-angiopoietin system plays a part in angiogenesis, synovial proliferation, and remodelling of RA pannus. Further experiments, including studies to examine the biological function of Tie-1 and Tie-2 and immunohistochemistry for angiopoietins, are necessary for a better understanding of the pathophysiology of RA synovitis.
The origin and differentiation of vascular cells within the inflamed synovium are not well understood. However, clearly, based on the serial analysis of surface antigens, it seems that many endogenous haematopoietic cell precursors are present in synovial tissue of RA.24 Among these, a high density of CD34 positive cells have been shown in peripheral blood and in synovial tissue.25 In addition to serving as a marker for mature endothelium, CD34 is also expressed during early stages of angiogenesis.26 ,27 Furthermore, it seems that CD34 positive cells in peripheral blood still retain a proliferative capacity as progenitor cells to both lymphocytes and endothelial cells.28 ,29 Interestingly, we found many luminal structures surrounded by CD34 positive cells within capillary-rich areas, which might be indicative of immature capillary endothelium. Although a lineage between CD34 and Tie receptors, which has already been shown in lymphopoietic cells,30 has not yet been reported in the angiogenic process, it is possible that CD34 positive endothelial progenitor cells pre-existing in, or infiltrating, synovial tissue from peripheral blood, differentiate into endothelial cells. Subsequent processes might include the induction of Tie receptors in the endothelium itself or in the surrounding undifferentiated cells for further growth of the vessels, in cooperation with the secreted angiopoietins. Elucidation of the mechanism underlying Tie receptor induced angiogenesis may allow the design of new treatments for RA.
In summary, we have shown here that Tie-1 and Tie-2 tyrosine kinase receptors are widely expressed in the proliferating synovium of RA, including synovial lining and stromal cells as well as the vascular system. We also showed that such expression is dependent on the proliferative activity of the RA synovium. Our results suggest the functional importance of Tie receptors in synovial proliferation and angiogenesis in RA synovitis.
Acknowledgments
We thank Mrs Motoki, Mrs Fukahori, and Mr Kawata for the preparation of histological sections, and Dr Kohno and Dr Kawabe for providing tissue samples and cultured synoviocytes, respectively.
References
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Universal Time: 10:45 | Local Time: 10:45 (0h GMT)
Select your timezone:
Room: E-Poster Hall
P-4.41 Predictors for renal outcome in living kidney donors: From data of Korean organ transplantation registry
Yunmi Kim, Korea
Assistant professor
Nephrology
Inje University Busan Paik Hospital
Abstract
Predictors for renal outcome in living kidney donors: From data of Korean organ transplantation registry
Yunmi Kim1, Min Ji Kim2, Jin Seok Jeon3, Heungman Jun4, Kyunghwan Jeong5, Jaeseok Yang6, Curie Ahn7, Chanil Park1, Taehee Kim1, Sun Woo Kang1, Yeong Hoon Kim1.
1Internal medicine, Inje University Busan Paik Hospital, Busan, Korea; 2Internal medicine, Daedong Hospital, Busan, Korea; 3Internal medicine, Soonchunhyang University Seoul Hospital, Seoul, Korea; 4Surgery, Inje University Ilsan Paik Hospital, Goyang, Korea; 5Internal medicine, Kyung Hee University College of Medicine, Seoul, Korea; 6Surgery, Seoul National University Hospital, Seoul, Korea; 7Nephrology, Seoul National University Hospital, Seoul, Korea
KOTRY study group.
Introduction: The safety of donors is one of the most important issues in living donor kidney transplantation. We aimed to investigate predictors of renal outcome in living kidney donors that can help guide management of living kidney donors.
Methods: We analyzed data of kidney donors who were registered to a nationwide prospective registry, the Korean Organ Transplantation RegistrY (KOTRY), from May 2014 to December 2016. Among a total of 1,497 living kidney donors, 456 donors were followed up until 2 years with available serum creatinine measurement after kidney transplantation. We analyzed factors related to renal outcome of donors. Chronic kidney disease (CKD) was defined as estimated glomerular filtration rate (eGFR) < 60 ml/min/1.73m2 or spot urine protein-to-creatinine ratio ≥ 150mg/g or spot urine microalbumin-to-creatinine ratio ≥ 30mg/g or 24-hour urine protein ≥ 150mg.
Results: At 2 years after kidney transplantation, CKD developed in 99 (21.7%) donors. Donors who had incident CKD were older (50.1 ± 10.8 vs. 42.5 ± 11.7 years-old), had more hypertension (12.1% vs. 5.0%), had higher serum uric acid (5.4 ± 1.5 mg/dL vs. 4.9 ± 1.4 mg/dL) and glucose level (102 ± 18 mg/dL vs. 97 ± 12 mg/dL), and lower predonation eGFR (88 ± 13 mL/min/1.73m2 vs. 106 ± 13 mL/min/1.73m2) than subjects who did not develop CKD. The eGFR decreased 0.4 ± 3.6 ml/min/1.73m2 per year since nephrectomy in incident CKD group, while it increased 2.2 ± 1.7 ml/min/1.73m2 per year in non-CKD group (p = 0.008). In multivariate logistic regression analysis, higher systolic blood pressure was associated with higher risk of CKD (Odds Ratio (OR), 1.322 per 10 mmHg increment; 95% Confidence Interval (CI), 1.036-1.686; p = 0.025), and higher predonation eGFR (OR, 0.906 per 1 ml/min/1.73m2 increment; 95% CI, 0.876-0.936; p < 0.001) and higher ratio of eGFR at discharge to predonation eGFR (OR, 0.603,1 per 0.1 increment; 95% CI, 0.428-0.849; p = 0.004) were related to lower risk of CKD.
Conclusion: Higher blood pressure was related to higher risk of CKD in kidney donors. Higher predonation eGFR and less decline of eGFR after single nephrectomy were predictors for long-term preservation of renal function.
This study was supported by a fund by Research of Korea Centers for Disease Control and Prevention (2014-ER6301-00, 2014-ER6301-01, 2014-ER6301-02, 2017-ER6301-00)..
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1
1
Compression socks help ankle swelling? Not sure if due to preg or lupus. Swelling happened overnight but BP norm. Severe joint pain 5 weeks
Compression socks help ankle swelling? Not sure if due to preg or lupus. Swelling happened overnight but BP norm. Severe joint pain 5 weeks
Here are some ...: If just happening overnight, one has to concern about DVT (deep vein thrombosis) although it's uncommon for bilaterally simultaneous occurrence. So, watch such swelling closely for potential progress, go to urgent care timely, & don't wait until the last minute. For the time being, wear compression + leg elevation will help, but not knowing its underlying causes. Best wish ... ...Read more
Dr. Robert Lowe
1,539 doctors shared insights
Painful Joints (Definition)
That term is not really a specific diagnosis, but rather somewhat of a general term. The medical term is arthralgias, which implies pain in multiple joint possibly coming from a single cause. Don't hesitate to be seen and evaluated for ...Read more
2
2
What is arthralgia?
What is arthralgia?
See below: Technically arthralgia is pain in the joints and arthritis is inflammation in the joints however, the terms are often used interchangeably. Not all pain in joints is arthritic though. For instance, joint pain can occur from viruses or even conditions like low thyroid (hypothyroid). ...Read more
3
3
What causes arthralgia?
What causes arthralgia?
It is joint pain: This is pain in the joint. It can be due to injury or inflammation. If there is more inflammation you can get swelling and this is then called arthritis.There are many causes for joint pain and it can even occur if the muscle strength about he joints is not good. There are lab tests to help tell if you have inflammation as well as your examination by your physician. or a rheumatologist ...Read more
4
4
Can arthralgia cause severe illness?
Can arthralgia cause severe illness?
Other way around: Arhtralgia simply means joint pain. It is a symptom that can occur, not cause, with some illnesses. ...Read more
5
5
What kind of dr do see for arthralgia?
What kind of dr do see for arthralgia?
Rheumatologist: Rheumatologist how specialize with joint disease, or you see your family doctor how will guide you .Good luck thanks. ...Read more
See 1 more doctor answer
8
8
What does the diffuse mean in arthralgias?
Major and minor jts.: Arthralgias means pain without obvious swellin of the involved joints.Arthitis is both pain as well as inflammatory swelling of joints. Diffuse arthralgias include pain from major joints like shoulder, elbow, wrist, hip, knee, ankle joints involvement as well as minor joints like finger joints, toe joints, foot joints, spine joints involvement and causing pain in those regions. Rheumatic fever has both. ...Read more
9
9
Difference betwen arthralgia&arthritis?
Pain vs Swelling: Arthralgia refers to only joint pain (arth = joint; -algia = pain). Arthritis refers to inflammation in the joint (arth- = joint; -itis = inflammed) which may or may not be accompanied by pain. There are many types of arthritis--most of which involve a disease process that is either chronic (osteoarthritis, ra, jia) or short-term or curable (reactive arthritis, septic arthritis). ...Read more
10
10
Difference between arthritis and arthralgia?
Difference between arthritis and arthralgia?
Inflammation: "arthritis" means joint inflammation while "arthralgia" means joint pain. You can have joint pain without joint inflammation, joint inflammation without joint pain, or have both together. ...Read more
11
11
What are the tests for arthritis - arthralgia?
What are the tests for arthritis - arthralgia?
Clinical eval +++: The most important 'test' is--as usual--the diagnostic tool between the physician's ears. Any well versed specialist in the field of arthritis (rheumatology) knows that hearing exactly what the details are given by the pt (history) and a careful, thorough exam of all parts of the body, will yield a dx, or at least what tests to order. Some: esr, crp, antibodies to own cells, cbc, etc. ...Read more
12
12
What is the difference between arthritis, arthralgia?
See below: Technically arthralgia is pain in the joints and arthritis is inflammation in the joints however, the terms are often used interchangeably. Not all pain in joints is arthritic though. For instance, joint pain can occur from viruses or even conditions like low thyroid (hypothyroid). ...Read more
See 1 more doctor answer
14
14
What are the main symptoms of fibromyalgia vs arthralgia?
What are the main symptoms of fibromyalgia vs arthralgia?
Fibromyalgia: Fibromyalgia(fm) versus arthalgia (muscle pain). Fm symtpom cluster is more specific: pain, allodynia [pressure sensitive], joint stiffness, fatigue insomnia, 9 paired 'tender points' on body, swallowing, bowel, bladder dysfunction. Depression is a common go along. 9:1 male to f ratio. 2-4% of pop. Might have it. Considered difficult to diagnose and treat at times. Arthralgia=simply muscle pain. ...Read more
See 1 more doctor answer
15
15
Have arthralgia -- what are some warm ups to do before working out to help?
Same as anyone else: For most people with joint pain, there is no need for any special type of warm-up. The same sorts of things that a non-arthritic person does should be adequate, except perhaps with more attention to areas that are particularly stiff or uncomfortable. Don't avoid exercise, but be gentle and listen to your body. ...Read more
16
16
What’s the Difference between Arthritis and Arthralgia. Which one is more serve?
What’s the Difference between Arthritis and Arthralgia. Which one is more serve?
Arthritis and: Arthralgia, literally means joint pain and is a symptom of the Arthritis is a joint disorder itself that involves inflammation of one or several joints. ...Read more
See 1 more doctor answer
18
18
What causes arthralgia and myalgia in dengue?
What causes arthralgia and myalgia in dengue?
Viral infection +: There is a viral infection and also bleeding that occurs. Like the flu viral muscle involvement occurs from the viral infection. Dengue also cause bleeding into tissue and this can contribute. When you have a viral infection the body responds with a variety of chemicals and cytokines and some of these increase the swelling, attracting inflammatory cells and alsorelease pain chemicals. ...Read more
19
19
What causes arthralgia and myalgia in dengue ?
What causes arthralgia and myalgia in dengue ?
Viruses: There are four different but related viruses that cause dengue fever. The viruses which cause fever, arthralgia, myalgia, and other symptoms (depending on which virus is present) are transmitted through mosquito bites. ...Read more
See 1 more doctor answer
20
20
Arthralgia symptoms after immune complex reaction. How soon does it end?
Arthralgia symptoms after immune complex reaction. How soon does it end?
Depends on cause: Serum sickness. Thiis is commonly seen after settings such as a reaction to a foreign antigen (drug, infection, etc) and once that antigen resolves the immune complex reaction subsites - time depends can be days, weeks or months. But with a chronic setting where the antigen persists like in an autoimmune reaction in lupus, then the immune complexes persists and the condition continues. ...Read more
Dr. Bruce Weisbrot
120 doctors shared insights
Joint Aches (Definition)
Discomfort emanating from the connection between two bones ...Read more
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The Most Known Benefits Of Cannabis 1
The Most Known Benefits Of Cannabis
Many reasons exist why lots more people are starting to uncover the lots of marijuana rewards. In truth, this herb is among one of nature’s great products, as it provides a number of organic substances that were employed for decades. Once the cannabis herb was initially identified by European explorers, it was used in a number of healing reasons. The majority of the herbal plants that were employed through these healing therapies are still being used these days. Should you be looking for the best widespread make use of this natural vegetation, then you have to give some thought to the way it impacts the human brain, the many different types of plant life which might be within the cannabis class give persons a whole new strategy to combat sickness, along with help them to with stress.
Nonetheless. This specific benefit from cannabis is actually one that many individuals neglect. One of the main explanations why so many people use the various advantages of this shrub is due to the actual way it enhances the in general function of your brain.
The Most Known Benefits Of Cannabis 2When it comes to pondering beneficially, among the finest means to make this happen is with the use of marijuana. Exactly why this specific chemical substance will help you imagine absolutely is simply because it can increase the all round chemical type sense of balance throughout the head. To be at optimum levels, the mind has about three main chemical like levels which require to keep nicely balanced. When one of them levels has run out of whack, the effect might be psychological issues like depressive disorder and terrible selection. So that you can overcome these signs and symptoms, most people choose cannabis.
The power of the harmful chemicals inside the neurological usually are not the sole thing that needs to be in equilibrium. Additionally, the amount of the necessary oxygen that could be moving to the head cells is also essential. Whenever the o2 which is running to this very area is reduced, the individual’s mind gets drained and the ability to think and carry out any sort of activity will likely be tremendously diminished. When any person has a lot air flowing on their mind cellular material, they will likely sense particularly exhausted and often will find it hard to feel, as well as other prevalent human brain functions. Too little oxygen and the brain is missing out on necessary substances, causing the mind to work improperly.
Other ways that cannabis can boost the mental faculties chemistry is by the reduction of the levels of dopamine. The dopamine on the human brain is in charge of muscles relaxation, along with frame of mind and appetite feelings. When someone provides extensive dopamine, they tend to enjoy pleasure and optimistic emotions and thoughts. If this substance stage declines, the individual will really feel a shed with their feeling as well as preference to engage in routines will minimize. This is the reason many people who suffer from major depression use weed on a regular basis.
The final of the marijuana mental faculties biochemistry boosting rewards is by the rise of serotonin. Serotonin is accountable for a, depressive disorders and nervousness number of other intellectual issues. As soon as the levels of serotonin are substantial, any person are often more prone to perform activities faster and also have a superior remembrance. However, whenever the levels of serotonin are small, people will be more very likely to really feel disheartened and often will execute a smaller amount perfectly in their activities. In some instances, one might notice that marijuana provides all of them with the “advantage” on the subject of rivalling against people in some tasks.
Some other unique primary advantages of weed stem from the point that it does not have many of the harmful unwanted effects that numerous prescribed drugs have. Some examples are things like memory decline and improvements in vision. As well as those two typical illnesses, you will find cognitive results at the same time, for instance paranoia and hallucinations. Without such harmful adverse reactions related to cannabis, you can easily understand why it is one of the top notch benefits associated with this kind of form of medication.
One last illustration of the many benefits of cannabis comes from the point that it could possibly basically help to lower the number of major depression the initial one is encountering. There are several people who will suffer from your key depressive episode everyday. In some cases, the person will not seek any type of treatment method in anyway, and can just quit hanging out in public places therefore they won’t should see any one. In an effort to beat their despair, other individuals will take a large package of your chemical type. Irrespective of the reasons an particular selects to use this substance, they will be aware that it may have significant side effects. Nonetheless, most people in this product can easily report some very nice advantages.
If you have any concerns concerning in which and how to use hemp gummies, you can call us at our own site.
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Type 2 Diabetes: Where Do I Start?
2019-01-04
You’ve just been diagnosed with type 2 diabetes and if we’re being honest, you’re probably nervous about the lifestyle changes you will have to make and don’t know where to begin. The good news is getting started on your new life with type 2 diabetes is simple. With just a few steps, you’ll begin to redefine normalcy and live a full life with diabetes.
Set Realistic Goals
You and your doctor are working towards a goal to make sure you’re able to manage diabetes well enough to live a full, healthy and happy life with it. An essential part of the beginning of type 2 diabetes management is understanding what your numbers mean and setting realistic goals for lowering your daily blood sugar numbers and A1C. Understand type 2 diabetes affects everyone differently, so ask your doctor what numbers are optimal for you.
This includes asking your doctor or another member of your diabetes care team what your ideal blood sugar numbers should be before your first meal of the day, two hours after your first bite of a meal, which ranges are too high or low, and what to do in the event your blood sugar is too high or low.
Build Your Support Team
When it comes to building your diabetes care team, always remember you are the most important person in it. While specialists certainly provide the expertise, only you fully understand how diabetes affects your body. Seek recommendations for endocrinologists, nutritionists, dietitians, diabetes educators and peer support groups from trusted sources such as your primary care doctor. When choosing members of your care team, ensure they respect your values, including cultural ones and provide a holistic approach to your treatment plan and address the mental and emotional tolls of diabetes self-management.
Also vital to your support team are the people who care about you the most. Whether this consists of family, friends, colleagues, or neighbors, identify loved ones you can confide in about your struggles, fears and successes with diabetes management. Those in this circle should be non-judgmental, supportive and help find solutions to your problems, even if they aren’t living with diabetes themselves. Research also shows people with diabetes who join peer support groups are more likely to manage diabetes well, less likely to experience diabetes complications and have a higher quality of life. The American Association of Diabetes Educators has a list of peer support resources available for those seeking both online and in-person help.
Find the Right Diet and Exercise Plan For You
The general advice for those living with type 2 diabetes is to eat a healthy diet and exercise regularly. But what does that mean for you? In short, whatever you make of it. Living with diabetes doesn’t mean cutting out cake, burgers, or your favorite guilty pleasures. It means adjusting in what quantities and the frequency in which you eat them. If you’re someone who’s had a negative view of healthy foods, living with diabetes can change that perspective for you. Healthy eating can be as simple as recreating your favorite dishes with healthier ingredients.
For example, if you enjoy creamy dishes typically high in fat and carbs such as chicken alfredo and pasta, make it at home instead of buying the canned sauce or pre-packaged meal. Substitute heavy cream for half-and-half, use fresh parmesan and garlic, cook chicken breast in extra virgin olive oil and substitute white pasta for whole-wheat or quinoa pasta. You can add flavor boosters using fresh or dried Italian herbs such as basil, parsley and oregano and control the amount of salt you add. Learning to cook healthy at home carries health benefits by helping you control your sodium, fat and carbohydrate intake, plus it’s fun!
If you’re not a gym person—don’t sweat it (pun intended). There’s no need to purchase an expensive gym membership you’re not going to use. In fact, exercise can be completely free! Lace up your shoes and go for a run, walk and jog around the neighborhood. If you don’t exercise already, set a goal for the amount of time you’re willing to dedicate to physical activity per day. If that’s five minutes around the block for the first week, awesome! Stick with it and build on your progress. The following week, you may want to bump it up to 10 minutes and so on.
Check out resources such as the Beyond Type 2 Food and Diabetes and Exercise pages to generate ideas on how to construct your diet, determine which foods and workouts suit you.
Identify the Costs of Diabetes Supplies and Care
Diabetes can be expensive. The American Diabetes Association published a report in April 2018 that stated people with diabetes spend over two times more on medical expenses per year than a person without diabetes. People with diabetes spend an average of $16,752 on medical expenses per year, with $9,601 of that directly attributed to diabetes care. These costs come from hospital inpatient care, prescription medicines, diabetes supplies and visits to the doctor.
Because of this, it’s extremely important to understand how your health insurance plan can help you cover the costs of diabetes management. Adequate coverage can be the difference in preventing serious complications. Read about health coverage in your state and see if you’re eligible for financial assistance. If brand-name diabetes medications and supplies are too expensive, ask your doctor to prescribe generic versions. Also, you can purchase some diabetes supplies such as blood glucose meters, lancets and test trips over-the-counter at your local pharmacy. Finally, research local health clinics that may provide low-
Being diagnosed with type 2 diabetes can be scary, but it’s not a death sentence and with proper management, you will be able to live your best life with it. This guide is meant to relieve the stress and confusion diagnosis brings. Another important reminder is diabetes does not define you. You are still a whole, entire person who deserves to enjoy everything life has to offer and with a positive outlook on your treatment plan, your support system and access to adequate resources, you will thrive with type 2 diabetes.
WRITTEN BY Beyond Type 2 Editorial Team, POSTED 01/04/19, UPDATED 12/05/22
This piece was authored collaboratively by the Beyond Type 2 Editorial Team.
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Int J Med Sci 2014; 11(6):620-625. doi:10.7150/ijms.8251
Research Paper
PIK3CA Gene Amplification and PI3K p110α Protein Expression in Breast Carcinoma
Mohammad Firoozinia1, Mohammad Zareian Jahromi2, Soheil Zorofchian Moghadamtousi1, Sonia Nikzad1, Habsah Abdul Kadir1 Corresponding address
1. Biomolecular Research Group, Biochemistry Program, Institute of Biological Sciences, Faculty of Science, University of Malaya, 50603 Kuala Lumpur, Malaysia
2. Institute of Bioscience, University Putra Malaysia, 43300 Serdang, Selangor, Malaysia
This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) License. See http://ivyspring.com/terms for full terms and conditions.
Citation:
Firoozinia M, Zareian Jahromi M, Moghadamtousi SZ, Nikzad S, Abdul Kadir H. PIK3CA Gene Amplification and PI3K p110α Protein Expression in Breast Carcinoma. Int J Med Sci 2014; 11(6):620-625. doi:10.7150/ijms.8251. Available from http://www.medsci.org/v11p0620.htm
File import instruction
Abstract
A family of PI3Ks is the lipid kinases, which enhance intracellular pools of phosphatidyl inositol 3,4,5-tri-phosphate (PIP3) through phosphorylating its precursor. Amplifications and deletions of genes, as well as somatic missense of the PIK3CA gene have been described in many human cancer varieties, including of the brain, colon, liver, lung and stomach.
Immunohistochemistry and Real-time quantitative PCR tests were used to determine the PIK3CA gene amplification (gene copy number) and to detect protein expression, respectively. The results obtained were analysed and the ratio of PIK3CA to β-actin gene copy number was calculated. Positive gene amplification of PIK3CA was appointed as a copy number of ≥4. Also, PI3K p110α protein expression was scored from 0 to 3+ and the scores of 2+ and 3+ were considered as positive for PI3K p110α protein expression.
We studied 50 breast carcinoma samples for PI3K p110α protein expression and PIK3CA gene copy numbers. In general, 36 out of 50 (72%) breast carcinoma samples showed a significant increase in PIK3CA gene amplification. 12 out of 50 (24%) showed positive staining, and 38 out of 50 (76%) showed negative staining for PI3K p110α expression.
We have identified no significant relationship between PIK3CA amplification, race (p= 0.630) and histological type (p=0. 731) in breast carcinoma, but correlation of PIK3CA amplification and age showed a significant relationship (p=0. 003) between them.
No significant relationship has been identified in correlation of PI3K p110α protein expression compared to age (p=0. 284), race (p=0. 546) and histological type (p=0. 285).
Amplification of PIK3CA was frequent in breast carcinoma and occurs in stages of breast carcinoma. Our result shows that there is a relationship between gene amplification and age in breast carcinoma. We suggest that PIK3CA is significant in breast tumorigenesis serve as a prevalent mechanism contributes to the oncogenic activation pathway of PIK3CA in breast cancer.
Keywords: Breast cancer, PI3 kinase, Real-time PCR, Expression
Introduction
Phopsphotidylinositol 3-kinase (PI3ks) is a grouping of lipid kinases to control signalling pathways occupied in cell proliferation, adhesion, survival, and motility. Phosphatidylinositol 3-kinase (PI3K), is a main downstream signalling component of tyrosine kinases (RTKs) as a growth factor receptor. Tainted mutation and expression of PI3-kinase/AKT pathway components have been occupied in diverse fellow malignancies [1,2]. Previously published article determined PTEN and epidermal growth factor receptor (HER3) as surrogate markers in patients, which have HER2-overexpressing MBC, and it has been suggested that these markers may affect in the PI3K pathway [3]. The previous published articles establish that the PIK3CA is furthermost oncogene mutated in breast carcinoma and provision an impress for PIK3CA in carcinogenesis [4].
So far, mutations of PIK3CA stated in breast cancers, which are gathered in two main hotspot areas in exons 9 and 20, consistent to tyrosine kinase and helical domains [4,5]. In more than 80% of the cases, mutations are gathered in the helical domain and kinase domain which encoded exon 9 and exon 20, respectively. To continue, several hotspot mutations of mentioned exons specifically H1047R, E545K and E542K were demonstrated to operate the PI3K/AKT pathway over the AKT phosphorylation [6-9]. However, this study has focused mainly on the amplification of PIK3CA in breast carcinomas. We defined the occurrence ratio of PIK3CA gene copy numbers in breast carcinoma in order to make a comparison with recent published data. Lately, it has been publicized that PI3K is linked to the cellular proliferation and transformation in some cancer cell lines, which contain breast carcinoma, myelogeneous leukemia and AIDS-related Kaposi Sarcoma, prostate carcinoma and hepatocellular carcinoma [10-14]. More recently, superior PI3K protein expression and activity have been identified in glioblastomas, colorectal and lung cancer [15,16]. In consequence, these findings recommended the significance of the PI3K in the development of malignant neoplasia. For that reason, we studied the expression layout of PI3K protein expression in 50 breast carcinoma.
Material and method
Tumor samples and cell lines
Formalin-fixed, paraffin-implanted tissue samples from 50 patients have been used for this study. The tumors selected for this study were 50 breast carcinoma. All tumours histological classification was established in the World Health Organization (WHO) system.
DNA isolation
Firstly, Paraffin-embedded tissue sections were treated at room temperature for 5 minutes with xylene, pursued by digestion with Proteinase K at 56ºC for 18 hours. Genomic DNA was consequently extracted employing QIAamp® DNA Mini Kit (Qiagen, Germany). The events were achieved matching to the directions of the manufacturer's.
Polymerase Chain Reaction (PCR)
Genomic DNA was amplified by real-time PCR using the specific PIK3CA gene amplifying primers. We have used β-actin as a reference gene for control. Primers and Taqman probes were as follows, PIK3CA, 5′-AAATGAAAGCTCACTCTGGAATTCC-3' (forward), and 5′-TGTGCAATTCCTATGCAATCG-3′ (reverse), and 5′-6-carboxyfluorescein-CACTGCACTGTTAATAACTCTCAGCAGGCAAA tetramethylrhodamine-3′ (Taqman probe) [17]. Also for β-actin, 5'-TCACCCACACTGTGCCCCATCTACGA-3′ (forward), 5′-TCGGTGAGGATCTTCATGAGGTA-3′ (reverse), and 5′-6-carboxyfluorescein-ATGCCCTCCCCCATGCCATCC-tetramethylrhodamine-3′ (Taqman probe) [17]. Entire primers as well as Taqman probes were procured from Operon Biotechnologies (Aitbiotech, Singapore). Final volume of 25µl was used for PCR reaction as referred in Table 1. The PCR cycling was designed by the following steps, denaturation at 95º C for 2 minutes, 50 cycles of 95º of centigrade for thirty seconds and 60º of centigrade for forty five seconds. The comparative PIK3CA copy number of the sample was calculated by considering 2.0 as the normal diploid DNA copy number. The cutoff value of PIK3CA copy number gain was set at more or equal to 4.0 copies [18,19].
Table 1
Protocol and amount of material used in real-time PCR
X1X2
Taq buffer with KCL2.5μl5μl
MgCl23μl6μl
dNTPs0.5μl1μl
Forward primer0.75μl1.5μl
Reverse primer0.75μl1.5μl
Taqman probe0.6μl1.2μl
Taq DNA polymerase1.25μl2.5μl
DNA2μl2μl
Double-distilled water13.6μl27.2μl
Total volume25μl50μl
To continue, for immunohictochemical analysis the slides were treated with 3-aminopropyltrimethoxysilane (APES). Paraffin-embedded tissue sections of thickness 4.0µm were cut using a Leica rotary microtome RM2135 (Leica Microsystems, Germany) and mounted on slides. The slides were stored at 4 ºC after drying. Briefly, the slides with paraffin sections were placed in 60ºC oven for 30 minutes. Then the tissue sections were deparaffinized and hydrated by crossing over xylene and a stratified series of ethanol. Antigen recovery as presented for 25 minutes at 100ºC in Tris-EDTA (pH9) buffer solution, into a microwave oven. After heat-induced epitope retrieval, the slides with tissue sections were allowed for 30 minutes to cool at room temperature. Then, tissue sections were washed in Tris-buffered saline with 0.1% Tween-20 (TBS-T), pH7.6. Then, incubated sections with 3% H2O2 solution for 10 minutes and after those sections were incubated in 3% BSA. After that primary antibody against PI3K (p110α 1:50) was enhanced and then incubated for 2 hours. Then, primary antibody enhancer (QIAgene) was enhanced and incubated about 20 minutes at room temperature. Then, tissues were embrocated with TBS-T and incubated in 3, 3′-diaminobenzidine (DAB) substrate chromogen system (UltraVision Plus Detection System; Thermo Fisher Scientific, Fermont, CA) for 5-20 minutes until the brown color end-products were observed and sections were washed in 2x dH2O. The tissue sections were finally counterstained with hematoxylin for 5 seconds and washed in running tap water for 2 minutes. Finally the tissues were dehydrated. Rabbit monoclonal anti-PI3K p110α antibody (clone C13F8, Cell signalling technology, USA) was used at a dilution of 1:50. Antigen detection was performed at 100ºC for 25 minutes at pH 6.0, 10mM sodium citrate buffer, in a microwave oven. Finally, tissue sections were incubated with anti-PI3K p110α antibody for one hour at room temperature.
The relationship between PIK3CA gene copy numbers and PI3K p110α protein expression and clinico-pathological records were evaluated by Fisher's exact test. Kruskal-Wallis and Mann-Whitney are the two statistical tests which were used for the correlation analysis and p˂ 0.05 was presumed as statistically significant. SPSS 20.0 parameters (SPSS Inc., USA) were used for statistical analysis.
Result
PIK3CA gene copy numbers and PI3K p110α protein expression in breast carcinoma
PIK3CA gene amplification has been studied in different type of human carcinomas, for example; uterine cancer [20], cell lung cancer [21], nasopharyngeal carcinoma [22] and endometrial cancer [23]. One of our aims was to determine the gene copy number rate of PIK3CA in breast carcinoma. Hence, genomic DNA from 50 breast carcinoma and 10 normal blood samples was used to determine the frequency of an increased copy number of PIK3CA gene. Our results suggest that, 36 out of 50 (72%) samples shows an increase in PIK3CA gene amplification in breast carcinoma and PIK3CA gene copy numbers were lower than 4, in 14 out of 50 (28%) samples. Results obtained from normal human blood samples showed that there were no significant positive gene copy numbers identified in normal blood DNA samples and PIK3CA gene copy numbers were lower than 4 in all samples.
We estimated expression of PI3K p110α in breast carcinoma in 50 breast carcinoma tissues. The immunohistochemical scores of 0 and 1+ staining were considered as negative and 2+ and 3+ staining were considered positive. As results shows, 12 out of 50 (24%) of breast carcinoma samples have positive staining and 38 samples (76%) were negative. Figure 1, shows negative control, weak (1+) and moderate (2+) staining of PI3K p110α protein in breast carcinoma tissue.
Figure 1
Immunostaining of PI3K p110α in breast carcinoma (Original Magnification, 100x) A) Moderate staining (2+) in invasive breast cancer tissues B) Weak staining (1+) in invasive breast cancer tissues C) Negative control staining in invasive breast cancer tissues.
Int J Med Sci Image (Click on the image to enlarge.)
Relationship between PIK3CA gene copy number, PI3K p110α protein expression, age, race and histological types
In the present study, the relationship between PIK3CA gene amplification, age, race and histological type was analysed in breast carcinoma. Statistical analysis showed that there is no significant relationship between PIK3CA gene amplification, race (p=0.630) and histological type (p=0.731) in breast carcinoma, but there is a significant relationship between PIK3CA gene amplification and age (p=0.003) in breast carcinoma (Table 2).
Also, we have done correlation between PI3K p110α protein expression, age, race and histological type in breast carcinoma, which statistical analysis showed that there is no significant relationship between PI3K p110α expression, age (p=0.284), race (p=0.546) and histological type (p=0.285) in breast carcinoma (Table 3).
Table 2
Correlation between PIK3CA gene copy numbers, age, race and histological types in breast carcinoma
PI3K Copy NoNumberMean RankP
Age*
=<482820.210.003
>482232.23
Race*
Group1820.00
Group22825.790.630
Group31027.30
Group4430.00
Histological Type**
I2027.30
II2023.700.731
III1025.50
*Mann-Whitney test / **Kruskal-Walley test
Table 3
Correlation between PI3K p110α expression, age, race and histological grade in breast carcinoma
PI3K p110αNumberMean RankP
Age*
=<482823.790.284
>482227.68
Race*
Group1823.50
Group22825.430.546
Group31023.90
Group4434.00
Histological type**
I2025.80
II2027.900.285
III1020.10
*Mann-Whitney test / **Kruskal-Walley test
Discussion
To find out gene copy numbers of the PIK3CA, we carried out real-time PCR over 50 breast tumor samples. Gene amplification is well accepted as a later occurrence in tumor progression [24,25].
Overall, we found a high frequency of PIK3CA gene copy numbers in breast carcinoma samples. Among the 50 cases, 36 (72%) showed a large amount of gene copy numbers in comparison to normal controls. Previously published data, specified PI3K pathway distorted in a large amount among breast carcinoma patients [26-28]. Though, the occurrence of gene copy number was much more than results identified in earlier studies (1-9-14%) [29,30]. PIK3CA amplification and mutation were nearly equally individual events and as they signify independent methods for enriching PI3K activity, an upper incidence of copy number may possibly clarify the inferior occurrence of PIK3CA amplification in this group compared to those in further reports. Among other types of cancers, genetic analysis of PIK3CA amplification were conducted in Japan, PIK3CA was over expressed in 73% of primary ovarian clear cell carcinomas [31]. In comparison with the previous published data, our data suggest that PIK3CA is significant in breast tumorigenesis, serve as a mutual mechanism contributes to the oncogenic activation of PIK3CA in breast cancer.
In breast carcinomas, PI3K over expression occurred in 24% of all tumor samples, thereby considered as not over expressed. More recently, studies informed that PI3K is not over expressed in melanocytic lesions [32]. Our data are consistent with the previous studies, whereas, p110β and p110α are all over expressed in untransformed cells and tissues, whereas p110δ expression is highly enriched in leukocytes. High levels of p110δ expression have been documented in some solid tumor cell lines, but the functional role is unknown [33]. PI3K pathway activation in breast carcinoma was distinguished using p-S6, p-AKT, and PTEN by evaluating of their expression through IHC. The expression of p-S6 and p-AKT was positive in 75% and 69% of breast carcinoma. There was No significant association between PI3K pathway status and breast carcinoma subtype for p-AKT [34].
Our data showed no significant association between PI 3-kinase expression and ages, races and histological types in breast carcinoma. Also, no relation between the PIK3CA gene copy number, race and histological type has been found, but there is a significant relation between PIK3CA gene copy number and age in breast carcinoma has reported, which may due post-transcriptional, translational and protein degradation regulation which shows some genes are produced but not expressed on the cell surface [35].
The PI3K pathway deviations are existing in a significant quantity of breast carcinoma patients. Accumulating evidence support that PI3K activation has been affiliated with persistence to ErbB2-targeted therapy, moreover standard cytotoxic therapy in breast carcinoma, and the addition of novel PI3K pathway inhibitors (e.g., PX-866, BEZ235, and XL147) which are expected to have superior therapeutic ability to treat patients resistant to standard therapies [36,37]. Although several PI3K activation biomarkers have been proposed such as p-Akt and PIP3, these biomarkers are either not specific or difficult to measure in clinical practice [38]. There was no significant correlation observed amongst PIK3CA mutation and age, differentiation, histological type and lymph node metastasis in a research has done in China [39]. Our research outcomes are not similar to the prior study, Saal et al. (2005); found positive significance between PIK3CA mutations and expression in breast cancer. We believe, variations in samples will be the reason of differences between our and the other studies, as their experiment was carried out on PIK3CA exons such as 1, 2, 4, 5, 7, 9, 12, 13, 18, 20, which were included intron-exon boundaries and their method were based on PCR as well as gene sequencing of exons so it can be the cause of inconsistency with our research. Our study also did not have any focus on mutations and we used primers for amplification of PIK3CA on exon 21. In contrast, another study done in exons 9 and 20 reported no significant relationship between PIK3CA mutations and some clinicopathologic characteristics, such as age, lymph node metastases, tumor size, ER and PR status, p53 expression and mutation in breast cancer [40].
Treatment and Survival
Based on survival statistics during of 5-year, which has been issued between 1975 to 2008 in the SEER Cancer Statistics Review; breast cancer therapy includes breast-conserving surgery (BCS) or mastectomy. Mastectomy is similar as long-term survival, when BCS is appropriately used for provincial or restricted cancers [41].
Limited of diagnosis are on age in women (20-45%), who decided to have breast reconstruction assume mastectomy elect, with each tissue flap or an implant or a mixture of the both [42-46].
Amongst women make a diagnosis in early stage (I or II) of breast carcinoma, 57% accept breast-conversing surgery, 36% assume a mastectomy , around 6% endure no surgical usage, and approximately 1% take no conduct. In contrast, across patients having late stage of breast cancer (III or IV), 13% accept breast-conserving surgery, 60% undertake mastectomy treatment, 18% assume no surgical demeanor, and 7% receive no treatment at all.
The totall comparative survival percentage in 5-year for patients (female) with breast cancer has enhanced from 75.1% to 90.0% between 1975 and 1977 to 2001 over 2007. The growth is mostly due to developments in therapy (ie, hormone therapy and chemotherapy), also to previously identified results from the extensive usage of mammography [47]. Moreover, to stage, epidermal growth factor receptor 2 (HER2) status in human, aspects which affect survival comprise hormone receptor status, and tumor grade.
Acknowledgements
Hereby, the authors would like to appreciate the University of Malaya for providing the research Grant (RP001-2012C).
Competing Interests
The authors have declared that no competing interest exists.
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Author contact
Corresponding address Corresponding author: Habsah Abdul Kadir. Biomolecular research group, Biochemistry Program, Institute of Biological Sciences, Faculty of Science Building, University of Malaya, 50603 Kuala Lumpur, Malaysia. Tel. (0060) 176788101; E-mail: habsahedu.my
Received 2013-12-1
Accepted 2014-3-12
Published 2014-4-22
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June 17, 2024
Fat Less Diet Plans
All About Healthy Diets
The Health Benefits of Coffee
2 min read
Drinking coffee can help prevent and treat several health conditions, including cancer. Its antioxidants may reduce inflammation, which in turn may reduce the risk of certain chronic diseases. Recent studies have shown that coffee may lower the risk of several cancers, including colorectal, liver and prostate cancer. However, coffee consumption is not recommended for those who are pregnant or at risk of bone fractures.
Studies show that drinking coffee reduces the risk of cardiovascular disease. People who drink three to five cups a day are 15% less likely to develop heart disease. This result was confirmed in a meta-analysis of studies involving more than 21,000 people. Coffee can also lower blood pressure. According to one study, drinking seven cups a day significantly reduced the risk of hypertension.
Coffee is a natural stimulant that increases alertness and concentration. Its high caffeine content makes it a great choice for drivers, as drinking coffee can reduce the distractions that often accompany driving. Moreover, studies have shown that drinking coffee has many health benefits, including a decreased risk of type 2 diabetes, Parkinson’s disease, heart disease, and stroke. Moreover, regular consumption of two to three cups a day may help improve health outcomes.
Studies on diabetes and drinking coffee have shown that people who consume it on a daily basis are at a 6% lower risk of developing type 2 diabetes than those who don’t. This may be due to coffee’s ability to protect the beta cells of the pancreas, which produce insulin. Furthermore, coffee’s high antioxidant content may improve insulin sensitivity and metabolism.
Drinking coffee is associated with several health benefits, including reduced risk of type 2 diabetes, a reduced risk of liver disease, and increased insulin sensitivity. However, the mechanisms behind these positive effects are not well understood. Currently, coffee is recommended only for moderate amounts as more studies are needed to determine the best dosage.
Drinking coffee may also help protect against neurodegenerative diseases, such as Parkinson’s disease and Alzheimer’s disease. Research has shown that people who drink coffee regularly have a significantly lower risk of developing these diseases, but the results aren’t conclusive. In addition, coffee can prevent or slow down the progression of depression and cognitive conditions in certain types of people. There are also studies that suggest that drinking more coffee may reduce the risk of developing certain types of liver cancer.
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Interested In Learning A Whole Lot About Massages? Check This Out!
BeanRosenthal3125 | 2022.02.17 09:07 | 조회 6
It is essential to create your entire body pleased occasionally. If you would like like a secure existence without soreness, massages will assist you to do this. Please read on for a few ideas on how restorative massage can get you in a better frame of mind and body, and just how it could help you stay there.
