Citric acid (citrate) is a weak acid that is formed in the tricarboxylic acid cycle or that may be introduced with diet. The evaluation of plasma citric acid is scarcely used in the diagnosis of human diseases. On the contrary urinary citrate excretion is a common tool in the differential diagnosis of kidney stones, renal tubular acidosis and it plays also a role in bone diseases. The importance of hypocitraturia should be considered with regard to bone mass, urine crystallization and urolithiasis. (PMID 12957820) The secretory epithelial cells of the prostate gland of humans and other animals posses a unique citrate-related metabolic pathway regulated by testosterone and prolactin. This specialized hormone-regulated metabolic activity is responsible for the major prostate function of the production and secretion of extraordinarily high levels of citrate. The key regulatory enzymes directly associated with citrate production in the prostate cells are mitochondrial aspartate aminotransferase, pyruvate dehydrogenase, and mitochondrial aconitase. testosterone and prolactin are involved in the regulation of the corresponding genes associated with these enzymes. The regulatory regions of these genes contain the necessary response elements that confer the ability of both hormones to control gene transcription. Protein kinase c (PKC) is the signaling pathway for the prolactin regulation of the metabolic genes in prostate cells. testosterone and prolactin regulation of these metabolic genes (which are constitutively expressed in all mammalian cells) is specific for these citrate-producing cells. (PMID 12198595) Citric acid is found in citrus fruits, most concentrated in lemons and limes, where it can comprise as much as 8% of the dry weight of the fruit. Citric acid is a natural preservative and is also used to add an acidic (sour) taste to foods and soft drinks. The salts of citric acid (citrates) can be used as anticoagulants due to their calcium chelating ability. Intolerance to citric acid in the diet is known to exist. Little information is available as the condition appears to be rare, but like other types of food intolerance it is often described as a "pseudo-allergic" reaction.
Cytidine monophosphate, also known as 5'-cytidylic acid and abbreviated CMP, is a nucleotide. It is an ester of phosphoric acid with the nucleoside cytidine. CMP consists of the phosphate group, the pentose sugar ribose, and the nucleobase cytosine. Cytidine monophosphate (CMP) is derived from cytidine triphosphate (CTP) with subsequent loss of two phosphates. The synthesis of the pyrimidines CTP and UTP occurs in the cytoplasm and starts with the formation of carbamoyl phosphate from glutamine and CO2. Next, aspartate undergoes a condensation reaction with carbamoyl-phosphate to form orotic acid. In a subsequent cyclization reaction, the enzyme Aspartate carbamoyltransferase forms N-carbamoyl-aspartate which is converted into dihydroorotic acid by Dihydroorotase. The latter is converted to orotate by Dihydroorotate oxidase. Orotate is covalently linked with a phosphorylated ribosyl unit with Orotate phosphoribosyltransferase (aka "PRPP transferase") catalyzing reaction, yielding orotidine monophosphate (OMP). Orotidine-5-phosphate is decarboxylated by Orotidine-5'-phosphate decarboxylase to form uridine monophosphate (UMP). UMP is phosphorylated by two kinases to uridine triphosphate (UTP) via two sequential reactions with ATP. CTP is subsequently formed by amination of UTP by the catalytic activity of CTP synthetase. Cytosine monophosphate (CMP) and uridine monophosphate (UMP) have been prescribed for the treatment of neuromuscular affections in humans. Patients treated with CMP/UMP recover from altered neurological functions. Additionally, the administration of CMP/UMP appears to favour the entry of glucose in the muscle and CMP/UMP may be important in maintaining the level of hepatic glycogen constant during exercise. [PMID:18663991].