In case you have been feeling especially stressed out, it just could be time to get a calming therapeutic massage. Massages are not just useful to chill out you emotionally but personally also. It helps to promote circulation and loosens up your muscle tissue. Forget about some of your stress levels having a massage therapy.
Make use of your thumbs when supplying a massage. Thumbs can drive much deeper easier than other fingertips can, and they also definitely get into the recipient's muscle groups properly. Be careful not to utilize your thumbs to force way too assertively, as that might be painful towards the person receiving the restorative massage!
Consider supplying your self or a person a foot massage therapy. Focusing on the bottoms initially can really unwind someone. Start off stroking the bottoms of your feet heading forward and backward in right outlines. Do these motions beginning with the hindfoot for the bases of the toes. Once the soles happen to be appropriately massaged, you can proceed to the feet as well as the top rated and midst of the foot.
Petrissage is the simplest way to relieve pressure making ache vanish. This method demands you to apply your fingertips along with your thumb. Seize hold of a muscles and press it for a couple of moments well before moving on to a different location. Look at the same regions a few times before the discomfort disappears.
Decrease all external audio when you are supplying a restorative massage. It can be tough to chill out if you find a lot of disturbance in the region in which the therapeutic massage is happening. This will help your level of relaxing during the process. Choose a spot or time that is certainly a lot more calm. Usually, enjoy soft music or white-noise to masquerade any exterior noises.
It is of the utmost importance that you are currently relaxed when receiving a restorative massage. Consider relaxation workout routines they are able to help your own muscles to slowly and gradually de-stress. As soon as the massage therapist commences the therapeutic massage, keep using serious breaths at times to maintain the muscle tissue peaceful and free.
Think about obtaining a massage therapist that could can come to your house or to your working environment. A number of people who do massages reduce your cost simply because they don't require work space and might vacation about to several places. This is good news for you personally mainly because it will set you back a lot less, and it's much more hassle-free.
When you are giving a therapeutic massage, try not to make use of the exact same cerebrovascular event repeatedly. This could make the total encounter mundane, as you wish to incorporate the maximum amount of transform in the treatment as possible. Alter your strategy, the stroke and the way hard you hit around the again, neck and thighs.
Do you suffer from high blood pressure? Be it genetic or caused by stress it might be dangerous. If you are searching for a way to decrease your blood pressure a lttle bit, try out having a massage therapy. Massages are a fantastic way to ease pressure and stress. They also have been proven to decrease people blood pressure levels substantially.
When you are giving an individual a therapeutic massage, continue to be peaceful. You don't want a masseuse possibly which is conversing your mind off of during the massage. Mother nature sounds or gentle music is all that needs to be noticed. In addition to these matters, you must conserve a peaceful environment.
Shiatsu massages are derived from China. There are numerous resemblances to traditional chinese medicine nonetheless, rather than using tiny needles, fingertips are employed. Strain points are focused to help you get to chill out. Shiatsu massages help increase your power.
The ft are an frequently overlooked region that should be massaged. There are lots of strain points in the feet that can chill out the entire body by and large and give the entire system a sense of wellness. Focus on a single ft . at one time and employ the maximum amount of stress when your partner allows.
If you're expectant, you can nevertheless have a massage when it is distributed by a certificate therapist. This is certainly the best way to cope with morning hours health problems, tension, back discomfort, sore boobies and inflamed ankles. You are able to continue it soon after birth to manage postpartum depressive disorders, weight-loss and newborn-transporting discomfort, too.
Recuperate little by little following enjoying a massage therapy. 강남안마 Keep off on right away jumping up in the table the moment the masseuse foliage the area. Take the opportunity to luxuriate in the comfortable, calm sense of the body. Available your eyesight, eat your surroundings, and then little by little stay up on the edge from the kitchen table. Rest an instant well before ranking.
If you're getting a massage, you shouldn't wait to speak to your massage therapist. If you have ache inside a a number of place, make sure they know. If you require more intensity in a few locations to sort out the kinks, then you will want to talk up and so the massage therapist will be aware of.
Permit your masseuse recognize your songs personal preferences. Many individuals enjoy calming tunes enjoying during their restorative massage, however some tend not to. If you prefer a quiet environment whilst you obtain your restorative massage, communicate up. You may also indicate a specific sort of tunes and even request ambient noises for example parrot music or sea surf.
You should make time to discover more about your body, especially its muscles and neural system. You will be able to provide much better massages once you know in which sensitive neurological endings are placed and also have a far better concept of in which muscle groups are. Additionally, you will understand the aches you experience much better as soon as you a little more about your system.
Should your fingers could make it to the spots, you would certainly be competent at giving on your own an ideal massage. Go ahead and take ideas from this report to the masseuse to see if they are willing to try some out on you. Your again has a huge part in your own life, so make sure you take better care of it.
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Date Updated: 03/30/2022
Tricyclic and tetracyclic antidepressants, also called cyclic antidepressants, are among the earliest antidepressants developed. They're effective, but they've generally been replaced by antidepressants that cause fewer side effects. However, cyclic antidepressants may be a good option for some people. In certain cases, they relieve depression when other treatments have failed.
Cyclic antidepressants are designated as tricyclic or tetracyclic, depending on the number of rings in their chemical structure — three (tri) or four (tetra).
How cyclic antidepressants work
Cyclic antidepressants ease depression by affecting chemical messengers (neurotransmitters) used to communicate between brain cells. Like most antidepressants, cyclic antidepressants work by ultimately effecting changes in brain chemistry and communication in brain nerve cell circuitry known to regulate mood, to help relieve depression.
Cyclic antidepressants block the reabsorption (reuptake) of the neurotransmitters serotonin (ser-o-TOE-nin) and norepinephrine (nor-ep-ih-NEF-rin), increasing the levels of these two neurotransmitters in the brain. Cyclic antidepressants also affect other chemical messengers, which can lead to a number of side effects.
Cyclic antidepressants approved to treat depression
The Food and Drug Administration (FDA) approved these tricyclic antidepressants to treat depression:
• Amitriptyline
• Amoxapine
• Desipramine (Norpramin)
• Doxepin
• Imipramine (Tofranil)
• Nortriptyline (Pamelor)
• Protriptyline
• Trimipramine
The FDA approved the tetracyclic antidepressant maprotiline to treat depression.
Sometimes cyclic antidepressants are used to treat conditions other than depression, such as obsessive-compulsive disorder, anxiety disorders or nerve-related (neuropathic) pain.
Possible side effects and cautions
Because of the different ways cyclic antidepressants work, side effects vary somewhat from medication to medication. Some side effects may go away after a time, while others may lead you and your doctor to try a different medication. Side effects may also be dependent on the dose, with higher doses often causing more side effects.
Some common possible side effects include:
• Drowsiness
• Blurred vision
• Constipation
• Dry mouth
• Drop in blood pressure when moving from sitting to standing, which can cause lightheadedness
• Urine retention
Other possible side effects include:
• Weight loss
• Increased appetite leading to weight gain
• Excessive sweating
• Tremor
• Sexual problems, such as difficulty achieving an erection, delayed orgasm or low sex drive
Generally speaking:
• Amitriptyline, doxepin, imipramine and trimipramine are more likely to make you sleepy than other tricyclic antidepressants are. Taking these medications at bedtime may help.
• Amitriptyline, doxepin, imipramine and trimipramine are more likely to cause weight gain than other tricyclic antidepressants are.
• Nortriptyline and desipramine appear to have better tolerated side effects than other tricyclic antidepressants do.
For antidepressants that cause sleepiness, be careful about doing activities that require you to be alert, such as driving a car, until you know how the medication will affect you.
Which antidepressant is best for you depends on a number of issues, such as your symptoms and any other health conditions you may have. Ask your doctor and pharmacist about the most common possible side effects for your specific antidepressant and read the patient medication guide that comes with the prescription.
Safety issues
Some tricyclic antidepressants are more likely to cause side effects that affect safety, such as:
• Disorientation or confusion, particularly in older people when the dosage is too high
• Increased or irregular heart rate
• More-frequent seizures in people who have seizures
Other issues to discuss with your doctor before you take a cyclic antidepressant:
• Antidepressants and pregnancy. Talk to your doctor about the risks and benefits of using specific antidepressants. Some antidepressants may harm your baby if you take them during pregnancy or while you're breast-feeding. If you're taking an antidepressant and you're considering getting pregnant, talk to your doctor or mental health professional about the possible risks. Don't stop taking your medication without contacting your doctor first, as stopping might pose risks for you.
• Drug interactions. When taking an antidepressant, tell your doctor about any other prescription or over-the-counter medications, herbs or other supplements you're taking. Some antidepressants can cause dangerous reactions when combined with certain medications or herbal supplements.
• Serotonin syndrome. Rarely, an antidepressant can cause high levels of serotonin to accumulate in your body. Serotonin syndrome most often occurs when two medications that raise the level of serotonin are combined. These include other antidepressants, certain pain or headache medications, and the herbal supplement St. John's wort.
• Signs and symptoms of serotonin syndrome include anxiety, agitation, high fever, sweating, confusion, tremors, restlessness, lack of coordination, major changes in blood pressure and a rapid heart rate.
• Seek immediate medical attention if you have any of these signs and symptoms.
• Safety and blood tests. Your doctor may recommend blood levels to determine the most effective dose. Some side effects and benefits of cyclic antidepressants depend on the dose. Overdose of cyclic antidepressants can be dangerous.
• Chronic health conditions. Cyclic antidepressants can cause problems in people with certain health conditions. For example, if you have glaucoma, an enlarged prostate, heart problems, diabetes, liver disease or a history of seizures, talk to your doctor about whether a cyclic antidepressant is a safe choice for you.
Suicide risk and antidepressants
Most antidepressants are generally safe, but the FDA requires that all antidepressants carry black box warnings, the strictest warnings for prescriptions. In some cases, children, teenagers and young adults under 25 may have an increase in suicidal thoughts or behavior when taking antidepressants, especially in the first few weeks after starting or when the dose is changed.
Anyone taking an antidepressant should be watched closely for worsening depression or unusual behavior. If you or someone you know has suicidal thoughts when taking an antidepressant, immediately contact your doctor or get emergency help.
Keep in mind that antidepressants are more likely to reduce suicide risk in the long run by improving mood.
Stopping treatment with cyclic antidepressants
Cyclic antidepressants aren't considered addictive. However, stopping antidepressant treatment abruptly or missing several doses can cause withdrawal-like symptoms. Symptoms may vary depending on how the drug works. This is sometimes called discontinuation syndrome. Work with your doctor to gradually and safely decrease your dose.
Withdrawal-like symptoms can include:
• Agitation, irritability or anxiety
• Nausea
• Sweating
• Flu-like symptoms, such as chills and muscle aches
• Insomnia
• Lethargy
• Headache
Finding the right antidepressant
People may react differently to the same antidepressant. For example, a particular drug may work better — or not as well — for you than for another person. Or you may have more, or fewer, side effects from taking a specific antidepressant than someone else does.
Inherited traits may play a role in how antidepressants affect you. In some cases, where available, results of special blood tests may offer clues about how your body may respond to a specific antidepressant. However, other variables besides genetics can affect your response to medication.
When choosing an antidepressant, your doctor takes into account your symptoms, any health problems, other medications you take, and what's worked for you in the past.
Typically, it may take several weeks or longer before an antidepressant is fully effective and for initial side effects to ease up. Your doctor may recommend dose adjustments or different antidepressants, but with patience, you and your doctor can find a medication that works well for you.
© 1998-2023 Mayo Foundation for Medical Education and Research (MFMER). All rights reserved. Terms of Use
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Kansas City MO Chiropractors May Help Scoliosis
Kansas City MO Chiropractors May Help Scoliosis
Kansas City Chiropractors May Help Scoliosis
Among common back conditions, scoliosis is one that has the potential to cause a great deal of discomfort and immobility. Between 5 million and 7 million people in the United States are affected by scoliosis. Kansas City MO chiropractors have the ability to provide relief to many scoliosis patients, making their day-to-day lives more manageable.
What is Scoliosis in Kansas City MO?
Scoliosis is a condition of the spine where a lateral or sideways curvature of greater than 10 degrees develops. Most of the time, the cause of this unique curvature is unknown, but in around 20 percent of the cases, things like neurological disease, trauma, or tumors are responsible. Scoliosis with no known cause is called idiopathic.
If someone has functional scoliosis, it means that a postural issue, muscle spasm or legs that are different lengths is the cause. This type of scoliosis can usually be remedied. If scoliosis is considered structural, various postural strategies are usually ineffective. Scoliosis is more common among girls and it typically develops between the ages of 10 and 15. It can also be passed down, so if a parent or sibling has it there is a higher likelihood of a younger child getting it.
Common Symptoms of Scoliosis
Some of the common symptoms of scoliosis include intense pain, reduced range of motion, reduced lung function, and reduced heart function. Psychological problems including decreased self-esteem are also a common issue among people that have scoliosis. Around 80 percent of people with scoliosis have a curvature of fewer than 20 degrees, but since it occurs most often during adolescence, it is possible to see large increases in curvature within a short period. Scoliosis is usually diagnosed through physical evaluation and x-rays to determine the extent of the spinal curvature.
Chiropractic Treatment for Scoliosis
Some of the most effective treatments performed by Kansas City chiropractors for scoliosis include spinal manipulation, electric muscle stimulation, and therapeutic exercise. This is an area that hasn’t received a lot of attention or research, but many patients with scoliosis that have had chiropractic treatment report an improvement in their condition.
Even if the spinal curvature is not completely corrected, any associated pain or issues that have been added to the scoliosis discomfort will be addressed. Sometimes the change in posture and gait created by scoliosis causes other areas to overcompensate, causing pain and leading to new issues. Your chiropractor at Leath Chiropractic will search for the underlying cause of all your structural aches and pains and find the solution that works best for your specific situation.
At Leath Chiropractic our team is here to help answer your questions. Please feel free to contact us today.
OFFICE HOURS
Monday
7:30am - 12:00pm
2:00pm - 5:00pm
Tuesday
Closed
Wednesday
7:30am - 12:00pm
2:00pm - 5:00pm
Thursday
9:00am - 12:00pm
2:00pm - 5:00pm
Friday
7:30am - 12:00pm
2:00pm - 5:00pm
Saturday
9:00am - 1:00pm
Sunday
Closed
Leath Chiropractic
6537 N Cosby Ave
Kansas City, MO 64151
(816) 587-7711
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Patient Education
March 29, 2023
Oftentimes, contact lens wearers will skimp on their lens care because some of the solutions are costly and it seems like a good way to save some hard-earned cash. But this is not a good idea. Cutt...
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We are frequently asked if it’s wise to have cataract surgery if you have Macular Degeneration.
Let’s start with some background.
1. Cataracts and Age-related Macular Degeneration (AMD) are both leading causes of visual impairment in the...
It's pretty common for eye doctors to have older patients come in asking if the white part of their eye, the sclera, has a growth or is turning a gray color.
Usually, the culprit is senile scleral plaque, which is commonly seen in people over...
Recent Census Bureau data shows a population of approximately 71 million baby boomers (the generation born from 1946-1964). What does that have to do with low vision you may ask? Approximately 40 million people worldwide have some sort of...
Age-related macular degeneration, often called ARMD or AMD, is the leading cause of vision loss among Americans 65 and older.
AMD causes damage to the macula, which is the central portion of the retina responsible for sharp central vision. AMD...
At some point, you might be the victim of one of these scenarios: You rub your eye really hard, you walk into something, or you just wake up with a red, painful, swollen eye. However it happened, your eye is red, you’re possibly in pain, and...
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optometrist, eye doctor, South Portland, ME
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Phone: (207) 799-3031 Fax: (207) 799-9005
Mon, Tue, Thur, Fri: 8:00am - 5:45pm
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Latest News
March 29, 2023
Oftentimes, contact lens wearers will skimp on their lens care because some of the solutions are costly and it seems like a good way to save some hard-earned cash. But this is not a good idea. Cutt...
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About problem sleepiness
What is problem sleepiness?
Problem sleepiness occurs when sleepiness during the day interferes with work or social functioning.
• Symptoms of problem sleepiness may include difficulty concentrating, falling asleep while driving, or problems with emotional control.
• There are a number of causes of problem sleepiness, including sleep disorders; other medical conditions; certain medications; substances like drugs, alcohol, or caffeine; or an altered sleep-wake cycle.
• Sleep disorders include narcolepsy, insomnia, sleep apnea, and restless legs syndrome.
• Sleepiness is a major cause of motor vehicle accidents, poor school performance, and depressed mood.
• Shift workers are especially susceptible to sleepiness and its risks.
• Treatment may consist of improving sleep hygiene and avoiding precipitating factors.
What is problem sleepiness?
Everyone feels sleepy at times. However, when sleepiness interferes with daily routines and activities, or reduces the ability to function, it is called "problem sleepiness." A person can be sleepy without realizing it. For example, a person may not feel sleepy during activities such as talking and listening to music at a party, but the same person can fall asleep while driving home afterward.
What are the symptoms for problem sleepiness?
You may have problem sleepiness if you:
• consistently do not get enough sleep, or get poor quality sleep;
• fall asleep while driving;
• have difficulty paying attention or concentrating at work, school, or home;
• have performance problems at work or school;
• are often told by others that you are sleepy;
• have difficulty remembering;
• have slowed responses;
• have difficulty controlling your emotions; or
• must take naps on most days.
What are the causes for problem sleepiness?
Sleepiness can be due to the body's natural daily sleep-wake cycles, inadequate sleep, sleep disorders, or certain drugs.
What are the treatments for problem sleepiness?
The treatment options for excessive sleepiness vary greatly, depending on the cause.
Obstructive sleep apnea
One of the most common treatments is continuous positive airway pressure (CPAP). This therapy employs a small bedside machine that pumps air through a flexible hose to a mask worn over your nose and mouth.
Newer versions of CPAP machines have smaller, more comfortable masks. Some people complain that CPAP is too loud or uncomfortable, but it remains the most effective OSA treatment available. It’s typically the first treatment a doctor will suggest for OSA.
Restless legs syndrome
RLS can sometimes be controlled with lifestyle changes. A leg massage or a warm bath before bedtime may help. Exercising early in the day may help with RLS and with your ability to fall asleep.
Your doctor may recommend iron supplements if it appears your iron levels are low. Your doctor may also prescribe medications to control RLS symptoms. If so, be sure to discuss any potential side effects with your doctor or pharmacist.
Narcolepsy
Narcolepsy symptoms may be treated with some lifestyle adjustments. Brief, scheduled naps may help. Sticking to a regular sleep-wake schedule every night and morning is also recommended. Other tips include:
• getting daily exercise
• avoiding caffeine or alcohol before bedtime
• quitting smoking
• relaxing before bed
All of these things can help you fall asleep and stay asleep better at night. This may help cut down on sleepiness during the day.
Depression
Treating depression can be done with a combination of therapy, medications, and lifestyle changes. Antidepressant drugs aren’t always necessary. If your doctor recommends them, they may be needed temporarily.
You may be able to ease depression through talk therapy and making certain lifestyle changes, such as exercising more, limiting alcohol, eating a nutritious diet, and managing stress.
Age-related sleep problems
The lifestyle changes that can help treat narcolepsy and insomnia can also help people experiencing age-related sleep problems. If lifestyle changes alone aren’t enough, talk with your doctor. They can prescribe sleep medications that can improve your quality of sleep.
Idiopathic hypersomnia
Since the cause of idiopathic hypersomnia isn’t known, treatment is focused on alleviating symptoms and may include stimulants, diet changes, or lifestyle changes.
The bottom line
Getting enough sleep is crucial to good health. If you can identify the cause of your excessive sleepiness and get treatment, you should find yourself feeling more energetic and with a better ability to concentrate during the day.
If your doctor doesn’t ask about your sleep routine, volunteer your symptoms of daytime sleepiness and discuss ways to overcome them. Don’t live with feeling tired every day when you might have a condition that’s easily and safely treated.
What are the risk factors for problem sleepiness?
Sleepiness is the desire to fall asleep. It's normal to feel sleepy at times, especially if you've been awake for a long time or haven't had enough sleep the night before. But when sleepiness interferes with your daily activities and causes problems at home, school or work, it can become a disorder called hypersomnolence.
Hypersomnolence usually involves extreme daytime sleepiness that affects your ability to function during the day. When you're hypersomnolent, it's hard for you to stay awake for more than a few hours at a time without taking a nap—even when you have the opportunity to sleep. Hypersomnolence can be caused by an underlying medical condition or by an emotional or behavioral problem.
It is a common symptom of several medical conditions, including depression, heart failure, chronic pain, and restless legs syndrome.
It can also be caused by certain medications such as antidepressants (SSRIs), amphetamines, and antihistamines. The problem sleepiness can also be a side effect of some over-the-counter medications such as cold medicine or pain relievers containing caffeine.
The four risk factors of problem sleepiness are:
1. Age: most people experience a decline in their ability to stay awake as they get older
2. Stress: stress can make you feel tired and sleepy
3. Sleep disorders: an untreated sleep disorder like insomnia can make it difficult for you to fall asleep and stay asleep throughout the night
4. Medical conditions: certain medical conditions such as heart disease, diabetes, cancer, or depression can increase your risk of experiencing problem sleepiness.
Symptoms
Difficulty concentrating during the day,Drowsiness during the day (including falling asleep at inappropriate times),Fatigue after waking up from sleep—or not feeling refreshed after sleeping enough hours for your body's needs,Having trouble waking up in the morning and/or falling asleep at night on a regular basis
Condition
Sleep Apnea,Insomnia,Shift Work Sleep Disorder (SWSD),Circadian Rhythm Disorders (CRDs),Narcolepsy,Sleep-Related Breathing Disorders (SRBDs)
Drugs
Trazodone (a selective serotonin reuptake inhibitor),Mirtazapine (a noradrenergic and specific serotonergic antidepressant),Nuvigil (modafinil)
Is there a cure/medications for problem sleepiness?
In general, medications do not help problem sleepiness, and some make it worse. Caffeine can reduce sleepiness and increase alertness, but only temporarily. It can also cause problem sleepiness to become worse by interrupting sleep.
While alcohol may shorten the time it takes to fall asleep, it can disrupt sleep later in the night, and therefore add to the problem sleepiness.
Medications may be prescribed for patients in certain situations. For example, the short-term use of sleeping pills has been shown to be helpful in patients diagnosed with acute insomnia. Long-term use of sleep medication is recommended only for the treatment of specific sleep disorders.
Video related to problem sleepiness
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Question: How do you catch HIV?
Contact between broken skin, wounds, or mucous membranes and HIV-infected blood or blood-contaminated body fluids. Deep, open-mouth kissing if both partners have sores or bleeding gums and blood from the HIV-positive partner gets into the bloodstream of the HIV-negative partner. HIV is not spread through saliva.
Is it easy to catch HIV?
HIV is not passed on easily from one person to another. The virus does not spread through the air like cold and flu viruses. HIV lives in the blood and in some body fluids. To get HIV, 1 of these fluids from someone with HIV has to get into your blood.
What are the chances of catching HIV?
Key pointsActivityRisk-per-exposureVaginal sex, male-to-female, no condom0.08% (1 in 1234)Vaginal sex, male-to-female, no condom, undetectable viral load0%Receptive anal sex, no condom1.38% (1 in 72)Receptive anal sex, no condom, undetectable viral load0%10 more rows•15 May 2020
How is HIV caused?
HIV infection is caused by the human immunodeficiency virus. You can get HIV from contact with infected blood, semen, or vaginal fluids. Most people get the virus by having unprotected sex with someone who has HIV. Another common way of getting it is by sharing drug needles with someone who is infected with HIV.
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|
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Skip to content
whey protein
What are the side effects of whey protein ?
on
5 Whey Protein Side effects
whey protein
Whey protein is one of the most popular and old dietary supplements that exist in the health and fitness industry, the way by which supplement eases the difficult task of meeting out daily intake is the reason why is so popular, apart from this is also the most researched supplement and the most consumed one as well as it gives a complete 25–27 gm of fast-digesting per serving.
whey protein
Although with lots of advantages, whey protein side effects can also cause some that you should always be aware of for better health awareness.hence these are 5 whey protein side effects that one should know about.
1. Digestive issues
it is made up of milk, which contains lactose, which is a type of sugar found in dairy, and with people who are lactose intolerant which is if their body cannot digest lactose, they can face some digestive issues related to lactose digestion such as a bloating, acidity, gas, vomiting and diarrhea which are a quite a
whey protein
serious problems one has to face if they are body cannot deal with lactose effectively, hence if you are someone who is lactose intolerance than avoiding consuming protein can potentially cause you some problems and uneasiness as well.
2. Hormonal issues
Since it is derived from milk, along with the goodness of essential nutrients milk has also added hormones that in some cases naturally present in them, or in the majority of cases, dairy farmers inject artificial hormones to the cows to extract large quantities of milk and hence the milk has also free flow of hormones like
whey protein
estrogen that enters the human body when one consumes it, now it may not hammer some people but for the people who are sensitive to hormonal imbalances may feel a lot of problems like acne, hair fall, oily skin, gut issues and P C O S(in women)
Thus if you are someone who is more sensitive towards hormonal changes, the addition of whey protein in your diet can make it a little worse for your body, thus avoiding could be the best case over here.
3. Kidney problems
Protein is essential for all human beings out there, from healthy muscle mass to bone health to hormones to skin and hair health, it is an important nutrient for the human body but if one person is consuming more than their body require it can lead to deterioration of kidney as the main function of kidneys is to filter out
whey protein
the blood and if you are loaded with a lot of protein, it will make a little difficult for the kidney to filter out the excess from your blood and as supplement gives you a high amount of protein easily, consuming more supplement daily can put you on that risky zone where your kidneys have might have to suffer.
4. Whey Protein side effects can make you ill
With the rise of supplements in the market, there is also the increase of fake supplement just like any other thing like mineral water or basic foods, now as is on the expensive side the margins involved are much more that gives birth to more delicacy and adulteration in supplement which can cause serious issues in one health,
especially to one's digestive health and liver and kidney health as these cheap and fake supplements are made with crap quality and if one is new to supplements there are high chances that any person can fall into the web.
5. Side effects May give you Acne
Since supplement is derived from milk, various Researchers suspect that there is a correlation between milk and acne, due to the fact that milk and milk products contain I G F-1, a growth-promoting hormone positively associated with the increase of estrogen factors linked to the appearance of acne and thus
whey protein
if you are someone who is little sensitive to dairy, consuming protein and whey protein side effects might give you some breakouts in the form of acne, which is never a good thing to have.
While protein is a great dietary supplement that anyone can add on the other side of whey protein, there are some protein side effects as mentioned above that can disturb one's body health and harmony, hence consuming in accordance with your health practitioner and regulating how your body reacts to it.
Leave your thought here
Please note, comments need to be approved before they are published.
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Back to Library
Myth-Busting the Causes of Obesity
by Ted Kyle, RPh, MBA
Fall 2016
The eternal question about obesity seems to be: what causes it?
It’s an important question. Without understanding the roots of a problem, the odds of solving it are pretty small. But this question doesn’t have a single, simple answer. That’s because it’s really a bunch of questions rolled up into one.
So let’s break that question down into smaller questions that have more satisfying answers.
Why do we have so much more obesity than we had in 1980?
The short answer to this question is that many things have changed in the world around us that combine to make everybody gain weight. Some people think sugar is the villain – especially in sugary sodas. That’s probably part of it. Some people say it’s all about days spent sitting in front of our glowing rectangles. That’s part of it. But the truth is those are just a few possibilities from a long list of suspects.
The Obesity Society tells us that many factors are contributing to the prevalence of obesity. Their infographic (below) gives you a glimpse of some of those factors. If you dig deeper you can find even more.
These factors are simply suspects. Any one of them may play a small role. Some of them may play a large role. Definitive proof is lacking to distinguish one from the other. Much remains to be learned. And anyone who tells you that it’s a simple matter of diet and physical activity just doesn’t understand the science of obesity.
Why does this person have obesity?
The short answer to that question is that the main reason is in his genes. The stock answer – because he made bad choices or lives a bad lifestyle – is simply wrong. Plenty of people make bad choices or live a bad lifestyle and never develop obesity. Plenty of people are very careful about their lifestyle choices and yet cannot shake their obesity.
Overwhelmingly, a person’s individual risk of obesity is inherited. A 2008 study and commentary found heritability estimated at 77 percent and a total (i.e., shared and non-shared) environmental effect of <25 percent. Estimates of the overall heritability of obesity vary – some as low as 50 percent. Some range much higher. But the bottom line is that genes play the largest role in determining how much fat an individual’s body stores.
Why is it so hard to overcome obesity?
The short answer to this question is that obesity is more than just one single disease. Back in 1971, the American government declared war on cancer and set out to find a cure. Tremendous progress means we’ve come to understand that cancer is a collection of many diseases divided into many different sub-types. Some are curable, some are manageable and some are really hard to deal with.
The smartest scientists working on obesity are learning that the same thing is true for obesity.
Opening the Blackburn Course in Obesity Medicine in Boston this year, Doctor Lee Kaplan presented a compelling rationale for moving past thinking that one size fits all in obesity prevention, diagnosis, or treatment. Kaplan started with a simple definition of obesity – excessive fat accumulation that presents a risk to health – and presented an expansive overview of the wide variety of ways that an unhealthy fat mass can become the set point for different individuals.
To make his point, Kaplan listed 57 potential varieties of obesity (pictured above) and then explored distinguishing characteristics of some of them.
Different pathologies mean that different people respond to different therapies very differently. In bariatric surgery, for example, the average response might be losing about 30 percent of body weight in a given population. But some patients will lose as much as half of their initial body weight. A few will lose very little and eventually regain it.
For every obesity treatment, we see a wide variety of responses. Medical nutrition therapy can bring dramatic responses in some people, alongside minimal responses in other people who initially seem very similar. A drug like liraglutide, which typically causes a loss of 5-10 percent of body weight, produces a loss of up to 30 percent in a few outliers.
The reasons for this diversity are only partially understood. Genetics, epigenetics, environmental factors, and behavioral factors all play a role. The one thing that is clear is that thinking one-size-fits-all in obesity is simply wrong.
Conclusion
No one treatment works for everyone. No one prevention strategy will be adequate to prevent obesity in the next generation. Dogged pursuit of understanding the complexity of this disease is the key. It’s key for developing targeted strategies that will actually work for preventing obesity’s diverse causes. It’s key for developing targeted treatments to relieve the suffering obesity causes in so many forms.
About the Author:
Ted Kyle, RPh, MBA, is a pharmacist and health marketing expert and is also Immediate-Past Chairman of the OAC National Board of Directors.
by Robert Kushner, MD Fall 2021 Disclaimer: Consult with your healthcare provider if you are interested in…
Read Article
Fall 2021 While we can’t always control what happens to us, we can choose how we respond.…
Read Article
The Obesity Action Coalition (OAC) and the American College of Physicians (ACP) are proud to offer a…
View Guide
Comprehensive obesity care requires teaming up with a qualified and compassionate medical professional. Find the right healthcare provider to talk about your weight and health at ObesityCareProviders.com.
Click Here
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In recent years, we have witnessed the rise of cannabis-infused products in the skin care market. This has gone hand-in-hand with the broader acceptance that cannabis has been acquiring both in society and legislation everywhere. Studies show that people who suffer from skin conditions or illnesses are growing more familiar with the health benefits brought by some cannabis components, such as cannabidiol — CBD.
CBD is a non-psychoactive component found in the cannabis plant. It is excellent for health issues due to its antioxidant, neuroprotective and anti-inflammatory properties. Doctors and dermatologists have been showing continuous interest in the possibilities of CBD as a treatment for skin-related issues. Damage provoked by oxidative stress and free radicals as we age, as well as psoriasis, acne, and eczema, could be successfully treated with the help of cannabidiol.
Unfortunately, it is still early as far as cannabis-related researches go. We still don’t know just how beneficial CBD could potentially be to treat all of these health issues. But what we have seen thus far does not disappoint.
Understanding Eczema
Eczema can be defined as a skin issue where the dermis becomes irritated and itchy. The term itself is both medically and commonly used, although it refers to a broader set of skin conditions.
As the National Eczema Association has revealed recently, approximately 30 million Americans suffer from eczema skin conditions. Dermatologists describe eczema as a skin condition where the skin barrier does not function at its best. This leads the skin to become increasingly dehydrated and inflamed. Symptoms of eczema include skin dryness and redness. Itchiness in the dermis is also very common. Although eczema is a hereditary skin condition, there are many external factors that may worsen it. If the environment triggers our allergies or irritates our skin, this might affect eczema in our body.
Eczema usually appears only as unsettling itchiness at different spots of our skin. It could be regular, or it could be temporary. In certain seasons of the year, the condition may be more sensitive to exposure. However, people with severe eczema might experience a far worse debilitating effect. To severely ailed patients, eczema could provoke major skin infections, as well as impairing the immune system. Mental health issues, such as anxiety and depression, could also be triggered by severe eczema.
What Are the Best Ways to Treat Eczema?
Treating eczema usually requires two very important steps. Dermatologists and skin care professionals consider that eczema first requires the skin barrier to be repaired, to improve skin hydration. After that, we should check on the inflamed skin. If there is a major rash on certain areas of the skin, these could lead to inflammation, which is why they must also be treated.
Eczema can typically be treated through gentle skin cleansers and moisturizers. Hydrocortisone creams are often employed in the treatment of eczema, as are steroid ointments. Oral immunosuppressants and UV light therapy are also widely used to treat this condition.
How CBD Can Be Used to Treat Eczema
Doctors consider that CBD is a component with several soothing and anti-inflammatory properties. This makes it very useful to treat skin conditions, such as eczema. Endocannabinoid is a component that we produce naturally in our body, and it can also be found in our skin. CBD can be used to quell eczema by applying it to our skin, and relying on the endocannabinoids and receptors from it.
In medical terms, the endocannabinoid system is part of our immune system. This helps explain why skin conditions like psoriasis and eczema could be a symptom of immune system debilitation. Since skin is the largest organ in our body, it could also be regarded as part of the immune system. The weakened endocannabinoid system in our skin could be the one causing the skin condition. CBD can then be used to influence our endocannabinoid system, thus helping treat eczema successfully.
Many dermatologists regard CBD as a great component for skin treatment. They consider it positive that CBD’s beneficial properties impact the root of the skin conditions, but also that its origins are natural and plant-based. It could be considered a mirror-image of a molecule which our body produces by itself, in that toxicity is low, whereas the potential effect it brings can be significant.
How to Apply CBD as a Treatment for Eczema
The endocannabinoid system in our body has a regulatory function, in the sense that it accelerates things and slows them down when necessary. CBD could then work as a preventative component, or be used when we feel we’re getting a flare-up. Doctors believe that the gravity of the skin condition could determine whether we should treat eczema only with topicals, or if a combination of topicals and comestibles can be used.
If the skin issue is merely a moderate one, dermatologists consider that topicals are probably the best choice to treat it. If we develop a very irritated skin with a continuous set of eczema flare-ups, which could be a chronic skin condition, topicals and comestibles will be required. Doctors are growing confident on the effects of CBD as a means to treat eczema, both in topical and indigestible solutions.
Which Form of CBD Works Best to Treat Eczema?
Doctors advise us to use the full spectrum form of CBD to soothe a skin condition such as eczema. This will allow us to gain all the benefits the cannabis plant has to offer to treat the condition and lessen its harms. When it comes to hemp-derived forms of CBD, doctors consider it’s not such an easy question to answer. The key thing to distinguish whether hemp and cannabis can be paired is if the CBD form is an isolate.
If we choose to apply a CBD isolate that has no traces of cannabinoids or any other terpenes, we can’t experience the full health effects the component has to offer. Data shows that something called the Entourage Effect has a beneficial impact when CBD is used to treat skin conditions. Unfortunately, this effect only shows in full spectrum CBD.
What Is the Future of CBD and Eczema?
Most professionals in the medical industry consider that eczema patients will be treated with CBD in the future. Studies consistently show that CBD has many anti-inflammatory effects when it’s employed to treat skin conditions. Not only it is beneficial in the treatment of eczema now, but it will probably become part of prescribed medications in the near future.
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top of page
Botox: More Than Just a Wrinkle Eraser
There is a confusion and misinformation among the general public regarding aesthetic injections, often incorrectly referred to as “botox”. This misnomer has led to the association of botox with images of unnatural, overly inflated faces. It is important to recognize that various injection-based treatments exist, each serving distinct purposes and delivering different outcomes.
This widespread misconception can be attributed, in part, to a lack of understanding about the true nature of botox and its mechanism of action. So, let’s delve deeper into the topic and explore botox and its diverse range of applications.
What is botox and how does it work?
How botox works | RJ CLINIC
Botox, or botulinum toxin, is a neurotoxin that is produced by the bacteria Clostridium botulinum. When injected into a muscle, it blocks the release of acetylcholine, a neurotransmitter responsible for muscle contraction. This prevents the muscle from contracting and causing wrinkles or other unwanted movements. Another common injection, filler, on the other hand, is injected to add volume and plumpiness, filling in hollow areas and smoothing out wrinkles.
Uses:
While it is often known for its ability to diminish wrinkles and fine lines on the face, botox offers a broader range of cosmetic and even medical uses beyond that.
Uses for botox | RJ CLINIC
Treat dynamic lines
Botox is most commonly used to treat dynamic wrinkles, which are caused by repetitive muscle movements, such as frowning, squinting or raising eyebrows. These wrinkles can create an older or fatigued appearance. By temporarily paralyzing and weakening the muscles involved for these movements, botox helps smoothen the skin and rejuvenate the face, resulting in a more youthful and revitalized look.
Face slimming
Botox can also be used to contour the face. An increasingly popular treatment is the use of botox injections to target the masseter muscles, aiding in slimming and refining the jawline, ultimately leading to a more feminine and aesthetically pleasing appearance. This treatment is particularly popular in Asian countries, where a V-shaped or heart- shaped face is considered more desirable than a square-shaped face.
Jaw Slimming with Botox | RJ CLINIC
The masseter muscle, a prominent muscle running along the side of the face, serves a pivotal role in the processes of chewing and jaw clenching. However, in certain individuals, various factors such as teeth grinding or clenching, chronic stress, or even genetic predisposition can contribute to the enlargement of the masseter muscle. This enlargement can lead to a more square-shaped jawline, which is often perceived as a characteristic associated with a masculine aesthetic.
To address this concern, botox injections are strategically administered to the masseter muscles, causing a temporary relaxation of the muscle fibers. By doing so, the injections effectively reduce the bulkiness and hypertrophy of the masseter muscles. The treatment helps to sculpt and contour the jawline, resulting in a softer and more feminine appearance.
The cosmetic benefits of botox injection for the masseter muscles extend beyond slimming and contouring the jawline. The procedure can also contribute to a more balanced and proportionate facial profile, enhancing overall facial harmony. Moreover, botox injections for masseter muscle reduction are known for their non- surgical and non-invasive nature, making them a popular choice among individuals seeking subtle yet effective facial enhancements.
Brow lift
Another application of botox involves the enhancement of the brow area, commonly known as a brow lift. By injecting small quantities of botox into the muscles responsible for pulling down the eyebrows, it becomes possible to achieve a lifted appearance and create a more defined, arched shape. This technique proves particularly beneficial and effective for individuals with naturally droopy eyebrows, as it helps to rejuvenate and revitalize their overall facial expression.
Treat gummy smile
Gummy smile treatment with botox | RJ CLINIC
Furthermore, botox offers a solution for those troubled by a gummy smile, a condition characterized by the excessive display of gum tissue when smiling. This aesthetic concern arises from hyperactive muscles that elevate the upper lips, resulting in the exposure of a significant portion of the gums. Thankfully, botox provides an effective treatment option for this condition. By temporarily relaxing the muscles responsible for elevating the upper lips, botox reduces the excessive display of gum tissue, thereby improving the harmony and balance of the smile.
Nose tip lift
Botox can also enhance the appearance of the nose tip. It is possible to relax the muscle responsible for pulling the nasal tip downward with botox injection, and effectively creating a “lift” for the nose tip. This technique proves advantageous for individuals seeking subtle changes to the shape and projection of their nose, without resorting to invasive surgical procedures.
Treat dimpled and receding chin
Dimpled chin treatment with botox | RJ CLINIC
Botox also offers a solution for those with a receding and dimpled chin caused by an overactive mentalis muscle. The mentalis muscle, when hyperactive, can result in a chin that appears dimpled and receded. Botox induces temporary relaxation, hence allowing for increased chin projection and reducing the appearance of dimpling.
Nefertiti Lift
The Nefertiti Lift is a cosmetic procedure names after Queen Nefertiti, an ancient Egyptian queen known for her elegant and defined jawline. The procedure involves the use of botox injections to rejuvenate and contour the neck and jawline, resulting in a more youthful and sculpted appearance.
Nefertitit lift treatment with botox | RJ CLINIC
The Nefertiti Lift primarily targets the platysma muscle, which is located in the neck and plays a significant role in supporting the lower face and neck. When platysma muscles are strong, it can create a downward pull, obscuring the jawline and forming vertical neck bands. This can result in an aged and less defined appearance. Nefertiti lift aims to counteract the downward forces caused by the muscle, thereby providing a lifting effect, creating more defined jawline and improved appearance of the neck.
“ Why is it that after multiple botox injections, I no longer see the same improvement that I saw with my initial injections?”
There are many brands of botulinum toxin A or botox available, with Dysport, Botox, and Xeomin being the most widely recognised, and then there are newer brands like Daxxify or Jeauveau.
Types of botox in malaysia | RJ CLINIC
The proteins present in botulinum toxin act as antigens, thereby provoking an immune response from the body, which results in the development of antibodies against the toxin. Consequently, with repeated treatments, the efficacy of botulinum toxin injections wanes, owing to the presence of these antibodies, which block the effect of the toxin.
There is an exception for this case, which is Xeomin. Xeomin was FDA-approved in 2011 and is often advertised as the “cleanest product” of Botox injections because Xeomin does not contain complexing protein that causes antibody formation.
Of course, there are also other factors that can affect the efficacy of botox injections, including changes in the dosage and injection technique.
Why is botox not permanent?
Botox effects only last 3 to 6 months because of neuronal plasticity, wherein fine nerve fibers emerge and reinnervate the muscle fibers, leading to recovery of muscle strength. On top of that, body can also form new connections between the nerve fibers and muscle fibers, known as motor end plates. Formation of new motor end plates can further aid in the restoration of normal muscle function.
Top of Form
Microbotox or mesobotox
Microbotox is a specialized form of botox injection that involves the use of diluted botox solutions to target a larger area of the skin with multiple injections. This technique allows for a more widespread, subtle effect on the skin’s surface while maintaining natural facial expressions.
The microbotox technique is used to reduce sweat, sebum (oil) and minimize pores due to the effect on sweat glands, sebaceous glands (oil glands) and erector pili muscle.
Medical uses of botox
In addition to its cosmetic uses, botox has a variety of medical applications. It can be used to treat chronic migraines, blepharospasm (involuntary eyelid twitching), cervical dystonia (neck muscle spasms), hyperhidrosis (excessive sweating), and spasticity (muscle stiffness and spasms)
Botox or fillers?
There are some common misconceptions about botox that need to be addressed. Firstly, it is important to understand that botox and fillers are two distinct treatments. While fillers work by filling in static lines and restoring lost volume, botox is used to relax muscles that cause wrinkles and dynamic lines.
Botox and filler comparison | RJ CLINIC
Botox works by temporarily paralyzing the muscles that cause wrinkles and fine lines, primarily in the upper part of the face, such as forehead and around the eyes. Results typically last for three to 6 months.
Dermal fillers are a popular cosmetic treatment used to address wrinkles and lines that are present even when the face is at rest. These lines, also known as static lines, develop as a result of a combination of factors, including aging, sun damage, loss of collagen and elastin and repetitive facial expression over time. Unlike dynamic wrinkles that appear with facial movement and are treated with botox to relax the underlying muscles, static lines are formed due to the loss of volume and skin elasticity. This is where dermal fillers come into play to help filling in the static lines and reducing their prominence.
While hyaluronic acid fillers can be dissolved by injecting hyaluronidase if there are any issues, there is no such solution available for botox. Therefore, if there are any undesirable outcomes from botox treatment, you have to wait for the effects to wear off naturally.
Do facial exercise work?
Facial exercises | RJ CLINIC
Facial exercise is a technique in which specific facial muscles are targeted and exercised in order to improve their tone and strengthen them. The aim is to make the face look firmer and more youthful, and to reduce the appearance of wrinkles and fine lines.
Proponents of facial exercise argue that by stimulating blood flow and circulation to the face, these exercises can help nourish the skin and promote a healthy glow. Some also claim that facial exercise can help release tension and stress and improve overall relaxation.
Facial exercise can involve a variety of movements and techniques, such as puckering the lips, raising the eyebrows, and performing certain facial expressions. Some people also use tools like facial massage rollers and gua sha stones to enhance the benefits of facial exercise.
However, there is currently NO strong scientific evidence to support these claims. In fact, overly vigorous facial movements can actually exacerbate wrinkles and fine lines.
One reason for this is that repeated facial movements can cause the muscles in the face to contract and pull on the skin, leading to formation of new wrinkles over time. Additionally, excessive stretching and tugging of the skin can damage its elasticity and contribute to the breakdown of collagen and elastin fibers, which are important for maintaining a smooth and youthful appearance.
If you are looking to reduce wrinkles and fine lines at home, it is generally recommended to focus on lifestyle habits like using sunscreen, eating healthy diet and staying hydrated, as well as using skincare products with proven anti-aging ingredients like retinol or retinoids and antioxidants.
Your anti-aging skincare
Anti Aging skincare | RJ CLINIC
Speaking of retinol and retinoids, they are well known and widely used as skincare for their antiaging benefits. However, there can be some confusion about the distinctions between them.
Retinol is a specific type of retinoid. Retinoids are a class of compounds derived from Vitamin A, and retinol is one of the forms. In comparison to prescription-strength retinoids or retinoic acid such as tretinoin (Retin-A), adapalene (Differin), and tazarotene (Tazorac), retinol is considered milder and available for purchase over the counter.
Retinol is available in various skincare products without the need for a prescription. Retinol is 20 times less potent than prescription-strength retinoids. It serves as a precursor to retinoic acid, which is responsible for the anti-aging effects when it undergoes conversion by the skin. Retinoic acid is the only form of ingredient that is bioavailable to the skin. To put it simply, retinoic acid does not require conversion by the skin to become effective- it starts working instantly.
Retinol, on the other hand, takes more time to produce visible results. However, this does not mean that OTC retinol is ineffective. The notion that “stronger is better” is a common misconception. The slow conversion of retinol makes it more tolerable for individuals with sensitive skin, while prescription-strength retinoids have higher potential for side effects such as skin irritation, dryness, and increased sensitivity.
Ultimately, both retinol and retinoic acid are effective; the difference lies in the time it takes for visible effects to appear, which varies based on individual tolerance. Along with retinol, retinyl palmitate and retinaldehyde are also considered to be less potent forms of retinoids.
These substances offer several benefits for the skin, including:
· Reduced wrinkles and fine lines: They stimulate collagen production, which helps improve skin elasticity and reduced the appearance of wrinkles and fine lines.
· Improved skin texture: Consistent use of retinol or retinoids can lead to smoother skin by promoting cell turnover and facilitating exfoliation.
· Reduced acne: Retinoids possess anti-inflammatory properties and can effectively clear out clogged pores, making them beneficial for treating acne.
As previously mentioned, retinol and retinoids can cause skin sensitivity, redness, dryness and flakiness, especially during the initial stages of use. To minimize these effects, it is advisable to begin with a low concentration and gradually increase it as your skin becomes more tolerant. You can also start by applying 2 to 3 times per week and then gradually increase the frequency to daily use, based on your skin’s tolerance. Additionally, it is important to incorporate daily sunscreen use when using retinol or retinoids since they can heighten the skin sensitivity to the sunlight. This precaution helps protect your skin from potential sun damage.
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Activation of protein kinase C (PKC) has been implicated in gastric carcinogenesis. Enzastaurin is an oral ATP-competitive inhibitor of the PKCβ isozyme. Although enzastaurin was initially advanced to the clinic based on its antiangiogenic activity, it is also known to have a direct effect on a variety of human cancer cells, inducing apoptosis by inhibiting the Akt signal pathway. However, data on enzastaurin for gastric cancer are limited. Therefore, this study was performed to assess the antitumor activity of enzastaurin on gastric cancer cells and to investigate the underlying antitumor mechanisms. Enzastaurin suppressed the proliferation of cultured gastric cancer cells and the growth of gastric carcinoma xenografts. Enzastaurin did not have an effect on gastric cancer cell cycle progression; however, it had a direct apoptosis-inducing effect through the caspase-mediated mitochondrial pathway. Glycogen synthase kinase 3β phosphorylation, a reliable pharmacodynamic marker of enzastaurin activity, and Akt phosphorylation were both decreased after treatment with enzastaurin. Although the p90 ribosomal S6 kinase (Rsk) was also dephosphorylated, Erk phosphorylation was not affected in the enzastaurin-treated gastric cancer cells. Enzastaurin activated Bad, one of the Bcl-2 proapoptotic proteins, through dephosphorylation at Ser112, and depletion of Bad activity resulted in resistance to enzastaurin-induced apoptosis and cytotoxicity in gastric cancer cells. These data suggest that enzastaurin induces apoptosis through Rsk-mediated and Bad-mediated pathways, besides inhibiting the Akt signal cascade. Furthermore, enzastaurin had synergistic or additive effects when combined with 5-fluorouracil, cisplatin, paclitaxel, or irinotecan. These results warrant further clinical investigation of enzastaurin for gastric cancer treatment. [Cancer Res 2008;68(6):1916–26]
Although the incidence of gastric adenocarcinoma has decreased significantly in Western countries, it is still among the most common malignancies in South America, in many former Eastern European countries, and across Asia. In Korea, according to statistics reported in 2005, gastric cancer was the most prevalent cancer in men (1). Although chemotherapy is commonly used in clinical practice, the prognosis of advanced gastric cancer is still poor and treatment is usually unsuccessful. In breast, lung, and colorectal cancers, the identification of novel molecular targets and the development of therapies specific to these targets have provided successful new approaches to treatment in clinical practice. However, targeted therapy has not been successful in the treatment of gastric cancer, and attempts to develop and apply new agents are urgently needed.
The protein kinase C (PKC) signaling pathway, which functions through serine/threonine kinase activity, plays a key role in tumor-induced angiogenesis, tumor growth, differentiation, cytokine secretion, migration, and apoptosis and is a possible target for anticancer therapy (2, 3). PKC activation contributes to tumor cell survival and proliferation and, as such, has been implicated repeatedly in the malignant progression of human cancers, such as B-cell lymphoma (4), malignant gliomas (2), and colorectal carcinomas (57). PKC is stimulated by vascular endothelial growth factor (VEGF) receptor activation and is an important mediator of VEGF, the most potent angiogenic factor identified in a variety of solid tumors (8).
Gastric cancer tumor tissue possesses a higher level of PKC activity than normal tissue (9). Two highly specific PKC inhibitors (RO-31-8220 and chelerythrine) have been shown to suppress the growth of gastric cancer cells through apoptosis induction and cell cycle quiescence (10). PKC has been implicated as having an important role in the development of invasive activity in gastric cancer (11). Recently, it was reported that the antisense targeting PKCα and PKCβ1 markedly inhibited gastric cancer cell growth and made gastric cancer cells more responsive to mitomycin C–induced or 5-fluorouracil (5-FU)–induced apoptosis (12). Given its proposed key role in tumorigenesis, PKC may be a promising target for gastric cancer growth inhibition.
Enzastaurin (LY317615.HCl), an acyclinc bisindolylmaleimide, was initially developed as an ATP-competitive selective inhibitor of PKCβ (13). In addition to its major target PKCβ, enzastaurin also potently inhibits other PKC isoforms, including PKCδ, PKCε, PKCγ, and PKCα (14). Although enzastaurin was initially developed for antiangiogenic cancer therapy (15), recent preclinical studies have shown that enzastaurin has a direct effect on a variety of human cancer cells, inducing apoptosis (14, 1618). Enzastaurin was also shown to target the phosphoinositide 3-kinase (PI3K)/Akt pathway and to inhibit glycogen synthase kinase 3β (GSK3β) phosphorylation (14). Based on these promising preclinical findings, a phase I clinical study that found that enzastaurin at 525 mg once daily was the recommended dose for further clinical trials was completed. At this 525 mg daily dose, a steady-state plasma concentration of enzastaurin and its analytes reached up to 8 μmol/L, with the a mean plasma exposure of 2.2 μmol/L (3). Currently, enzastaurin is being evaluated in several phase II or phase III clinical trials.
However, the role of enzastaurin in gastric cancer remains unknown. The results of our study show that enzastaurin is cytotoxic to gastric cancer cells. These findings strongly support further clinical evaluation of enzastaurin. Furthermore, our data show that enzastaurin induces gastric cancer cell apoptosis by a mechanism not previously reported through the p90 ribosomal S6 kinase (Rsk) and Bad-mediated pathways, in addition to inhibiting the Akt signaling cascade.
Drugs and Reagents
Enzastaurin was provided by Eli Lilly Company. Other chemotherapeutic drugs were obtained as follows: 5-FU and cisplatin from Choongwae Pharma Company, paclitaxel from BMS Korea, and irinotecan from CJ Pharmaceutical Company. Enzastaurin was initially dissolved in DMSO (Sigma Chemical Co.) at a concentration of 5 mmol/L and stored in small aliquots at −20°C.
Antibodies to caspase-3, caspase-9, Erk, phosphorylated Erk, Akt, phosphorylated Akt, p90 Rsk, phosphorylated Rsk (Thr359/Ser363), GSK3β, phosphorylated GSK3β, Bad, phosphorylated Bad (Ser112), and phosphorylated Bad (Ser136) were purchased from Cell Signaling Technology. Antibodies to caspase-8 and poly(ADP-ribose) polymerase (PARP) were provided by BD PharMingen. Antibodies to Bax, Bak, Bcl-XL, Mcl-1, and cytochrome c were obtained from Santa Cruz Biotechnology. The antibody to Bcl-2 was from DakoCytomation.
Cell Lines and Culture
Human gastric cancer cell lines (SNU-1, SNU-5, SNU-16, SNU-216, SNU-484, SNU-601, SNU-620, SNU-638, SNU-668, and SNU-719) were obtained from the Korea Cell Line Bank (19) and grown in RPMI 1640 supplemented with 10% fetal bovine serum and gentamicin (10 μg/mL). All cell lines were incubated under standard culture conditions (20% O2 and 5% CO2; 37°C).
Cell Growth Inhibition Assays
Tetrazolium dye [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, MTT; Sigma] assays were used to evaluate the growth inhibitory effects of enzastaurin, as described in prior studies (20, 21). Cells were seeded on 96-well plates, incubated for 24 h, and then treated with drugs for 72 h at 37°C. After drug treatment, MTT solution was added to each well and incubated for 4 h at 37°C before the medium was removed. DMSO was then added and shaken for 30 min at room temperature. Cell viability was determined by measuring absorbance at 550 nm in a microplate reader (Spectra Classic, Tecan Co.). Experiments were performed in groups of six for each drug concentration and were repeated thrice.
Xenograft Mouse Model
To determine the in vivo activity of enzastaurin, 6-wk-old female athymic nude mice (Harlan Sprague-Dawley, Inc.) were injected s.c. in the back with SNU-16 or SNU-484 cells in 100 μL PBS. When the tumor reached 100 mm3, enzastaurin was suspended in 10% acacia (Fisher Scientific) in water and given at a dose of 75 mg/kg by oral gavage twice daily. Control groups were treated only with vehicle. Tumor burden was measured twice a week with a caliper (calculated volume = length × width × height × π / 6).
Cell Cycle Analysis
Cells were washed twice in PBS, fixed in 70% ethanol, and stored at −20°C until required for analysis. Before analysis, cell suspensions were washed with PBS, digested with RNase A (50 μg/mL) for 15 min at 37°C, and then stained with propidium iodide (50 μg/mL). The cell DNA contents (10,000 cells per experimental group) were determined using a FACSCalibur flow cytometer (Becton Dickinson Biosciences) equipped with a ModFit LT program (Verity Software House, Inc.), as previously described (20).
Annexin V Binding Assay for Apoptosis
After the cells were exposed to enzastaurin for 72 h, the degree of apoptosis was assessed by the Annexin V binding assay as instructed by the manufacturer (BD PharMingen). The harvested cell suspension was incubated with Annexin V for 15 min at room temperature in the dark and then analyzed by flow cytometry, as described previously (20). Single-variable analysis, which used Annexin V–FITC only, was performed due to the self-fluorescence of enzastaurin within the propidium iodide spectrum.
Terminal Deoxyribonucleotidyl Transferase–Mediated dUTP Nick End Labeling Assay for Apoptosis
Three core tissue biopsies (4 mm in diameter) were taken from each individual paraffin-embedded tissue sample (donor blocks) and arranged in a new recipient paraffin block (tissue array block) using a trephine apparatus (Superbiochips Laboratories). Each tissue array block contained samples of all animals. Sections of 4 μm were cut from each triplicate tissue array blocks, deparaffinized, and dehydrated. Immunohistochemical detection of apoptosis was carried out using an Apoptag in situ Apoptosis Detection kit (Chemicon International) following the procedures provided by the manufacturer.
Western Blot Analysis
Cultured cells were washed with ice-cold PBS and suspended in an extraction buffer [20 mmol/L Tris-Cl (pH 7.4), 100 mmol/L NaCl, 1% NP40, 0.5% sodium deoxycholate, 5 mmol/L MgCl2, 0.1 mmol/L phenylmethylsulfonyl fluoride, 0.1 mmol/L pepstatin A, 0.1 mmol/L antipain, 0.1 mmol/L chymostatin, 0.2 mmol/L leupeptin, 10 μg/mL aprotinin, 0.5 mg/mL soybean trypsin inhibitor, and 1 mmol/L benzamidine] on ice for 15 min. Samples containing equal amounts of total protein were resolved in a SDS-polyacrylamide denaturing gel, transferred to nitrocellulose membranes, and probed with antibodies. Detection was performed using an enhanced chemiluminescence system (Amersham Pharmacia Biotech).
For total protein extraction from frozen tissue, mouse tissues frozen in liquid nitrogen after excision were powdered with mortar and pestle. Radioimmunoprecipitation assay buffer [50 mmol/L Tris-Cl (pH 8.0), 150 mmol/L NaCl, 1% NP40, 0.5% sodium deoxycholate, 0.1% sodum dodecyl sulfate, 1 mmol/L EDTA, 1 mmol/L phenylmethylsulfonyl fluoride, 1 mmol/L Na3VO4, 1 mmol/L NaF, 1 μg/mL aprotinin, 1 μg/mL leupeptin, and 1 μg/mL pepstatin] was added to powdered tissue. Samples were vortexed and then incubated for 45 min on ice. Samples were homogenized and centrifuged at 14,000 × g for 10 min. Then, Western blot analysis was performed using the same method.
Analysis of Cytochrome c Release
For detecting the mitochondrial cytochrome c release into the cytosol, cells were harvested at each experimental time point, resuspended with isotonic isolation buffer [10 mmol/L HEPES, 1 mmol/L EDTA, 250 mmol/L sucrose (pH 7.6)], and collected by centrifugation. Cells were then suspended in hypotonic isolation buffer [10 mmol/L HEPES, 1 mmol/L EDTA, 50 mmol/L sucrose (pH 7.6)] and disrupted by passing through a 27-gauge needle 5 to 10 times. After adding hypertonic isolation buffer [10 mmol/L HEPES, 1 mmol/L EDTA, and 450 mmol/L sucrose (pH 7.6)] to balance the tonicity of the buffer, cells were centrifuged at 16,000 × g for 20 min, and the supernatant was used for the cytosol protein extraction.
Transfection with Small Interfering RNA
Two independent small interfering RNA (siRNA) vectors that target the DNA sequence of Bad (Bad1 AAGAAGGGACTTCCTCGCCCG, Bad 2 GACGAGTTTGTGGACTCCTTT; Qiagen Co.) were used in this experiment, and a nonspecific siRNA (nonhomologous to any known gene sequence) was used as a negative control. SNU-620 cells were transfected with these siRNAs for 4 h using the Lipofectamine Plus reagent (Invitrogen) according to the manufacturer's protocol and recovered in fresh medium containing 10% fetal bovine serum for 12 h. Cells were then treated with enzastaurin or DMSO, and the proportion of apoptotic cells (sub-G1 fraction) was determined by flow cytometry.
Analysis of Drug Combination Effects (Isobologram Analysis)
Analyses of drug interactions were performed by constructing an envelope of additivity using the isobologram method of Steel and Peckham, as described previously (21, 22). Based on available dose-response curves, the combined effects of enzastaurin and other cytotoxic chemotherapeutic agents were analyzed at IC50. Three isoeffect curves were drawn as follows.
Mode I line. When the dose of drug A is chosen, there remains an increment of effect to be produced by drug B. If two drugs were to act independently, the addition is performed by taking the increase in doses, starting from 0, that give log survivals which add up to IC50 (heteroaddition).
Mode II(A) line. When the dose of drug A is chosen, an isoeffect curve can also be calculated by taking the dose increment of drug B that gives the required contribution to the total effect up to the limit, in this case, IC50 (isoaddition).
Mode II(B) line. Similarly, when the dose of drug B is chosen, an isoeffect curve can be calculated by taking the dose increment of drug A that gives the required contribution to IC50 (isoaddition).
With combination of graded doses of drug A and a chosen dose of drug B, a single dose-response curve can be drawn. When the experimental IC50 concentration in this drug combination falls left of the envelope (Supplementary Fig. S1, point P1), the two drugs have supraadditive (synergistic) interaction. When the experimental data point is within the envelope, the combination is considered to be noninteractive (additive; Supplementary Fig. S1, point P2). Finally, when the data point is in the area to the right of the envelope, the combination is considered to be antagonistic (Supplementary Fig. S1, point P3 or point P4).
Actual IC50 values were obtained from growth inhibition curves after cancer cells were exposed to a variety of concentrations of enzastaurin or other cytotoxic agents, alone or in combination. When combined, two drugs were applied simultaneously for 72 h.
Statistical analysis. Comparison of quantification of terminal deoxyribonucleotidyl transferase–mediated dUTP nick end labeling (TUNEL) assay or percentage of surviving cells were analyzed by two-tailed Mann-Whitney U test or Student's t test. Statistical analysis to compare tumor sizes in xenograft-bearing mice was performed with Student's two-tailed t test. Differences between groups were considered statistically significant if P < 0.05.
Enzastaurin suppresses gastric cancer cell proliferation in vitro and in a xenograft mouse model. Although enzastaurin was initially introduced for clinical development due to its antiangiogenic activity, it was also shown to have a direct antiproliferative effect on human tumor cells (14). We therefore evaluated the ability of enzastaurin to suppress gastric cancer cell proliferation in culture. Indeed, enzastaurin suppressed the proliferation of gastric cancer cells and showed a wide variety of IC50 values. SNU-620 cells were the most sensitive to enzastaurin (IC50, 3.56 μmol/L) and SNU-1, SNU-5, SNU-16, and SNU-484 cells had a low micromolar range of IC50 values (3.78–6.35 μmol/L). However, enzastaurin was not very cytotoxic with SNU-216 and SNU-719 with IC50 values of >250 μmol/L after 72 hours of exposure (Fig. 1A).
Figure 1.
Antiproliferative activity of enzastaurin in human gastric cancer cells. A, in vitro inhibition of gastric cancer cell proliferation. The effects of enzastaurin on the proliferation of a variety of human gastric cancer cell lines were determined using the MTT assay. Cells were seeded into 96-well culture plates, treated with enzastaurin for 3 d, and then treated with MTT solution for 4 h. The cell viability was determined by measuring absorbance. Points, mean of three experiments; bars, SD. B, tumor growth suppression in a xenograft mouse model of human gastric cancer. Athymic nude mice bearing SNU-484 gastric cancer xenografts were treated with 75 mg/kg enzastaurin twice daily by gavage after tumors reached a mean tumor volume of 100 mm3 (n = 6 for each group). Vehicle control-treated animals received 10% acacia on the same schedule. Tumor volume was measured twice a week using a caliper. Tumor growth was significantly suppressed by enzastaurin treatment. *, P < 0.05 as determined by Student's t test.
Figure 1.
Antiproliferative activity of enzastaurin in human gastric cancer cells. A, in vitro inhibition of gastric cancer cell proliferation. The effects of enzastaurin on the proliferation of a variety of human gastric cancer cell lines were determined using the MTT assay. Cells were seeded into 96-well culture plates, treated with enzastaurin for 3 d, and then treated with MTT solution for 4 h. The cell viability was determined by measuring absorbance. Points, mean of three experiments; bars, SD. B, tumor growth suppression in a xenograft mouse model of human gastric cancer. Athymic nude mice bearing SNU-484 gastric cancer xenografts were treated with 75 mg/kg enzastaurin twice daily by gavage after tumors reached a mean tumor volume of 100 mm3 (n = 6 for each group). Vehicle control-treated animals received 10% acacia on the same schedule. Tumor volume was measured twice a week using a caliper. Tumor growth was significantly suppressed by enzastaurin treatment. *, P < 0.05 as determined by Student's t test.
Close modal
We next sought to assess the in vivo efficacy of enzastaurin using a mouse model of human gastric cancer. The phase I clinical trials for enzastaurin have shown that p.o. administration at 525 mg/d yields ∼2 μmol/L mean steady-state plasma exposure of enzastaurin and its analytes (3). In the tumor xenograft-bearing mice, plasma enzastaurin concentration is ∼2 μmol/L at a dose of 75 mg/kg given p.o. by gavage twice daily (14). At this dose of enzastaurin, tumor growth in the enzastaurin-treated group was significantly suppressed compared with the control group in the SNU-484 xenograft-bearing mice (P < 0.05; Fig. 1B). Enzastaurin treatment also significantly suppressed the growth of SNU-16 gastric cancer xenograft (P < 0.05; data not shown).
Enzastaurin inhibits gastric cancer cell proliferation without cell cycle specificity and induces direct apoptosis. After demonstrating that enzastaurin had antiproliferative effects on gastric cancer cells, we next sought to examine the effects of enzastaurin on cell cycle progression. The cell cycle profiles of the gastric cancer cells were analyzed, and enzastaurin was found to have little effect on the cell cycle progression of SNU-620 and SNU-484. However, the sub-G1 population increased with the passage of time and in a dose-dependent manner after enzastaurin treatment; this result suggests that enzastaurin induced apoptosis (Fig. 2A). Protein profiling of enzastaurin-treated gastric cancer cells showed cleavage of caspase-3 and PARP. The amount of cleaved forms of these proteins increased in a time-dependent and dose-dependent manner after enzastaurin treatment (Fig. 2B,, top). Consistent with these data, the Annexin V binding assay confirmed a dose-dependent enzastaurin-induced apoptosis in SNU-620 and SNU-484 cells (Fig. 2B , bottom left). Taken together, these analyses show that enzastaurin induced direct apoptosis in human gastric cancer cells in the low micromolar range (2.5–10 μmol/L) without cell cycle–specific inhibition.
Figure 2.
Enzastaurin inhibits gastric cancer cell proliferation without cell cycle specificity and induces direct apoptosis through a mitochondrial pathway. A, effects of enzastaurin on cancer cell cycle distributions. Gastric cancer cells (SNU-620 and SNU-484) were treated with DMSO or enzastaurin (2.5, 5, or 10 μmol/L) for the indicated times and then collected for analysis. After 72 h, the cells were fixed with 70% ethanol, stained with propidium iodide, and subjected to flow cytometric analysis. Proportions of cells in the G1, S, and G2-M phase were quantified using the ModFit LT program (Verity Software House); total percentages of G1, S, and G2-M phases are 100% in our data. The fraction of sub-G1 content was separately calculated as a percentage of total gated events. B, enzastaurin-induced apoptosis: Western blot and Annexin V binding assay. SNU-620 and SNU-484 cells were treated with DMSO or enzastaurin up to 48 h as indicated. Equal amounts of whole-cell extracts were resolved by SDS-PAGE and analyzed by Western blotting with antibodies specific for caspase-3 or PARP (Western blot analysis; top); Annexin V staining was performed in SNU-620 and SNU-484 cells treated with DMSO or enzastaurin for 72 h and then analyzed by flow cytometry. The percentage of cells stained with Annexin V–FITC increased in enzastaurin-treated gastric cancer cells (bottom left); total protein was extracted from frozen xenograft tumors. The induction of caspase-3 activation by enzastaurin was shown using Western blot analysis (bottom right). C, enzastaurin-induced apoptosis: TUNEL assay from enzastaurin-treated or control group. Apoptosis was measured in paraffin-embedded xenograft tumors, and representative images of TUNEL immunohistochemistry are shown. The number of apoptotic cells was counted. Columns, mean of TUNEL-positive cells; bars, SE. Ten fields per slide and three slides per individual animal were counted (P < 0.05 as determined by Mann-Whitney U test). D, the change of initiator caspases and release of cytochrome c from mitochondria to cytosol in enzastaurin-treated SNU-620 cells. SNU-620 cells were treated with enzastaurin for the indicated times. Equal amounts of whole-cell extracts were resolved by SDS-PAGE, and Western blot analysis was performed with antibodies specific for caspase-8 and caspase-9. Neither caspase-8 nor caspase-9 active fragments were detected (left); after incubating SNU-620 cells with DMSO or enzastaurin for 48 h, cytosolic proteins were separated and the level of cytosolic cytochrome c was determined by Western blotting (right).
Figure 2.
Enzastaurin inhibits gastric cancer cell proliferation without cell cycle specificity and induces direct apoptosis through a mitochondrial pathway. A, effects of enzastaurin on cancer cell cycle distributions. Gastric cancer cells (SNU-620 and SNU-484) were treated with DMSO or enzastaurin (2.5, 5, or 10 μmol/L) for the indicated times and then collected for analysis. After 72 h, the cells were fixed with 70% ethanol, stained with propidium iodide, and subjected to flow cytometric analysis. Proportions of cells in the G1, S, and G2-M phase were quantified using the ModFit LT program (Verity Software House); total percentages of G1, S, and G2-M phases are 100% in our data. The fraction of sub-G1 content was separately calculated as a percentage of total gated events. B, enzastaurin-induced apoptosis: Western blot and Annexin V binding assay. SNU-620 and SNU-484 cells were treated with DMSO or enzastaurin up to 48 h as indicated. Equal amounts of whole-cell extracts were resolved by SDS-PAGE and analyzed by Western blotting with antibodies specific for caspase-3 or PARP (Western blot analysis; top); Annexin V staining was performed in SNU-620 and SNU-484 cells treated with DMSO or enzastaurin for 72 h and then analyzed by flow cytometry. The percentage of cells stained with Annexin V–FITC increased in enzastaurin-treated gastric cancer cells (bottom left); total protein was extracted from frozen xenograft tumors. The induction of caspase-3 activation by enzastaurin was shown using Western blot analysis (bottom right). C, enzastaurin-induced apoptosis: TUNEL assay from enzastaurin-treated or control group. Apoptosis was measured in paraffin-embedded xenograft tumors, and representative images of TUNEL immunohistochemistry are shown. The number of apoptotic cells was counted. Columns, mean of TUNEL-positive cells; bars, SE. Ten fields per slide and three slides per individual animal were counted (P < 0.05 as determined by Mann-Whitney U test). D, the change of initiator caspases and release of cytochrome c from mitochondria to cytosol in enzastaurin-treated SNU-620 cells. SNU-620 cells were treated with enzastaurin for the indicated times. Equal amounts of whole-cell extracts were resolved by SDS-PAGE, and Western blot analysis was performed with antibodies specific for caspase-8 and caspase-9. Neither caspase-8 nor caspase-9 active fragments were detected (left); after incubating SNU-620 cells with DMSO or enzastaurin for 48 h, cytosolic proteins were separated and the level of cytosolic cytochrome c was determined by Western blotting (right).
Close modal
The effects of enzastaurin therapy on tumor cell apoptosis were also examined in a xenograft mouse model (SNU-484). In Western blot analysis using protein extraction from frozen xenograft tumors, the induction of caspase-3 activation was shown in enzastaurin-treated SNU-484 xenograft-bearing mice (Fig. 2B,, bottom right). We also performed TUNEL assay on paraffin-embedded xenograft tumors and used tissue arrays, which allowed direct comparison between tissues from different animal groups. The results of TUNEL assay indicated increased levels of apoptosis in enzastaurin-treated animals compared with control animals (P < 0.05; Fig. 2C).
Enzastaurin activates the mitochondrial pathway during apoptosis in gastric cancer cells. Two major apoptotic pathways, the death receptor pathway (extrinsic pathway) and the mitochondrial pathway (intrinsic pathway), have been well characterized in mammalian cells. Over the course of these pathways, activation of the death receptor first triggers caspase-8 activation, whereas the release of mitochondrial cytochrome c activates caspase-9 as an initial caspase, all of which subsequently induce the activation of effector caspases, such as caspase-3, caspase-6, and caspase-7 (23). As shown in Fig. 2B, caspase-3 was activated in gastric cancer cells, and, thus, we next examined the activation of initiator caspases (caspase-8 and caspase-9) in enzastaurin-treated SNU-620 cells. Although active fragments of caspase-8 or caspase-9 were not detected in the Western blotting, the amount of the caspase-9 proform decreased with time. This result suggests that enzastaurin-induced apoptosis is associated with the activation of caspase-9. However, the amount of the caspase-8 proform did not change after enzastaurin treatment (Fig. 2D,, left). In addition, enzastaurin induced the cytochrome c release from the mitochondria to the cytosol in SNU-620 cells (Fig. 2D , right). These results show that enzastaurin treatment led gastric cancer cells to undergo apoptosis through a mitochondrial pathway.
The proapoptotic Bcl-2 family proteins (Bax and Bak) have been shown to be required for the disruption of mitochondria and intrinsic death of cancer cells, whereas the antiapoptotic Bcl-2 family proteins (Bcl-2, Bcl-XL, and Mcl-1) can prevent cell death by interfering with the action of Bax and Bak. Therefore, the change in the expression of the Bcl-2 family proteins was examined after treating the SNU-620 or SNU-484 cells with DMSO or enzastaurin. The expression levels of Bax and Bak were not changed after enzastaurin treatment in both cell lines. Enzastaurin suppressed both Bcl-2 and Bcl-XL expression at 2.5 μmol/L in the SNU-620 cells but had no effect on these proteins in the SNU-484 cells. The levels of Mcl-1 were not significantly changed at 2.5 to 5 μmol/L of enzastaurin, but were suppressed at a higher dose of enzastaurin (10 μmol/L) in both cell lines (Supplementary Fig. S2).
Enzastaurin blocks phosphorylation of Akt and p90 Rsk. We sought to examine whether pathways known to be influenced by PKC activity might be affected in gastric cancer cells by enzastaurin treatment. PKC activity has been connected to many intracellular signaling pathways, including the ras-Erk signaling axis and the PI3K/Akt pathway (14). Although Rsk is activated by Erk, Rsk can also be influenced by a PKC-dependent and Erk-independent pathway (2426). In a previous report, treatment of HCT116 colon cancer cells and U87MG glioblastoma cells with enzastaurin failed to inhibit Erk activity, but enzastaurin inhibited Akt phosphorylation in these cell lines (14). Similarly, treatment of SNU-620 and SNU-484 cells with enzastaurin did not suppress Erk activity in the Western blot analysis. By contrast, enzastaurin showed a clear concentration-dependent reduction of AktSer473 and RskThr359/Ser363 phosphorylation (Fig. 3A). Enzastaurin also suppressed the expression of phosphorylated GSK3β, a downstream target of the Akt pathway, in both gastric cancer cell lines (Fig. 3B).
Figure 3.
Enzastaurin suppresses Rsk and Akt phosphorylation. A and B, enzastaurin-induced Rsk, Akt, and GSK3β dephosphorylation. Whole-cell extracts were prepared from SNU-620 and SNU-484 cells treated with DMSO or enzastaurin for the indicated times and were subjected to Western blot analysis.
Figure 3.
Enzastaurin suppresses Rsk and Akt phosphorylation. A and B, enzastaurin-induced Rsk, Akt, and GSK3β dephosphorylation. Whole-cell extracts were prepared from SNU-620 and SNU-484 cells treated with DMSO or enzastaurin for the indicated times and were subjected to Western blot analysis.
Close modal
Enzastaurin induces Bad-mediated apoptosis through the Rsk pathway in gastric cancer cells. It is well known that the activation of both ras-Erk and PI3K/Akt signaling pathways promotes cancer cell survival and, along with the cell death machinery, leads to the phosphorylation and inactivation of Bad, a proapoptotic member of the Bcl-2 family proteins. Rsk can also phosphorylate Bad via a PKC-dependent and Erk-independent pathway (2426). Survival-promoting cytokines suppress the activity of the Bad protein by inducing the phosphorylation of Bad at two critical sites, Ser112 and Ser136, which leads to the dissociation of Bad from prosurvival Bcl-2 proteins and the association of Bad with members of the 14-3-3 family of proteins (27). The regulation of Bad by these phosphorylation events suggests that Bad is a point of convergence for multiple signaling pathways that cooperate in cell death or survival. Akt phosphorylates Bad on Ser136, whereas Erk or Rsk phosphorylate Bad on Ser112, respectively (2426). Because enzastaurin suppressed the phosphorylation of Akt and Rsk, we next evaluated whether Bad activity was affected in enzastaurin-treated gastric cancer cells using Western blot analysis. As shown in Fig. 4A, Ser112 phosphorylation of Bad was readily detectable and decreased in a concentration-dependent manner after enzastaurin treatment. Because Erk phosphorylation was not decreased in enzastaurin-treated cells (Fig. 3A), enzastaurin-induced Rsk dephosphorylation is thought to activate Bad via dephosphorylation of Bad at Ser112. These data suggest that activation of Bad through its dephosphorylation at Ser112 is a crucial mechanism for enzastaurin-mediated gastric cancer cell apoptosis.
Figure 4.
Enzastaurin induces Bad-mediated apoptosis through the Rsk pathway in gastric cancer cells. A, enzastaurin-induced Bad dephosphorylation at Ser112. Whole-cell lysates of SNU-620 and SNU-484 cells after treatment of DMSO or enzastaurin for the indicated times were subjected to Western blot analysis. Bad protein phosphorylated at Ser136 was not detected in the extracts of gastric cancer cells (data not shown). B, knockdown of Bad by siRNAs. SNU-620 cells were transfected with the nonspecific control vector or siRNA vectors against Bad (Bad1 and Bad2). Immunoblotting showed a stable decrease in the total Bad expression after the transfection of Bad siRNAs. C, the change of enzastaurin-induced apoptosis after depletion of Bad expression. SNU-620 cells were transfected with the nonspecific control vector or siRNA vectors against Bad (Bad1 and Bad2). Apoptosis (sub-G1 proportion) was analyzed 48 or 72 h after DMSO or enzastaurin treatment by flow cytometry. D, the change of enzastaurin-induced cytotoxicity after depletion of Bad expression. SNU-620 cells transfected with siRNA vectors were seeded into six-well culture plates and then treated with DMSO or enzastaurin (10 μmol/L). After 72 h, surviving cell numbers were counted by hemocytometer (P < 0.05 as determined by Student's t test).
Figure 4.
Enzastaurin induces Bad-mediated apoptosis through the Rsk pathway in gastric cancer cells. A, enzastaurin-induced Bad dephosphorylation at Ser112. Whole-cell lysates of SNU-620 and SNU-484 cells after treatment of DMSO or enzastaurin for the indicated times were subjected to Western blot analysis. Bad protein phosphorylated at Ser136 was not detected in the extracts of gastric cancer cells (data not shown). B, knockdown of Bad by siRNAs. SNU-620 cells were transfected with the nonspecific control vector or siRNA vectors against Bad (Bad1 and Bad2). Immunoblotting showed a stable decrease in the total Bad expression after the transfection of Bad siRNAs. C, the change of enzastaurin-induced apoptosis after depletion of Bad expression. SNU-620 cells were transfected with the nonspecific control vector or siRNA vectors against Bad (Bad1 and Bad2). Apoptosis (sub-G1 proportion) was analyzed 48 or 72 h after DMSO or enzastaurin treatment by flow cytometry. D, the change of enzastaurin-induced cytotoxicity after depletion of Bad expression. SNU-620 cells transfected with siRNA vectors were seeded into six-well culture plates and then treated with DMSO or enzastaurin (10 μmol/L). After 72 h, surviving cell numbers were counted by hemocytometer (P < 0.05 as determined by Student's t test).
Close modal
To confirm the direct involvement of Bad in enzastaurin-induced apoptotic cell death, we analyzed the effect of silencing endogenous Bad protein by siRNA in SNU-620 cells. Transfections of two independent siRNAs targeting Bad (Bad1 and Bad2) strongly silenced endogenous Bad, compared with transfections of nonspecific siRNA (Fig. 4B). When SNU-620 cells were transfected with Bad siRNAs, the extent of enzastaurin-induced apoptosis and cytotoxicity were markedly reduced compared with those cells transfected with the control siRNA (Fig. 4C and D). Taken together, these results suggest that enzastaurin-induced apoptosis and cytotoxicity in gastric cancer cells were mediated through Bad activation via the Rsk pathway.
Enzastaurin is also known to exert its anticancer activity by inhibiting signals through the Akt pathway (14, 17, 18); our data also showed decreased phosphorylation of Akt in enzastaurin-treated gastric cancer cells (Fig. 3A). However, although the phosphorylated Bad (Ser136) antibody readily detected the phosphorylated Bad control protein (from Cell Signaling Technology, Inc.), the Bad protein phosphorylated at Ser136 from the extracts of gastric cancer cells was not detected (data not shown). Thus, the association between the Akt pathway and the Bad activity could not be confirmed.
The combination of enzastaurin and cytotoxic chemotherapeutic drugs shows additive or synergistic activity in gastric cancer cells. The combined effects of enzastaurin and cytotoxic chemotherapeutic agents (5-FU, cisplatin, paclitaxel, and irinotecan) were tested using the isobologram method in SNU-620 and SNU-484 cells (Fig. 5). The simultaneous exposure of enzastaurin and these additional cytotoxic agents over a period of 72 hours produced additive or synergistic interactions.
Figure 5.
IC50 isobolograms of enzastaurin plus other chemotherapeutic agents show additive or synergistic interaction in SNU-620 and SNU-484 cells. SNU-620 (A) or SNU-484 cells (B) were exposed to various concentrations of enzastaurin or other cytotoxic agents (5-FU, cisplatin, paclitaxel, and irinotecan) for 72 h, alone or in combination, simultaneously. Left, dose-response curves of enzastaurin and other chemotherapeutics drugs. MTT assays were used to evaluate the growth-inhibitory effects of drug combinations. Right, envelopes of additivity, surrounded by solid (), dashed (), and dotted lines (·····), were constructed from the dose-response curves. Points, mean values for three independent experiments.
Figure 5.
IC50 isobolograms of enzastaurin plus other chemotherapeutic agents show additive or synergistic interaction in SNU-620 and SNU-484 cells. SNU-620 (A) or SNU-484 cells (B) were exposed to various concentrations of enzastaurin or other cytotoxic agents (5-FU, cisplatin, paclitaxel, and irinotecan) for 72 h, alone or in combination, simultaneously. Left, dose-response curves of enzastaurin and other chemotherapeutics drugs. MTT assays were used to evaluate the growth-inhibitory effects of drug combinations. Right, envelopes of additivity, surrounded by solid (), dashed (), and dotted lines (·····), were constructed from the dose-response curves. Points, mean values for three independent experiments.