Cystathionine is a dipeptide formed by serine and homocysteine. Cystathioninuria is a prominent manifestation of vitamin-B6 deficiency. The transsulfuration of methionine yields homocysteine, which combines with serine to form cystathionine, the proximate precursor of cysteine through the enzymatic activity of cystathionase. In conditions in which cystathionine gamma-synthase or cystathionase is deficient, for example, there is cystathioninuria. Although cystathionine has not been detected in normal human serum or plasma by most conventional methods, gas chromatographic/mass spectrometric methodology detected a mean concentration of cystathionine in normal human serum of 140 nM, with a range of 65 to 301 nM.567 Cystathionine concentrations in CSF have been 10, 1, and 0.5 uM, and "not detected." Only traces (i.e., <1 uM) of cystathionine are present in normal CSF.587. gamma-Cystathionase deficiency provided the first instance in which, in a human, the major biochemical abnormality due to a defined enzyme defect was clearly shown to be alleviated by administration of large doses of pyridoxine. The response in gamma-cystathionase-deficient patients is not attributable to correction of a preexisting deficiency of this vitamin. (OMMBID, Chap. 88).
Deoxyadenosine is a derivative of the nucleoside adenosine. It is composed of adenine attached to a deoxyribose moiety via a N9-glycosidic bond. Deoxyribose differs from ribose by the absence of oxygen in the 3' position of its ribose ring. Deoxyadenosine is a critical component of DNA. When present in sufficiently high levels, deoxyadensoine can act as an immunotoxin and a metabotoxin. An immunotoxin disrupts, limits the function, or destroys immune cells. A metabotoxin is an endogenous metabolite that causes adverse health effects at chronically high levels. Chronically high levels of deoxyadenosine are associated with adenosine deaminase (ADA) deficiency, an inborn error of metabolism. ADA deficiency damages the immune system and causes severe combined immunodeficiency (SCID). People with SCID lack virtually all immune protection from bacteria, viruses, and fungi. They are prone to repeated and persistent infections that can be very serious or life-threatening. These infections are often caused by "opportunistic" organisms that ordinarily do not cause illness in people with a normal immune system. The main symptoms of ADA deficiency are pneumonia, chronic diarrhea, and widespread skin rashes. The mechanism by which dATP functions as an immunotoxin is as follows: because deoxyadenosine is a precursor to dATP, a buildup of dATP in cells inhibits ribonucleotide reductase and prevents DNA synthesis, so cells are unable to divide. Since developing T cells and B cells are some of the most mitotically active cells, they are unable to divide and propagate to respond to immune challenges. High levels of deoxyadenosine also lead to an increase in S-adenosylhomocysteine, which is toxic to immature lymphocytes.
Galactitol or dulcitol is a sugar alcohol that is a metabolic breakdown product of galactose. Galactose is derived from lactose in food (such as dairy products). When lactose is broken down by the enzyme lactase it produces glucose and galactose. Galactitol has a slightly sweet taste. It is produced from galactose in a reaction catalyzed by aldose reductase. When present in sufficiently high levels, galactitol can act as a metabotoxin, a neurotoxin, and a hepatotoxin. A neurotoxin is a compound that disrupts or attacks neural cells and neural tissue. A hepatotoxin as a compound that disrupts or attacks liver tissue or liver cells. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of galactitol are associated with at least two inborn errors of metabolism, including galactosemia and galactosemia type II. Galactosemia is a rare genetic metabolic disorder that affects an individual's ability to metabolize the sugar galactose properly. Excess lactose consumption in individuals with galactose intolerance or galactosemia activates aldose reductase to produce galactitol, thus depleting NADPH and leading to lowered glutathione reductase activity. As a result, hydrogen peroxide or other free radicals accumulate causing serious oxidative damage to various cells and tissues. In individuals with galactosemia, the enzymes needed for the further metabolism of galactose (galactose-1-phosphate uridyltransferase) are severely diminished or missing entirely, leading to toxic levels of galactose 1-phosphate, galactitol, and galactonate. High levels of galactitol in infants are specifically associated with hepatomegaly (an enlarged liver), cirrhosis, renal failure, cataracts, vomiting, seizure, hypoglycemia, lethargy, brain damage, and ovarian failure.