Close modal
PKC is involved in signal transduction pathways that regulate growth factor response, tumor cell proliferation, and apoptosis. PKC therefore represents an attractive and promising target for cancer treatment. Although implicated in gastric cancer pathogenesis, the therapeutic value of targeting the PKC signaling pathway in gastric cancer is to date unknown. We therefore investigated the cytotoxicity and antitumor effects of enzastaurin in gastric cancer. Although SNU-216 and SNU-719 were resistant to enzastaurin, growth of other gastric cancer cells was effectively inhibited by enzastaurin. Specially, SNU-1, SNU-5, SNU-16, SNU-484, and SNU-620 had a low micromolar range of IC50 values (3.78–6.35 μmol/L; Fig. 1A); this range was similar to that of colon carcinoma, glioblastoma, prostate cancer, cutaneous T-cell lymphoma, and myeloma cell lines (14, 17, 18). When combined with cytotoxic agents commonly used in the treatment of advanced gastric cancer, enzastaurin showed synergistic or additive activities at clinically significant concentrations (1–3 μmol/L), as shown in Fig. 5. Oral dosing with enzastaurin to yield plasma concentrations similar to those achieved in clinical trials also significantly suppressed the growth of human gastric cancer cell xenografts (Fig. 1B).
To date, there is no report on the effects of enzastaurin on cancer cell cycle progression. In a previous report, stauroporine and its analogues with high specificity for PKC had differential effects on cell cycle progression in A549 lung cancer cells. Staurosporine and UCN-01 retarded A549 cells in G0-G1. However, CGP 41251 had no effect on any phase of the A549 cell cycle, as enzastaurin inhibited SNU-620 and SNU-484 cell growth in a noncycle-specific manner (Fig. 2A). These findings show that PKC inhibitors differ with respect to the mechanisms by which they interfere with the cell cycle (28). Our data suggest that enzastaurin induces in vitro cell growth inhibition in gastric cancer through direct induction of apoptosis without affecting cell cycle progression. This apoptotic induction by enzastaurin was mediated through the activation of caspases in the gastric cancer cells. The increased level of the cytosolic cytochrome c protein and the decreased level of caspase-9 proform, after enzastaurin treatment, reveal that a mitochondrial apoptotic pathway was involved in enzastaurin-induced gastric cancer cell death (Fig. 2D). Enzastaurin-induced apoptosis was also shown in tumor xenograft-bearing mice (Fig. 2B and C). In MM.1S myeloma cells, down-regulation of Mcl-1, but not Bcl-2 and Bcl-XL, was observed after enzastaurin treatment (2.5–5 μmol/L; ref. 16). However, Mcl-1 expression levels were not changed significantly at 2.5 to 5 μmol/L of enzastaurin in SNU-620 and SNU-484 cells, but its expression was suppressed at a higher dose (10 μmol/L). Both Bcl-2 and Bcl-XL expression in SNU-620 cells were decreased at lower doses of enzastaurin (2.5 μmol/L; Supplementary Fig. S2). These results show that enzastaurin affects the expression of the antiapoptotic Bcl-2 family proteins differently according to the specific cell type evaluated.
The mechanisms associated with enzastaurin-induced apoptosis in cancer cells are not clear. Recent studies have emphasized the importance of the PI3K/Akt signaling pathway in enzastaurin-induced apoptosis in human cancer cell lines. These studies showed that the expression of phosphorylated Akt and GSK3β, one of the Akt downstream targets, was decreased by enzastaurin treatment. They also suggested that GSK3β is a reliable pharmacodynamic marker for enzastaurin activity (14, 17, 18). Akt activation, which is mediated through phosphorylation, maintains a survival signal that protects cells from apoptosis by phosphorylating proapoptotic proteins, such as caspase-9, Bad, and the cell regulatory protein GSK3β; in addition to indirectly modulating p53 and nuclear factor-κB, it also mediates growth factor–induced cell proliferation (18). Therefore, suppression of Akt phosphorylation may be an important mechanism associated with enzastaurin-induced tumor cell death. However, experiments with in vitro kinase assays showed that enzastaurin caused virtually no inhibition of Akt (14). Thus, it was suggested that enzastaurin may indirectly suppress the Akt signaling pathway through its inhibitory effect on PKC proteins (14). However, the mechanisms underlying enzastaurin activity, linking the PKC and Akt pathways, are still unknown and remain to be elucidated.
In our study, the expression of both phosphorylated Akt and GSK3β was also decreased by enzastaurin treatment; this finding is consistent with previous reports. Additionally, our experiments showed a new mechanism involved in enzastaurin-induced apoptosis in gastric cancer cells—the Bad pathway. Bad is one of the proapoptotic Bcl-2 family member proteins and is inactivated by phosphorylation at two critical sites, Ser112 and Ser136. When phosphorylated at Ser112 or Ser136, Bad is complexed to the cytosolic 14-3-3 protein and fails to interact with the antiapoptotic Bcl-XL protein, thus favoring cell survival (27). In our experiments, Bad activation (dephosphorylation) was confirmed in enzastaurin-treated gastric cancer cells (Fig. 4A). In addition, the depletion of Bad conferred resistance to enzastaurin-induced apoptosis and cytotoxicity in the gastric cancer cells (Fig. 4C and D). Because Erk phosphorylation was not decreased, dephosphorylation of Bad at Ser112 is thought to be mediated by Rsk inactivation in enzastaurin-treated gastric cancer cells (2426). However, a phosphorylated Bad at Ser136, which is mediated by the Akt pathway, was not detected in our experiments. One explanation for this finding is that the expression of phosphorylated Bad at Ser136 in gastric cancer cells is below the limit of detection with the antibody we have used (from Cell Signaling Technology, Inc.). However, weak or absent phosphorylation on Ser136 might be a common phenomenon shared by diverse tumor cells. One study showed efficient Bad phosphorylation at Ser136 in normal melanocytes, whereas it was only minimally detected in melanoma cell lines, although the levels of Bad protein were similar in the two cell types (29). Another study reported a similar phenomenon (30). Thus, the association between Akt and Bad cannot be confirmed in our study; further investigation of the mechanisms underlying Akt-associated apoptotic induction in enzastaurin-treated cancer cells need to be performed. Suggesting mechanisms for enzastaurin-induced apoptosis in gastric cancer, including the newly identified Rsk-mediated and Bad-mediated pathways, are illustrated in Fig. 6.
Figure 6.
Schematic representation of mechanisms of enzastaurin-induced apoptosis in gastric cancer cells. Enzastaurin inhibits PKC activity and phosphorylation of Akt, GSK3β, Rsk, and Bad, leading to apoptotic induction and inhibition of tumor cell proliferation.
Figure 6.
Schematic representation of mechanisms of enzastaurin-induced apoptosis in gastric cancer cells. Enzastaurin inhibits PKC activity and phosphorylation of Akt, GSK3β, Rsk, and Bad, leading to apoptotic induction and inhibition of tumor cell proliferation.
Close modal
In summary, enzastaurin induced gastric cancer cell death via mitochondria and caspase-mediated pathways without cell cycle specificity. We showed that enzastaurin induced apoptosis in gastric cancer cells via a newly identified mechanism through Rsk-mediated and Bad-mediated pathways, in addition to the Akt signaling cascade. Furthermore, enzastaurin had synergistic or additive activity with other cytotoxic agents in gastric cancer cells. Our data provide a platform for further evaluation of the novel and orally available PKCβ inhibitor, enzastaurin, as a potential therapeutic agent for the treatment of gastric cancer.
Note: Supplementary data for this article are available at Cancer Research Online (http://cancerres.aacrjournals.org/).
Grant support: Seoul National University Bundang Hospital Research grant 02-2007-030 and Eli Lilly Company.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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Supplementary data
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Sunblock, Sunscreen, and SPF.. What Exactly Are They?
You have probably been exposed to the concept of sun protection from your mother insisting you put on sunscreen and wait a few minutes before jumping into the water. You’ve probably also used sunblock, sunscreen, and SPF interchangeably to mean sun protection; but what exactly are they and what are their differences? While they do fall into the category of sun protection, they each have different functions.
Terms
1. Ultraviolet Rays (UV Rays) are solar energy radiation. UV Rays may not only cause damage over time, but can also leave immediate burning to skin if it is left unprotected over a period of time, depending on the amount of sun exposure. They are proven to be human carcinogens.
2. UVA Rays are long wavelength radiation, responsible for 95% of radiation that reaches the Earth's surface and can penetrate into our skin and is responsible for most skin damage.
3. UVB Rays are medium wavelength radiation that are mostly blocked by the Earth's atmosphere but can still cause delayed tanning and burning of the skin.
Sun Protection and Why We Need It
The most obvious reason for using sun protection is to prevent burning from the heat of the sun. Sun protection products don't necessarily lessen the heat that we feel from the sun, but they act as barriers or layers that shield us from the damage that we can get from that heat. Our sun emits solar energy radiation that are harmful to us even though we don't see them so sun protection is vital to keeping our skin healthy.
Skin cancer (melanoma) can develop from lack of protection from harmful UV rays. According to skincancer.org, "On average, a person’s risk for melanoma doubles if they have had more than five sunburns, but just one blistering sunburn in childhood or adolescence more than doubles a person’s chances of developing melanoma later in life."
Sun protection is definitely not something to be taken lightly. After all, our skin is the largest organ of our bodies and the one that is most exposed, so it just makes sense that we care for it as much as we care for our internal wellbeing.
Sunblock
Sunblock, as the name suggests, acts as a blocker and barrier against solar energy radiation that is more popularly known as UV (Ultraviolet) rays. In the past, most sun protection was really just sunblock. Sunblocks are those thick creams that our parents would smother on us and leave us looking white and ashy, although many invisible sunblocks have come out that don't leave this ugly white cast. Sunblock's main purpose is to physically block UV rays. They sit on top of the skin, leaving a film composed of oxides that block the harmful rays. That layer deflects the UV rays instead of allowing the radiation to penetrate the skin.
Sunscreen
Sunscreens, unlike sunblocks, act more like a filter. Sunscreen is a filter that lessens the amount of radiation that gets through to our skin and also uses chemicals to transform the harmful UV rays into something non-damaging to our skin. Sunscreens are made up of chemicals such as avabenzone and oxybenzone that work well to transform harmful UV rays but since they use strong chemicals, some may have negative reactions to this. A lot of people prefer sunscreens over sunblocks because they feel lighter on the skin and aren't as sticky as good ol' sunblocks do.
SPF
Finally we have SPF. SPF isn't another type of sun protection product. The US FDA describes it as "... a measure of how much solar energy (UV radiation) is required to produce sunburn on protected skin (i.e., in the presence of sunscreen) relative to the amount of solar energy required to produce sunburn on unprotected skin. As the SPF value increases, sunburn protection increases."
We all have heard the common misconception that the higher the SPF, the longer we have to reapply sun protection. While it is partly true, it isn't exactly a direct relation. The amount of time with sun exposure is not directly related to SPF, but rather SPF is directly related to the amount of sun exposure one gets. For example, your exposure to solar energy for one hour at 9:00 in the morning is just the same amount of sun exposure for 15 minutes under the sun at 1:00 in the afternoon. This means you may need to reapply more sun protection if you are exposed at peak sun exposure times. As a general rule, it is best to get the highest SPF you can get your hands on.
Choosing the One For You
Before going out to buy your next sun protection staple, it would be helpful to take note of these considerations and how they might work with your skin and your lifestyle. If you have very sensitive skin, it would seem that sunblocks are a better option as they do not have skin-penetrating chemicals that may irritate the skin.
Use of sun protection is not only for pool and beach days out. We are exposed to the harmful UV rays every single day. A quick grocery run or working beside the window can be harmful to our skin without appropriate sun protection. This damage can build up over time and may lead to premature aging or even, in bad cases, melanoma. Daily use of sun protection on the face and the most exposed areas of our body would be beneficial.
Helpful Reminders
• Sun exposure from 10 AM to 3 PM is most harmful. Apart from wearing sunblock and/or sunscreen, put on proper clothing (sun hat, long-sleeve clothing or rash guards, etc) and try to stay in a shaded area.
• Get a broad-spectrum SPF product with a water-resistant formula.
• Don't skimp on the product, apply an ample amount.
• Reapply every two hours (individuals with lighter skin tones may need to reapply more often).
• Avoid any type of sun protection products for babies 6 months and below. Use rash guards or a sun hat instead.
• The higher the SPF, the better.
Happy (protected) splashing! ☀️ #uniquelycolorful
References:
FDA | Healthline | Skincancer.org | IntermountainHealthcare
Image Sources
Kampus Production | Rachel Cheng
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Is stomach pain after eating a sign of diabetes?
People with diabetes may experience stomach pain sign after eating due to a condition called gastroparesis, which is more common in people with diabetes. Gastroparesis is a condition that affects how the stomach empties, and it can be caused by nerve damage from high blood sugar, leading to slowed or non-functioning stomach muscles. This can result in symptoms such as nausea, vomiting, bloating, and postprandial fullness. Gastroparesis can also lead to complications in blood sugar control and may cause other digestive issues such as heartburn, reflux, and trouble controlling blood sugar[1].
Many people are quite in the know of the common symptoms of diabetes such as
• urinating often
• feeling very thirsty
• feeling very hungry, even though you are eating
• extreme fatigue
• blurry vision
• cuts/bruises that are slow to heal
• tingling, pain, or numbness in the hands/feet
• weight loss (type 1)
• dry, itchy skin
• Increased hunger
• unexplained weight loss
• genital itching or thrush
• blurred eyesight
• slow-healing cuts and wounds
• presence of ketones in the urine
• feeling tired and weak and
• feeling irritable or having other mood changes.
But not so many people know that abdominal discomfort after eating is a lesser-known sign of diabetes. When this happens, it could indicate gastroparesis, a complication where food gets stuck in the stomach due to nerve damage caused by fluctuating blood sugar. Here are symptoms of gastroparesis:
• Feeling full quickly after eating
• Abdominal pain, bloating, or nausea
• Undigested food in vomit
• Weight loss due to poor food absorption
Tips to manage gastroparesis:
• Eat smaller, more frequent meals: 4-5 smaller meals are easier to digest than 2-3 large ones.
• Avoid irritants: Limit fatty, fried, and cheesy foods.
• Add fiber: Fruits, vegetables, and whole grains aid digestion.
• Skip fizzy drinks: They bloat and cause discomfort.
• Quit smoking and limit alcohol: Both worsen stomach issues.
• Control blood sugar levels: Crucial for managing gastroparesis.
Note: Be aware of key diabetes symptoms: excessive thirst, frequent urination, fatigue, weight loss, genital itching, blurred vision.
What are the other causes of stomach pain after eating?
Stomach pain after eating can be caused by various factors, including:
• Food Allergy or Intolerance: Food allergies and intolerances can lead to symptoms such as gas, bloating, cramping, and diarrhea, resulting in stomach pain after eating.
• Gastritis: Inflammation of the stomach lining can cause stomach pain, sickness, vomiting, and indigestion.
• Inflammatory Bowel Disease (IBD): IBD causes the gut to become inflamed and can lead to stomach pain and other symptoms.
• Gastroesophageal Reflux Disease (GERD): Acid reflux or GERD can cause pain after eating, along with symptoms such as heartburn, nausea, and a burning sensation in the throat.
• Overeating or Difficult-to-Digest Foods: Consuming large meals or foods that are difficult to digest can result in stomach pain.
• Infectious Pathogens: Viruses, bacteria, and toxic substances can cause stomach pain after eating.
• Digestive Problems: Indigestion, constipation, and diarrhea can also lead to abdominal pain after eating.
Last Updated on February 9, 2024 by shalw
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Get in touch:
Avoid These 3 Common Mistakes in Your Weight Loss Journey
Are you feeling overwhelmed and intimidated by the gym? As a new trainee, it’s common to be confused about where to start and how to achieve your goals. With the overwhelming amount of information on social media, it’s easy to fall into the trap of making mistakes that hinder your progress. In this article, we’ll highlight three of the most common mistakes people make with their training when trying to lose weight, and how working with a personal trainer can help you avoid them.
Trying to Do Too Much
One of the most common mistakes people make is trying to do too much at once. This can leave you feeling overwhelmed and discouraged when you don’t see the results you were hoping for. To avoid this, start by defining your weight loss goals and work with a personal trainer to create a personalized plan that aligns with your objectives. It’s important to stay focused on your plan and not get distracted by trendy exercises or fad diets. Remember, the key to success is consistency, and a personal trainer can help keep you accountable and motivated.
You Don’t Value Recovery
Recovery is a crucial part of any weight loss journey. It’s important to give your body the time it needs to recover after a workout to avoid injuries and burnout. Many people make the mistake of not prioritizing recovery, which can lead to frustration and slow progress. A personal trainer can help you create a recovery plan that includes proper sleep, hydration, nutrition, and even soft-tissue work. By prioritizing recovery, you’ll see faster progress and avoid setbacks.
Lacking Patience
Patience is key when it comes to weight loss. Many people make the mistake of expecting immediate results and get discouraged when they don’t see progress right away. However, sustainable weight loss takes time, and it’s important to stay committed and patient. A personal trainer can help you set realistic goals and create a plan that focuses on long-term success. Remember, consistency is key, and a personal trainer can help you stay motivated and accountable.
In conclusion, weight loss can be a challenging journey, but working with a personal trainer can help you avoid common mistakes and achieve your goals. By focusing on a personalized plan, prioritizing recovery, and staying patient, you’ll see progress and success in your weight loss journey. Remember, it’s never too late to start your journey, and a personal trainer can help you every step of the way.
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Life Extension Magazine®
Mason jar of clean vegetables suggested by Suzanne Somers
Issue: Feb 2011
Suzanne Somers’s New Mission to Lift the Veil of Scientific Ignorance
Life Extension® has published solid scientific data showing that age-related diseases can be postponed or prevented altogether. Celebrity Life Extension® member Suzanne Somers’s new book, Sexy Forever, examines seven key nutrients everyone should take to safely induce long-term weight loss.
Scientifically reviewed by Dr. Gary Gonzalez, MD, in May 2022. Written by: Life Extension Editorial Staff.
Suzanne Somers’s New Mission to Lift the Veil of Scientific Ignorance
What will it take for the public to understand that the diseases of aging can be postponed or prevented altogether?
For 31 years, we at Life Extension® have published solid scientific data documenting that healthy lifestyle choices can slash disease risk.
Yet as we begin year 2011, two-thirds of Americans are overweight or obese. Their youth is being robbed by an epidemic of metabolic syndrome and diabetes that sharply increases incidences of cancer, vascular occlusion, arthritis, dementia, and virtually every other age-related disorder.
Membership in the Life Extension Foundation is at an all-time high, but we reach only a minute fraction of the American population. The vast majority of individuals today wallow in a state of ignorance about what they should be doing to protect their vital health.
While we at Life Extension can point to our extensive track record of scientific achievements, the public remains largely unimpressed. When a famous celebrity, however, appears on national television to espouse many of these same anti-aging strategies, the average person stops to notice.
There is something in the human psyche that prompts people to emulate what celebrities do - whether it’s good or bad.
In the case of Suzanne Somers, she has turned her life around by removing toxic compounds from her environment, eating organic foods, meticulously keeping her hormones in natural balance, having her blood regularly tested, and taking the appropriate supplements.
Suzanne is by no means the only prominent personality doing this. After all, Hollywood has long emphasized youthful appearances - and those involved in show business are perhaps the earliest examples of humans taking aggressive steps to thwart degenerative changes both inward and outward.
What differentiates Suzanne from our many other celebrity members is that she shouts from the rooftops the many virtues she has attained by following a meticulous science-based youth restoration program.
In her latest book titled Sexy Forever, Suzanne reveals to the public much of the data that Life Extension members view as commonsense approaches to protect against age-related illness.
What impresses us is the ability of Suzanne Somers to appear in the national media and enlighten the world as to how humans can successfully intervene into pathological aging processes. By lifting the veil of scientific ignorance, Suzanne can singlehandedly educate the public about proven methods to avoid diseases that needlessly cripple and kill millions of Americans each year.
The following is an excerpt from the chapter titled Supplement to Speed Weight Loss in Sexy Forever.
Supplement to Speed Weight Loss
Supplement to Speed Weight Loss
Experts Weigh In: A Brief Interview with Cristiana Paul
Cristiana Paul, MS, is an independent nutrition consultant in the Los Angeles area and my personal nutritionist. She is an avid reviewer of nutrition research and educates doctors and patients on nutritional therapies and assessments for optimal health. She is also a contributor to the fourth edition of The Textbook of Natural Medicine. Nutrition is the fuel our bodies need to operate. With inferior nutrition our health suffers and we are set up for disease. I asked her how we can stay healthy (and consequently thin) in our toxic environment.
Christiana Paul: For our bodies to function optimally and efficiently we need to consume a diet balanced with the right amounts of protein, good fat, unrefined carbohydrates, and lots and lots of various forms of fiber (soluble and insoluble). All these aspects are important to maximize fat burning and support body renewal and function. Most of us need to supplement because we do not get enough nutrients due to poor diet and the deficiency of our soils. The most important supplements are vitamins, minerals, and essential fatty acids, but a few others also play important roles. Relative to weight control, here are some good examples of supplements that may be useful because they are very involved in fat and carbohydrate burning:
Carnitine
This supplement helps fat transport in the mitochondria, where it has a chance to be burned. Carnitine is mostly found in red meat, which many people avoid, and it is also synthesized in the body, but sometimes not enough to support optimal fat burning. A urine test can tell us if we need to supplement. Typical doses are 500 to 1,000 mg/day. It may be especially helpful when taken an hour or two prior to exercise.
Lipoic Acid
This plays a role in blood glucose control. If you have elevated or highly fluctuating glucose levels (such as in hypoglycemia) you may consider supplementing with 100 to 1,200 mg (based on a doctor’s or nutritionist’s evaluation). The bottom line is that lipoic acid will help you burn glucose more efficiently, and in that sense it helps with weight control.
CoQ10
There is a blood test for coenzyme Q10 that tells us if we need to supplement. If you take a statin or red yeast rice, the body’s production of CoQ10 is impaired, so you need to supplement even more. CoQ10 is a key factor in energy production and helps us burn fats and carbs more efficiently. In fact, it was shown to help normalize elevated blood glucose in some cases. It also supports heart health and protects the brain. Typical doses are 30 to 100 mg.
Most people are not aware that correcting nutritional deficiencies with a good multivitamin/multimineral and omega-3 supplement will make them much more efficient at burning fat, sugar, and carbohydrates and will also reduce cravings. Blood and urine testing can help a physician analyze each person’s needs for supplementation. At the very minimum you want to take a basic multivitamin/multimineral in a formula that has good absorbable ingredients and no unwanted contaminants. You also want the nutrients to be in a form that they occur in nature if they are available—for example, natural folate (not folic acid), natural mixed tocopherols for vitamin E (not just alpha-tocopherol), natural mixed carotenoids (not just beta-carotene), natural vitamin B12 (methylcobalamin or adenosylcobalamin, not cyanocobalamin or hydroxycobalamin), and chelated minerals.
Most people need to supplement with omega-3 fats because their diets provide an excess of omega-6 fats (from cooking oils and animal fats), and it’s important to choose fish oil, flaxseed oil, or algae (for vegetarians) that are clean of environmental contaminants (mercury, PCBs) and oxidized fats. Frankly, it is a good idea to ask for a certificate of analysis from the manufacturer for everything you take.
Extracts from green tea were shown in studies to help boost weight loss. It probably does this through a few complementary actions: it boosts the metabolic rate (an increase of 4 percent per twenty-four hours when taking an extract of 370 mg EGCG per day) and it keeps adrenaline elevated longer than normal (which helps fat release from body stores and may reduce hunger). More sustained adrenaline levels may help a person feel more energetic, and he or she may be more likely to exercise or do something physical. For a person with excess adrenaline production (or who has a difficult time breaking it down, such as those with COMT mutations) green tea may increase adrenaline levels to an unhealthy range. On the other hand, for people who are tired all the time because their adrenal glands do not produce adequate amounts of adrenaline, green tea may be helpful. You can drink it or take extracts that contain the equivalent of 2 to 3 cups of green tea in a pill (for example 500 mg EGCG).
Supplement to Speed Weight Loss
Also, keep in mind that the body needs tyrosine (an amino acid found in proteins) to make adrenaline. Supplementing with tyrosine (1 to 2 g/day) may boost production of adrenaline and work synergistically with green tea. Too much adrenaline at night is not good, so it’s important to make sure that supplements are not affecting your sleep quality. Poor sleep leads to weight gain and health problems, and this effect can be increased by the addition of coffee.
Fiber is important, so try to get 35 to 50 g of fiber daily from both soluble and insoluble forms (read the label, it will tell you). Variety is important with fiber, and avoiding the artificial colors and sweeteners added to most commercial brands is also important. Fiber will keep you full longer and help you eat less. It slows down the absorption of sugar, thus reducing insulin production in response to meals. Keep in mind that insulin influences the fat cells to reduce the release of their fat content and also slows down certain fat-burning enzymes. This is not because insulin is an evil hormone but because it is supposed to signal that the body has plenty of glucose, telling it: “Burn the glucose first and save the fat from body storages for later.” So you see, if you eat excess carbohydrates and sugar all day long, you impair your ability to tap into your fat stores.
Fiber also reduces fat and cholesterol and sugar absorption, and it may lower blood levels of cholesterol and triglycerides. Fiber helps detoxify, supports regular bowel movements, and reduces risks of many cancers. I cannot speak enough about the fiber benefits for weight control and health.
Suzanne Somers: I have been looking for supplements from nature that can speed up and enhance your ability to lose weight. With the help of top bioscientists, I’ve discovered a supplement that does just that. This is a science-based product and when I read about the incredible results, all from natural ingredients, I knew I had to make the results available to everyone.
The Sexy Forever Weight Loss Formula includes:
1. LuraLean®
2. Phaseolus vulgaris
3. Irvingia
4. Green tea phytosome
LuraLean®
LuraLean®
This ingredient helps control the absorption of some calories if taken before the two heaviest meals of the day. By maintaining its viscous structure throughout the digestive tract, LuraLean® is able to stop the absorption of ingested fats and carbohydrates. LuraLean® is a fiber composed of specially processed glucomannan—a water-soluble polysaccharide derived from a tuberous plant that grows only in the remote mountains of northern Japan.
This translates into weight reduction. One clinical study showed that without any dietary changes (participants ate and drank whatever they wanted), those taking LuraLean® lost 5.5 pounds after eight weeks compared to a 1.5-pound weight gain in the placebo group. In a similar study, those taking LuraLean® (twice a day before breakfast and dinner) lost 7.04 pounds compared to a gain of almost 1 pound in the placebo arm of the study. These studies showed substantial reductions in blood triglycerides, cholesterol, and LDL (bad cholesterol) levels in the LuraLean® groups compared to increases in these dangerous blood fats in the placebo arms.
Looking at the blood test results of typical healthy twenty-one-year-olds, scientists noticed that they had very low levels of blood glucose, cholesterol, and triglycerides. Even if people do not change their diet, by the time they reach age fifty their blood glucose, triglycerides, and cholesterol are usually much higher. Fifty-year-olds typically weigh more than when they were twenty-one, especially in the abdominal region of their bodies. There are correlations between blood glucose and triglyceride levels and unwanted weight gain.
To put it simply, the same calories a twenty-one-year-old can safely ingest become increasingly toxic as we age. This is because aging causes us to lose the metabolic capacity to utilize ingested calories in efficient energy-expending ways. Not only do these calories induce body fat storage, but they also increase vascular disease risks. That is why taking LuraLean® before the two heaviest meals of the day is so important. It helps impede absorption of excess sugars and fats in your diet, while helping to reduce the amount of food you consume with each meal.
Phaseolus Vulgaris
Phaseolus Vulgaris
Researchers at the UCLA School of Medicine have successfully used extracts from the white kidney bean (Phaseolus vulgaris) to target alpha amylase. A study was done where thirty obese adults took either a placebo or the Phaseolus vulgaris extract. After eight weeks, those taking the white bean extract lost 3.8 pounds in weight, and more important, 1.5 inches of abdominal fat. The group taking the Phaseolus vulgaris also had a three-fold reduction in triglyceride levels compared with the placebo group, which helps corroborate the role of weight loss and simultaneous reduction in artery-clogging triglyceride levels.
Another more impressive study of Phaseolus vulgaris showed that those who consumed the most carbohydrates lost the most weight. In this study, subjects who supplemented with Phaseolus vulgaris and consumed the highest levels of dietary starch lost 8.7 pounds compared with only 1.7 pounds in the control group over four weeks. Even more impressive was the 3.3 inches of belly fat lost in the Phaseolus vulgaris group versus only 1.3 inches in the controls. In a double-blind study on sixty overweight volunteers, half the study participants received Phaseolus vulgaris while the other half were given a placebo. Both groups were placed on a 2,000–2,200-calorie diet. After only thirty days, those taking Phaseolus vulgaris lost 6.5 pounds of weight and 1.2 inches in waist size compared with 0.8 pounds and 0.2 inches in the placebo group.
As we age, it becomes increasingly difficult to keep belly fat off. At the same time, we are challenged to keep blood glucose levels in optimal ranges. The exploding rates of type 2 diabetes and obesity are a testament to the dual problem of weight gain caused by the absorption of too many calories from simple carbohydrates.
Irvingia
Irvingia is a West African plant extract (from Irvingia gabonesis) that has been shown to help support leptin sensitivity in overweight people. Fat cells (called adipocytes) secrete leptin, a hormone that tells your brain you’ve eaten enough. Leptin also helps with the breakdown of stored (triglyceride) fat in our fat cells. Overweight people have higher blood levels of leptin, indicating that their cells have become resistant to leptin. In a published study, irvingia demonstrated beneficial effects on leptin blood levels, followed by a weight loss of over 20 pounds on average in ten weeks and an average reduction in waist circumference of about 6 inches. Study subjects taking irvingia reported consuming fewer calories, which makes sense, based on the enhanced leptin sensitivity brought about by this plant extract. Irvingia also has alpha-amylase-inhibiting properties similar to Phaseolus vulgaris. Inhibiting amylase helps slow the rate of carbohydrate absorption, reducing the caloric impact of starchy and sugary foods.
Green Tea Phytosome
Large meals overload the bloodstream with calories and later cause a rebound increase in appetite when blood sugar levels plummet in response to excess release of insulin. One way of stopping this after-meal glucose-insulin rebound is to take nutrients that neutralize the carbohydrate-degrading enzyme alpha-amylase before meals.
Scientific data suggests that irvingia also helps support healthy adiponectin levels. Adiponectin is a hormone that helps maintain the insulin sensitivity of our energy-producing cells. Large fat cells found in overweight people produce less adiponectin. This means that these individuals need to be concerned about maintaining enough adiponectin to support insulin sensitivity, something that we lose during normal aging.
Most people don’t know this, but the majority of body fat consists of triglycerides that are stored in our fat cells. A reason that weight loss and triglyceride reduction go hand in hand is that triglycerides make up the bulk of our fat storage. We get triglycerides directly from the fat we eat, and also from the conversion of excess glucose in our blood to triglycerides stored in our fat cells. In the latter instance, glucose is converted to triglycerides by an enzyme called glycerol-3-phosphate dehydrogenase. Irvingia inhibits glycerol-3-phosphate dehydrogenase, reducing the amount of ingested sugars that are converted to body fat.
Green Tea Phytosome
We all know about the great benefits of green tea. Aging robs us of the ability to efficiently burn fat as energy. Instead we store fat in our adipocytes (fat cells). The components responsible for green tea’s weight loss benefits are polyphenol compounds that increase metabolic energy expenditure and hence calorie burning. The problem is getting enough of green tea’s polyphenols absorbed into the blood. But a group of Italian researchers created a proprietary green tea phytosome that increased the polyphenols’ ability to be absorbed into the bloodstream. In a human clinical trial using this green tea phytosome, the weight loss effects were substantial. This study involved one hundred overweight subjects, half of whom received the green tea phytosome. Both groups were placed on reduced-calorie diets (approximately 1,850 calories/day for men and 1,350 calories/day for women).
Suzanne Somers, Sexy Forever
After ninety days on the reduced-calorie diet, the control group lost 9.9 pounds. The group taking the green tea phytosome, on the other hand, lost a whopping 30.1 pounds—more than triple the weight loss of the control group! There was a 10 percent reduction in the green tea phytosome group’s belly size compared with a 5 percent reduction in the control group. Male participants did even better in this category, showing a 14 percent reduction in waist circumference compared with a 7 percent reduction in the control group.
What’s so interesting about this study is that it shows that people can lose considerable weight (9.9 pounds) by eating fewer calories. Yet when this green tea phytosome was added, the total amount of weight lost tripled (to 30.1 pounds) while twice as much belly fat disappeared. Scientists attribute these remarkable benefits to the ability of green tea to boost resting metabolic rates and reduce the absorption of dietary fats, which makes this green tea phytosome an ideal nutrient to take before heavy meals.
If you are going to turn your life around by eliminating toxic foods, adding these four supplements can boost your ability to lose weight more quickly and safely, with no drugs or stimulants.
For further information on Sexy Forever’s online companion, visit www.SexyForeverPlan.com
Excerpt from Sexy Forever by Suzanne Somers. Published by Crown, Copyright 2010 Suzanne Somers©.
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• 1
Keywords: CELLS ; BLOOD ; CELL ; Germany ; THERAPY ; VIVO ; GENERATION ; SYSTEM ; DISEASE ; POPULATION ; TISSUE ; MARKER ; BIOLOGY ; DISCOVERY ; CELL THERAPY ; MARKERS ; STEM-CELLS ; cord blood ; EXPANSION ; STEM ; FETAL CALF SERUM ; CELL BIOLOGY ; mesenchymal stromal cells ; Genetic ; ANIMAL SERUM ; AUTOLOGOUS SERUM ; BOVINE SERUM ; clinical-scale expansion ; closed process ; CULTURE-CONDITIONS ; good manufacturing practice ; IN-VITRO DIFFERENTIATION ; mononuclear cell separation ; regenerative medicine ; Sepax ; unrestricted somatic stem cell
Abstract: Background aims. The discovery of unrestricted somatic stem cells (USSC), a non-hematopoietic stem cell population, brought cord blood (CB) to the attention of regenerative medicine for defining more protocols for non-hematopoietic indications. We demonstrate that a reliable and reproducible method for good manufacturing practice (GMP)-conforming generation of USSC is possible that fulfils safety requirements as well as criteria for clinical applications, such as adherence of strict regulations on cell isolation and expansion. Methods. In order to maintain GMP conformity, the automated cell processing system Sepax (Biosafe) was implemented for mononucleated cell (MNC) separation from fresh CB. After USSC generation, clinical-scale expansion was achieved by multi-layered CellSTACKs (Costar/Corning). Infectious disease markers, pyrogen and endotoxin levels, immunophenotype, potency, genetic stability and sterility of the cell product were evaluated. Results. The MNC isolation and cell cultivation methods used led to safe and reproducible GMP-conforming USSC production while maintaining somatic stem cell character. Conclusions. Together with implemented in-process controls guaranteeing contamination-free products with adult stem cell character, USSC produced as suggested here may serve as a universal allogeneic stem cell source for future cell treatment and clinical settings
Type of Publication: Journal article published
PubMed ID: 20370349
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• 2
Keywords: IN-VIVO ; BONE-MARROW ; PROGENITOR CELLS ; VASCULATURE ; FLOW-CYTOMETRY ; PERIPHERAL-BLOOD ; GENE-THERAPY ; PRECURSORS ; PROTOCOL ; MESENCHYMAL STEM-CELLS
Abstract: BACKGROUND AIMS: Endothelial progenitor cells (EPCs) specifically home to sites of malignant growth, rendering them attractive for anti-cancer therapies. Data are conflicting on the phenotype and quantitative contribution toward tumor angiogenesis based on differing culture assays to outgrow EPCs. To evaluate the origin and early phenotype of EPCs and to define a population with enhanced tumor-targeting capacity, we evaluated a hierarchy of cord blood-derived EPCs modeling the multi-step nature of tumor homing. METHODS: CD34(+) mononuclear cells were isolated from fresh cord blood and cultured to derive endothelial colony-forming cells (ECFCs). Human umbilical vein endothelial cells (HUVECs) served as control. Using intra-vital microscopy, the recruitment was analyzed in mice bearing C6 xenografts. Adhesion, migration, transmigration and differentiation were further addressed. RESULTS: Within the primary passage, ECFCs underwent a rapid maturation from a CD45(+) and CD31(+) phenotype to a CD45(-) and endothelial marker positive phenotype. Assessing in vivo tumor recruitment, ECFCs had the highest activity in all steps analyzed. In vitro, ECFCs demonstrated significantly higher adhesion under static and flow conditions. Similarly, ECFCs exhibited highest migratory and trans-migratory activity toward tumor-conditioned medium. On subcutaneous implantation, only ECFCs formed blood vessels covered with perivascular cells, similar to HUVECs. CONCLUSIONS: Our study indicates that ECFCs emerge from a CD45(+) and CD31(+) progenitor and rapidly mature in culture. ECFCs have a significantly higher potential for tumor targeting than non-cultured CD34(+) cells and HUVECs. They are ideal candidates for future cell-based anti-cancer therapies.
Type of Publication: Journal article published
PubMed ID: 23491253
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• 3
Keywords: CELLS ; EXPRESSION ; tumor ; BLOOD ; CELL ; Germany ; human ; IN-VIVO ; THERAPY ; VIVO ; FOLLOW-UP ; POPULATION ; GENE ; DRUG ; gene therapy ; MICE ; TRANSDUCTION ; gene transfer ; GENE-TRANSFER ; MARKER ; FLOW ; BIOLOGY ; MATURATION ; TARGET ; HUMANS ; resistance ; VECTOR ; MARKERS ; STEM-CELLS ; FLOW-CYTOMETRY ; HEMATOPOIETIC PROGENITOR CELLS ; HEMATOPOIETIC-CELLS ; PERIPHERAL-BLOOD ; MULTIDRUG-RESISTANCE ; MULTIDRUG-RESISTANCE-1 GENE ; P-GLYCOPROTEIN ; EX-VIVO ; LINEAGE ; RESISTANCE 1 GENE ; SEVERE COMBINED IMMUNODEFICIENCY ; DRUGS ; REPOPULATING CELLS ; in vivo ; progenitor cell ; VARIETIES ; MDR1 gene therapy ; myeloid differentiation ; P-GLYCOPROTEIN EXPRESSION ; peripheral blood ; TRANSDUCED CELLS
Abstract: Background The objective of multidrug resistance-1 (MDR1) gene therapy is protection of the myeloid cell lineage. It is therefore important to examine the effect of retroviral transduction on myeloid maturation. Transfer of the human MDR1 gene can confer resistance to a variety of cytostatic drugs. For a safe application in humans it is paramount to follow-up the development of transduced cells. Methods We transduced human mobilized peripheral blood progenitor cells (PBPC) with a viral vector containing the human MDR1 cDNA and transplanted the transduced cells into non-obese diabetic severe combined immunodeficient (NOD/SCID) mice. The progeny of the transduced cells was analyzed in detail by flow cytometry. Results A detailed analysis by four-color flow cytometry showed that MDR1 transgene-expressing CD33(+) myeloid cells were preferentially negative for the maturation-associated myeloid markers CD11b and CD10, while the untransduced CD33(+) myeloid cells expressed significantly higher proportions of these Ag (PB 〈 0.01 each). There was no difference in the expression of B- or T-lymphoid Ag among the MDR1-transduced and untransduced lymphoid cells. Discussion These data indicate that retroviral MDR1 gene transfer results in preferential P-glycoprotein expression in myeloid progenitor cells, which is the target cell population for myelotoxicity of cytostatic drugs
Type of Publication: Journal article published
PubMed ID: 17148033
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• 4
• 5
Keywords: CELLS ; EXPRESSION ; IN-VITRO ; proliferation ; tumor ; IN-VIVO ; MODEL ; THERAPY ; DISEASE ; DISEASES ; GENE ; MICE ; TRANSPLANTATION ; BONE-MARROW ; NOD/Scid mice ; MOUSE ; MOUSE MODEL ; cord blood ; ONCOLOGY ; interaction ; BLOOD PROGENITOR CELLS ; SDF-1 ; FATE ; REPOPULATION ; mesenchymal stromal cells ; ENGRAFTMENT ; NOD/SCID/B2M(NULL) MICE
Abstract: Abstract Background aims. Transplantation of allogeneic hematopoietic stem cells (HSC) within the framework of hematologic oncology or inherited diseases may be associated with complications such as engraftment failure and long-term pancytopenia. HSC engraftment can be improved, for example by co-transplantation with mesenchymal stem cells (MSC). Recently, a new multipotent MSC line from umbilical cord blood, unrestricted somatic stem cells (USSC), has been described. It was demonstrated that USSC significantly support proliferation of HSC in an in vitro feeder layer assay. Methods. A NOD/SCID mouse model was used to assess the effect of USSC on co-transplanted CD34(+) cells and look for the fate of transplanted USSC. The migration potential of USSC was studied in a Boyden chamber migration assay and in vivo. Quantitative real-time polymerase chain reaction (qRT-PCR) for CXCR4, CD44, LFA1, CD62L, VLA4, RAC2, VLA5A and RAC1 were performed. NMR1 nu/nu mice were used for a tumorigenicity test. Results. After 4 weeks, homing of human cells (CD45(+)) to the bone marrow of NOD/SCID mice was significantly increased in mice co-transplanted with CD34(+) cells and USSC (median 30.9%, range 7-50%) compared with the CD34(+) cell-only control group (median 5.9%, range 3-10%; P = 0.004). Homing of USSC could not be shown in the bone marrow. A cell-cell contact was not required for the graft enhancing effect of USSC. An in vivo tumorigenicity assay showed no tumorigenic potential of USSC. Conclusions. This pre-clinical study clearly shows that USSC have an enhancing effect on engraftment of human CD34(+) cells. USSC are a safe graft adjunct.