Ethanol is a clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. Indeed, ethanol has widespread use as a solvent of substances intended for human contact or consumption, including scents, flavorings, colorings, and medicines. Ethanol has a depressive effect on the central nervous system and because of its psychoactive effects, it is considered a drug. Ethanol has a complex mode of action and affects multiple systems in the brain, most notably it acts as an agonist to the GABA receptors. Death from ethanol consumption is possible when blood alcohol level reaches 0.4%. A blood level of 0.5% or more is commonly fatal. Levels of even less than 0.1% can cause intoxication, with unconsciousness often occurring at 0.3-0.4 %. Ethanol is metabolized by the body as an energy-providing carbohydrate nutrient, as it metabolizes into acetyl CoA, an intermediate common with glucose metabolism, that can be used for energy in the citric acid cycle or for biosynthesis. Ethanol within the human body is converted into acetaldehyde by alcohol dehydrogenase and then into acetic acid by acetaldehyde dehydrogenase. The product of the first step of this breakdown, acetaldehyde, is more toxic than ethanol. Acetaldehyde is linked to most of the clinical effects of alcohol. It has been shown to increase the risk of developing cirrhosis of the liver, multiple forms of cancer, and alcoholism. Industrially, ethanol is produced both as a petrochemical, through the hydration of ethylene, and biologically, by fermenting sugars with yeast. Small amounts of ethanol are endogenously produced by gut microflora through anaerobic fermentation. However most ethanol detected in biofluids and tissues likely comes from consumption of alcoholic beverages. Absolute ethanol or anhydrous alcohol generally refers to purified ethanol, containing no more than one percent water. Absolute alcohol is not intended for human consumption. It often contains trace amounts of toxic benzene (used to remove water by azeotropic distillation). Consumption of this form of ethanol can be fatal over a short time period. Generally absolute or pure ethanol is used as a solvent for lab and industrial settings where water will disrupt a desired reaction. Pure ethanol is classed as 200 proof in the USA and Canada, equivalent to 175 degrees proof in the UK system.
gamma-Aminobutyric acid (GABA) is an inhibitory neurotransmitter found in the nervous systems of widely divergent species, including humans. It is the chief inhibitory neurotransmitter in the vertebrate central nervous system. In vertebrates, GABA acts at inhibitory synapses in the brain. It acts by binding to specific transmembrane receptors in the plasma membrane of both pre- and postsynaptic neurons. This binding causes the opening of ion channels to allow either the flow of negatively-charged chloride ions into the cell or positively-charged potassium ions out of the cell. This will typically result in a negative change in the transmembrane potential, usually causing hyperpolarization. Three general classes of GABA receptor are known (PMID: 10561820). These include GABA-A and GABA-C ionotropic receptors, which are ion channels themselves, and GABA-B metabotropic receptors, which are G protein-coupled receptors that open ion channels via intermediaries known as G proteins (PMID: 10561820). Activation of the GABA-B receptor by GABA causes neuronal membrane hyperpolarization and a resultant inhibition of neurotransmitter release. In addition to binding sites for GABA, the GABA-A receptor has binding sites for benzodiazepines, barbiturates, and neurosteroids. GABA-A receptors are coupled to chloride ion channels. Therefore, activation of the GABA-A receptor induces increased inward chloride ion flux, resulting in membrane hyperpolarization and neuronal inhibition (PMID: 10561820). After release into the synapse, free GABA that does not bind to either the GABA-A or GABA-B receptor complexes can be taken up by neurons and glial cells. Four different GABA membrane transporter proteins (GAT-1, GAT-2, GAT-3, and BGT-1), which differ in their distribution in the CNS, are believed to mediate the uptake of synaptic GABA into neurons and glial cells. The GABA-A receptor subtype regulates neuronal excitability and rapid changes in fear arousal, such as anxiety, panic, and the acute stress response (PMID: 10561820). Drugs that stimulate GABA-A receptors, such as the benzodiazepines and barbiturates, have anxiolytic and anti-seizure effects via GABA-A-mediated reduction of neuronal excitability, which effectively raises the seizure threshold. GABA-A antagonists produce convulsions in animals and there is decreased GABA-A receptor binding in a positron emission tomography (PET) study of patients with panic disorder. Neurons that produce GABA as their output are called GABAergic neurons and have chiefly inhibitory action at receptors in the vertebrate. Medium spiny neurons (MSNs) are a typical example of inhibitory CNS GABAergic cells. GABA has been shown to have excitatory roles in the vertebrate, most notably in the developing cortex. Organisms synthesize GABA from glutamate using the enzyme L-glutamic acid decarboxylase and pyridoxal phosphate as a cofactor (PMID: 12467378). It is worth noting that this involves converting the principal excitatory neurotransmitter (glutamate) into the principal inhibitory one (GABA). Drugs that act as agonists of GABA receptors (known as GABA analogs or GABAergic drugs), or increase the available amount of GABA typically have relaxing, anti-anxiety, and anti-convulsive effects. GABA is found to be deficient in cerebrospinal fluid and the brain in many studies of experimental and human epilepsy. Benzodiazepines (such as Valium) are useful in status epilepticus because they act on GABA receptors. GABA increases in the brain after administration of many seizure medications. Hence, GABA is clearly an antiepileptic nutrient. Inhibitors of GAM metabolism can also produce convulsions. Spasticity and involuntary movement syndromes, such as Parkinson's, Friedreich's ataxia, tardive dyskinesia, and Huntington's chorea, are all marked by low GABA when amino acid levels are studied. Trials of 2 to 3 g of GABA given orally have been effective in various epilepsy and spasticity syndromes. Agents that elevate GABA are also useful in lowering hypertension. Three grams orally have been effective in controlling blood pressure. GABA is decreased in various encephalopathies. GABA can reduce appetite and is decreased in hypoglycemics. GABA reduces blood sugar in diabetics. Chronic brain syndromes can also be marked by deficiencies of GABA. Vitamin B6, manganese, taurine, and lysine can increase both GABA synthesis and effects, while aspartic acid and glutamic acid probably inhibit GABA effects. Low plasma GABA has been reported in some depressed patients and may be a useful trait marker for mood disorders. GABA has an important role in embryonic development, especially facial development, as substantiated by the association of a cleft palate in transgenic mice deficient in GAD67 (glutamate decarboxylase). A recent Japanese population study reported linkage in patients with a nonsyndromic cleft lip with or without a cleft palate and specific GAD67 haplotypes (PMID: 23842532). Unusually high levels of GABA (especially in the brain) can be toxic and GABA can function as both a neurotoxin and a metabotoxin. A neurotoxin is a compound that damages the brain and/or nerve tissue. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of GABA are associated with at least five inborn errors of metabolism, including D-2-hydroxyglutaric aciduria, 4-hydroxybutyric aciduria/succinic semialdehyde dehydrogenase deficiency, GABA-transaminase deficiency, homocarnosinosis, and hyper beta-alaninemia. Nearly all of these conditions are associated with seizures, hypotonia, intellectual deficits, macrocephaly, encephalopathy, and other serious neurological or neuromuscular problems. Increased levels of GABA seem to alter the function of the GABA-B receptor, which may play a role in the tonic-clonic seizures that are often seen in patients with the above disorders.
Glycerylphosphorylethanolamine, also known as gpea, belongs to the class of organic compounds known as organic phosphoramides. These are organic compounds containing the phosphoric acid amide functional group. Glycerylphosphorylethanolamine is soluble (in water) and a moderately acidic compound (based on its pKa). Glycerylphosphorylethanolamine has been found in human brain, prostate and liver tissues. Within the cell, glycerylphosphorylethanolamine is primarily located in the cytoplasm. Glycerylphosphorylethanolamine exists in all living organisms, ranging from bacteria to humans. In humans, glycerylphosphorylethanolamine is involved in phospholipid biosynthesis pathway. Glycerylphosphorylethanolamine is a membrane breakdown product resulting from the cleavage of the lipid group from glycerophosphoethanlomine fatty acids (i.e. phosphatidylethanolamine). It acts as a growth stimulant for hepatocytes.
Homovanillic acid is a dopamine metabolite occurring in human biofluids. A high proportion of patients with neuroblastoma excrete increased amounts of it in their urine. Homovanillic acid is a major catecholamine metabolite. It is used as a reagent to detect oxidative enzymes.(Wikipedia).