Type of Publication: Journal article published
PubMed ID: 20950214
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• 6
Keywords: THERAPY ; TRANSPLANTATION ; T-CELLS ; NK cells ; CANCER-PATIENTS ; GENE-EXPRESSION ANALYSIS ; PHASE-II ; ACUTE MYELOID-LEUKEMIA ; EX-VIVO EXPANSION ; LARGE-SCALE
Abstract: BACKGROUND AIMS: Ex vivo expansion of natural killer (NK) cells is a strategy to produce large numbers of these effector cells for immunotherapy. However, the transfer of bench-top expansion protocols to clinically applicable methods is challenging for NK cell-based therapy because of regulatory aspects and scale-up issues. Therefore, we developed an automated, large-scale NK cell expansion process. METHODS: Enriched NK cells were expanded with interleukin-2 and irradiated clinical-grade Epstein-Barr virus-transformed lymphoblastoid feeder cells with the use of an automated system in comparison to manual expansion, and the cells were investigated for their functionality, phenotype and gene expression. RESULTS: Automated expansion resulted in a mean 850-fold expansion of NK cells by day 14, yielding 1.3 (+/-0.9) x 10(9) activated NK cells. Automatically and manually produced NK cells were comparable in target cell lysis, degranulation and production of interferon-gamma and tumor necrosis factor-alpha and had similar high levels of antibody-dependent cellular cytotoxicity against rituximab-treated leukemic cells. NK cells after automated or manual expansion showed similar gene expression and marker profiles. However, expanded NK cells differed significantly from primary NK cells including upregulation of the functional relevant molecules TRAIL and FasL and NK cell-activating receptors NKp30, NKG2D and DNAM-1. Neither automatically nor manually expanded NK cells showed reduced telomere length indicative of a conserved proliferative potential. CONCLUSIONS: We established an automated method to expand high numbers of clinical-grade NK cells with properties similar to their manually produced counterparts. This automated process represents a highly efficient tool to standardize NK cell processing for therapeutic applications.
Type of Publication: Journal article published
PubMed ID: 25881519
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• 7
Abstract: BACKGROUND AIMS: Natural killer (NK) cells can rapidly respond to transformed and stressed cells and represent an important effector cell type for adoptive immunotherapy. In addition to donor-derived primary NK cells, continuously expanding cytotoxic cell lines such as NK-92 are being developed for clinical applications. METHODS: To enhance their therapeutic utility for the treatment of B-cell malignancies, we engineered NK-92 cells by lentiviral gene transfer to express chimeric antigen receptors (CARs) that target CD19 and contain human CD3zeta (CAR 63.z), composite CD28-CD3zeta or CD137-CD3zeta signaling domains (CARs 63.28.z and 63.137.z). RESULTS: Exposure of CD19-positive targets to CAR NK-92 cells resulted in formation of conjugates between NK and cancer cells, NK-cell degranulation and selective cytotoxicity toward established B-cell leukemia and lymphoma cells. Likewise, the CAR NK cells displayed targeted cell killing of primary pre-B-ALL blasts that were resistant to parental NK-92. Although all three CAR NK-92 cell variants were functionally active, NK-92/63.137.z cells were less effective than NK-92/63.z and NK-92/63.28.z in cell killing and cytokine production, pointing to differential effects of the costimulatory CD28 and CD137 domains. In a Raji B-cell lymphoma model in NOD-SCID IL2R gammanull mice, treatment with NK-92/63.z cells, but not parental NK-92 cells, inhibited disease progression, indicating that selective cytotoxicity was retained in vivo. CONCLUSIONS: Our data demonstrate that it is feasible to generate CAR-engineered NK-92 cells with potent and selective antitumor activity. These cells may become clinically useful as a continuously expandable off-the-shelf cell therapeutic agent.
Type of Publication: Journal article published
PubMed ID: 27887866
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• 8
Keywords: EXPRESSION ; IN-VITRO ; THERAPY ; DIFFERENTIATION ; DOWN-REGULATION ; BONE-MARROW ; culture ; STEM-CELLS ; SAFETY ; LONG-TERM CULTURE ; senescence ; POTENCY ; EXPANSION ; fetal bovine serum ; HUMAN SERUM ; adipose tissue-derived mesenchymal stromal cells ; CALF SERUM ; HUMAN PLATELET LYSATE ; replicative aging
Abstract: BACKGROUND AIMS: Mesenchymal stromal cells (MSC) are promising candidates for innovative cell therapeutic applications. For clinical-scale manufacturing, different supplements have been evaluated as alternatives for the commonly used fetal bovine serum (FBS). We have reported previously that pooled human AB serum (HS) accelerates the proliferation of adipose tissue-derived MSC (ASC) while maintaining key functions of MSC biology such as differentiation, immune suppression and growth factor secretion. ASC expanded in FBS-supplemented culture media undergo replicative aging that is associated with a progressive loss of differentiation capacity but without indications of cellular transformation. The effects of HS media on ASC long-term culture, however, remain poorly characterized. METHODS: Long-term cultures of ASC in FBS and HS media were analyzed with respect to proliferation, marker expression, differentiation and immune suppression. RESULTS: Despite signs of an accelerated proliferation, extended life span and clonogenic capacity of ASC cultivated in HS-supplemented media, HS and FBS cultures revealed no significant differences with respect to differentiation potential and expression of senescence markers. Anchorage-independent growth, which is indicative of tumorigenic properties, was not observed in either culture conditions. Similarly, immune suppressive activities were maintained. Donor variation regarding differentiation potential and marker expression became apparent in this study independent of the culture supplement or culture duration. CONCLUSIONS: We have demonstrated that the use of pooled allogeneic HS maintains the characteristics of ASC even after long-term expansion, further demonstrating that the use of HS is an alternative to FBS.
Type of Publication: Journal article published
PubMed ID: 22300364
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• 9
Keywords: ADHERENS JUNCTIONS, ADIPOSE-TISSUE, ADULT, adult stem cells, ADULT STEM-CELLS, animal, BIOLOGY, biot
Abstract: As an archetype of human adult stem cells that can readily be harvested, enriched and expanded in vitro, mesenchymal stromal cells (MSC) have been reported to be of significance for regenerative medicine. The literature is replete with reports on their developmental potentials in pre-clinical model systems. Different preparative protocols have been shown to yield MSC-like cell cultures or even cell lines, from starting materials as diverse as bone marrow, fat tissue, fetal cord blood and peripheral blood. However, MSC are still ill-defined by physical, phenotypic and functional properties. The quality of preparations from different laboratories varies tremendously and the cell products are notoriously heterogeneous. The source and freshness of the starting material, culture media used, presence of animal sera, cytokines, cell density, number of passages upon culture, etc., all have a significant impact on the (1) cell type components and heterogeneity of the initial population, (2) differential expansion of specific subsets, with different potentials of the end products, and (3) long-term functional fate of MSC as well as other types of progenitor cells that are co-cultivated with them. Consequently, there is an urgent need for the development of reliable reagents, common guidelines and standards for MSC preparations and of precise molecular and cellular markers to define subpopulations with diverse pathways of differentiation and divergent potentials
Type of Publication: Journal article published
PubMed ID: 18574765
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• 10
Keywords: CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; proliferation ; tumor ; BLOOD ; CELL ; Germany ; DIFFERENTIATION ; MOLECULES ; RELEASE ; ACTIVATION ; DENDRITIC CELLS ; T cell ; T cells ; T-CELL ; T-CELLS ; FLOW ; BIOLOGY ; MOLECULE ; culture ; cytokines ; MATURATION ; STIMULATION ; ASSAY ; NUMBER ; METASTATIC MELANOMA ; PHENOTYPE ; VACCINE ; IMMUNOTHERAPY ; ADAPTIVE IMMUNITY ; FLOW-CYTOMETRY ; INTERFERON-GAMMA ; COLONY-STIMULATING FACTOR ; SURFACE EXPRESSION ; T-cell response ; CYTOKINE ; ELISA ; cancer vaccine ; LEVEL ; methods ; dendritic cell ; microbiology ; coagulation activation ; IL-6 ; MEDICINE ; MONOCYTES ; biotechnology ; E2 ; response ; discussion ; NORWAY ; CELL BIOLOGY ; LIGATION ; red ; CD86 ; DC maturation ; dendritic cell differentiation ; dendritic cell function ; platelet contamination ; T-HELPER-CELLS ; VITRO LIPOPOLYSACCHARIDE-CHALLENGE
Abstract: Background Monocytapheresis has been established to collect a sufficient number of monocytes (MO) for differentiation to dendritic cells (DC) as a cancer vaccine. Platelets (Plt) are invariably found as a contaminant in the final monocytapheresis product. The aim of this study was to investigate DC differentiation under the influence of Plt with regard to their function and phenotype. Methods MO were isolated and co-cultured with autologous Plt at different MO:Plt ratios (1:1.7, 1:5, 1:15, 1:45 and 1:135) in the presence of interleukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor (GM-CSF). IL-12p70 release after ligation of CD40L was determined in the supernatant by enzyme-linked immunosorbent assay (ELISA). For T-cell stimulation, tetanus toxoid was added to immature DC and maturation was induced by adding cytokines (IL-1, IL-6, tumor necrosis factor- and prostaglandin E2). Stimulated T cells were analyzed for activation and proliferation as well as for intracellular cytokines by flow cytometry. Results All DC cultures were strongly positive for CD83. At a contaminating concentration of 5 Plt/MO, matured DC showed the highest expression of HLA-DR, CD80 and CD86, inducing a strong T-cell proliferation with high production of IL-4 and interferon-. The highest level of IL-12p70 production was observed by the same DC group. Discussion Plt did not negatively influence DC maturation but enhanced the expression of co-stimulatory molecules and the release of IL-12. Functionally this was reflected by a strong T-cell response that involved T-helper 1 (Th1)- as well as Th2-biased T cells. Our findings show that controlling the Plt concentration may provide important advantages for the generation of DC for use in immunotherapy
Type of Publication: Journal article published
PubMed ID: 18985478
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Exercise During Menopause: Best Workouts During the Transition
Menopause is a natural part of every woman's life, and it's essential to recognize that each woman's experience is unique. The symptoms can be quite diverse, ranging from hot flashes to anxiety and sleep issues, making it challenging for many of us to feel our best during this time. But here's some encouraging news: you have the power to embrace healthy habits that can make a significant difference in coping with these changes and supporting your body through menopause.
One fantastic step you can take is incorporating exercise into your routine. It can be a wonderful starting point to help you feel more balanced and empowered throughout this transformative journey.
Why Exercise is important during Menopause
During the menopause transition, as our bodies go through changes, our ovaries cease to produce estrogen. This brings forth a range of symptoms like hot flashes, sleep disturbances, and brain fog. However, it's crucial to know that it also heightens the risk of heart disease, stroke, and osteoporosis. Taking care of ourselves during this time becomes even more vital, as we navigate through these transformations and prioritize our health and well-being.
According to the Centers for Disease Control and Prevention (CDC), most of us women should strive for at least 150 minutes of moderate aerobic activity or 75 minutes of vigorous aerobic activity per week to stay healthy and active. Let's make fitness a part of our lives and enjoy the wonderful benefits it brings!
Variety of Exercises to Embrace During Menopause
Cardio
Incorporating aerobic activities that engage your large muscle groups and elevate your heart rate is such a fantastic idea! The options for cardio are endless, and you can choose from a wide variety of activities. In fact, almost any activity counts, which means you have the freedom to enjoy and embrace what truly brings you joy. Whether it's dancing, cycling, brisk walking, or any other fun activity, let's get moving and savor the benefits of staying active!
• Walking
• Jogging
• Biking
• swimming
It's all about taking small steps, building your strength and confidence along the way. Remember, every little effort counts, and you've got this! Let's embark on this journey together and enjoy the amazing progress we'll make!
Strength Training
As we go through menopause, our risk of osteoporosis shoots up because we need estrogen to help build strong bones. That's why incorporating strength training into our routine becomes especially crucial. These exercises work wonders by not only building bone and muscle strength but also burning body fat and giving our metabolism a boost. Let's embrace strength training to keep our bones strong, our bodies fit, and our spirits soaring! We've got the power to take charge of our health and well-being!
When working out at home, consider using dumbbells and resistance tubing to get those muscles working. If you're hitting the gym, you have the option to use weight machines or free weights. The key is to pick a level of resistance that challenges your muscles in about 12 repetitions, and then you can gradually progress from there. It's all about finding the right balance and embracing the strength-building journey with confidence and determination.
Yoga and meditation
Yoga poses can bring relief, calming your nerves, centering your mind, and easing symptoms like:
• Hot flashes
• Irritability
• fatigue
Remember that every woman's menopause journey is different, and that means your symptoms are unique to you. So, finding relief is all about customizing your approach. Embrace a relaxation technique that suits you best, whether it's practicing deep breathing, indulging in yoga, or finding tranquility through meditation. This is your time to focus on self-care and discover what brings you comfort and peace. Embrace these moments of relaxation, and let them nourish your mind, body, and soul. You deserve all the care and support during this transformative phase.
Dancing
If running on a treadmill isn't your cup of tea, why not try a delightful dance class? Dancing can be a fantastic way to build muscle, stay flexible, and have fun while doing it.
• Jazz
• Ballet
• Ballroom
• Salsa
Exercise doesn't have to feel like all hard work. You can add fun and calorie-burning cardio sessions to your routine, benefiting your body and having a blast at the same time! Let's make fitness enjoyable and rewarding for our amazing selves!
There are so many different dance styles to choose from, so find one that suits your groove and let yourself dance your way to health and happiness!
Be realistic
Setting goals is key to avoiding frustration on our fitness journey. Make sure your goals are realistic, attainable, and specific. Instead of just saying, "I'll exercise more," be clear and precise, like:
"I'll take a 30-minute walk at lunch three days a week."
"I'll join a fun group cycling class."
"I'll make time to play tennis with a friend once a week."
By setting these achievable goals, we'll stay motivated and see wonderful progress on our path to a healthier and happier self. How about recruiting a friend or your spouse as a workout buddy? Having someone by your side can keep you motivated and accountable on your fitness journey. Together, you can cheer each other on, share the joys of progress, and support each other through challenges.
Let's make exercising a delightful bonding experience, filled with laughter and encouragement. With a workout buddy, we'll stay on track and achieve our goals with even more fun and success!
Stay motivated
When it comes to managing certain menopausal symptoms, there are steps we can take to support our physical well-being. Let's explore these empowering ways to navigate through this transformative phase with grace and comfort!
• Adjust your thermostat to a cooler setting.
• Dress in light, breathable layers of clothing.
• Keep a fan nearby to help ease hot flashes and night sweats.
It's essential to be aware that our risk for various medical conditions like breast cancer, type 2 diabetes, and heart disease can increase during and after menopause. But fear not! We have the power to make a positive impact on our health. By staying committed to regular workouts and maintaining a healthy weight, we can help reduce these risks and embrace a brighter, healthier future.
Let your creativity flow
Absolutely, staying physically active is important, but let's not forget about nurturing our creativity! This is the perfect time to explore artistic pursuits. Join a painting class or be a part of a knitting group to immerse yourself in a new creative adventure. It will bring a sense of accomplishment and fulfillment.
Not only that, but engaging in a creative outlet will also help us shift our focus away from bothersome symptoms. So, let's embrace the joy of creativity and watch our spirits soar! You deserve to express yourself and find joy in the beauty of your creations.
Remember that staying active is important every day, but it doesn't mean we have to work out intensely every single day. We can find a balance that works for us! You might go for a walk daily, and on 3-4 days a week, add some variety like a fun class, weights session, swim, or bike ride. It's all about making it enjoyable! Group classes can be energizing with the vibrant atmosphere, while a solo run can be your personal escape and meditation. So, let's commit to our fitness journey, invite some friends along, or make new ones, and keep it exciting by mixing up our activities.
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Can You Overdose On Codeine Phosphate?
Codeine phosphate is a widely prescribed medication for the relief of moderate to severe pain. It belongs to a class of drugs known as opioid analgesics, which work by changing the way the brain and nervous system respond to pain signals. While codeine phosphate can be effective in managing pain when used correctly, there is also a risk of overdose.
An overdose occurs when an individual takes more than the recommended dose or takes it more frequently than prescribed. This can lead to serious health consequences, including respiratory depression, coma, and even death.
Understanding the signs and symptoms of codeine phosphate overdose, as well as ways to prevent and treat it, is crucial for anyone who uses this medication.
In this article, we will explore whether it is possible to overdose on codeine phosphate and what steps can be taken to avoid such an outcome.
Understanding Codeine Phosphate and its Effects on the Body
The pharmacological properties of codeine phosphate and its impact on the human body have been extensively studied in scientific literature. Codeine phosphate is classified as an opioid analgesic, which means it is a type of pain medication that works by binding to specific receptors in the central nervous system. This results in a decrease in pain sensation, but also produces other physiological effects such as respiratory depression, sedation, and euphoria.
While codeine phosphate can be effective for managing certain types of pain when used appropriately under medical supervision, its abuse potential and long-term effects on the body are concerning. Codeine abuse may lead to physical dependence and addiction over time, as well as various health complications such as liver damage, gastrointestinal problems, and respiratory issues.
Additionally, chronic use of codeine phosphate may result in tolerance development where higher doses are required to achieve the same level of pain relief. It is important to note that misuse or abuse of prescription opioids like codeine phosphate has become a major public health concern worldwide due to their potential for overdose and death.
Recognizing the signs and symptoms of codeine phosphate overdose is crucial for timely intervention and preventing fatalities.
Recognizing the Signs and Symptoms of Codeine Phosphate Overdose
This section delves into the identification of observable indications and symptoms that can suggest an adverse reaction stemming from significant ingestion of codeine phosphate. There are several risk factors associated with codeine phosphate overdose, including taking higher doses than prescribed, combining it with other substances such as alcohol or benzodiazepines, and having a history of substance abuse or addiction.
In case of a codeine phosphate overdose, emergency response is crucial to prevent further harm. Symptoms of an overdose may include:
• shallow breathing
• confusion
• extreme drowsiness
• slow heartbeat
• cold and clammy skin
• blue lips and nails
• seizures or convulsions
If any of these symptoms are observed in someone who has recently taken codeine phosphate, immediate medical attention should be sought by calling 911 or local emergency services. It is important to note that prompt action can save lives in cases of opioid overdoses.
To prevent codeine phosphate overdose from happening in the first place, there are several measures individuals can take. These will be discussed in the subsequent section about preventing codeine phosphate overdose.
Preventing Codeine Phosphate Overdose
Prevention of adverse reactions resulting from significant ingestion of codeine phosphate can be achieved through various measures. One important step is safe dosing, which involves following the prescribed dosage and not exceeding it. It is crucial to note that individuals have different tolerance levels for codeine, and taking more than the recommended dose can lead to serious consequences, including overdose.
Another vital aspect in preventing codeine phosphate overdose is identifying risk factors. These may include a history of substance abuse or addiction, underlying medical conditions such as liver or kidney disease, and concurrent use of other medications. Healthcare providers should carefully evaluate these risk factors before prescribing codeine phosphate and monitor patients closely during treatment.
By following safe dosing guidelines and identifying potential risk factors, healthcare providers can help prevent codeine phosphate overdose and ensure patient safety.
In the subsequent section about treating codeine phosphate overdose, we will explore the steps that healthcare providers can take if an individual does experience an overdose.
Treating Codeine Phosphate Overdose
Effective management of excessive ingestion of codeine phosphate is crucial to prevent serious complications, including respiratory depression and even death. Emergency procedures should be initiated immediately upon recognizing the symptoms of overdose, which include drowsiness, confusion, pinpoint pupils, shallow breathing, and slow heart rate.
The following steps can help in treating codeine phosphate overdose:
1. Administration of naloxone: Naloxone is an opioid antagonist that can quickly reverse the effects of codeine phosphate and other opioids.
2. Airway management: In severe cases of overdose, patients may require intubation or mechanical ventilation to support their breathing.
3. Gastric lavage: This procedure involves flushing out the stomach contents to remove any remaining unabsorbed medication.
4. Supportive care: Patients with codeine phosphate overdose may need close monitoring in intensive care units for several days due to potential long-term effects such as liver damage and cognitive impairment.
Prompt recognition and appropriate treatment can improve the prognosis for individuals who have ingested excessive amounts of codeine phosphate. However, it is essential to seek medical attention immediately upon suspecting an overdose to avoid potentially fatal consequences.
Frequently Asked Questions
How is codeine phosphate different from other painkillers?
Codeine phosphate is a type of opioid pain medication that is commonly prescribed for moderate to severe pain relief. Compared to other painkillers, codeine has a lower potency and may be less effective in managing chronic pain.
However, it still remains an important option for those who cannot tolerate stronger opioids or non-opioid medications. Codeine works by binding to specific receptors in the brain and spinal cord, which blocks pain signals.
While codeine can be an effective treatment option when used appropriately, it also carries significant risks of addiction, dependency, and overdose if misused or taken in high doses. Therefore, it is essential to take this medication exactly as prescribed by a healthcare provider and avoid using it for prolonged periods without medical supervision.
Can codeine phosphate be used to treat other conditions besides pain?
Codeine phosphate is primarily used as a pain medication, but it can also be effective in treating other conditions. Alternative uses for codeine phosphate include treatment of coughs, diarrhea, and irritable bowel syndrome. However, the effectiveness of codeine phosphate for these conditions varies and there are potential side effects to consider.
Common side effects of codeine phosphate use include drowsiness, constipation, nausea, vomiting, and respiratory depression. Contraindications to codeine phosphate use include asthma or other breathing problems, liver or kidney disease, and a history of drug abuse or addiction. Precautions should be taken when using this medication with certain other drugs such as alcohol or sedatives.
Dosing guidelines vary depending on the severity of the condition being treated and should only be followed under medical supervision to avoid possible overdose.
What is the recommended dosage of codeine phosphate?
The recommended dosage of codeine phosphate varies depending on the age, weight, and severity of the pain being treated. The usual adult dose for pain relief is 15-60mg every four to six hours, with a maximum daily dose of 240mg.
However, elderly patients or those with hepatic or renal impairment may require lower doses to avoid potential side effects such as respiratory depression, dizziness, nausea, and constipation.
It is important to follow the recommended dosage guidelines and not exceed the maximum daily dose as this can lead to overdose and potentially life-threatening consequences.
Patients should also be aware of any other medications they are taking that may interact with codeine phosphate and increase its effects.
Is it safe to take codeine phosphate with other medications?
Possible interactions and precautions should be taken into consideration when taking codeine phosphate with other medications. Codeine phosphate can interact with a range of drugs, including antidepressants, sedatives, muscle relaxants, and certain painkillers. These interactions may lead to increased side effects or reduced effectiveness of either medication.
Additionally, patients with certain medical conditions such as liver disease or respiratory problems should exercise caution when taking codeine phosphate as it can exacerbate these conditions. It is important to consult with a healthcare professional before taking any new medications in conjunction with codeine phosphate to ensure safe and effective use.
How long does it take for codeine phosphate to leave the body?
Codeine phosphate is a commonly prescribed medication for pain relief. The length of time it takes for the drug to leave the body can vary depending on several factors.
Codeine phosphate withdrawal may occur when someone stops taking the medication, and this may be accompanied by symptoms such as restlessness, anxiety, insomnia, muscle aches, and sweating. The detox process from codeine phosphate usually lasts between one to two weeks but can take longer in some cases.
Factors affecting codeine phosphate elimination include age, weight, liver function, and metabolic rate. It is essential to follow the doctor’s instructions carefully while taking codeine phosphate and not exceed the prescribed dosage to avoid potential complications or overdose.
Conclusion
Codeine phosphate is a commonly prescribed pain medication that can be effective when used properly. However, an overdose of this drug can be fatal and requires immediate medical attention. Understanding the signs and symptoms of a codeine phosphate overdose is essential to preventing serious complications.
Some common signs of codeine phosphate overdose include difficulty breathing, confusion, extreme drowsiness or lethargy, seizures, and loss of consciousness. It is important to note that these symptoms may not appear immediately after taking the drug but may develop gradually over time.
Preventing codeine phosphate overdose involves following proper dosage instructions as prescribed by a healthcare provider. It is also essential to avoid mixing this medication with alcohol or other drugs that can depress the central nervous system. If you suspect someone has overdosed on codeine phosphate, seek emergency medical care immediately.
In conclusion, while codeine phosphate can provide relief from pain when used appropriately, it is crucial to understand the potential risks associated with an overdose of this drug. Recognizing the signs and symptoms of an overdose and taking steps to prevent such an event are key in ensuring patient safety.
If you or someone you know struggles with addiction to prescription medications like codeine phosphate, seeking professional help from a healthcare provider or addiction specialist can provide valuable support in overcoming this challenge.
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You won’t believe this.
Apple cider vinegar is taken by many individuals. It has many benefits to the body ad can help lower blood sugar to an acceptable level. Many individuals use this drink to lower their blood sugar every night.
ACV has been taken more and more in recent years due to the benefits that the body will receive. This product has many benefits for the body and can even lower blood sugar to a healthy level if it is consumed properly. This is especially great for those who can not control their blood sugar. It is very important for people to control and maintain their blood sugar levels.
many experts recommend that individuals take ACV to help their body get control of its blood sugar level. High blood sugar can cause many issues throughout the body and could lead to many serious diseases if it is not handled properly.
* Additional Disclaimer: All content provided by this newsletter is for informational and educational purposes only and is not meant to represent trade, investment, or healthcare recommendations.
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Cited 0 times in
간외담도폐쇄에 대한 Kasai 술식 후 생존 결과 및 예후인자
Other Titles
Kasai Operation for Extrahepatic Biliary Atresia - Survival and Prognostic Factors
Authors
윤찬석 ; 한석주 ; 박영년 ; 정기섭 ; 오정탁 ; 최승훈
Citation
Journal of the Korean Association of Pediatric Surgeons (소아외과), Vol.12(2) : 202-212, 2006
Journal Title
Journal of the Korean Association of Pediatric Surgeons (소아외과)
ISSN
1225-9047
Issue Date
2006
Keywords
Biliary atresia ; Portoenterostomy ; Survival ; Prognosis
Abstract
The prognostic factors for extrahepatic biliary atresia (EHBA) after Kasai portoenterostomy include the patient's age at portoenterostomy (age), size of bile duct in theporta hepatis (size), clearance of jaundice after operation (clearance) and the surgeon's experience. The aim of this study is to examine the most significant prognostic factor of EHBA after Kasai portoenterostomy. This retrospective study was done in 51 cases of EHBA that received Kasai portoenterostomy by one pediatric surgeon. For the statistical analysis, Kaplan-Meier method, Logrank test and Cox regression test were used. A p value of less than 0.05 was considered to be significant. Fifteen patients were regarded as dead in this study, including nine cases of liver transplantation. There was no significant difference of survival to age. The age is also not a significant risk factor for survival in this study (Cox Regression test; p = 0.63). There was no significant difference in survival in relation to the size of bile duct. However, bile duct size was a significant risk factor for survival (Cox Regression test; p = 0.002). There was a significant difference in relation to survival and clearance (Kaplan-Meier method; p = 0.02). The clearing was also a significant risk factor for survival (Cox Regression test; p = 0.001). The clearance of jaundice is the most significant prognostic factor of EHBA after Kasai portoenterostomy.
Files in This Item:
T200600668.pdf Download
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pediatrics (소아청소년과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers
Yonsei Authors
Park, Young Nyun(박영년) ORCID logo https://orcid.org/0000-0003-0357-7967
Oh, Jung Tak(오정탁)
Chung, Ki Sup(정기섭)
Choi, Seung Hoon(최승훈)
Han, Seok Joo(한석주) ORCID logo https://orcid.org/0000-0001-5224-1437
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/109573
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Invisalign Treatment Boron CA 93516
invisalign treatment
What is Invisalign?
Invisalign Treatment Boron CA 93516 Invisalign is a kind of dental braces that utilize clear tray aligners. They’re made of Invisalign’s own blend of plastic, and made in their own centers based upon mold and mildews of your mouth. The aligners are a solid item of plastic that is solid sufficient to tax details parts of your teeth to gradually move them into a far better placement.
To get Invisalign, you first need to have an assessment with your dentist. They’ll take a look at your smile, your total oral health, and take perceptions of your mouth. After that, Invisalign makes their aligners unique to your mouth for a customized fit. Your dentist develops your total treatment strategy and functions as your partner in obtaining the outcomes you want.
Invisalign uses a series of aligner trays that are replaced every one to two weeks. Each replacement tray will certainly feel a little different, as it’s made to proceed moving and moving your teeth.
You require to use Invisalign trays for a lot of your day (20– 22 hours/day) in order to see outcomes. They’re easily gotten rid of for eating, cleaning, flossing, or for unique occasions.
Though it’s a strong item of plastic, Invisalign aligners are braces, not retainers, due to the fact that they actively relocate your teeth to shape your mouth and jaw. Retainers simply hold your teeth in place.
For comparison, typical metal bracket supports typically set you back $2,000–$6,000.
Once again, all of these costs rely on your individual instance. Very crooked teeth or a mouth with an overbite will certainly require more time to slowly relocate the teeth into an optimal position, whether you use Invisalign or typical dental braces.
Just how does Invisalign function?
Invisalign makes use of sophisticated 3-D computer-imaging innovation to determine a complete treatment strategy from the first setting of your teeth to the last desired placement. Clear aligners are tailor-made for your teeth based on these results. Each is help a pair weeks, and then changed by the following in the collection, so your teeth will slowly relocate to the last excellent placement.
What are the major advantages of Invisalign?
The Invisalign aligners are almost clear, so it’s likely individuals will not also see you’re using dental braces. And, unlike dental braces, you can eat and drink all of the foods you appreciate, and brush and floss as you generally would just by getting rid of the aligners. Ultimately, Invisalign doesn’t make use of any steel brackets or wires that can aggravate your mouth – this also suggests you’ll spend less time in the dentist’s chair due to the fact that you will not require to come in for changes.
Can I most likely to any kind of dentist for treatment with Invisalign?
Dentists that provide individuals with Invisalign are called for to undertake training sessions to end up being a skilled Invisalign carrier. Additionally, these dental professionals should take part in recurring training courses that will gain them the classification of “Preferred Provider.” When choosing the best dentist for your procedure, ask them if they’re a recommended supplier, or if they’ve been properly trained to treat you with Invisalign.
Is Invisalign agonizing?
Invisalign has the ability to straighten your teeth without the discomfort related to the cables used in dental braces. It’s possible for you to experience a momentary pain or stress during the first few days of each aligner. This is typical and alright – it simply suggests the treatment is working and your teeth are getting closer to their last location.
Exist certain people that Invisalign isn’t ideal for?
Invisalign is appropriate for many teenagers and grownups. The only people that Invisalign isn’t ideal for are those who still have primary teeth or second molars that have not erupted. Your dentist or orthodontist will certainly be able to figure out if Invisalign treatment is right for you if you assume you’re a prospect.
Are there foods I should avoid while making use of Invisalign aligners?
No. Given that the aligners can be eliminated, you have much more flexibility in what you can consume or consume. Both important points that need to be prevented while putting on Invisalign aligners is eating gum and smoking, as it can discolor the aligners.
I used to wear dental braces and my teeth have considering that shifted. Can Invisalign assist? Most of the more than 1 million users of Invisalign have actually used dental braces in their past and have actually experienced changing afterward. Invisalign can usually correct the problem without having to go via the social awkwardness related to wearing steel dental braces.
How much does Invisalign set you back?
Like the majority of medical treatments, the price of Invisalign can vary depending upon numerous aspects, including how hard your case is, for how long your treatment is, where you live, and your insurance protection. The national average for treatment is about $5,000, yet this can vary anywhere from $3,500 to $8,000.
Invisalign is a kind of braces that use clear tray aligners. The Invisalign aligners are virtually clear, so it’s most likely individuals won’t also notice you’re using braces. Dentists who use patients with Invisalign are called for to undergo training sessions to become a skilled Invisalign company. Invisalign is able to correct your teeth without the pain connected with the cables used in dental braces. The two primary things that must be stayed clear of while wearing Invisalign aligners is chewing gum and smoking, as it can tarnish the aligners. Invisalign Treatment Boron CA 93516
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1.
Pharmaceutical Technology ; 45(9):26-28, 2021.
Article in English | EMBASE | ID: covidwho-2169917
2.
Transplant Cell Ther ; 2022 Oct 21.
Article in English | MEDLINE | ID: covidwho-2150218
ABSTRACT
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), disproportionately affects immunocompromised and elderly patients. Not only are hematopoietic cell transplantation (HCT) and chimeric antigen receptor (CAR) T-cell recipients at greater risk for severe COVID-19 and COVID-19-related complications, but they also may experience suboptimal immune responses to currently available COVID-19 vaccines. Optimizing the use, timing, and number of doses of the COVID-19 vaccines in these patients may provide better protection against SARS-CoV-2 infection and better outcomes after infection. To this end, current guidelines for COVID-19 vaccination in HCT and CAR T-cell recipients from the American Society of Transplantation and Cellular Therapy Transplant Infectious Disease Special Interest Group and the American Society of Hematology are provided in a frequently asked questions format.
3.
JAAD Case Reports ; 2022.
Article in English | ScienceDirect | ID: covidwho-2159235
4.
Vnitr Lek ; 68(7): 444-448, 2022.
Article in English | MEDLINE | ID: covidwho-2114787
ABSTRACT
Kidney transplant recipients are a very vulnerable population at risk of severe course and death from Covid-19. Several antiviral drugs are now available for the treatment of nonhospitalized individuals with mild to moderate Covid-19 and hospitalized patients with severe disease. The combination of monoclonal antibodies is also available to be used as pre-exposure prophylaxis in elderly patients. Previously used monoclonal antibodies for post-exposure prophylaxis are no longer effective because of the new mutations and are no longer recommended. Although the immune response to Covid-19 vaccines is impaired in kidney transplant recipients, the effectiveness of the Covid-19 vaccines was described even in this immunocompromised group. Therefore vaccination, together with anti-epidemic measures, remains the most important tool to prevent Covid-19.
Subject(s)
COVID-19 Vaccines , COVID-19 , Kidney Transplantation , Aged , Humans , Antibodies, Monoclonal , COVID-19/prevention & control , COVID-19 Vaccines/administration & dosage , Kidney Transplantation/adverse effects , Vaccination
5.
Vaccines (Basel) ; 10(10)2022 Oct 10.
Article in English | MEDLINE | ID: covidwho-2071922
ABSTRACT
The mortality rate after novel coronavirus infection, which causes severe acute respiratory distress syndrome (SARS-CoV-2), is much higher in kidney transplant recipients (KTRs) compared to the general population. Seroconversion after vaccination is also lower, and breakthrough infection is much higher. Many studies reported seroconversion rate after a booster (third) dose of vaccine but clinical outcomes received less attention. Here, we reported the impact of an mRNA vaccine booster dose on clinical outcomes of KTRs with SARS-CoV-2 infection. A total of 183 KTRs with SARS-CoV-2 infection were identified. Of 183 KTRs, 146 KTRs had sufficient data for analysis and were included in this study. Forty-eight patients (32.9%) received zero to 1 doses of vaccine (Group 1), thirty-one (21.2%) received two doses (Group 2), and sixty-seven (45.9%) received a booster dose (Group 3). Pneumonia developed in 50%, 23%, and 10% in Group 1, 2, and 3 (p < 0.001). Hospital admission requirement was 81%, 48%, and 12% (p < 0.001). Mortality rate was 26%, 3%, and 3% (p = 0.001). A multivariate analysis showed that only diabetes adversely affects mortality while the booster dose of the vaccine significantly reduced mortality. The booster dose of the vaccine is strongly recommended in all KTRs especially those with diabetes. Our study also suggested the timing of the booster dose vaccine to be administered within 4 months after the second dose.
6.
Open Access Macedonian Journal of Medical Sciences ; 10(E):1169-1173, 2022.
Article in English | EMBASE | ID: covidwho-2066702
ABSTRACT
BACKGROUND: The implementation of the vaccine on a large scale has almost reached all provinces in Indonesia. East Kalimantan, one of the provinces affected by COVID-19, has also implemented a vaccine program. Seroprevalence surveys are essential to describe the success of vaccine program based on antibody titer test. AIM: This study aims to determine the anti-SARS-CoV-2 antibody titer value based on the type of vaccine received by the academic community in Samarinda, one of the cities most affected by COVID-19 in East Kalimantan. METHODOLOGY: The study was population-based. The study sampled 100 people from the community. Participants must be in good health, aged 16–60, with a positive COVID-19 test, no comorbid illnesses or other chronic problems, no blood transfusions, and most importantly, have received the least initial dosage of immunization. The data will be analyzed using SPSS 26 and STATA 16. A normality test and Tobit regression test to determine the antibody distribution in each vaccine type. RESULTS: The results showed that Moderna COVID-19 Vaccine provided a significant (p = 0.001) increase in antibody prediction of 1090 U/ml (95% CI: 764–1416), while Pfizer provided a significant (p = 0.000) rise of 766 U/ ml (95% CI: 307–1226). CONCLUSION: According to the results of a seroprevalence survey conducted among the academic community in East Kalimantan, receivers of inactivated vaccinations outnumbered those of mRNA and vector-based vaccines. It can be determined that booster immunizations for students and academic staff are required to guard against COVID-19 infection. As boosters, both Moderna’s COVID-19 Vaccine and Pfizer’s COVID-19 Vaccine are strongly recommended.
7.
American Journal of Transplantation ; 22(Supplement 3):931, 2022.
Article in English | EMBASE | ID: covidwho-2063524
ABSTRACT
Purpose: Most developing countries do not have access to high-efficiency mRNA vaccine. In Thailand, the first and most available vaccines were inactivated, and later on, viral vector vaccine. Here, we reported the efficacy of inactivated and viral vector vaccine in preventing severe disease and death in kidney transplant recipients. Method(s): This is a retrospective study comprised 45 kidney transplant recipients with Covid-19 infection. Patients were classified into 2 groups based on vaccination status before COVID-19 infection. Patients in group 1 were vaccinated with either inactivated or viral vector vaccine and patients in group 2 were unvaccinated. Group 1 was also subdivided into fully and partially vaccinated. All patients received the same standard of care. Outcomes of interest were rate of death, pneumonia and requirement of oxygen therapy. Result(s): There were 23 patients (51%) in group 1 [7 fully vaccinated (5 inactivated, 2 viral vector), 16 partially vaccinated (all viral vector)] and 22 patients (49%) in group 2. All of baseline characteristics including recipient factors, donor factors, immunologic factors and immunosuppressive regimens were similar between groups except only mean recipient age was older in group 1 (55 +/- 11 years in group 1 VS 48 +/- 15 years in group 2, p = 0.035). Of 45 patients in this study, 11 patients died (24%). Significantly more death occurred in group 2. Three patients (all partially vaccinated) and 8 patients died in group 1 and group 2 respectively (13% VS 36%, p = 0.03). No patient receiving full vaccination died. Pneumonia developed equally in both groups (70% VS 71%, p = 0.89). There was a trend toward less oxygen requirement in group 1 (50% VS 74% p = 0.10) as well as less ventilator requirement (9% VS 19% p = 0.48). Conclusion(s): Inactivated and viral vector COVID-19 vaccines have good efficacy in mortality reduction in kidney transplant recipients. Even partial vaccination can exert some protection against death. However, to achieve better prevention, full vaccination should be encouraged to all kidney transplant recipients.
8.
American Journal of Transplantation ; 22(Supplement 3):696, 2022.
Article in English | EMBASE | ID: covidwho-2063494
ABSTRACT
Purpose: Recent data has shown poor antibody response to SARS-CoV-2 vaccination among adult kidney transplant (tx) recipients, with seroconversion ranging between 22%-58% after two mRNA vaccine doses. Here, we evaluated the antibody and T cell response to SARS-CoV-2 vaccination and evaluate the effects of intensified immunosuppression on such response in pediatric (ped) kidney tx recipients. Method(s): Between April and November 2021, 31 ped renal tx patients (pts)aged 13-22 years old had SARS-CoV-2 spike IgG assessment after receiving 2 doses of SARS-CoV-2 mRNA or 1 dose of viral vector vaccine. Pts were evaluated by their level of immunosuppression: A) standard immunosuppression (tacrolimus, mycophenolate mofetil +/- steroids) or B) intensified immunosuppression (standard immunosuppression + solumedrol pulse, IVIG, rituximab, and/or tocilizumab within 11 months prior to and up to 5 months after SARS-CoV-2 vaccination). A subgroup of 18 pts had SARS-CoV-2 Tc assessment post-vaccination. Result(s): 23 of 31 (74.2%) pts seroconverted at a median assessment time of 83 days (IQR 43-124) post-vaccination. There was no difference in the use of steroid-based or steroid-free immunosuppression between the two groups or the type of vaccine received (Table 1). 15 of 17 (88.2%) of those who received standard immunosuppression seroconverted post-vaccination compared to 8 of 14 (57.1%) in those who received intensified immunosuppression (Table 1;p = 0.10). In a subgroup of pts who had SARS-CoV-2 spike-specific Tc testing, 7 of 7 (100%) in the standard immunosuppression group had positive Tc compared to 7 of 11 (63.6%) in the intensified immunosuppression group (Table 1, p = 0.12). There was no leukopenia or difference in the WBC count in either group at the time of Tc testing (Table 1;p = 0.97). No pts developed symptomatic SARS-CoV-2 infection. Conclusion(s): Ped renal tx recipients appear to have higher rates of seroconversion after the standard 2-dose mRNA or 1-dose viral vector SARS-CoV-2 vaccination compared to adult renal tx recipients. The intensified immunosuppression group appears to have a trend towards lower SARS-CoV-2 spike IgG and Tc conversion, however, results are limited by the small sample size. Larger studies are needed to better understand the humoral and cellular response to SARS-CoV-2 vaccination in this group. (Figure Presented).