Glyoxylic acid or oxoacetic acid is an organic compound that is both an aldehyde and a carboxylic acid. Glyoxylic acid is a liquid with a melting point of -93°C and a boiling point of 111°C. It is an intermediate of the glyoxylate cycle, which enables certain organisms to convert fatty acids into carbohydrates. The conjugate base of glyoxylic acid is known as glyoxylate (PMID: 16396466). In humans, glyoxylate is produced via two pathways: (1) through the oxidation of glycolate in peroxisomes and (2) through the catabolism of hydroxyproline in mitochondria. In the peroxisomes, glyoxylate is converted into glycine by glyoxylate aminotransferase (AGT1) or into oxalate by glycolate oxidase. In the mitochondria, glyoxylate is converted into glycine by mitochondrial glyoxylate aminotransferase AGT2 or into glycolate by glycolate reductase. A small amount of glyoxylate is converted into oxalate by cytoplasmic lactate dehydrogenase. Glyoxylic acid is found to be associated with primary hyperoxaluria I, which is an inborn error of metabolism. Under certain circumstances, glyoxylate can be a nephrotoxin and a metabotoxin. A nephrotoxin is a compound that causes damage to the kidney and kidney tissues. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. High levels of glyoxylate are involved in the development of hyperoxaluria, a key cause of nephrolithiasis (commonly known as kidney stones). Glyoxylate is both a substrate and inductor of sulfate anion transporter-1 (SAT-1), a gene responsible for oxalate transportation, allowing it to increase SAT-1 mRNA expression, and as a result oxalate efflux from the cell. The increased oxalate release allows the buildup of calcium oxalate in the urine, and thus the eventual formation of kidney stones. As an aldehyde, glyoxylate is also highly reactive and will modify proteins to form advanced glycation products (AGEs).
Folic acid is a member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by dihydrofolate reductase. These folic acid congeners are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids, methylated tRNA, and generate and use formate. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia.
Glucose is a monosaccharide containing six carbon atoms and an aldehyde group and is therefore referred to as an aldohexose. The glucose molecule can exist in an open-chain (acyclic) and ring (cyclic) form, the latter being the result of an intramolecular reaction between the aldehyde C atom and the C-5 hydroxyl group to form an intramolecular hemiacetal. In water solution both forms are in equilibrium and at pH 7 the cyclic one is the predominant. Glucose is a primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. In animals glucose arises from the breakdown of glycogen in a process known as glycogenolysis. Glucose is synthesized in the liver and kidneys from non-carbohydrate intermediates, such as pyruvate and glycerol, by a process known as gluconeogenesis.
Glycine is a simple, nonessential amino acid, although experimental animals show reduced growth on low-glycine diets. The average adult ingests 3 to 5 grams of glycine daily. Glycine is involved in the body's production of DNA, phospholipids and collagen, and in release of energy. Glycine levels are effectively measured in plasma in both normal patients and those with inborn errors of glycine metabolism. (http://www.dcnutrition.com/AminoAcids/) Nonketotic hyperglycinaemia (OMIM 606899) is an autosomal recessive condition caused by deficient enzyme activity of the glycine cleavage enzyme system (EC 2.1.1.10). The glycine cleavage enzyme system comprises four proteins: P-, T-, H- and L-proteins (EC 1.4.4.2, EC 2.1.2.10 and EC 1.8.1.4 for P-, T- and L-proteins). Mutations have been described in the GLDC (OMIM 238300), AMT (OMIM 238310), and GCSH (OMIM 238330) genes encoding the P-, T-, and H-proteins respectively. The glycine cleavage system catalyses the oxidative conversion of glycine into carbon dioxide and ammonia, with the remaining one-carbon unit transferred to folate as methylenetetrahydrofolate. It is the main catabolic pathway for glycine and it also contributes to one-carbon metabolism. Patients with a deficiency of this enzyme system have increased glycine in plasma, urine and cerebrospinal fluid (CSF) with an increased CSF: plasma glycine ratio. (PMID 16151895).
Fructose 6-phosphate is an important intermediate in the Carbohydrates pathway. The interconversion of glucose-6-phosphate and fructose-6-phosphate, the second step of the Embden-Meyerhof glycolytic pathway, is catalyzed by the enzyme phosphoglucose isomerase (PGI). In gluconeogenesis, fructose-6-phosphate is the immediate precursor of glucose-6-phosphate (wikipedia).
Glutathione is a compound synthesized from cysteine, perhaps the most important member of the body's toxic waste disposal team. Like cysteine, glutathione contains the crucial thiol (-SH) group that makes it an effective antioxidant. There are virtually no living organisms on this planet-animal or plant whose cells don't contain some glutathione. Scientists have speculated that glutathione was essential to the very development of life on earth. glutathione has many roles; in none does it act alone. It is a coenzyme in various enzymatic reactions. The most important of these are redox reactions, in which the thiol grouping on the cysteine portion of cell membranes protects against peroxidation; and conjugation reactions, in which glutathione (especially in the liver) binds with toxic chemicals in order to detoxify them. glutathione is also important in red and white blood cell formation and throughout the immune system. glutathione's clinical uses include the prevention of oxygen toxicity in hyperbaric oxygen therapy, treatment of lead and other heavy metal poisoning, lowering of the toxicity of chemotherapy and radiation in cancer treatments, and reversal of cataracts. (http://www.dcnutrition.com/AminoAcids/) glutathione participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase. It is also important as a hydrophilic molecule that is added to lipophilic toxins and waste in the liver during biotransformation before they can become part of the bile. glutathione is also needed for the detoxification of methylglyoxal, a toxin produced as a by-product of metabolism. This detoxification reaction is carried out by the glyoxalase system. Glyoxalase I (EC 4.4.1.5) catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II (EC 3.1.2.6) catalyzes the hydrolysis of S-D-Lactoyl-glutathione to glutathione and D-lactate. GSH is known as a substrate in both conjugation reactions and reduction reactions, catalyzed by glutathione S-transferase enzymes in cytosol, microsomes, and mitochondria. However, it is also capable of participating in non-enzymatic conjugation with some chemicals, as in the case of n-acetyl-p-benzoquinone imine (NAPQI), the reactive cytochrome P450-reactive metabolite formed by acetaminophen, that becomes toxic when GSH is depleted by an overdose (of acetaminophen). glutathione in this capacity binds to NAPQI as a suicide substrate and in the process detoxifies it, taking the place of cellular protein thiol groups which would otherwise be covalently modified; when all GSH has been spent, NAPQI begins to react with the cellular proteins, killing the cells in the process. The preferred treatment for an overdose of this painkiller is the administration (usually in atomized form) of N-acetylcysteine, which is used by cells to replace spent GSSG and renew the usable GSH pool. (http://en.wikipedia.org/wiki/glutathione).
Glycerol 3-phosphate is a chemical intermediate in the glycolysis metabolic pathway. It is commonly confused with the similarly named glycerate 3-phosphate or glyceraldehyde 3-phosphate. Glycerol 3-phosphate is produced from glycerol, the triose sugar backbone of triglycerides and glycerophospholipids, by the enzyme glycerol kinase. Glycerol 3-phospate may then be converted by dehydrogenation to dihydroxyacetone phosphate (DHAP) by the enzyme glycerol-3-phosphate dehydrogenase. DHAP can then be rearranged into glyceraldehyde 3-phosphate (GA3P) by triose phosphate isomerase (TIM), and feed into glycolysis. The glycerol 3-phosphate shuttle is used to rapidly regenerate NAD+ in the brain and skeletal muscle cells of mammals (wikipedia).
Glucuronic acid is a carboxylic acid that has the structure of a glucose molecule that has had its sixth carbon atom (of six total) oxidized. The salts of glucuronic acid are known as glucuronates. Glucuronic acid is highly soluble in water. In humans, glucuronic acid is often linked to toxic or poisonous substances to allow for subsequent elimination, and to hormones to allow for easier transport. These linkages involve O-glycosidic bonds. The process is known as glucuronidation, and the resulting substances are known as glucuronides (or glucuronosides). Glucuronidation uses UDP-glucuronic acid (glucuronic acid linked via a glycosidic bond to uridine diphosphate) as an intermediate. UDP-glucuronic acid is formed in the liver of all animals.
Guanidoacetic acid is a metabolite in the Urea cycle and metabolism of amino groups, and in the metabolic pathways of several amino acids. This includes glycine, serine, threonine, arginine and proline metabolism. Guanidinoacetic acid is also a precursor of creatine, an essential substrate for muscle energy metabolism.