9.
American Journal of Transplantation ; 22(Supplement 3):440, 2022.
Article in English | EMBASE | ID: covidwho-2063396
ABSTRACT
Purpose: Organ transplant recipients (OTR) have worse outcomes from COVID-19 and weaker antibody responses to vaccination than do immunocompetent individuals. Data on clinical outcomes among OTR with breakthrough COVID-19 are urgently needed, given decreased vaccine efficacy against the B.1.617.2 (Delta) variant. We compared crude case fatality rates (CFR) between fully vaccinated and unvaccinated kidney transplant recipients (KTR) with COVID-19. Method(s): We identified KTR with COVID-19 at our institution between 3/1/20 and 11/17/21. Multi-organ transplant recipients, KTR who received additional ("booster") doses, and those with partial or unknown vaccination status were excluded due to small numbers. KTR were considered fully vaccinated 2 weeks after receiving either the second dose of an mRNA vaccine series (Moderna, Pfizer-BioNTech) or one dose of the Janssen viral vector vaccine. Demographics, clinical characteristics, and in-hospital or hospice care mortality were extracted from electronic medical records. Result(s): Among 109 KTR with COVID-19, 19 were fully vaccinated at symptom onset. Vaccinated KTR with COVID-19 were older (median: 63.5 vs. 57.5 years, P<0.05) and waited longer to seek care after symptom onset (median: 6 vs. 3 days, P<0.05). Comorbidities and time from transplant were comparable between the two groups. CFR was higher among vaccinated KTR (26% vs. 10%, HR 0.34, 95%CI 0.11-1, P=0.05;Fig. 1), although the difference was not significant after adjustment for age (aHR 0.53, 95%CI 0.17-1.61, P>0.1). All fatal breakthrough infections occurred when the Delta variant accounted for >98% of COVID-19 cases in our HHS region. Conclusion(s): Vaccinated OTR remain at high risk for fatal COVID-19. Younger OTR are likely more immunoprotected than older OTR, which-combined with the emergence of the Delta variant and easing of restrictions-may have contributed to the observed shift toward older age among KTR with breakthrough COVID-19 and the high resultant CFR. Vaccinated OTR may delay seeking care for breakthrough symptoms due to a false sense of security. Our findings highlight the importance of pretransplant vaccination, and, among OTR, the need for ongoing preventive measures (masks, social distancing, vaccination of close contacts, post-vaccine education) and additional vaccine doses. OTR should be linked to care immediately after exposure or onset of symptoms consistent with COVID-19, given the availability of anti-spike monoclonal antibodies for prevention or treatment. (Figure Presented).
10.
Appl Biochem Biotechnol ; 2022 Oct 12.
Article in English | MEDLINE | ID: covidwho-2060052
ABSTRACT
In the current scenario of the coronavirus pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), considerable efforts have been made to control the pandemic by the development of a strong immune system through massive vaccination. Just after the discovery of the genetic sequences of SARS-CoV-2, the development of vaccines became the prime focus of scientists around the globe. About 200 SARS-CoV-2 candidate vaccines have already been entered into preclinical and clinical trials. Various traditional and novel approaches are being utilized as a broad range of platforms. Viral vector (replicating and non-replicating), nucleic acid (DNA and RNA), recombinant protein, virus-like particle, peptide, live attenuated virus, an inactivated virus approaches are the prominent attributes of the vaccine development. This review article includes the current knowledge about the platforms used for the development of different vaccines, their working principles, their efficacy, and the impacts of COVID-19 vaccines on thrombosis. We provide a detailed description of the vaccines that are already approved by administrative authorities. Moreover, various strategies utilized in the development of emerging vaccines that are in the trial phases along with their mode of delivery have been discussed along with their effect on thrombosis and gastrointestinal disorders.
11.
Emerg Microbes Infect ; 11(1): 2689-2697, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-2051172
ABSTRACT
The rapid widespread Omicron subvariant BA.5 of SARS-CoV-2 has become a potential imminent pandemic threat, but available vaccines lack high efficacy against this subvariant. Thus, it is urgent to find highly protective vaccination strategies within available SARS-CoV-2 vaccines. Here, by using a SARS-CoV-2 pseudovirus neutralization assay, we demonstrated that the aerosol inhalation of adenoviral vector COVID-19 vaccine after two dose of inactivated vaccine (I-I-Ad5) led to higher levels of neutralizing antibodies against D614G strain (2041.00[95% CI, 1243.00-3351.00] vs 249.00[149.10-415.70]), Omicron BA.2 (467.10[231.00-944.40] vs 72.21[39.31-132.70]), BA.2.12.1(348.5[180.3-673.4] vs 53.17[31.29-90.37]), BA.2.13 (410.40[190.70-883.3] vs 48.48[27.87-84.32]), and BA.5 (442.40 vs 56.08[35.14-89.51]) than three inactivated vaccine doses (I-I-I). Additionally, the level of neutralizing antibodies against BA.5 induced by I-I-Ad5 was 2.41-fold higher than those boosted by a third dose of RBD subunit vaccine (I-I-S) (p = 0.1308). The conventional virus neutralizing assay confirmed that I-I-Ad5 induced higher titre of neutralizing antibodies than I-I-I (116.80[84.51-161.5] vs 4.40[4.00-4.83]). In addition, I-I-Ad5 induced higher, but later, anti-RBD IgG and IgA in plasma than I-I-I. Our study verified that mucosal immunization with aerosol inhalation of adenoviral vector COVID-19 vaccine may be an effective strategy to control the probable wave of BA.5 pandemic in addition to two inactivated vaccines.
Subject(s)
COVID-19 , Viral Vaccines , Humans , COVID-19 Vaccines , SARS-CoV-2 , Antibodies, Neutralizing , Antibodies, Viral , COVID-19/prevention & control , Vaccines, Inactivated , Adenoviridae/genetics
12.
Headache ; 62(8): 1046-1052, 2022 09.
Article in English | MEDLINE | ID: covidwho-2019281
ABSTRACT
BACKGROUND: Coronavirus disease 2019 (COVID-19) vaccine-related side effects are a key concern with the emergence of various types of vaccines in the market. We aimed to assess the frequency and characteristics of headache following different types of COVID-19 vaccines. METHODS: Fully vaccinated people were recruited by a convenience sample through an online survey from September 1 to December 1, 2021. Detailed analysis of headache following vaccination was investigated. Participants with a history of pre-existing headaches were telephone interviewed by a neurologist to ascertain the type of headache. RESULTS: A total of 1372 participants participated (mean age 32.9 ± 11.1). The highest frequency of headache was reported with the adenoviral vector type (302/563, 53.6%), followed by mRNA vaccines (129/269, 48%) and then the inactivated type (188/540, 34.8%). Recipients of the adenoviral vector type had a significantly longer latency between vaccination and the headache onset (median 8 h [5:12]) than recipients of the inactivated type (median 4 h [2:8], p < 0.001). Headache intensity was significantly higher with the adenoviral vector type (median 6 [5:8]) than with the inactivated type (median 5 [4:7], p < 0.001). Adenoviral vector vaccines would increase the likelihood of headache by 2.38 times more than inactivated vaccines (odds ratio [OR] 2.38, 95% confidence interval [CI] 1.83-3.04, p < 0.001). Female sex and thyroid disease were significantly associated with headache related to COVID-19 vaccines (OR 1.52, 95% CI 1.16-1.99; OR 3.97, 95% CI 1.55-10.2, respectively). CONCLUSION: Recipients of the COVID-19 vaccine should be counseled that they may experience headaches, especially after the adenoviral vector type. However, the intensity of such headache is mild to moderate and can resolve within a few days. Based on the current study design and the potential recall bias, these results may not be generalizable and should be preliminary.
Subject(s)
COVID-19 Vaccines , COVID-19 , Headache , Adult , COVID-19/epidemiology , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Female , Headache/epidemiology , Headache/etiology , Humans , Surveys and Questionnaires , Young Adult
13.
Pathog Dis ; 80(1)2022 10 03.
Article in English | MEDLINE | ID: covidwho-2017915
ABSTRACT
Effective vaccination is a key element in the exit strategy from the current severe acute respiratory syndrome-CoV coronavirus-2 (SARS-CoV-2) pandemic, and may also offer protection against severe disease from future variants of concern. Here, we prospectively monitored T-cell responses over time, using ELISpot interferon-γ (INF-y) release assays, and B-cell responses, using serological tests, after vaccination and booster with BioNTech/Pfizer mRNA (Pfizer) and Janssen vector (Janssen/Johnson & Johnson) vaccines in hospital health care workers. Vaccine recipients were divided into seropositive and seronegative individuals at baseline, in order to determine the effect of natural immunity on vaccine-induced immune kinetics. We found that convalescent individuals mounted higher spike-specific INF-y-secreting T-cell responses and B-cell-mediated IgG responses, after receiving the Janssen vaccine or the first dose of the Pfizer vaccine. IgG levels corresponded to the virus neutralization capacity as measured by VNT assay. At 8 months postvaccination, spike-specific cellular immunity waned to low levels in individuals with or without prior natural immunity, whereas waning of humoral immunity occurred predominantly in naive individuals. The booster shot effectively reinduced both cellular and humoral immune responses. To conclude, our data supports the implemented single-dose mRNA booster strategy employed in the Netherlands. Furthermore, the level of pre-existing natural immunity may be factored into determining the optimal time window between future booster vaccines.
Subject(s)
COVID-19 , Viral Vaccines , Antibodies, Viral , COVID-19/prevention & control , Health Personnel , Humans , Immunity, Cellular , Immunity, Humoral , Immunoglobulin G , Interferon-gamma , Kinetics , RNA, Messenger , SARS-CoV-2 , Vaccination
14.
J Formos Med Assoc ; 2022 Aug 18.
Article in English | MEDLINE | ID: covidwho-1996350
ABSTRACT
The appropriate interval between heterologous prime adenoviral vectored vaccination and boost mRNA vaccination remains unclear. We recruited 100 adult participants to receive a prime adenoviral vectored vaccine (ChAdOx1, AstraZeneca) and a boost mRNA vaccine (mRNA-1273, Moderna) 12 weeks apart and checked their serum SARS-CoV-2 anti-spike IgG titers and neutralizing antibody titers against B.1.1.7 (alpha) and B.1.617.2 (delta) variants on the 28th day after the boost dose. Results were compared with our previous study cohorts who received the same prime-boost vaccinations at 4- and 8-week intervals. Compared to other heterologous vaccination groups, the 12-week interval group had higher neutralizing antibody titers against SARS-CoV-2 variants than the 4-week interval group and was similar to the 8-week interval group at day 28. Adverse reactions after the boost dose were mild and transient. Our results support deploying viral vectored and mRNA vaccines in a flexible schedule with intervals from 8 to 12 weeks.
15.
Journal of General Internal Medicine ; 37:S256, 2022.
Article in English | EMBASE | ID: covidwho-1995808
ABSTRACT
BACKGROUND: Despite COVID-19 vaccines' demonstrated effectiveness in mitigating COVID-related hospitalizations and death, large numbers of Americans, including U.S. veterans, have not completed the primary vaccine series or the third/booster dose. The Veterans Health Administration (VHA) is the largest integrated health care system in the U.S. Identifying subgroups of veterans that have not completed COVID-19 vaccination and booster/third doses may inform targeted interventions to decrease disparities and promote vaccine completion. METHODS: We included veterans enrolled at VHA facilities from Jan 1, 2021 (first COVID-19 vaccinations available for highest risk veterans per CDC guidelines) through December 22, 2021. The VA COVID-19 Shared Data Resource was linked to the Corporate Data Warehouse to provide vaccination and other COVID-related clinical information, as well as demographic and social determinants data. The main study outcome was completion of the COVID-19 primary vaccine series (two doses of either mRNA vaccine or one dose of the viral vector vaccine). Secondary outcome was completion of the booster or third dose among eligible veterans. Univariate descriptive statistics determined the proportion of veterans completing vaccination by subgroup of interest;relative risks calculated statistical significance. RESULTS: Of 6,235,555 veterans, 9.5% were women;mean age was 62.9 years (+/-16.8 years);31.2% were of non-White racial/ethnic minority groups;6.7% were Hispanic. Of these, 61.7% completed primary vaccination series. Primary vaccination rates were significantly lower in younger veterans ≤ 49 years (47.2%) compared to those >50 years (67.7%). In addition, lower primary vaccination rates were found in women vs. men (57.1% vs. 62.5%);those residing in highly rural vs. urban locations (53.9% vs. 64.5%);Native Americans (56%) compared to Black/African American (64.8%), Hispanic (63.9%) or White (61.6%) veterans;those reporting food insecurity vs. not (54.9% vs. 64.3%);housing insecurity vs. not (51.6% vs. 65.1%);having had a positive vs. negative COVID-19 test prior to vaccination (45.5% vs. 71.6%);and not assigned a primary care team vs. assigned (45.2% vs. 64.5%), (all pvalues < 0.001). Of 3,672,322 eligible veterans, 33.5% received their booster/ third doses as of 12/22/21. Subgroups at risk for not having received booster/ third doses were the same as for the primary series, with the youngest veterans (18-49 years) having the lowest rates of booster/third doses compared to veterans > 50 years (16.1% vs. 36.9%). CONCLUSIONS: Based on VA data, substantial proportions of veterans remain unvaccinated-or under-vaccinated, especially younger veterans, women, Native Americans, those with food or housing insecurity, prior COVID-19, and those not assigned to primary care. Impactful interventions, including health care staff encouraging vaccine completion among more vulnerable subgroups, are needed to avoid further disparities related to adverse COVID19 outcomes.
16.
Front Public Health ; 10: 929445, 2022.
Article in English | MEDLINE | ID: covidwho-1993896
17.
Biochimica Clinica ; 46(1):16-33, 2022.
Article in Italian | EMBASE | ID: covidwho-1988757
ABSTRACT
The COVID-19 pandemic has prompted an unprecedented race to find the means to contrast the SARS-CoV-2 infection, resulting in a huge common effort to develop an efficacious vaccine as soon as possible and an exceptional acceleration of the review process to ensure its safety and efficacy. Many technological platforms are currently under investigation or have already been approved, including those based on the inactivated virus, mRNA- or DNA-based vaccines expressing viral antigens, recombinant SARS-CoV-2 proteins and vector-based vaccines exploiting chimeric adenoviruses. The emergence of new viral variants has represented ad additional challenge and has induced the entire scientific community to potentiate the monitoring process of the ongoing vaccination campaigns. In this scenario, laboratory medicine certainly plays a pivotal role not only in the diagnosis of the infection but also in monitoring the immune response to vaccines and in the detection and prevention of clinically significant adverse events, ultimately contributing to the determination of the biological and clinical efficacy of the available vaccines. This review offers an overview of the most recent and updated data on anti-SARS-CoV-2 vaccines and the technological principles behind them as well as on the resources that laboratory medicine can offer to support the vaccination campaigns. All these aspects represent a rapid step forward in the clinical field which transcends the COVID-19 outbreak and that will certainly pave the way for the future scientific research.
18.
Microbiol Spectr ; 10(4): e0249521, 2022 08 31.
Article in English | MEDLINE | ID: covidwho-1986343
ABSTRACT
We investigated how differences in age, sex, or vaccine type can affect humoral and cellular immune responses after vaccination with vector (ChAdOx1 nCoV-19), mix-and-match (first, ChAdOx1 nCoV-19, and second, BNT162b2), or mRNA (BNT162b2 or mRNA-1273) vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Venous blood was collected from 573 subjects (vector, 396; mix-and-match, 96; and mRNA, 81) before the first vaccination (T0), 7 to 8 weeks (vector) or 3 to 4 weeks (mRNA) after the first vaccination (T1), and 3 to 4 weeks after the second vaccination (T2). The humoral and cellular immune responses were evaluated using Elecsys anti-SARS-CoV-2 (Roche), Alinity SARS-CoV-2 IgG II Quant (Abbott), cPass SARS-CoV-2 neutralization antibody detection (GenScript), and QuantiFERON SARS-CoV-2 (Qiagen) kits. At T1, the levels of the receptor-binding domain antibodies (RBD Ab) and neutralizing antibodies (NAb) decreased with aging, but interferon gamma release (IGR) levels increased. The RBD Ab, NAb, and IGR levels were higher in females than in males at T1 and T2. The NAb levels were higher in the mix-and-match and mRNA vaccine groups than in the vector vaccine group at T2. The RBD Ab and IGR levels were higher in the mRNA vaccine group than in the vector or mix-and-match vaccine groups at T2. The optimal cutoffs for RBD Ab and NAb, which were used to determine the presence of T cell responses, were 5.7 binding antibody units per milliliter (BAU mL-1) and 12.0 IU mL-1, respectively. Age, sex, and vaccine type affected the humoral and cellular immune responses, and T cell responses could be estimated from RBD Ab and NAb levels. IMPORTANCE There have been few studies that comprehensively evaluated factors affecting immune responses and the correlation between humoral and cellular immune responses after vector, mix-and-match, and mRNA vaccines against SARS-CoV-2. Therefore, we analyzed the effects of age, sex, and the different vaccine regimens on the immune responses to vaccination against SARS-CoV-2. The correlation between humoral and cellular immune responses and the cutoffs were derived for RBD antibodies and neutralizing antibodies to predict the presence of the cellular immune responses. In this comprehensive study, we demonstrated that there were differences in the immune responses induced after vaccination depending on the age and sex of an individual. Among the three vaccine regimens, the mix-and-match and mRNA vaccines induced the most robust immune responses. Finally, the proposed optimal cutoffs for RBD and neutralizing antibodies may be useful for predicting cellular immune responses when assays for cellular immune responses are not available.
Subject(s)
COVID-19 , Viral Vaccines , Antibodies, Neutralizing , Antibodies, Viral , BNT162 Vaccine , COVID-19/prevention & control , COVID-19 Vaccines , ChAdOx1 nCoV-19 , Female , Humans , Immunity, Cellular , Male , RNA, Messenger , SARS-CoV-2/genetics , Vaccination , Vaccines, Synthetic , mRNA Vaccines
20.
JAAD Case Rep ; 28: 18-20, 2022 Oct.
Article in English | MEDLINE | ID: covidwho-1977458
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October 19, 2023 | Infectious disease research
Multi-omic profiling of pathogen-stimulated primary immune cells
Authors: Renee Salz, Emil E. Vorsteveld, Caspar I. van der Made, Simone Kersten, Merel Stemerdink, Tsung-han Hsieh, Musa Mhlanga, Mihai G. Netea, Pieter-Jan Volders, Alexander Hoischen, Peter A.C. ’t Hoen
Objectives To perform long-read transcriptome and proteome profiling of pathogen-stimulated peripheral blood mononuclear cells (PBMCs) from healthy donors. We aim to discover new transcripts and protein isoforms expressed during immune responses to diverse pathogens. Methods PBMCs were exposed to four microbial stimuli for 24 hours: the TLR4 ligand lipopolysaccharide (LPS), the TLR3 ligand Poly(I:C), heat-inactivated Staphylococcus aureus, Candida albicans, and RPMI medium as negative controls. Long-read sequencing (PacBio) of one donor and secretome proteomics and short-read sequencing of five donors were performed. IsoQuant was used for transcriptome construction, Metamorpheus/FlashLFQ for proteome analysis, and Illumina short-read 3’-end mRNA sequencing for transcript quantification. Results Long-read transcriptome profiling reveals the expression of novel sequences and isoform switching induced upon pathogen stimulation, including transcripts that are difficult to detect using traditional short-read sequencing. We observe widespread loss of intron retention as a common result of all pathogen stimulations. We highlight novel transcripts of NFKB1 and CASP1 that may indicate novel immunological mechanisms. In general, RNA expression differences did not result in differences in the amounts of secreted proteins. Interindividual differences in the proteome were larger than the differences between stimulated and unstimulated PBMCs. Clustering analysis of secreted proteins revealed a correlation between chemokine (receptor) expression on the RNA and protein levels in C. albicans- and Poly(I:C)-stimulated PBMCs. Conclusion Isoform aware long-read sequencing of pathogen-stimulated immune cells highlights the potential of these methods to identify novel transcripts, revealing a more complex transcriptome landscape than previously appreciated.
Journal: Biorxiv
DOI: 10.1101/2023.09.13.557514
Year: 2023
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Table of Contents
ORIGINAL ARTICLE
Year : 2019 | Volume : 1 | Issue : 1 | Page : 8-14
Multicentric, randomized, double-blind, comparative study in STEMI patients to establish clinical biosimilarity of biosimilar tenecteplase with reference product
1 Medical Affairs Group, DALC, Reliance Life Sciences, Navi Mumbai, Maharashtra, India
2 Clinical Research Group, DALC, Reliance Life Sciences, Navi Mumbai, Maharashtra, India
Date of Submission18-Oct-2018
Date of Decision08-May-2019
Date of Acceptance14-Jun-2019
Date of Web Publication13-Dec-2019
Correspondence Address:
Dr. Prasad Apsangikar
Reliance Life Sciences, R-282, TTC Area of MIDC, Thane Belapur Road, Rabale, Navi Mumbai - 400 701, Maharashtra
India
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Source of Support: None, Conflict of Interest: None
DOI: 10.4103/ACCJ.ACCJ_6_18
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Abstract
Objectives: Tenecteplase (TNK) is an established third-generation class 1A thrombolytic. The objective of the present study was to establish clinical biosimilarity of TNK biosimilar in a comparative phase III study with the reference product in the patients of ST elevation myocardial infarction (STEMI). Materials and Methods: In the double-blind, randomized, comparative clinical study 105 individuals were enrolled (70 in biosimilar TNK arm and 35 in the reference arm). Primary endpoint was thrombolysis in myocardial infarction (TIMI) 3-flow rate of the infarct-related artery at 90 min and all-cause mortality rate at 30 days' post dosing. Secondary endpoints considered were 50% resolution of elevated ST segment at 90 min, re-infarction till day 30, change in the left ventricular ejection fraction at day 30, events of ventricular tachyarrhythmias till day 30, and comparative pharmacokinetics. Immunogenicity was assessed along with the evaluation of safety at day 30. Results: TIMI grade 3-flow rate was achieved in 29 (43.28%) individuals in biosimilar arm and 14 (41.18%) individuals in the reference arm. The difference between the groups was statistically not significant (P = 0.8396). Four (5.71%) all-cause mortality were reported in biosimilar TNK arm compared to 2 (5.71%) in reference arm (all-cause mortality rate at 30 days' post dosing) and the difference between the two arms was statistically not significant (P = −1.00). Conclusion: Biosimilar TNK demonstrated biosimilar equivalence with the reference product in terms of the efficacy and safety analysis in this Phase III study and may be considered as a suitable alternative to reference TNK in patients with STEMI.
Keywords: STEMI, tenecteplase, thrombolysis, thrombolysis in myocardial infarction
How to cite this article:
Apsangikar P, Chaudhry S, Naik M, Deoghare S, Joseph J. Multicentric, randomized, double-blind, comparative study in STEMI patients to establish clinical biosimilarity of biosimilar tenecteplase with reference product. Ann Clin Cardiol 2019;1:8-14
How to cite this URL:
Apsangikar P, Chaudhry S, Naik M, Deoghare S, Joseph J. Multicentric, randomized, double-blind, comparative study in STEMI patients to establish clinical biosimilarity of biosimilar tenecteplase with reference product. Ann Clin Cardiol [serial online] 2019 [cited 2023 Jun 10];1:8-14. Available from: http://www.onlineacc.org/text.asp?2019/1/1/8/273002
Introduction Top
Tenecteplase (TNK) is a genetically engineered variant of the alteplase molecule. Three different mutations result in an increase of the plasma half-life, of the resistance to plasminogen-activator inhibitor[1] and of the thrombolytic potency against platelet-rich thrombi. Among available agents in clinical practice, TNK is the most fibrin-specific molecule and can be delivered as a single bolus intravenous injection. Several large-scale clinical trials have enrolled more than 27,000 patients with acute myocardial infarction (AMI). TNK is equivalent to front-loaded alteplase in terms of mortality and is the only bolus thrombolytic drug for which this equivalence has been formally demonstrated.[1] TNK appears more potent than alteplase when symptoms duration lasts more than 4 h. In addition, TNK significantly reduces the rate of major bleeds and the need for blood transfusions.[1] According to a recent experience published, data of 15,222 patients who had STEMI and received weight-adjusted TNK injection were analyzed. Overall, 95.43% of patients had clinically successful thrombolysis (CST).[2] In the different subgroups, hypertensives, diabetics, smokers, and hyperlipidemic patients had CST rates comparable to the general patient data. CST rates were significantly lower in the elderly patients (>70 years; 92.11%; P < 0.0001), in patients with history of ischemic heart disease (93.86%; P¼ 0.0004) and in patients receiving delayed treatment (>6 h after onset of chest pain; 85.38%; P < 0.0001).[2] The efficacy of a half-dose TNK strategy compared to full-dose TNK and primary percutaneous coronary intervention in the elderly where it was shown to have similar efficacy.[3]
Biosimilars can have a major impact on the affordability and availability of premium biologics in all markets.[4] Apart from the physicochemical and biological characterization compared to the innovator product, it is equally important to establish the clinical similarity of the biosimilar with the innovator product according to the guidelines and geographical regulations. The present study is the phase III double-blind comparative clinical study of TNK biosimilar from Reliance life Sciences (TenecteRel™) to establish the clinical biosimilarity with innovator reference TNK.
Materials and Methods Top
This was a double-blind, prospective, multi-center, randomized, two-arm, parallel group, active-control, comparative clinical study to evaluate efficacy and safety of biosimilar TNK/reference TNK in patients with ST-segment elevation myocardial infarction (STEMI). The study was approved by the Drug Controller General of India office, and the Clinical Trials Registry India (CTRI) registration number is CTRI/2016/09/007230. A total of 105 individuals were enrolled in the study, i.e., 70 individuals in biosimilar TNK arm and 35 individuals in the reference arm across 14 centers in India. The primary efficacy endpoint was the rate of thrombolysis in myocardial infarction (TIMI) 3-flow of the infarct-related artery at 90 min and all-cause mortality rate at 30 days' post dosing. A sample size of 105 individuals in a 2:1 ratio (Biosimilar TNK/reference TNK) was based on previous studies with angiographic endpoint, patency rate of 55%–65% at 90 min for a power of 80%. The innovator TNK being well established clinically, with an appropriate statistical plan approved from the regulatory authorities the individuals were distributed in 2:1 ratio for an enhanced exposure to the biosimilar TNK.
The centralized randomization provided by reliance statistical team was followed across all sites and individuals were assigned to the treatment groups according to randomization.
All individuals who had given written informed consent to participate in the study were assigned a sequential individual number at the screening visit. Individuals were randomly assigned to the two treatment groups in a 2:1 ratio. The randomization schedule was generated by statistician at Reliance Life Sciences. Once individual was found to be eligible for randomization, the site requested a randomization code for the subject. Randomization was managed centrally. The individual identification number was a unique number containing site number and patient number.
Of these 105 individuals, 101 individuals completed 90-min evaluation post dosing without any major protocol deviations that could affect efficacy assessments. Hence, these 101 individuals were included in per protocol population. All randomized individuals received study medication as per study protocol and were considered for intent to treat (ITT)/safety population. The first 24 individuals (12 individuals in each arm) were considered for pharmacokinetic analysis. A total of 57 patients on biosimilar TNK arm and 28 patients on reference arm completed the study. [Table 1] shows the individual disposition.
Table 1: Summary of subject disposition [ITT population (n=105)]
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Male and female individuals in the range of 18–65 years of age who presented with chest pain and/or equivalent symptoms within 6 h and diagnosis of ST-elevation myocardial infarction (STEMI) who were ready to consent and adhere to the study visit schedule and requirements were enrolled for the study. Individuals with left bundle branch block (LBBB), history of contraindication to the use of thrombolytics were excluded. individuals with internal active bleeding or known history of hemorrhagic diathesis, any known history of stroke or stroke of unknown origin in preceding 6 months, history of intracranial tumor, arteriovenous malformation, cerebral aneurysm, major surgery, parenchymal biopsy, ocular surgery and/or significant trauma within the past 2 months (this includes any trauma associated with the current AMI), high-risk individuals as per TIMI risk scoring[5] and individual with any other contraindications for thrombolysis were excluded from the study.
TNK (biosimilar TNK and reference TNK) was administered by single intravenous recommended dose based on the weight of the individual over approximately 10 s. A preexisting intravenous line could be used for administration of TNK in 0.9% sodium chloride solution only. Antithrombotic adjunctive therapy with platelet inhibitors and anticoagulants was allowed according to the relevant treatment guidelines for the management of patients with ST-elevation myocardial infarction. Unfractionated heparin or enoxaparin and antiplatelet agents were allowed as a concomitant therapy as per institutional standards. Acetylsalicylic acid was initiated as soon as possible after symptom onset.
Statistical analyses were performed using the SAS® statistical software (Version: 9.3; SAS® Institute Inc., USA). Comparative analysis was performed for primary and secondary endpoint data. Primary endpoint analysis, the proportion of individuals with rate of TIMI 3 flow of the infarct-related artery at 90 min and all-cause mortality rate at 30 days' post dosing between the treatment groups was estimated with their 95% confidence intervals.
The pharmacokinetic assessment was done in the first 24 individuals (12 individuals in each arm). A total of 14 samples (5 ml each) were collected for pharmacokinetic assessment. First sample (predose) was collected just prior to drug administration (0.00 h) and subsequent samples were collected at 5, 10, 20, 30, 45 min, 1, 1.5, 2, 3, 4, 5, 6 and 8 h after the drug administration. Individuals were hospitalized for at least first 48 h after drug administration for efficacy, safety, and pharmacokinetic assessments. Laboratory investigations, electrocardiogram (ECG), and echocardiography were performed as per study schedule. The angiogram at 90 min was done after considering the clinical condition, other investigations such as ECG and risks associated with the procedure for individual subjects. The investigator decided the need of angiogram to evaluate the perfusion status based on the above considerations. The pharmacodynamic assessment was based on the ST elevation resolution at 90 min and cardiac enzymes level. The study duration for individual subjects was up to 30 days and subjects will be followed at 6 months and 1 year for survival data.
The primary endpoint was TIMI 3-flow rate of the infarct-related artery at 90 min and all-cause mortality rate at 30 days' post dosing. As the primary endpoint data for TIMI perfusion grades were individual to investigator assessment, the main primary endpoint was all-cause mortality rate at 30 days post dosing. Secondary endpoints considered were 50% resolution of elevated ST segment at 90 min, re-infarction till day 30, changes in the left ventricular ejection fraction assessed by echocardiography at day 30, events of ventricular tachyarrhythmias as determined at each ECG time-point till day 30, change from baseline in cardiac enzymes level, pharmacokinetic parameters assessment after the first dose, immunogenicity assessment at day 30 and evaluation of safety based on adverse events, physical examinations, vital signs, ECGs, echocardiography and safety laboratory tests at study visit (day 30).
Results Top
Efficacy Results Top
In biosimilar TNK arm, the mean age of the individuals was 52.5 years, mean height was 161.7 cm and mean weight was 64.5 kg. Of 70 individuals randomized in study arm, 54 (77.14%) individuals were male and 16 (22.86%) individuals were female.
In reference arm, the mean age of the individuals was 50.0 years, mean height was 162.7 cm and mean weight was 66.9 kg. Of 70 individuals randomized in biosimilar TNK arm, 33 (94.29%) individuals were male and 2 (5.71%) individuals were female.
The demographic characteristics of the individuals enrolled in biosimilar TNK and reference arms were comparable for age, height, and weight [Table 2].
Table 2: Demographics and Baseline Characteristics
Click here to view
In biosimilar TNK arm, the mean age of the individuals was 52.5 years, mean height was 161.7 cm and mean weight was 64.5 kg. Of 70 individuals randomized in biosimilar TNK arm, 54 (77.14%) individuals were male and 16 (22.86%) individuals were female. In reference arm, the mean age of the individuals was 50.0 years, mean height was 162.7 cm and mean weight was 66.9 kg. Of 70 individuals randomized in the reference arm, 33 (94.29%) individuals were male and 2 (5.71%) individuals were female. The demographic characteristics of the individuals enrolled in biosimilar TNK and reference arms were comparable for age, height, and weight [Table 2].
History of preexisting risk factor has been included in study listings. Cardiac enzyme levels (creatine phosphokinase [CPK], CPK MB, Troponin T, and Troponin I) were monitored at baseline, 8, 16, 24, 48 h and predischarge. Cardiac enzyme levels were comparable between the groups.
During the study, vital signs were monitored at regular intervals and were comparable in the study and innovator groups.
Change in the left ventricular ejection fraction was assessed by echocardiography performed at baseline (within 48 h after admission) to day 30. The mean change from baseline in the left ventricular ejection fraction was 5.1% in biosimilar TNK arm and 6.0% in the reference arm. The difference between the two arms was statistically not significant (P = 0.6692). All patients enrolled in the study were with a definitive diagnosis of ST-elevation myocardial infarction (STEMI).
All parameters required for assessment of TIMI risk score (age, history of diabetes, hypertension or angina, systolic blood pressure <100 mmHg, Heart rate >100, Killip Class II-IV, Weight <67 kg, anterior ST elevation or LBBB and Time to treatment >4 h) were evaluated separately at baseline. However, analysis of TIMI risk score was not done as it was not required as per protocol defined study eligibility criteria.
Of 105 individuals enrolled in the study, angiography was performed in 101 individuals (i.e., 67 individuals in biosimilar TNK arm and 34 individuals in reference arm] at any time point. Of these 101 individuals, TIMI grade 3-flow rate was achieved in 29 (43.28%) individuals in biosimilar TNK arm and 14 (41.18%) individuals in the reference arm. The difference between the groups was statistically not significant (P = 0.8396) [Table 3].
Table 3: Summary of TIMI grade 3 flow rate of the infarct related artery (PP population)
Click here to view
Out of 105 enrolled individuals (ITT/safety population), 29 (41.43%) individuals in biosimilar TNK arm and 14 (40.00%) individuals in reference arm achieved TIMI grade 3-flow rate. The difference between the groups was statistically not significant (P = 0.8884). In this study, total 06 deaths were reported i.e. 04 (5.71%) in biosimilar tenecteplase arm and 02 (5.71%) in reference arm. Of these 8 reported deaths in one year, 6 deaths were reported within 30 days of administration of the investigational product. Of these, 4 (5.71%) deaths were reported in biosimilar TNK arm compared to 2 (5.71%) deaths in reference arm (all-cause mortality rate at 30 days' post dosing). As shown in [Table 4], the difference between the all-cause mortality rate at 30 days' post dosing between the two arms was statistically not significant (P = 1.00).
Table 4: All-cause mortality rate at 30 days post dosing (ITT population)
Click here to view
In terms of secondary endpoints, resolution of elevated ST segment was evaluated at 90 min ECG compared to baseline. In biosimilar TNK arm, 30 (42.86%) individuals achieved 50% resolution of elevated ST segment at 90 min compared to 14 (40.00%) individuals in reference arm. The difference in the two arms was statistically not significant (P = 0.7748). Myocardial re-infarction was monitored at each ECG evaluation time point till day 30. A total of 3 events of myocardial re-infarction (2 events at 90 min and 1 event at 24 h) were reported in biosimilar TNK arm compared to 1 event (at 60 min) reported in reference arm. Change in the left ventricular ejection fraction was assessed by echocardiography performed at baseline (within 48 h after admission) to day 30. The mean change from baseline the in left ventricular ejection fraction was 12.2% in biosimilar TNK arm and 14.4% in reference arm. The difference between the two arms was statistically not significant (P = 0.6715). The incidence of ventricular tachyarrhythmias was comparable in biosimilar TNK and reference arm at each ECG evaluation time point from baseline to day 30. The change in serum levels of all cardiac enzymes (CPK, CPK MB, Troponin T, and Troponin I) was comparable between the two arms at all evaluation time points. The descriptive statistics of baseline and end of the study for left ventricular ejection fraction did not show any statistically significant difference between both the groups.
For pharmacokinetic analysis, ratio analysis was performed for Ln-transformed pharmacokinetic parameters Cmax, AUC0-8, and AUC0-∞. Ln-transformed pharmacokinetic parameters Cmax, AUC0-8, and AUC0-∞ were evaluated considering the 90% confidence interval [Table 5]. For biosimilar TNK and reference product, mean Cmax was 12440 and 10916 ng/mL, AUC0-8 was 10815 and 8771 (ng × h/mL), and AUC0-∞ was 10953 and 9023 (ng × h/mL), respectively. The median tmax observed for both biosimilar TNK and reference product was 5 min. The median t1/2 observed for biosimilar TNK, and reference product was 0.84 and 1.123 h, respectively. The difference could be attributed to the less number of patients in the control group. The inter-individual variability of biosimilar TNK was much lower for Cmax compared to the reference. The inter-individual variability, whereas it was comparable for AUC0-8 and AUC0-∞ between both the arms. The ratios of the mean of Ln-transformed data (T/R ratio) for lnCmax, lnAUC0-8, and lnAUC0-∞ were 124.88, 124.50, and 121.94, respectively. The descriptive pharmacokinetics is given in [Table 5]. TNK being fibrin specific binds to fibrin in thrombus in the coronary artery/arteries depending on the extent of pathological thrombosis. Hence, serum concentration of TNK is likely to be variable because of its preferential distribution depending on the pathological thrombus and its extent.[6]
Table 5: Descriptive Pharmacokinetic Parameters
Click here to view
Safety results
In this study, a total of 103 adverse events were reported out of which 66 were reported in the biosimilar TNK arm and 37 were reported in the reference arm. There were 37 (52.86%) individuals in biosimilar TNK arm and 17 (51.43%) individuals in the reference arm who had at least one treatment-emergent adverse event (TEAE). There were 1 (1.43%) individual in biosimilar TNK arm and 2 (5.71%) individuals in the reference arm with at least one TEAE related to study medication. There were 6 (8.57%) individuals in the biosimilar TNK arm and 2 (5.71%) individuals in the reference arm with at least one serious adverse event (SAE). A total of 9 SAEs were reported during this study. SAE term of one event was split into two separate terms for the medical dictionary of regulatory affairs (MedDRA) coding. Therefore, 9 SAEs were coded into 10 SAE terms (of which, 8 were reported in the biosimilar TNK arm and 2 were reported in the reference arm). Out of these, 3 SAEs were assessed as related (1 definitely related and 2 possibly related) to the investigational product, and 7 SAEs were unrelated to study medication. No individuals from biosimilar TNK or reference arm were discontinued from the study due to the adverse event. All adverse events were classified according to MedDRA version 19.1. The percentage of individuals with adverse events in each arm was compared, and the difference between the two arms was statistically nonsignificant (P > 0.05). The summary of all adverse events is presented in [Table 6].
Table 6: Overall summary of adverse events (ITT)
Click here to view
According to system organ class in the biosimilar TNK arm, the most commonly reported (incidence ≥5%) TEAEs were related to General disorders and administration site conditions 11 (15.71%), respiratory, thoracic and mediastinal disorders 11 (15.71%), investigations 8 (11.43%), cardiac disorders 7 (10.00%), gastrointestinal disorders 4 (5.71%), nervous system disorders 4 (5.71%), and vascular disorders 4 (5.71%). In the reference arm, the most commonly reported (incidence ≥5%) TEAEs were related to general disorders and administration site conditions 10 (28.57%), gastrointestinal disorders 5 (14.29%), respiratory, thoracic and mediastinal disorders 3 (8.57%), cardiac disorders 2 (5.71%), infections and infestations 2 (5.71%), musculoskeletal and connective tissue disorders 2 (5.71%), and nervous system disorders 2 (5.71%). In biosimilar TNK arm, the reported cardiovascular adverse events included bradycardia 1 (1.43%), cardiac tamponade 1 (1.43%), cardiogenic shock 2 (2.86%), sinus tachycardia 1 (1.43%), ventricular fibrillation 1 (1.43%), and ventricular tachycardia 3 (4.29%). In reference arm, the reported cardiovascular adverse events included sinus tachycardia 1 (2.86%) and ventricular tachycardia 1 (2.86%).
In this study, a total of 8 deaths were reported, i.e., 06 (8.02%) in biosimilar TNK arm and 2 (5.71%) in reference arm. Of these 8 reported deaths, 6 deaths were reported within 30 days of administration of the investigational product. Of these, 4 (5.71%) deaths were reported in biosimilar TNK arm compared to 2 (5.71%) deaths in reference arm (all-cause mortality rate at 30 days' post dosing). The difference between the all-cause mortality rate at 30 days' post dosing between biosimilar TNK and reference arms was statistically not significant (P = 1.00). Overall, out of eight reported deaths, five were cardiorespiratory and three were noncardiac.