Homogentisic acid, also known as melanic acid, is an intermediate in the breakdown or catabolism of tyrosine and phenylalanine. It is generated from the compound p-hydroxyphenylpyruvate through the enzyme p-hydroxyphenylpyruvate dehydrogenase. The resulting homogentisic acid is then broken down into 4-maleylacetoacetate via the enzyme homogentisate 1,2-dioxygenase. Homogentisic acid is also found in other organisms. For instance, it can found in Arbutus unedo (strawberry-tree) honey, in the bacterial plant pathogen Xanthomonas campestris as well as in the yeast Yarrowia lipolytica where it is associated with the production of brown pigments. Homogentisic acid can be oxidatively dimerized to form hipposudoric acid, one of the main constituents of the 'blood sweat' of hippopotamuses. When present in sufficiently high levels, homogentisic acid can function as an osteotoxin and a renal toxin. An osteotoxin is a substance that causes damage to bones and/or joints. A renal toxin causes damage to the kidneys. Chronically high levels of homogentisic acid are associated with alkaptonuria (OMIM: 203500), an inborn error of metabolism. Alkaptonuria is a rare inherited genetic disorder in which the body cannot process the amino acids phenylalanine and tyrosine. It is caused by a mutation in the enzyme homogentisate 1,2-dioxygenase (EC 1.13.11.5), which leads to an accumulation of homogentisic acid in the blood and tissues. Homogentisic acid and its oxidized form benzoquinone acetic acid are excreted in the urine, giving it an unusually dark color. The accumulating homogentisic acid (and benzoquinone acetic acid) causes damage to cartilage (ochronosis, leading to osteoarthritis) and heart valves as well as precipitating as kidney stones and stones in other organs. More specifically, homogentisic acid can be converted to benzoquinone acetic acid (BQA), and the resulting BQA can be readily converted to polymers that resemble the dark skin pigment melanin. These polymers are deposited in the collagen, a connective tissue protein, of particular tissues such as cartilage. This process is called ochronosis (as the tissue looks ochre); ochronotic tissue is stiffened and unusually brittle, impairing its normal function and causing damage. Homogentisic acid is the primary precursor of melanin synthesis in Vibrio cholerae.


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Sussex theater to debut new original production
Jon Bleiweis
jbleiweis@dmg.gannett.com
The Bethany Area Repertory Theater is set to premiere its latest production, "An Affair to Forget" at the Dickens Parlour Theatre.
The play, written by the group's resident playwright, Bob Davis, is the final part of a trilogy of comedies featuring the Tomlinson family during different holiday celebrations.
While the trilogy's first two plays — "We Gather Together" and "Good King Succotash" — revolve around the family's Thanksgiving and Christmas, respectively, "An Affair to Forget" features a July 4 wedding.
The six-show run takes place April 21-23 and 28-30. Shows start at 7:30 p.m.
The play follows what Davis calls a dysfunctional family through their relationships. Anything that could possibly go wrong at the wedding does, he said.
"This isn't just theater," Davis said. "This is what happens in a lot of families and it's very funny."
The play is directed by first-time director Veronica Bona. She has been in BART plays in the past — including the trilogy's first two shows — and Davis said the group tries to get people involved in all aspects of the theater.
Bona is excited to make her directorial debut and believes there's something for everyone in "An Affair to Forget."
"You've got in-laws and outlaws and everybody in this world should feel connected to a part of this play," she said. "It takes you out of reality and into hilarity."
"An Affair to Forget" is the penultimate show of BART's off-season offerings before the summer. The season concludes with a production of Stephen Sondheim's "A Funny Thing Happened on the Way to the Forum" in June.
On Twitter @JonBleiweis and Facebook at Facebook.com/byjonbleiweis
"An Affair to Forget"
When: 7:30 p.m. April 21-23, 28-30
Where: Dickens Parlour Theatre, 35715 Atlantic Ave, Millville
Web: dptmagic.com

redpajama_set_name: RedPajamaCommonCrawl


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Home Site Directory Contacts Subscription RSS Twitter
Home » Commemorative coins of Ukraine and souvenir products
600 Years to the city of Chernivtsi
Putting into circulation : 20 May 2008
Denomination Metal Weight, g Diameter, mm Quality class of coinage Edge Mintage, pcs Actual, pcs
5 nickel silver 16.54 35,0 special uncirculated corrugated 45000 45000
Series: Ancient cities of Ukraine
The coin is dedicated to the city of Chernivtsi, an administrative, economic and cultural centre, one of picturesque cities of Ukraine, which is located on both banks of the river Prut in the foothills of the Carpathian Mountains. The first written mention of Chernivtsi was found in the charter of a Moldavian landlord Oleksander Dobryi in 1408, though according to archeological data this settlement above the river Prut was founded much earlier.