Discussion Top
Following ST-segment elevation myocardial infarction (STEMI), early and complete epicardial reperfusion is associated with improved survival.[7] TNK is a third generation thrombolytic, a mutant of t-PA, modified in such a way that it has decreased plasma clearance, increased fibrin specificity and reduced sensitivity to plasminogen activator inhibitor-1.[8] The apparent improvement in side effects coupled with the ease of the administration of TNK t-PA makes it an attractive option in multiple settings.[8] The American College of Chest Physicians recognizes TNKase as a Class 1A recommendation in the treatment of STEMI patients within 12 h from the onset of symptoms.[9]
Ease of administration, rapid action (three times faster than tPA), potency (13.5-fold more potent in lysing platelet-rich clotsin vivo than tPA), weight-adjusted dosing - 0.53 mg/kg, highest fibrin specificity, reduced plasma clearance, high PAI-1 resistance (80-fold more than tPA), and less ICH make TNK a favored thrombolytic or best amongst the equals[10] and is preferred to be used in high risk subset of diabetics.[11]
Following the U.S. and EU guidelines, biosimilarity to a reference product has been demonstrated through analytical data, animal testing and one or more clinical studies, including the assessment of immunogenicity and pharmacokinetics or pharmacodynamics. Further to the detailed characterization with physicochemical and biological orthogonal testing, the present study was designed to establish the clinical biosimilarity of TenecteRel™ (TNK) with that of innovator reference TNK in patients with ST-segment elevation myocardial infarction (STEMI). This was a prospective, multi-center, randomized, two-arm, parallel group, active-control, and comparative clinical study. The demographic characteristics of the individuals enrolled in biosimilar and reference TNK arms were comparable for age, height, and weight. The primary endpoints of the study, i.e., TIMI Grade 3-flow rate and 30 days' mortality were comparable in both treatments arms. Overall, TIMI Grade 3-flow rate was comparable between both the arms. Biosimilar TNK was also comparable to the reference product with respect to other efficacy parameters including 50% resolution of elevated ST segment at 90 min, change in left ventricular ejection fraction, changes in cardiac enzyme levels, myocardial re-infarction, and ventricular tachyarrhythmias. These findings support the comparable efficacy profile of biosimilar and reference TNK. Pharmacokinetics was assessed in the light of efficacy and safety profile of the two arms and the observed results have no bearing on the safety and efficacy profile of the drug as evident from its their comparable efficacy and safety profile. Further, the lower variability of biosimilar TNK for Cmax compared to reference, indicates a favorable pharmacokinetic profile of the Test formulation. As per the available literature, the safety observations are consistent with the known safety profile of TNK. Several studies have reported the similar adverse events observed during this study and therefore, considering the disease condition and the safety profile of the study medication, the SAEs in this study do not raise any new safety concern. Immunogenicity samples from all individuals were negative for antidrug antibodies against TNK. There were no apparent immunologically mediated safety or efficacy concerns reported in this study, and the results were consistent with the available literature on TNK.[11]
Conclusion Top
TenecteRel™ (biosimilar TNK) has comparable efficacy profile to that of reference innovator TNK as evident from the efficacy variables analyzed between the treatment arms. The comparable adverse events support the similar safety profile. Overall, both drugs were well tolerated. The observed safety profile is in line with a known safety profile of TNK. No major safety concerns were noted during this study with biosimilar or reference TNK. Therefore, based on this comparability, TenecteRel™ (biosimilar TNK) may be considered as a suitable alternative to reference TNK in patients with ST-segment elevation myocardial infarction (STEMI).
Acknowledgment
We would like to acknowledge the investigators who participated in the study across the country and were instrumental in conducting and completion of the trial to generate data. Any opinions, findings, and conclusions expressed in this material are those of the authors.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References Top
1.
Melandri G, Vagnarelli F, Calabrese D, Semprini F, Nanni S, Branzi A. Review of tenecteplase (TNKase) in the treatment of acute myocardial infarction. Vasc Health Risk Manag 2009;5:249-56. Back to cited text no. 1
2.
Iyengar SS, Nair T, Hiremath JS, Jadhav U, Katyal VK, Kumbla D, et al. Pharmacologic reperfusion therapy with indigenous tenecteplase in 15,222 patients with ST elevation myocardial infarction – The Indian registry. Indian Heart J 2013;65:436-41. Back to cited text no. 2
3.
Shavadia HJ, Bainey K, Tyrrell B, Brass N, Paterson C, Knapp D, Wels RC. half-dose tenecteplase compared to conventional stsegment myocardial infarction (stemi) reperfusion strategies in the elderly: An observational analysis. Can J Cardiol 2015;31:S20-1. Back to cited text no. 3
4.
Guillermin A, Yan DJ, Perrier A, Marti C. Safety and efficacy of tenecteplase versus alteplase in acute coronary syndrome: A systematic review and meta-analysis of randomized trials. Arch Med Sci 2016;12:1181-7. Back to cited text no. 4
5.
Morrow DA, Antman EM, Charlesworth A, Cairns R, Murphy SA, de Lemos JA, et al. TIMI risk score for ST-elevation myocardial infarction: A convenient, bedside, clinical score for risk assessment at presentation: An intravenous nPA for treatment of infarcting myocardium early II trial substudy. Circulation 2000;102:2031-7. Back to cited text no. 5
6.
Reliance Life Sciences. TenecteRelTM (Tenecteplase) Clinical Study Report. Ver. 1. Reliance Life Sciences; 2017. p. 1-45. Back to cited text no. 6
7.
Yuri B, Pride C, Michael Gibson. Efficacy and safety of single-bolus tenecteplase compared with front-loaded alteplase in Chinese patients with acute myocardial infarction. J Geriatr Cardiol 2007;4:142-3. Back to cited text no. 7
8.
Iyengar SS, Godbole GS. Thrombolysis in the era of intervention. J Assoc Physicians India Suppl 2011;59:26-30. Back to cited text no. 8
9.
Iyengar SS, Nair T, Hiremath J, Dutta AL, Jadhav U, Katyal VK, et al. Pharmacological reperfusion therapy with tenecteplase in 7,668 Indian patients with ST elevation myocardial infarction – A real world Indian experience. J Assoc Physicians India 2017;65:43-7. Back to cited text no. 9
10.
Saran RK, Sethi R, Nagori M. Tenecteplase – The best among the equals. Indian Heart J 2009;61:4454-8. Back to cited text no. 10
11.
Sathyamurthy I, Jayanthi K, Iyengar SS, Hiremath JS, Kumbla D, Ramesh B. Efficacy and safety of tenecteplase in diabetic and non-diabetic patients of STEMI – Indian registry data. J Assoc Physicians India 2010;58:229-30. Back to cited text no. 11
Tables
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]
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Asthma Versus Allergies
May 1, 2023
Asthma Verses Allergies
More than 25 million people in the U.S. have asthma, according to a recent study by the Cleveland Clinic. Of those, over 15 million have asthmatic reactions caused by common allergens, ranking allergic asthma as the most common form of asthma in America. But how can you tell the difference between a chronic asthma condition and an asthmatic reaction induced by allergies? Read on to find out the signs and causes of asthma and allergic asthma, as well as how to diagnose and treat these conditions.
What’s the difference between allergies and asthma?
Allergies occur when the immune system encounters a particular substance (an allergen) and mistakenly identifies it as a threat. The body then produces immunoglobulin E antibodies that bind to the allergen, releasing powerful chemical substances that, though created to protect the body, trigger symptoms such as runny nose, nasal congestion, hives and itchy eyes. Common allergy conditions include dermatitis, eczema, hay fever and conjunctivitis.
Asthma is a chronic lung disease that can make it difficult for patients to breathe properly. It affects people of all ages and usually develops in childhood, although it can also appear later in adulthood. During an asthmatic episode (known as an asthma attack), airways in the lungs begin to constrict and, in some cases, produce mucus that can limit the amount of air that can flow freely through the lungs. Asthma symptoms include wheezing, coughing and shortness of breath.
Asthma can be caused by non-allergenic factors including infections of the airway, stress, certain medications, smoke and air temperature. Additionally, a person can experience an asthmatic episode as a result of encountering pollen, dust mites, mold, pet dander and other allergens. This is known as allergic asthma — the most common form of asthma in children and adults.
How do I know if I have asthma or allergic asthma?
The only way to know if you have a chronic asthma condition or allergic asthma is to get tested by a physician. To test for allergic asthma, doctors typically utilize a skin test, which involves making a small prick on skin of a patient’s arm or back and applying allergens next to the exposed area. This form of testing is highly accurate and can check up to 40 different allergen substances at once. Blood testing is also sometimes used to screen for allergies.
There are three main testing methods for asthma: FeNO testing, spirometry and peak flow testing. FeNO testing involves the patient breathing into a machine that measures the nitric oxide levels in their breath, which signifies whether the lungs are inflamed. Spirometry testing also requires the patient to blow into a machine, but it focuses on measuring how fast the patient can breathe in and out, as well as how much air they can hold in their lungs. In a peak flow test, the patient is asked to blow into a small handheld device that measures how fast they can breathe in and out. Peak flow testing may be done several times over a number of weeks to see if there are any changes in the patient’s breathing before an asthma diagnosis is reached.
What treatment options are available?
After getting a diagnosis, you and your doctor can work together to develop a treatment plan that best serves your needs.
The most common treatment for asthma is a prescription inhaler: a medicine-filled canister that works to deliver medication straight to the lungs in order to narrow the muscles in the airways to allow for more oxygen to flow. Inhalers are designed to be carried on your person at all times and come in two variations — dry powder or metered dose. Another common treatment method is a nebulizer, which is a specialized machine that uses a mask to convert asthma medication into a mist that can be easily inhaled into the lungs.
For allergic asthma, common treatment options include OTC allergy medications such as nasal steroid sprays, decongestants, saline nasal sprays and antihistamines. In more severe cases of allergic asthma, a doctor may prescribe an epinephrine inhaler. In addition to these short-term treatment options, a doctor may recommend an allergy shot, which works by introducing a small dose of allergens into your body to help your immune system build up a tolerance over time.
The most important factor in managing asthma and allergic asthma is knowing your triggers and doing your best to avoid them. It is highly recommended to carry an emergency inhaler with you at all times in the event of an asthma attack.
If you or someone in your family are experiencing symptoms of chronic asthma or allergies, visit Midwest Express Clinic to receive a comprehensive diagnosis and develop a personalized relief plan with one of our expert providers. To find a clinic nearest you, visit midwestexpressclinic.com/locations.
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Exactly what you need to eat to lose weight and live longer
Beyond obesity, our diet can lead to a wide range of health problems
Low fat, high protein, paleo, keto; Diet fads come and go, but as any credible nutritionist will tell you, the truth about diet remains the same: the key to a long, healthy life is a balanced diet. It sounds simple enough, but the latest statistics reveal a shocking truth. According to the Food Standards Agency, unhealthy diets account for a staggering 13 per cent of all deaths in the UK.
A poor diet causes obesity, high blood pressure, high cholesterol and type 2 diabetes, all risk factors for cardiovascular disease. Obesity is also linked to 13 different types of cancer, including postmenopausal breast cancer and bowel cancer. And it’s not just costing us our health: excess weight also costs the UK approximately £74 billion each year in direct NHS costs, lost workforce productivity and reduced life expectancy.
The impact of poor diet
Beyond obesity, there are a variety of other problems that can result from an unhealthy diet. Skin conditions such as psoriasis are exacerbated by high intakes of sugar and saturated fat, nutritional deficiencies can affect hair health, and there is growing evidence that a balanced diet is important for sleep. A large study found that a lack of key nutrients, such as calcium, magnesium, and vitamins A, C, D, E, and K, is associated with sleep problems.
And then there is our mental health. According to findings in the British Medical Journal, healthy eating patterns, such as the Mediterranean Diet, which includes many whole foods, healthy fats, fiber and lean protein, are associated with better mental health than unhealthy eating patterns, such as typical western diet. , which includes many processed foods, sugar and saturated fats. In fact, several Australian studies have found significant reductions in depressive symptoms among participants when diet quality was improved.
What needs to change?
So how bad is our diet? In the UK we consume, on average, twice the recommended amount of added sugar (it should be no more than 5 per cent of caloric intake), just three of our five daily intakes of fruit and vegetables, just 19g of fiber up to date. day (the recommendation is 30g/day) and just over a third of the recommended 280g/week of fish. The blame for this could be laid at many doors – the lack of access to healthy, affordable food, the need for stricter legislation on processed foods – but ultimately we have a responsibility to ourselves and to those we feed to eat a healthy and balanced diet. diet.
And it is well worth the effort. A 2022 study found that switching from a typical Western diet to one with a higher intake of whole grains, legumes, fish, fruits, vegetables and nuts while reducing red and processed meats, sugary drinks and refined grains could increase life expectancy by 10.7 years. for women and 13 years for men.
Fortunately, all it takes to turn things around is some basic nutritional knowledge, a well-stocked pantry, and a little time spent planning and preparing meals. Your path to a healthier, more balanced diet starts here.
What is a balanced diet?
A balanced diet is one that meets all of a person’s nutritional needs, with the appropriate combination of macronutrients (carbohydrates, proteins and fats) and micronutrients (vitamins and minerals). According to nutritionist and author Dale Pinnock, also known as “the medicinal chef” and creator of the new online weight management program The Metabolic Fix. It simply means a return to basics.
“Focus on building your diet around whole foods, the kind of things your great-grandparents would have eaten. Fruits, vegetables, nuts, seeds, whole grains, lean proteins and high-quality vegetables and healthy fats. If you do it right, you will win 95 percent of the battle.”
This sounds like good old-fashioned common sense, so how are we getting it so wrong? According to a recent government report, to get the country’s diet back on track, fruit and vegetable consumption would have to increase by 30 percent, fiber consumption by 50 percent, while foods high in saturated fat, salt and sugar would have to be eliminated. decreased by 25 percent and meat consumption fell by 30 percent. It is worth considering this information in the context of your own diet to see where improvements can be made.
Why is a balanced diet important?
A balanced diet is the cornerstone of good health. In the short term, you will sleep better, feel more alert and positive, and have sustained energy throughout the day. In the long term, eating well improves gut health, supports immunity, and protects against many chronic diseases, such as heart disease, diabetes, and cancer. But it’s not just about the obvious health benefits of a balanced diet, there are also wider lifestyle benefits to be had.
“You may be more inclined to exercise or hydrate properly if you take the time to consider your dietary options,” says registered dietitian Ro Huntriss. “Spending more time on meals and what you eat can also make cooking or eating a more social time and can improve relationships, if this is something you enjoy doing together with your partner, family or friends.”
The importance of calorie/energy balance
Traditional thinking holds that our weight is simply a function of the calories we eat versus the calories we burn, also known as the energy/balance equation, but as Huntriss points out, the picture is more complex than this and what we eat must be considered. along with the amount we eat.
“Fruits and vegetables are rich in nutrients but low in calories, so they can be consumed in relatively large quantities. Whole grain carbohydrates provide slow-release energy throughout the day, reducing cravings. Eating enough lean, plant-based protein helps keep you full and supports muscle mass, which in turn supports your metabolic rate, meaning you can burn energy while you’re at rest. “Healthy fats are nutritionally important, but they should be consumed in smaller quantities as they are high in calories.”
A balanced diet can help you lose weight
Focusing on the quality of our diet instead of traditional calorie restriction is an idea that is gaining ground for weight loss.
“The food choices we make influence all the important factors of weight control,” says Pinnock, “from the hormones used in food metabolism, such as insulin, leptin and ghrelin, to how effectively we we can exercise and recover, and how well we sleep. and manage stress.”
Another crucial element when it comes to losing weight is satiety or how full we feel after eating. Restrictive or very low-calorie diets can make us feel hungry all the time. On the contrary, by consuming lean protein at every meal and including fiber and healthy fats, our appetite is much better regulated and we are less likely to experience cravings and subsequently overeat. For example, a slice of whole wheat toast topped with canned sardines and served with a tossed salad provides fabulous nutrition, is very filling, and provides only 350 calories.
The importance of portion control
Overeating any food will jeopardize the variety of your diet since you won’t be as hungry for other foods and may have other negative consequences.
“Portion control is an integral part of a balanced meal,” advises Pinnock. “Overeating any food, healthy or not, can lead to weight gain.”
In fact, there are some healthy foods that are extremely caloric, so it’s important to watch portion sizes when monitoring your weight. For example, walnuts contain 180 calories per 30g and a medium-sized avocado has 320 calories.
An easy way to control portions when trying to lose weight is to use the 20 percent rule. Try eating 20 percent less food than usual, wait, and then eat more only if you’re really still hungry.
What are the components of a balanced diet?
The best practical way to ensure you are eating a balanced diet is to think about the relative proportions of the different food groups that make up your meal. Pinnock has a foolproof method for this called the perfect plate system.
“Fill half your plate with non-starchy vegetables, such as leafy greens, broccoli, and cauliflower. Fill a quarter of your plate with high-fiber, slow-burning carbohydrates, such as brown rice, quinoa, or root vegetables. In the remaining quarter, have a serving of high-quality protein: meat, fish, eggs, tofu or tempeh. Composing meals this way will increase satiety hormones, stabilize blood sugar, and provide a high level of variety in your diet.”
How to Eat a Balanced Diet When Life Gets Hectic
Lack of time is often cited as the main obstacle to eating a balanced diet; In fact, our best intentions can go out the window when we’re busy. Don’t worry, our experts have some top tips to stay on track when you’re short on time.
“I’m a fan of batch cooking, as organization is key,” says Pinnock. “When you have a little time on the weekend, cook your favorite meals in three, four, or even five times the normal amount and then freeze individual portions. You will soon fill your freezer with healthy homemade food.”
Huntriss swears by planning and shopping ahead each week and eliminating unhealthy snacks. “Plan your meals and snacks for the week and buy the ingredients you need in advance to meet them. This avoids the temptation of takeout and ready meals. Choose healthy snacks such as Greek yogurt, fruit, vegetables with hummus or a handful of nuts. “It’s very easy to focus on balanced meals and continue mindless snacking, which can sabotage your diet.”
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-2,522,475,609,893,697,500
|
상세검색
최근 검색어 전체 삭제
다국어입력
즐겨찾기0
156897.jpg
KCI등재 학술저널
Immediate Moderate Intensity Treadmill Exercise After Restraint Stress Induced ERK-mediated Anxiety and Depression
PURPOSE Chronic stress cause physical and mental function disorders such as anxiety and depression. One of the effective ways to relieve this stress is regular moderate intensity exercise. However effect of exact role of moderate intensity exercise on physical and mental function is not clear. This study aim to investigate the effect of immediate moderate intensity exercise after stress on anxiety, depression-like behavior and motor ability. METHODS Six-week-old male wister rat were divided into three group which were control(CT) group, restraint stress (RS) group and treadmill exercise after restraint stress (EX) group. RS and EX group were subjected to re-straint stress (1h/day) for 5 days, while CT group were stay in normal condition. Immediate after restraint stress, EX group were subjected to treadmill-running (30min/day) for 5 days immediate after restraint stress. Free mov-ing tests and open field tests were used to analyze behavior and athletic competence such as anxiety and de-pression, and phosphorylation levels of ERK were assessed using western blotting of the brain hippocampus. RESULTS In free moving test, freezing time of EX group were increased compared to RS group(p<.05) and CT group(p<.05). On the other hand, Velocity of EX group were decreased compared to RS group(p<.05) and CT group(p<.05). In open field test, velocity, distance and frequency in center of RS group were lower than CT group(p<.05) and EX group were lower than ST group(p<.01). Phosphorylation of ERK were increased on EX group. CONCLUSIONS Immediate moderate intensity treadmill exercise after restraint stress increased anxiety and depression-like behavior and decreased motor ability. Furthermore, the activity of ERK protein associated with stress and depression was increased by immediate exercise after stress. The results suggest that immediate exer-cise after stress can lead to mental and physical depression.
서론
연구방법
결과
논의
결론
Acknowledgments
Conflicts of Interest
References
로딩중
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Longitudinal association between infant disorganized attachment and childhood posttraumatic stress symptoms.
@article{Macdonald2008LongitudinalAB,
title={Longitudinal association between infant disorganized attachment and childhood posttraumatic stress symptoms.},
author={Helen Z Macdonald and Marjorie Beeghly and Wanda Grant-Knight and Marilyn Augustyn and Ryan W. Woods and Howard J Cabral and Ruth Rose-Jacobs and Glenn N Saxe and Deborah A. Frank},
journal={Development and psychopathology},
year={2008},
volume={20 2},
pages={493-508}
}
The purpose of this study was to evaluate whether children with a history of disorganized attachment in infancy were more likely than children without a history of disorganized attachment to exhibit symptoms of posttraumatic stress disorder (PTSD) at school age following trauma exposure. The sample consisted of 78 8.5-year-old children from a larger, ongoing prospective study evaluating the effects of intrauterine cocaine exposure (IUCE) on children's growth and development from birth to… CONTINUE READING
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1
Is Oral Thrush A Progressive Disease & Alternative Treatments For It?
Oral yeast infection or oral thrush is a fungal infection caused by an overgrowth of the Candida fungus in the mouth, generating white plaques on the tongue and inside the cheeks. This fungus is normally found in our body both in the vaginal region, in the skin and the mouth, however, when the defenses (immune system and normal microflora) are low, the fungus can proliferate, generating this disease, being more common in babies and older people.
This infection has a cure and its treatment is carried out with the use of mouthwashes, antifungal and maintaining proper oral hygiene, and should be guided by a general practitioner or dentist.(1)
Is Oral Thrush A Progressive Disease?
Is Oral Thrush A Progressive Disease?
Oral thrush mostly does not lead to further serious health conditions. However, it may be very uncomfortable. For example, if the fungus spreads to your digestive tract, it may cause discomfort during swallowing. If left untreated, it may continue lasting for months to years. It should not be taken lightly, as there can be some root causes of oral fungal diseases that may have severe consequences.(2)
Alternative Treatments For Oral Thrush
Repeated episodes of oral thrush also a symptom of immune deficiency. Therefore, try to build your immune system through a healthy diet. Also, maintain good oral hygiene, exercise regularly and promote proper rest. You can use a few simple alternative treatments to control the infection and reduce symptoms.
Brush Your Teeth Twice A Day: If you do not have good oral hygiene, brushing your teeth twice a day and flossing daily are necessary and can cure oral thrush.
Consume Unsweetened Yogurt: Plain yogurt contains active cultures that return a healthy pH balance and normal bacterial flora in the mouth. Although yogurt does not cure thrush in adults, it may help your body to kill enough bacteria and it is a good start for treatment.
Acidophilus Bacteria: Taking acidophilus daily is a good treatment for thrush. Acidophilus is a powder that is generally presented as a capsule, available in health food or vitamin stores. Acidophilus contains ingredients similar to yogurt, which works in the same way, allowing your body to repel oral candidiasis bacteria in adults.
Salt: Salt can be used as an effective oral thrush remedy. It produces a fungus-unfriendly condition inside your mouth. Salt can aid in relieving the symptoms fast. Mixing one teaspoon of table salt in lukewarm water (about one cup) to gargle and then spit. It is also good to apply a little salt inside the oral cavity and on the tongue and keep it for some time (not more than several seconds). Then rinse thoroughly with lukewarm water.
Baking Soda: You can use baking soda as a safe and cost-effective oral thrush treatment. This destroys the yeast triggering the infection. Moreover, it helps maintain a good pH level in the mouth by neutralizing acids.
Coconut Oil: Coconut oil also has shown good effectiveness fighting against oral thrush aiding to eliminate the fungus and reduce the associated discomfort.
Cinnamon: Cinnamon is another effective home remedy to combat this oral yeast infection. The Candida albicans development can be regulated by its strong antifungal effects.
Apple Cider Vinegar: This has enzymes to restrict infection of candida helping to restore the pH level of the body which helps to fight against the fungus overgrowth causing infection. Besides, it aids in boosting your immune response and providing a robust defense to counter candida infection.
Tea Tree Oil: This oil is also very effective in treating oral yeast infection. It has strong antifungal action to control fungal growth allowing rapid recovery.
Further, limit your intake of sugary foods to prevent the growth of yeast. If you smoke, quit smoking as it can worsen the symptoms. Suck on ice or fresh ice to reduce discomfort. Regularly visit the dentist, specifically if you are diabetic or have dentures.(3)(4)(5)
References:
1. Rahmani F, Rezaei N. Refractory Oral Thrush. Pediatric Immunology: Springer; 2019:383-385.
2. Taylor M, Raja A. Oral Candidiasis (Thrush). StatPearls [Internet]: StatPearls Publishing; 2019.
3. Seboe P, Haller DM, Sommer JM, Excoffier S, Gaboreau Y, Maisonneuve H. General practitioners’ perspectives on the use of nonpharmacological home remedies in two regions in Switzerland and France. Swiss medical weekly. 2018;148:w14676.
4. De Silva T, Weerasekera M, Edirisinghe D, et al. Patients with Diabetes; Their Perception and Practices towards Oral Health. 2016.
5. Dilhari A, Weerasekera MM, Siriwardhana A, et al. Candida infection in oral leukoplakia: an unperceived public health problem. Acta Odontologica Scandinavica. 2016;74(7):565-569.
Also Read:
Team PainAssist
Team PainAssist
Written, Edited or Reviewed By: Team PainAssist, Pain Assist Inc. This article does not provide medical advice. See disclaimer
Last Modified On:May 6, 2020
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How To Tell If You Have Low Testosterone
Men usually suspect that they may have low testosterone when they start experiencing certain symptoms, such as lack of energy, a decrease in sex drive, or any of the symptoms listed here.
Some men will look up these symptoms online, while others may talk to their doctor about the symptoms.
Ultimately, whichever route you take, you will land up at the same point – you need a blood test.
This blood test will check the key indicators of low testosterone in your body, such as total testosterone.
Your doctor, endocrinologist, or medical facilitator will then make a decision, based on these indicators and your lab results.
Some doctors may resist giving you a blood test – if this occurs, read Dealing With Doctors That Resist Testosterone Replacement Therapy.
If you need help understanding the information provided in blood test results for low testosterone, see Understanding Your Blood Test Results For Low Testosterone.
/* ]]> */
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Since 1995 - Non Profit Healthcare Advice
Conversion disorder or stroke?
04/16/2007
Question:
Apologizes for reiterating questions already asked; weâre looking for more answers. Also sorry for writing too much, thought it would be better w/ a broader picture.
2 ½ months ago mom had severe r-sided weakness and fell to floor at work. 911 was called and arrived immediately. B/c her face was drooping and drooled, speech completely slurred, couldnât move at all, and BP was dangerously high â firemen said stroke and rushed her to hospital. She stayed overnight w/ several tests (CAT scan, MRI of neck and head, MRA, EKG, etc ?). Everything showed clearâ¦although she still had symptoms â along w/ r-sided weakness in leg, arm, shoulder, and hand, also had comprehension problems and couldnât understand commands. Mixed up words and it took awhile to formulate sentences.
Started intensive Speech, PT, and OT (recomm. by Dr. in hospital). All therapists agreed she displayed symptoms of stoke patient. Hand specialist performed pressure test showing she had less than 50% strength in r-hand. Wasnât able to go back to work since therapy was all she could do in one day, was extremely weak and grew tired very easily, and used mostly fine motor skills at work.
Second week we visited an Internal Dr. someone recommended. Mom didnât have reg. treating physician â since only 55 ys, in good health, doesnât smoke/drink, and takes vitamins and eats only healthy food daily. Only medical history was what we gave him (never had major health prob.s except for a few visual disturbances w/ jagged prism of colors some months prior to event, and old injuries caused by car accidents; and only family history is her dad had several strokes and seizures in the recent past…although he has also always been healthy).
So during visit, Dr. became very skeptical of situation b/c of tests run in the hospital. Wanted to write off her condition as being a âconversion disorder.â We didnât know anything about it, so went w/ it. Also said didnât want to write it in chart b/c he was still going to treat it as a stroke. Since BP was still extremely high and her blood work came back, went ahead and prescribed: an aspirin a day, blood pressure, heart, cholesterol, and anti-depressant medications. Also scheduled more tests.
Next week: more therapy, took meds, did some research on CD, and went back to Dr. Until now seen him about 4 times and every visit he gets more condescending and even down-right rude at times. He dismissed everything we told him including visual prob.s and therapistsâ reports. Says just about everything except calling her a liar to her faceâ¦.when we asked about his diagnosis. She works extremely hard in therapy and isnât someone you can just look at and tell has had a stroke, so at times people are questionable. He wants to see surveillance video from work and even claims being fatigued has nothing to do w/ stroke and that she should be fine by now.
Mom is very strong, independent, happy, educated person and feels heâs claiming all symptoms are basically âin her headâ. She doesnât get stressed easily and b/c we are spiritual we hand over our problems to God instead of becoming overly worried about themâ¦.so sheâs not the type to do something like this just for attention and never has been.
Then visited neurologist who ordered EEG w/ another MRI. Was polite and wanted to wait for new results before making any conclusions. First test not back, but we do have the MRI report. Iâve tried to read as much as possible but feel like Iâm going in circles. Her Dr. is not an end-all bad guy and at times can be charming, but is just stubborn and big-headed sometimes and doesnât want to back down. If possible donât want to change Dr.s this late, but will if all it means is better bed-side manners. Have another follow-up w/ him next week and was just wondering if you could help us interpret results or if you have any comments.
MRI findings: along with technical terms stating that she does have âsignificant bilateral foraminal stenosisâ and bone spurs, concerning her brain it states that âthere does appear to be some slight periventricular white matter changes in the deep white matter of the left frontal region.â
Does this mean that she had a stoke, and if notâ¦was it definitely a conversion disorder? What do we do next? Thanks for your time and consideration.
Answer:
Despite the extensive information provided, I cannot tell you if your mother’s event represents a conversion disorder or a stroke. The recent MRI and EEG results will be very helpful, but may still leave a lingering doubt. If the report is as you have written, it is not clear if they saw something in the left hemisphere that they feel is consistent with a new ischemic lesion (stroke) or not. It will probably be necessary for your neurologist to review the films him/herself to determine whether this lesion is related to the symptoms. The findings are in a location where they could potentially be related to the symptoms.
In either case, the symptoms are real–your mother is not normal, with right sided weakness. The problem lies in that the expected test results were not seen (an obvious stroke on the MRI). This is a difficult circumstance in medicine–physicians are troubled when they can’t clearly explain the symptoms.
A conversion disorder is defined by somatic symptoms without a clear cause, and thus is a consideration for your mother. Part of the definition is that the patient is not willingly “faking” the symptoms–they consider the symptoms quite real and are not actively trying to have or portray the symptoms. Typically, the physical symptoms are indicative of a psychological conflict or stress that the person cannot deal with cognitively, and the body’s way of dealing with the stress is to manifest physical symptoms. These conversion disorder symptoms typically get better if the conflict/stress is identified and the patient is able to confront and deal with the stressor. Often this is not obvious, and so conversion disorders are hard to treat. The lack of voluntary control of symptoms separates conversion disorder from malingering, in which symptoms are voluntarily portrayed for a secondary gain (a classic example of malingering is a student portraying illness to get out of taking an exam they didn’t study for).
Let’s presume for a minute that it is indeed a conversion disorder. As to how individual physicians deal with a potential conversion disorder, there is certainly a variety of responses. Some become frustrated with the patient and family. Some are quite uncomfortable being in a position where they can’t explain the symptoms with a biological problem. Some physicians and some allied health personnel are not aware of (or have never seen) a conversion disorder, and thus might inappropriately insist that a biological cause exists. A frank discussion of the symptoms with the physician, and trying to come to an understanding of the future care plan may be helpful.
I hope this helps.
For more information:
Go to the Stroke health topic.
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1a01aa77535b9ecfb87b9fc36adbcd2f
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2,569,067,446,898,378,000
|
Menopausal or Not? Discover the Role of Blood Tests
Menopause is a natural stage of life that marks the end of a woman’s reproductive years. It typically occurs between the ages of 45 and 55, but it can happen earlier or later. Blood tests are used to measure the levels of hormones in a woman’s blood to check for menopause. What it is: Menopause […]
Unlocking the Mystery: Understanding Women’s Hormones and Fertility Tests
Women’s hormones test is a group of blood tests used to measure the levels of various hormones in a woman’s body. The most commonly measured hormones include estrogen, prolactin, follicle-stimulating hormone (FSH), and luteinizing hormone (LH). If you are experiencing symptoms related to hormonal imbalances, such as hot flashes, irregular periods, or infertility, a women’s […]
Ovulation: Tracking Your Fertility with Blood Tests
What is Ovulation and when do you ovulate? Ovulation is the process of releasing a mature egg from the ovary into the fallopian tube. This process usually happens once in every menstrual cycle and is necessary for conception to take place. The ovary, which contains thousands of immature eggs, starts to prepare an egg for […]
Understanding the ovarian cancer tumour marker
Ovarian cancer symptoms: Ovarian cancer can be difficult to detect in its early stages because the symptoms are often vague and can be caused by other conditions as well. However, some common symptoms of ovarian cancer include: Abdominal bloating or swelling Pelvic pain or pressure Difficulty eating or feeling full quickly Changes in bowel habits, […]
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6e3c8d3593f3f69280bb5502b214ab8e
|
-3,768,779,100,375,232,500
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Can CBD Help with Anger Management? A Comprehensive Guide
This article explores the potential benefits of using CBD for anger management. We will provide a comprehensive guide for beginners, including an overview of CBD, how it works, its potential benefits, and risks and side-effects. Additionally, we will examine the existing research on CBD and anger management and provide testimonials and success stories from individuals using CBD for anger issues.
Proudly powered by WordPress | Theme: Courier Blog by Crimson Themes.
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|
9222580d47c553ea90dc0f5e416f8f3a
|
7,976,144,840,703,623,000
|
Skip to main content
Dietary regulation of PI3K/AKT/GSK-3β pathway in Alzheimer’s disease
Abstract
Alzheimer’s disease (AD) is characterized by the formation of senile plaques and neurofibrillary tangles composed of phosphorylated Tau. Several findings suggest that correcting signal dysregulation for Tau phosphorylation in AD may offer a potential therapeutic approach. The PI3K/AKT/GSK-3β pathway has been shown to play a pivotal role in neuroprotection, enhancing cell survival by stimulating cell proliferation and inhibiting apoptosis. This pathway appears to be crucial in AD because it promotes protein hyper-phosphorylation in Tau. Understanding those regulations may provide a better efficacy of new therapeutic approaches. In this review, we summarize advances in the involvement of the PI3K/AKT/GSK-3β pathways in cell signaling of neuronal cells. We also review recent studies on the features of several diets and the signaling pathway involved in AD.
Introduction
Alzheimer’s disease (AD) is neuro-pathologically characterized by the damage of neurons and synapses as well as the formation of senile plaques from amyloids and neurofibrillary tangles (NFTs) composed of hyper-phosphorylated Tau, which is the most prevalent cause of age-related dementia [13]. Soluble amyloid species, including oligomers, may alter hippocampal synaptic plasticity and impair memory [4, 5]. The hyper-phosphorylated Tau is the principal component of helical filaments in intracellular NFTs. Amyloid-beta (Aβ) deposition occurs prior to the accumulation of the hyper-phosphorylated Tau in the AD brain. Soluble Aβ oligomers isolated from the brain extract of patients with AD accelerate Tau hyper-phosphorylation [6, 7]. In spite of the observations representing the pathophysiological roles of soluble Aβ species in AD pathogenesis, how Aβ induces the hyper-phosphorylation of Tau in AD brains remains an unanswered question. Although research efforts have provided insights into the biology of AD, the underlying routes mediating the progressive decline in cognitive function are still poorly understood. The precise molecular events that control the death of neuronal cells with Aβ are unclear.
The characterization of full-length Tau has shown that the Tau protein can undergo many transitional conformations, and each of the conformations may represent a potentially toxic object. Accumulation of the misfolded Tau intermediates in the human brain causes tauopathies, the most common form of AD [8]. The PI3K/AKT/GSK-3β pathway appears to be crucial for AD because it promotes protein hyper-phosphorylation in Tau. In particular, glycogen synthase kinase-3β (GSK-3β) plays a key role in the neuronal response to stress by phosphorylating and compromising the transcriptional activity of the cAMP response element binding, which regulates the transcription of the brain-derived neurotrophic factor (BDNF) and other neuropeptides that are important in the regulation of long-term memory and in the maintenance of synaptic plasticity, thereby contributing to the pathology of neuronal degeneration [9, 10]. Furthermore, GSK-3β is probably the most documented kinase implicated in the abnormal hyper-phosphorylation of Tau protein.
Several potential preventive factors against AD have been suggested by epidemiological research, including modifiable lifestyle factors such as diet [11]. Researchers have demonstrated that dietary choices can play an important role in the neuroprotection of AD. Because many factors in life influence brain function, several interventions might be promising in the prevention of brain dysfunction in AD [12]. The main objective of this article is to review the studies linking potential protective factors to pathogenesis of AD, focusing particularly on the roles of the PI3K/AKT/GSK-3β pathway.
Tau phosphorylation involved in the PI3K/AKT/GSK-3β signaling pathway
Tau proteins are essential in assembly as well as maintenance of the structural integrity of microtubules [1315]. However, Tau is abnormally hyper-phosphorylated and aggregated in AD. Aβ induces neuronal death and hyper-phosphorylation of the Tau protein (Figure 1), which is the main event responsible for NFT formation in AD brains [16]. Previous studies have demonstrated differential roles of Tau phosphorylation at several phosphorylation sites. It is apparent that Tau phosphorylation at various sites influences Tau activity. A consequence of Tau hyper-phosphorylation in AD is a reduction in its ability to bind microtubules, a destabilization of microtubule network, NFT formation, and ultimately neuronal death [17]. Disordered microtubule-associated Tau proteins are susceptible to aggregation. Aberrant Tau hyper-phosphorylation is implicated in neurodegeneration in AD. Several kinases and phosphatases have been identified to regulate the phosphorylation of Tau. Tau has been found to be phosphorylated at over 30 serine/threonine residues in the brains of patients with AD, and approximately one half of these are canonical sites for proline-directed protein kinases, including GSK-3β, cyclin-dependent kinase 5, and p38 mitogen-activated protein kinase (p38-MAPK) [18, 19]. These kinases are involved primarily in Tau hyper-phosphorylation [20, 21]. Tau phosphorylation at the proline-rich region, which is located upstream of the microtubule-binding domains, inhibits its microtubule assembly activity moderately and promotes its self-aggregation slightly [22]. Tau phosphorylation at the C-terminal tail region increases its activity and promotes its self-aggregation markedly [23]. Tau phosphorylation at both of these regions plus the microtubule-binding region nearly diminishes its activity and disrupts microtubules. Abnormally hyper-phosphorylated Tau disengages from microtubules and then increased cytosolic concentrations of unbound Tau occur, resulting in NFT [24, 25]. Hyper-phosphorylated Tau is the major component of the paired helical filaments that accumulate in degenerating neurons in AD and other neurodegenerative diseases.
Figure 1
figure 1
Schematic representation of PI3K/AKT/GSK-3β signaling pathway in neuronal cells of Alzheimer’s disease. Examples of molecules known to act on the regulatory pathways are shown. Note that some critical pathways have been omitted for clarity. 5-HT, 5-hydroxytryptamine, serotonin; BDNF, brain-derived neurotrophic factor; CDK5, cyclin-dependent kinase 5; GSK-3β, glycogen synthase kinase-3β; IKK, IκB kinase; NF-κB, nuclear factor-kappa-B; p38-MAPK, p38 mitogen-activated protein kinase; PI3K, phosphoinositide-3 kinase; PP2A, protein phosphatase 2A; TrkB, tropomyosin-receptor-kinase B; TSP1, thrombospondin-1.
AKT inhibition may contribute to the decrease of Tau phosphorylation at Thr212 and Ser214 because these two sites are substrates of AKT[26, 27]. AKT phosphorylation is catalyzed mainly by phosphoinositide-3 kinase (PI3K)-phosphoinositide-dependent protein kinase-1 (PDK1). Phosphatidylinositol 3,4,5-triphosphate (PIP3) is the major second messenger of the PI3K pathway that mediates receptor tyrosine kinase signaling to the survival kinase AKT. Increased levels of PIP3 at the membrane cause pleck-strin-homology (PH) domain-containing proteins such as AKT and PDK1 to colocalize, resulting in the kinase-mediated phosphorylation and activation [28]. Thus, activated PI3K induces the activation of AKT, which phosphorylates various biological substrates, including GSK-3β. PI3K/AKT signaling pathway dysfunction causes GSK-3β activity increase and leads to Tau hyper-phosphorylation, the main component of NFT [29]. GSK-3β has been shown to phosphorylate Tau in intact cells on multiple sites, some of which are aberrant in the abnormally hyper-phosphorylated Tau protein, a critical event in AD pathogenesis. Accordingly, a PI3K inhibitor (such as wortmannin) increases Tau hyper-phosphorylation [30, 31]. In addition, a study has suggested that PI3K/AKT signaling is attenuated in the brains of patients with AD [32]. Generally, under an AKT-activated process, complete activation requires Ser473, so levels of Ser473 phosphorylation represent the degree of AKT phosphorylation. GSK-3β is rendered inactive when it is phosphorylated at Ser9 by activated AKT[33]. Schematic structures of human AKT 1 and GSK-3β protein are shown in Figure 2. The activated AKT phosphorylates target proteins involved in cell survival, cell cycling, angiogenesis, and metabolism for neuroprotection (Figure 1). In other words, selective downregulation of the AKT concurrent with elevated GSK-3β activity may be linked to brain dysfunctional pathogenesis. It has been shown that AKT activation may play a therapeutic role in neurodegenerative diseases [34]. AKT is an important regulator of cell survival and apoptosis. GSK-3β is ubiquitously active and is a critical effector of PI3K/AKT cellular signaling. Thus, several cellular processes such as cell metabolism, cell death, and survival depend on GSK-3β [35, 36].
Figure 2
figure 2
Schematic structures of human AKT1 and GSK-3β protein. The predicted consensual domain structures for each protein are depicted. The functionally important sites including the sites of protein phosphorylation are shown. Note that the sizes of protein are modified for clarity. GSK-3β, glycogen synthase kinase-3β; PH, pleck-strin-homology.
Protein phosphatase 2A (PP2A) is the major protein phosphatase in the brain that dephosphorylates Tau at several phosphorylation sites, thereby stopping the ability of Tau to inhibit microtubule assembly and to self-assemble into helical filaments and NFTs [37]. PP2A activity has been shown to be decreased in AD brains [38]. GSK-3β antagonized by PP2A regulates Tau phosphorylation at many sites. PP2A has been reported to dephosphorylate GSK-3β at Ser-9 [39]. In contrast, activation of GSK-3β can inhibit PP2A. The mammalian target of rapamycin (mTOR) also regulates the activity of PP2A, and the inhibition of the mTOR activates the PP2A [40]. When the PI3K/AKT/mTOR signaling is affected, a regulatory interaction between PP2A and GSK-3β, which ensures the steady Tau phosphorylation, changes [41]. This equilibrium seems to be established by the regulatory coupling of mTOR by a dephosphorylation of GSK-3β mediated by PP2A. Another regulatory factor for PP2A activity is peptidyl-prolyl cis-trans-isomerase 1 (Pin1), a phosphorylation-dependent prolyl cis/trans isomerase. This isomerase has been shown to stimulate the dephosphorylation of Tau by PP2A [42]. In Pin1 knockout mice, Tau is hyper-phosphorylated [43]. Pin1 also regulates Tau stability and phosphorylation dynamics [44]. Pin1 promotes amyloid precursor protein (APP) turnover by inhibiting GSK-3β activity [45]. Pin1 changes are a constant feature of AD pathology and could serve as a biomarker of the onset or spread of AD neuropathology [46]. Overexpressing Pin1 or preventing Pin1 inhibition might be a new approach to block tauopathy.
Some dietary agents may contribute to the regulation of the PI3K/AKT/GSK-3β pathway
Several medicinal herbs and foods may regulate the activity of the PI3K/AKT/GSK-3β pathway. Achyranthes bidentata Blume is a commonly prescribed Chinese medicinal herb. The Achyranthes bidentata polypeptides might exert their protective effects against neuronal apoptosis through modulation of the PI3K/AKT/GSK-3β pathway [47]. Phyllanthus niruri also activates the PI3K/AKT pathway. Puerarin, the main isoflavone glycoside found in the Chinese herb, functions through activation of PI3K/AKT signaling [48]. GSK-3β has been shown to be significantly inhibited by the treatment of berberine extracted from Coptis chinensis Franch, a Chinese medicinal herb [49]. In addition, dietary long-chain omega-3 polyunsaturated fatty acids may affect membrane-associated signaling proteins such as AKT[50]. Unfortunately, however, we have found no clinical application in the literature of these dietary agents against AD treatment. Lithium increases cell survival by inducing BDNF and thereby stimulating activity in anti-apoptotic pathways, including the PI3K/AKT pathway, which has been proposed to function as a neuroprotective agent that prevents neuronal apoptosis [5153]. Lithium is also known to both directly and indirectly regulate GSK-3β through activation of the PI3K/AKT and MAPK signaling pathways in neurons. This regulation of GSK-3β is believed to be one of the main mechanisms by which lithium effects its neuroprotective role, as regulation of the kinase leads to downstream expression of anti-apoptotic and cell survival genes. Lithium has been involved in GSK-3β-related reduction in glutamate activity involved in neuronal survival [54, 55].
Leptin signaling also induces the activation of the ubiquitous nutrient-sensitive PI3K/AKT/mTOR pathway. Studies have demonstrated that leptin induces the activation of AKT via phosphorylation of AKT at Ser473. As a consequence, AKT activation ensues upon leptin signaling, which results in inhibition of GSK-3β through phosphorylation at Ser9 residue [56]. Obviously, leptin also activates the serine/threonine kinase mTOR in the hypothalamus through the PI3K/AKT pathway [57]. The mTOR is an evolutionary conserved kinase that controls translation of several mRNA transcripts involved in cell growth and cell proliferation. Pathways activated by leptin terminate in the phosphorylation of the Tau kinase GSK-3β at Ser9 residue, leading to the inhibition of its kinase activity. Therefore, leptin induced activation of AKT, p38-MAPK, and Tau kinase GSK-3β signal transduction pathways [58]. Branched-chain amino acid leucine activates the intracellular mTOR signaling pathway [59], which is critical for initiating the protein translation process [60]. The dried root of Anthriscus sylvestris has been used in traditional drugs for the treatment of various diseases. Anthricin, which is a natural product isolated from A. sylvestris, is an inhibitor of mTOR [61].
Potential therapeutic approach of the dietary agents for the neuroprotection in Alzheimer’s disease via the inhibition of Tau-phosphorylation
The culinary herb sage (Salvia officinalis) may be effective for patients with mild to moderate AD [62]. Rosmarinic acid, a major ingredient of sage, reduced a number of events induced by Aβ, including Tau protein hyper-phosphorylation. These data show the neuroprotective effect of sage against Aβ-induced toxicity, which could validate the traditional use of this spice in the treatment of AD. The clinical relevance has been emphasized by the observation that patients did not experience any adverse effect while taking sage. Pharmacological activities of sage relevant to AD include antioxidant activity, anti-inflammatory effects, and cholinesterase inhibition and particularly its reputation for aiding memory [63]. However, despite these promising clinical observations, the precise mechanism for this herb remains elusive. Rosmarinic acid is also a major ingredient of lemon balm (Melissa officinalis), a plant that has shown promising signs of therapeutic activity in patients with AD. Main activities of rosmarinic acid include anti-inflammatory, antioxidant, antibacterial, and antiviral properties [64].
Curcumin, a component of turmeric, can also improve structure and plasticity of synapse and enhance learning and memory abilities [65]. Interestingly, curcumin enhances synaptic plasticity and cognitive function in rats [66], suggesting that curcumin may represent a potent therapeutic agent which exerts multiple beneficial effects. It is suggested that the neuroprotection of curcumin might be mediated via the PI3K/AKT signaling pathway [67]. Genistein potentiates the anti-cancer effects of gemcitabine in human osteosarcoma via the downregulation of the AKT pathway [68]. Long-term treatment with lithium has been shown to modify performance deficits in transgenic mice expressing human APP by inhibiting GSK-3β [69]. This improvement in performance was associated with an increased AKT activation and an improved GSK-3β phenotype in neurons.
Ghrelin amends the effect of high glucose on decreased neuronal Tau hyper-phosphorylation, which has a positive correlation with the degree of cognitive dysfunction. Leptin also increases synaptogenesis and aids in memory formation in the hippocampus and is purported to be a cognitive enhancer. Epidemiological studies have implicated decreased leptin levels in the pathogenesis of AD. The leptin levels are inversely related to the risk of developing dementia of the AD type [70]. Evidence suggests that leptin facilitates spatial learning and memory [71, 72] and also increases neurogenesis in mice. Leptin decreases hyper-phosphorylation of Tau by the activation of the signal transduction pathway coupled to leptin receptors, which eventually mitigates Tau phosphorylation. It was shown that leptin is more potent than insulin at mitigating Tau phosphorylation [73, 74]. Thus, neuroprotecton in AD could be performed by certain diets and medicines involved in the PI3K/AKT/GSK-3β pathway (Figure 3).
Figure 3
figure 3
Potential molecular targets based on the predominant PI3K/AKT/GSK-3β pathway. The targets suggest that certain diets and medicines may contribute to neuro-protection via modulating the function of AKT and GSK-3β in Alzheimer’s disease. Note that some critical events have been omitted for clarity. 5-HT, 5-hydroxytryptamine, serotonin; BDNF, brain-derived neurotrophic factor; GSK-3β, glycogen synthase kinase-3β; IKK, IκB kinase; NF-κB, nuclear factor-kappa-B; PI3K, phosphoinositide-3 kinase; PUFA, polyunsaturated fatty acid; SSRI, selective serotonin reuptake inhibitor; TrkB, tropomyosin-receptor-kinase B; TSP1, thrombospondin-1.
Perspective
Clarification of the molecular mechanisms by which extracellular Aβ induces the hyper-phosphorylation of Tau in the pathogenic pathway of AD is essential, and Tau may be responsive to pharmacological intervention before neurodegeneration occurs. Tau is abnormally hyper-phosphorylated at multiple phosphorylation sites, and thus loses its ability to bind to microtubules and is part of pathological lesions characterizing tauopathies in AD. Experimental studies have shown that Aβ induces Tau hyper-phosphorylation in a number of cell types. Incompetent activation of AKT/GSK-3β signaling may be relevant to Aβ-induced Tau phosphorylation. A coordinated regulation of PP2A and GSK-3β seems to ensure balanced Tau phosphorylation. This may help in preventing severe changes in Tau phosphorylation. It is conceivable that different pathways function in concert with Tau phosphorylation in the AD brain. Understanding the effects of Aβ on the hyper-phosphorylation of Tau may provide a new therapeutic approach. However, the pathology of AD is complex and may involve several different biochemical pathways, including defective Aβ protein metabolism and inflammatory, oxidative, and hormonal pathways. Consequently, these pathways are all potential targets for AD treatment and prevention strategies.
Diet usually consists of complex combinations of lipids or nutrients that might act synergistically or antagonistically. One of the pleiotropic properties of these foods could explain their disease protective potentials, which could be mediated through modulation of the PI3K/AKT/GSK-3β pathway. Although the precise mechanisms have not yet been clarified, correcting PI3K/AKT/GSK-3β signal dysregulation by certain dietary agents in the central nervous system may be a potential therapeutic approach for some patients with AD. Further mechanistic studies are needed in order to understand the precise molecular mechanisms and to determine whether an adequate dietary intake is related to improved brain function and to determine the role it plays regarding the preservation of brain health. Long-term clinical studies are mandatory to elucidate the effect of treatment in the management of AD.
Abbreviations
AD:
Alzheimer’s disease
APP:
Amyloid precursor protein
Aβ:
Amyloid-beta
BDNF:
Brain-derived neurotrophic factor
GSK-3β:
Glycogen synthase kinase-3β
mTOR:
Mammalian target of rapamycin
NFT:
Neurofibrillary tangle
p38-MAPK:
p38 mitogen-activated protein kinase
PDK1:
PI3K-phosphoinositide-dependent protein kinase-1
PI3K:
Phosphoinositide-3 kinase
Pin1:
Peptidyl-prolyl cis-trans-isomerase 1
PIP3:
Phosphatidylinositol 3,4,5-triphosphate
PP2A:
Protein phosphatase 2A.
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Acknowledgments
This work was supported by grants-in-aid from the Ministry of Education, Culture, Sports, Science and Technology in Japan and was supported in part by a grant from Nakagawa Masashichi Shoten Co., Ltd (Nara City, Nara, Japan).
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Correspondence to Satoru Matsuda.
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Yasuko Kitagishi and Satoru Matsuda contributed equally to this work.
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Kitagishi, Y., Nakanishi, A., Ogura, Y. et al. Dietary regulation of PI3K/AKT/GSK-3β pathway in Alzheimer’s disease. Alz Res Therapy 6, 35 (2014). https://doi.org/10.1186/alzrt265
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• DOI: https://doi.org/10.1186/alzrt265
Keywords
• Curcumin
• Berberine
• Rosmarinic Acid
• PP2A Activity
• Dietary Agent
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4,085,588,765,105,359,400
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What are CBD’s medical advantages?
What are CBD’s medical advantages?
Everyone benefits from both mental and physical health. It’s critical to maintain good health in order to live a happier life. People are becoming increasingly health aware. They might readily locate any of the options by conducting an internet search. They can learn how to eat well, do home workouts, and get a variety of other health-related advice. Some may recommend taking supplements, but doing so on a regular basis or without the guidance of a medical professional can have negative consequences for your health. Natural vitamins will always protect you from negative side effects. The cbd oil for pain is a hemp-based supplement.
CBD oil is being used by a growing number of people due to its numerousHere are some advantages to consider if you’re wondering why:
Alleviate pain:
The ability to reduce pain is one of the major advantages of CBD oil. Endocannabinoids create the neurotransmitter, which binds to cannabinoid receptors in the neurological system. The immune system, sleep, and pain are all regulated by this system. The cbd oil for pain interacts with the receptor and helps to relieve chronic pain, inflammation, muscular discomfort, and nerve pain.
cbd oil for pain
Anxiety and depression can be reduced:
Anxiety and depression illnesses affect the majority of people. They are frequently treated with prescription medicines, which can have negative side effects such as headaches, sleeplessness, and sleepiness. CBD oil, on the other hand, treats anxiety as well as sadness. This type of disease can be treated safely and organically.CBD oil is also used to treat post-traumatic stress disorder in youngsters.
Neuroprotective:
CBD interacts with the brain’s signalling system and the endocannabinoid system, making it useful in the treatment of neurological illnesses. CBD oil lowers muscle spasticity in persons with multiple sclerosis and is beneficial in treating epilepsy, brain stroke, and Parkinson’s disease.
Acne Control:
Acne is a widespread problem that affects people of all ages, from teenagers to adults. Bacteria, underlying inflammation, sebum production, and oil release in the skin are all elements that contribute to acne. CBD oil can help with this because of its anti-inflammatory qualities and ability to lower sebum production. CBD oil Toronto will undoubtedly persuade you of its numerous advantages.
Keep your heart healthy:
The next most important issue that people encounter is heart disease. This CBD oil has various health benefits, including cardiac, circulation, and blood pressure control. High blood pressure, on the other hand, is linked to a variety of health problems, including heart attacks and strokes.
Share
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Biologic effects of dental materials. 3. Toxicity and antimicrobial effect of endodontic antiseptics in vitro.
@article{Spngberg1973BiologicEO,
title={Biologic effects of dental materials. 3. Toxicity and antimicrobial effect of endodontic antiseptics in vitro.},
author={Lena Sp{\aa}ngberg and B Engstr{\"o}m and Kaare Langeland},
journal={Oral surgery, oral medicine, and oral pathology},
year={1973},
volume={36 6},
pages={856-71}
}
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Nuclear medicine techniques
Radionuclide ventriculography (sometimes known as MUGA) is a test that uses very small amounts of radioactive materials, called tracers, to make your heart and blood vessels visible. This test evaluates heart function. Perfusion scans will show the blood flow through the heart muscle and may detect areas of poor blood flow ischaemia . For both tests, tracers are injected into your vein and are tracked through the heart using special cameras or scanners.
You will usually be tested when you are resting and possibly again with exercise, or after taking certain medicines. You may be asked not to have any food or drink containing caffeine or alcohol for several hours before the tests. You should take your daily medicine, unless otherwise instructed.
Nuclear medicine techniques only carry a very low risk of complications, as the amount of radiation is so small.
© Siemens
Patient having the MUGA scan
© Texas Heart Institute
Example of a MUGA scan
Return to Common tests for heart failure
ESC Guidelines for Heart Failure
What patients need to know
This guide for patients from the European Society of Cardiology aims to provide an overview of the latest evidence-based recommendations for the diagnosis and treatment of heart failure.
In particular, it should help patients to understand the:
• main types of heart failure
• medicines used to treat heart failure
• devices that may be appropriate
• importance of rehabilitation
• management by a multidisciplinary team
• importance of self-care in managing your own condition
Learn more
AN ANIMATED JOURNEY THROUGH HEART FAILURE
A series of 9 simple, captivating animations explaining heart failure and its treatment.
These narrated animations explain how a healthy heart works, what happens to it in heart failure and how various treatments work to improve your health.
PATIENT AND CAREGIVERS VIDEOS
In this section you can watch, listen or read interviews with other people with heart failure and their caregivers.
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heartfailurematters.org is a European Society of Cardiology website
The heartfailurematters.org website was developed under the direction of the Heart Failure Association of the European Society of Cardiology (ESC). The ESC is a world leader in the discovery and dissemination of best practices in cardiovascular medicine. Our members and decision-makers are healthcare professionals who volunteer their time and expertise to represent professionals in the field of cardiology in Europe and beyond.
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Supplementary MaterialsBelow may be the image is definitely a web link to a higher resolution version Supplementary Shape 1: Viability of goat early-staged follicles predicated on trypan blue staining (nonviable cells). major, and supplementary) follicles are generally seen in goats (Lucci et al. 1999). 30 m (JPG 301?kb) 441_2008_613_Fig2_ESM.jpg (295K) GUID:?E1DAE269-8767-424D-B49C-B0E3F47FC4BC Supplementary Structure 1: Experiment 1: osmotic tolerance of early-staged follicles to NaCl, sucrose, and ethylene glycol (sucrose) ahead of freezing (DOC 33?kb) 441_2008_613_MOESM4_ESM.doc (33K) GUID:?98C6B494-F285-44AE-901C-19997838E397 Supplementary Structure 3: Test 3: comparison between sluggish and fast chilling of early-staged follicles Evista pontent inhibitor (sucrose) (DOC 33?kb) 441_2008_613_MOESM5_ESM.doc (33K) GUID:?41B8F450-149E-4D7C-85CE-0CFAE6173C07 Supplementary Structure 4: Test 4: in vitro culture of early-staged follicles (sucrose) (DOC 34?kb) 441_2008_613_MOESM6_ESM.doc (34K) GUID:?B721C734-963D-4022-97EE-1CCDABD3EFBE Abstract Isolated caprine early-staged follicles were submitted to osmotic tolerance tests in the current presence of sucrose, ethylene glycol (EG), or NaCl solutions and were subjected to and cryopreserved (by sluggish or fast chilling) in MEM alone or MEM supplemented with Evista pontent inhibitor sucrose, EG (1.0 or 4.0?M), or both. When follicles had been Evista pontent inhibitor subjected to 1.5?M NaCl, just 2% from the follicles were viable, whereas 87% from the follicles were viable after contact with 4.0?M EG. Concerning exposure time, the best percentage of practical follicles was obtained when follicles were exposed for 10?min to 1 1.0?M EG?+?0.5?M sucrose; exposure for 60 s to 4.0?M EG?+?0.5?M sucrose also maintained high percentage viability in follicles. Slow cooling in the presence of 1.0?M EG?+?0.5?M sucrose (75%) or rapid Evista pontent inhibitor cooling in the presence of 4.0?M EG?+?0.5?M sucrose (71%) resulted in a significantly higher proportion of viable follicles than all other treatments (at 40?m Open in a separate window Fig.?2 Viability based on trypan blue staining of isolated caprine early-staged follicles exposed to NaCl (experiment 1; ((((((((non-viable cells). a Positive control, Triton X-100 treated secondary follicle. b Viable secondary follicle. c Non-viable secondary follicle. 50?m (JPG 240?kb) Supplementary Figure 2(295K, jpg)Viability of goat early-staged follicles based on staining with Hoechst (all nuclei) and ethidium homodimer-1 (nuclei from dead cells). a, b Representative image of a viable primordial follicle. c, d Representative image of two non-viable primordial follicles. Follicle contains a viable oocyte, whereas fewer than 90% of granulosa cells are viable. Follicle contains three oocytes of which one has deteriorated, and fewer than 90% of granulosa cells are viable (oocytes). Note that polyovular healthy early-staged (primordial, primary, and secondary) follicles are commonly observed in goats (Lucci et al. Rabbit Polyclonal to GAS1 1999). 30 m (JPG 301?kb) Supplementary Scheme 1(29K, doc)Experiment 1: osmotic tolerance of early-staged follicles to NaCl, sucrose, and ethylene glycol (sucrose) prior to freezing (DOC 33?kb) Supplementary Scheme 3(33K, doc)Experiment 3: comparison between slow and rapid cooling Evista pontent inhibitor of early-staged follicles (sucrose) (DOC 33?kb) Supplementary Scheme 4(34K, doc)Experiment 4: in vitro culture of early-staged follicles (sucrose) (DOC 34?kb) Acknowledgements The authors thank Arend Rijneveld and Frans van Kooi for logistical help, Dr. Damien Paris for the English review, and two anonymous reviewers for their helpful suggestions. Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. Footnotes Electronic supplementary material The online version of this article (doi:10.1007/s00441-008-0613-9) contains supplementary material, which is available to authorized users..
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Recipe for a Successful Diet
Mark Sagor
/
Categories:
EAP
How do you like the idea of a diet that lets you eat as much as you want to and still realize a healthy weight loss? A diet which doesn’t require you to keep track of calories or points?
If you like this idea read on, because not only is there such a diet, but a prestigious medical journal has just published research which demonstrates the strategy’s effectiveness.
Before telling you about it I want to say that there is absolutely nothing wrong with counting points or calories as a dieting approach. It is an effective approach for a lot of people and, over the years I have been very impressed with the success of the Weight Watcher program which is firmly based in counting points.
Having said that, counting calories is not an approach which works for everyone (no approach does). So it’s always a good idea to have different weight loss strategies available so you can find the option that will work best for you.
Let’s return to the results of a new study published in the Journal of the American Medical Association. This was a large and well-designed study ($8 million in funding from the National Institute of Health) that carefully followed more than 600 people.
The researchers found that “people who cut back on added sugar, refined grains and highly processed foods while concentrating on eating plenty of vegetables and whole foods- without worrying about counting calories or limiting portion sizes lost significant amounts of weight over the course of a year.”
This result was equally true whether people followed diets that were mostly low in fat or mostly low in carbohydrates.
In other words, the research strongly supports the idea that it is diet quality, not diet quantity, which helps people lose and manage their weight most effectively in the long run.
What is unique about this weight-loss study was the fact that the researchers did not set specific or restrictive carbohydrate, fat or calorie limits on people. They told participants to eat as much as they wanted to of whole foods in order to avoid feeling hungry. As you might imagine the people in the study were relieved, as well as surprised, when they learned they did not need to focus on restricting or counting calories.
This is not to say that calories don’t matter. By the end of the study the participants ultimately ended up consuming fewer calories. The key point is that they accomplished this, not by counting calories, but by eating enough whole and nutritious foods to satisfy their hunger.
Recipe for a Successful Diet
-Unlimited fresh and whole foods
-Very small amount of added sugar
-Small pinch of processed foods
-Less refined grains
Combine these ingredients to lose weight, feel healthier and not feel hungry in the process.
If you would like additional information or support for implementing this approach to weight management (or any other approach for that matter) remember that many companies have Employee Assistance Programs (EAPS) that feature health coaching as part of their services to provide professional and personalized guidance on nutrition and diet.
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ABSTRACT
• Aarskog-Scott syndrome, or faciogenital dysplasia (FGDY), is an inherited disorder characterized by a distinguishing set of craniofacial and skeletal anomalies, disproportionate short stature, and urogenital malformations.
• X-linked recessive and autosomal dominant inheritance patterns have been described in FGDY, indicating the presence of genetic heterogeneity. Linkage mapping and positional cloning efforts in the proximal short arm of the X chromosome (Xp11.21) led to the isolation of the gene involved in the X-linked Aarskog-Scott syndrome (FGD1).
• In addition to a chromosomal translocation breakpoint, two different single-base insertional frameshift mutations in the FGD1 gene have been identified in patients with familial Aarskog-Scott syndrome.
• FGD1 encodes a guanine nucleotide exchange factor (GEF) that specifically activates Cdc42, a member of the Rho (Ras homology) family of the p21 GTPases. By activating Cdc42, FGD1 protein stimulates fibroblasts to form filopodia, cytoskeletal elements involved in cellular signaling, adhesion, and migration. Through Cdc42, FGD1 protein also activates the c-Jun N-terminal kinase (JNK) signaling cascade, a pathway that regulates cell growth, apoptosis, and cellular differentiation.
• FGD1 contains additional motifs commonly associated with signaling proteins, including a pleckstrin homology (PH) domain, an evolutionarily conserved phosphatidylinositol-3-phosphate-binding FYVE domain, and two potential Src-homology 3 (SH3) binding sites. These additional domains may function to regulate the activity and/or location of the FGD1 protein.
• Within the developing mouse skeleton, FGD1 protein is expressed in precartilaginous mesenchymal condensations, the perichondrium and periostium, proliferating chondrocytes, and osteoblasts. These results suggest that FGD1 signaling may play a role in the biology of several different skeletal cell types including mesenchymal prechondrocytes, chondrocytes, and osteoblasts. The characterization of the spatiotemporal pattern of FGD1 expression in mouse embryos has provided important clues to the understanding of the pathogenesis of Aarskog-Scott syndrome.
• It appears likely that the primary defect in Aarskog-Scott syndrome is an abnormality of FGD1/Cdc42 signaling resulting in anomalous embryonic development and abnormal endochondral and intramembranous bone formation.
CLINICAL FEATURES, DIAGNOSIS, AND THERAPY
In 1970, Dagfinn Aarskog observed the association of disproportionate short stature and certain anomalies of the face, hands, feet, and genitalia in seven males from two generations of the same family.1 A year later, Scott reported three brothers with similar features.2 Since these initial reports, well over 100 cases of Aarskog-Scott syndrome, or faciogenital dysplasia (FGDY), have been published.3,4 Two reports of similarly affected brothers with osteochondritis dissecans and facial anomalies had been made earlier.6,7 Aarskog observed that the inheritance of this condition was compatible with an X-linked recessive disorder.1 Most families segregating this disorder have displayed an apparent X-linked recessive pattern of inheritance.3 However, the observation that several pedigrees demonstrated apparent male-to-male transmission has suggested an autosomal dominant form of FGDY.8,9 Therefore, genetic heterogeneity is probable.
Physical Features of the Disorder
The Aarskog-Scott syndrome phenotype consists of a characteristic set of facial and skeletal anomalies, disproportionate short stature, and urogenital malformations. ...
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Select your timezone:
P11.42 (247.8 in Journal) Early Experience of 48-hour Normothermic Machine Perfusion in Human Kidneys Applying Urine Recirculation
Annemarie Weissenbacher, Austria
Consultant Surgeon
Department of Visceral, Transplant and Thoracic Surgery
Medical University of Innsbruck
Abstract
Early experience of 48-hour normothermic machine perfusion in human kidneys applying urine recirculation
Franka Messner1, Silvia Gasteiger1, Marlene Pühringer1, Afshin Soleiman2, Dietmar Öfner1, Stefan Schneeberger1, Annemarie Weissenbacher1.
1Department of Visceral, Transplant and Thoracic Surgery, Medical University of Innsbruck, Innsbruck, Austria; 2INNPATH, Institute of Pathology, Tirol Kliniken Innsbruck, Innsbruck, Austria
Introduction: Normothermic machine perfusion (NMP) of the kidney has been studied extensively during the past decade. Short-term kidney NMPhas demonstrated promising results, however currently transplant logistics cannot be improved and for organ treatment longer preservationperiods might be necessary. As a proof of principle, we aimed to achieve 48-hour NMP by applying urine recirculation (UR) with a commerciallyavailable perfusion device.
Methods: Discarded human kidneys were normothermically perfused on the XVIVO Kidney Assist perfusion device. The perfusate comprisedpacked red cells and 5% albumin. For volume management UR was applied. Air (21% O2) and CO2 were used for oxygenation of the circuit andmonitored with an in-line blood gas analyzer. Perfusate and urine samples as well as hemodynamics were regularly assessed.
Results: Five discarded human kidneys underwent kidney NMP following hypothermic machine perfusion (HMP) and static cold storage. All butone kidneys were DBD organs. Median donor age (range) was 62 (41-68) years. Median (IQR) CIT and HMP were 19.9 (12.1) h and 5 (7.2) h. AnNMP duration of 48 h could be achieved in all kidneys. All kidneys were urinating throughout with a median (IQR) output of 22.5 (30.5) ml/h.Overall median (IQR) arterial flow was 695 (383) ml/min. Median (IQR) pH was 7.2 (0.2). Overall median (IQR) perfusate sodium, chloride andpotassium were 161 (14.7) mmol/L, 124.5 (11.5) mmol/L, and 6.5 (2.7) mmol/L. Median (IQR) perfusate lactate over time was 109 (55.2) mg/dL.Median perfusate sodium and chloride were significantly higher than corresponding urine values (sodium: 130 (27) mmol/L, chloride: 120.5(11.8) mmol/L) over time (P = 0.02 and 0.04). Median arterial flow over time was significantly higher in NMP kidneys with lower perfusate sodiumlevels (p<0.001, correlations coefficient Spearman’s rho -0.461).
Conclusions: This early experience underlines the feasibility of extended ex-situ kidney NMP by applying UR. Hemodynamic stability and urineexcretion were achieved for 48 hours.
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Home » Frequently asked Questions on Health » Corneal grafting for myopia
Corneal grafting for myopia
Q: Kindly enlighten me if corneal grafting can be done to get normal vision for an extremely high myopic(>-12 D) and high astigmatic person in case other surgeries like LASIK are not suitable or fail.
A:Corneal grafting is not a refractive procedure and is not done unless there is corneal disease such as Kerotocunus.
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Posted: May 19th, 2017
You are responsible for reviewing the nursing unit’s refrigerator. Which of the following drug, if found inside the fridge, should be removed?
You are responsible for reviewing the nursing unit’s refrigerator. Which of the following drug, if found inside the fridge, should be removed?
A. Nadolol (Corgard)
B. Opened (in-use) Humulin N injection
C. Urokinase (Kinlytic)
D. Epoetin alfa IV (Epogen)
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Is Procrastination a Sign of ADHD in Adults?
Procrastination is a common behaviour characterised by the delay or postponement of tasks or decisions. While many regard it as a universal experience, for adults, it may sometimes stem from underlying psychological conditions, such as Attention Deficit Hyperactivity Disorder (ADHD). ADHD is a neurodevelopmental disorder traditionally associated with children but increasingly recognised in adults, with symptoms that include inattention, impulsiveness, and hyperactivity. These symptoms can adversely affect an adult's ability to manage time and may lead to habitual procrastination.
The link between adult ADHD and procrastination is not explicit as a diagnostic criterion, but the intersection of ADHD's core symptoms with procrastinatory behaviour is frequently observed in clinical settings. This includes challenges with organisational skills, prioritisation, and completion of tasks. Adults living with ADHD may find that procrastination is not a mere bad habit but rather a part of their daily struggle with focus and task initiation, leading to negative emotions and reduced productivity. Especially in cases of more severe ADHD, the tendency to procrastinate can be pronounced, requiring tailored management strategies to overcome.
Key Takeaways
• Procrastination in adults can be indicative of ADHD, affecting task management and productivity.
• ADHD in adults presents with symptoms that can contribute to habitual procrastination.
• Addressing procrastination in ADHD involves understanding the psychological impacts and developing specific management strategies.
Understanding ADHD in Adults
Attention deficit hyperactivity disorder (ADHD) in adults is characterised by persistent patterns of inattention or hyperactivity-impulsivity that interfere with functioning or development. Diagnosis can be challenging, as ADHD presents differently in adults compared to children.
Symptoms and Diagnosis
Adult ADHD encompasses a range of inattentive and hyperactive symptoms. For diagnosis, clinicians typically look for:
• Inattentive Symptoms:
• Often fails to give close attention to details or makes careless mistakes in work
• Frequently has difficulty sustaining attention in tasks or play activities
• Regularly does not seem to listen when spoken to directly
• Often does not follow through on instructions and fails to finish tasks
• Hyperactivity Symptoms:
• Often fidgets with or taps hands or feet or squirms in seat
• Frequently leaves seat in situations when remaining seated is expected
• Commonly feels restless or acts as if "driven by a motor"
For a diagnosis, the presence of such symptoms must be consistent for at least six months and they must be seen to clash with the individual's level of development.
ADHD Subtypes and Presentations
ADHD manifestations are divided into three subtypes. A proper diagnosis will identify one of the following presentations:
• Predominantly Inattentive Presentation: Where inattention symptoms stand out
• Predominantly Hyperactive-Impulsive Presentation: Where hyperactivity and impulsiveness predominate
• Combined Presentation: When both inattentive and hyperactive-impulsive symptoms are equally present
Understanding these presentations is crucial for tailoring treatment according to the subtype of ADHD diagnosed in an adult.
Procrastination and Its Relation to ADHD
Procrastination is often more than merely putting off tasks; for adults with ADHD, it can be a pervasive and distressing aspect of their lives. This section explores the chronic patterns of postponement and unpacks the psychological underpinnings related to ADHD.
Chronic Procrastination
Chronic procrastination in the context of ADHD manifests as a consistent, repetitive delay of tasks across various areas of life. It is not limited to everyday procrastination, which might occur sporadically for most individuals. Instead, adults with ADHD might experience academic procrastination, where educational pursuits are continuously deferred, or decisional procrastination, where the inability to make timely decisions impacts their effectiveness. The correlation between ADHD and chronic procrastination is frequently attributed to executive dysfunction, where individuals have trouble planning, organising and prioritising.
• Everyday procrastination: Struggling with daily responsibilities.
• Academic procrastination: Delay in academic-related tasks.
• Decisional procrastination: Difficulty in making prompt decisions.
The Psychology Behind Procrastination
Procrastination is not merely a time management issue; it is deeply rooted in the psychological profile of an adult with ADHD. It can stem from an aversion to tasks viewed as uninteresting or complex, leading to a lack of motivation. Additionally, impulsivity, a core symptom of ADHD, exacerbates the tendency to seek out immediate rewards over long-term goals, thus preferring more enjoyable activities over pending tasks. Despite understanding the importance of these tasks, the individual's ADHD brain may struggle with organising thoughts and prioritising tasks, which can result in postponement.
Challenges in Daily Living
Adults with ADHD may face significant challenges in managing daily activities due to procrastination. This often manifests in poor time management and negatively impacting relationships and workplace performance.
Trouble With Time Management
Adults with ADHD frequently struggle with time management. They can find it difficult to assess how much time tasks will take and may have trouble starting or completing tasks promptly. This is not simply due to poor planning but is also a result of difficulties with organising and prioritising their workload. Key strategies to address these issues include:
• Creating a structured schedule: Listing daily tasks with specific time allocations.
• Setting reminders: Using alarms or apps to prompt action on tasks.
Impact on Relationships and Workplace Performance
Procrastination linked to ADHD can seriously undermine one's relationships and workplace performance. The inability to complete projects by deadlines can increase stress and diminish a person's professional reputation in the workplace. In personal relationships, procrastination may lead to conflict or disappointment when commitments are unmet. Strategies to improve this include:
• Clear communication: Ensuring expectations are understood.
• Task delegation: Sharing responsibilities to manage workload effectively.
Managing ADHD and Overcoming Procrastination
Effective management of ADHD and its associated procrastination in adults requires a structured approach that includes practical strategies and clinical interventions. By utilising a combination of self-management techniques and professional treatments, individuals with ADHD can enhance their self-control and productivity.
Strategies for Better Self-Control
Individuals with ADHD often struggle with self-control, which can lead to a tendency to procrastinate. Establishing a daily routine can bolster organisation and reduce the likelihood of task avoidance. A helpful technique is the Pomodoro method, where tasks are divided into manageable intervals, traditionally 25 minutes long, followed by a short break. This can prevent feelings of overwhelm and aid in maintaining motivation.
Organisational tools are also indispensable for managing procrastination:
• To-do lists: can help an individual keep track of tasks.
• Prioritisation, such as labelling tasks by urgency, can direct attention effectively.
• Scheduling: blocking out time for specific tasks in a planner can help allocate attention where needed.
Role of Medication and Therapies
Medication, particularly stimulant medications, can play a significant role in the treatment of ADHD. They typically work by increasing the levels of certain neurotransmitters in the brain to improve concentration and impulse control, thus reducing procrastination.
Medication types to consider include:
• Methylphenidate
• Dexamfetamine
• Atomoxetine
Each medication comes with its own potential side effects, and it is crucial that they are prescribed and monitored by a healthcare professional. In addition to medication, therapy is often recommended. Cognitive-behavioural therapy (CBT) can support individuals in understanding and changing their procrastination behaviours. Occupational therapy may assist in developing organisational skills and strategies to manage daily activities more effectively.
The Psychological Impact of ADHD
Adults with ADHD often experience a range of psychological effects that stem from the core symptoms of the disorder itself. These effects include challenges to mental health, such as anxiety and depression, and can lead to a cycle of stress and emotional strain associated with procrastination and task avoidance.
Effects on Self-esteem and Mental Health
Adults with Attention Deficit Hyperactivity Disorder (ADHD) may find their self-esteem is frequently compromised by the ongoing difficulties they face in managing day-to-day tasks. Chronic inattention and impulsivity, characteristic of ADHD, often lead to missed deadlines and forgotten commitments, contributing to feelings of underachievement and failure. These experiences can erode self-confidence, sometimes resulting in low self-esteem. Mental health professionals recognise that this pattern of repeated struggles can also precipitate anxiety and depression, as individuals with ADHD may consistently perceive themselves as underperforming in various aspects of life.
The Emotional Toll of ADHD Related Procrastination
Procrastination is not simply a habit for those with ADHD but a direct consequence of the disorder's symptoms. The tendency to postpone tasks results in a build-up of functions that can seem insurmountable. This backlog can induce stress, guilt, and shame, further exacerbating the cycle of procrastination. The emotional toll is palpable, as adults with ADHD may berate themselves for their perceived laziness or inability to start or complete tasks. This cycle of avoidance and self-criticism can be particularly damaging and often calls for intervention by mental health professionals to break the pattern and develop more effective coping strategies.
Frequently Asked Questions
Identifying ADHD in adults can be challenging as it often presents differently than in children. Understanding these signs, particularly procrastination, is crucial in addressing adult ADHD effectively.
What are the primary indicators of ADHD in adults?
The key signs of ADHD in adults include inattention, hyperactivity, and impulsivity. However, symptoms may manifest as difficulty in managing time, staying organised, setting goals, and maintaining focus on tasks.
How does procrastination differ in adults with ADHD compared to those without?
In adults with ADHD, procrastination often stems from issues with executive function, such as task initiation and time management. For those without ADHD, procrastination might be due to a lack of interest or temporary avoidance of unpleasant tasks.
Can prolonged procrastination be a symptom of adult ADHD?
Yes, prolonged procrastination can be indicative of adult ADHD, mainly when it's associated with other symptoms like difficulty concentrating, restlessness, and impulsiveness, which disrupt day-to-day functioning.
In adults with ADHD, how does task paralysis manifest?
Task paralysis in adults with ADHD typically presents as an overwhelming inability to start or complete tasks, often leading to severe procrastination and compounded by a sense of frustration and decreased self-esteem.
What role does dopamine play in ADHD-related procrastination?
Dopamine, a neurotransmitter involved in motivation and reward, plays a significant role in ADHD. Its dysregulation in adults with ADHD can result in seeking immediate gratification, thus contributing to procrastination due to the inability to stay motivated for longer, less rewarding tasks.
Could consistent procrastination in adults be mistaken for laziness when it's actually attributable to ADHD?
Consistent procrastination in adults may often be misconstrued as laziness. However, when it is linked to ADHD, such behaviour is usually not a choice but rather a part of the symptomatic challenges associated with the condition, including issues with executive function.
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6e3c8d3593f3f69280bb5502b214ab8e
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-2,117,925,296,355,909,000
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Valproate activates bovine leukemia virus gene expression, triggers apoptosis, and induces leukemia/lymphoma regression in vivo.
A. Achachi, A.-F. Florins, N. Gillet, Christophe DEBACQ, Jean-Pierre Urbain, G. M. Foutsop, Fabian VANDERMEERS, A. Jasik, M. Reichert, P. Kerkhofs, L. Lagneaux, Arsène Burny, R Kettmann, L. Willems
Résultats de recherche: Contribution à un journal/une revueArticleRevue par des pairs
Résumé
[en] Leukemogenic viruses like human T-lymphotropic virus and bovine leukemia virus (BLV) presumably persist in the host partly by latent integration of the provirus in a fraction of infected cells, leading to accumulative increase in the outgrowth of transformed cells. Furthermore, viral infection also correlates with a blockade of the apoptotic mechanisms concomitant with an apparent latency of the host cell. Conceptually, induction of viral or cellular gene expression could thus also be used as a therapeutic strategy against retroviral-associated leukemia. Here, we provide evidence that valproate, an inhibitor of deacetylases, activates BLV gene expression in transient transfection experiments and in short-term cultures of primary B-lymphocytes. In vivo, valproate injection into newly BLV-inoculated sheep did not abrogate primary infection. However, valproate treatment, in the absence of any other cytotoxic drug, was efficient for leukemia/lymphoma therapy in the sheep model leading to decreased lymphocyte numbers (respectively from 25.6, 35.7, and 46.5 x 10(3) cells per mm3 to 1.0, 10.6, and 24.3 x 10(3) cells per mm3 in three leukemic sheep) and tumor regression (from >700 cm3 to undetectable). The concept of a therapy that targets the expression of viral and cellular genes might be a promising treatment of adult T cell leukemia or tropical spastic paraparesis/human T-lymphotropic virus-associated myelopathy, diseases for which no satisfactory treatment exists so far.
langue originaleAnglais
journalProceedings of the National Academy of Sciences of the United States of America
Volume102
Numéro de publication29
Les DOIs
Etat de la publicationPublié - 2005
Modification externeOui
Empreinte digitale
Examiner les sujets de recherche de « Valproate activates bovine leukemia virus gene expression, triggers apoptosis, and induces leukemia/lymphoma regression in vivo. ». Ensemble, ils forment une empreinte digitale unique.
Contient cette citation
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Why Those Expensive Spa Massages Count Every Pound!
It known today that a lot of of our diseases are psycho-somatic in the. What this means is that it should be our emotional well-being leading to health and well-being. Our illnesses are tied to the stress that feeling, based on to face in our daily lives.
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Truth: Studies show that massage reduces your heart rate, lowers blood pressure, increases circulation and lymph flow, relaxes muscles, makes you more alert and capable of working more effectively and reduces stress, anxiety and nerves.
Although 건마 can cover a collection of different in the body which a massage chair may not achieve, no-cost offer similar benefits. With today’s current technology, most chairs are fashioned to mimic certain massage styles like shiatsu massage. They can loosen and penetrate deep into the muscles, straightening out those lumps very much like a hand massage does.
However, happen to be a involving factors you need to ensure before getting into pregnancy massage therapies. Talk to your medical professional. Let your son or daughter give the go ahead to have a massage. Several high risk pregnancies additional conditions such as hypertension, high blood pressure it’s tough history of pre-term pregnancies which can adversely affect a woman’s body and lead to complications in case the body isn’t treated everything needed. A doctor always be able to reply your questions and advice you appropriately.
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{
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{
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{
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}
}
}
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b755ed28a90d11d590ef646404f4afc5
|
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