Retail price, Hryvnas: 51
On the coin obverse there is a depiction of a fret lantern (on the right), one of the symbols of the city, a fragment of the conventionalized ornament (on the left), which decorates the roof of Chernivtsi university and above there are: the small National Emblem of Ukraine and inscriptions: НАЦІОНАЛЬНИЙ/ БАНК/ УКРАЇНИ/ 5/ ГРИВЕНЬ/ 2008 (National Bank of Ukraine/ 5/ Hryvnia/ 2008) and the NBU Mint logotype.
On the coin reverse there is depicted a composition made of the outstanding historical and architectural monuments of the city and the inscription: ЧЕРНІВЦІ (Chernivtsi), beneath - 600/ років (600/ years).
Designer: Volodymyr Atamanchuk
Engraver: Volodymyr Atamanchuk
© National bank of Ukraine
Address: 9 Instytutska St., Kyiv 01601
Tel 0-800-505-240 (a 24-hour service), e-mail: nbu@bank.gov.ua
Created by "Softline" (Ukraine)


Have you ever been in an interview thinking "What am I doing here?" ... its probably a good thing if you have not been in such a scenario. I have been unfortunate enough to be in such a situation while being on both sides of the table viz., interviewee and interviewer. Being the interviewer is much more fun and a lot more relaxing.
Will post more my experiences as soon as I manage to reconcile those resumes.


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Q: Making Site A Use Site B's wp-content Folder I'm trying to synchronize two WordPress sites and on my way I've faced few challenges. One of the challenges is to either synchronize the wp-content folder of two sites or make one site use the wp-content of other site for ADDING and RETRIEVING multimedia content.
Normally a Wordpress site uses its own wp-content folder but how can we customize the WordPress so that it uses other site's wp-content folder.
Visuallization:-

Constraints:-

*

*Site A and Site B are on different shared web hostings. Each having its own Cpanel.

redpajama_set_name: RedPajamaStackExchange


It is a fact well known that elderly persons provide a large market for the travel industry globally. This can be attributed to a variety of contributory factors key of them been the availability of time to take vacations and capital thanks to solid pension schemes in developed countries which improves pensioners' financial independence and purchasing power considering that travel is not a cheap venture. However the likelihood of seniors to travel more than the younger generation cannot only be attributed to the availability of time and money alone. . Old age is characterized of numerous physical as well as mental health and psychological challenges. Scientific research has proved that travel brings with it numerous health benefits to this class of persons.
Travel and travel related activities involve numerous bodily movements. A walk through the park, the museum, historical sites, a swim in the warm ocean waters at a scenic beach, a late evening dance to some nice, slow, soft and soothing music provide the much needed exercise consequently contributing to the much needed bodily fitness.
A large percentage of persons within this class are retirees. Persons no longer engaged in active service. As such they spend most of their time idle resulting to reduced brain activity which is a major predisposing factor to mental conditions such as dementia. Viewing new sceneries and engaging tour guides while on travel to learn more increases their brain activity. Most of them are also subjected to loneliness in the event they happen to lack proper social and emotional support. This leads to depression and other related psychological conditions. Travelling exposes them to new life experiences and encounters hence reducing the chances of being lonely.
Elderly travel though advised should be precautionary. Pre-travel research and preparation is paramount. Visit your doctor for advice before travel, get the necessary prescriptions and travel insurance. Subscribe to activities that your state of health can accommodate to avoid injuries and always keep in touch with your relatives in case of an emergency.
Travel industry players benefit as much as the elderly creating a mutually beneficial relationship. As such 'prey like capitalization' such as asking them to pay more for travel insurance is quite regrettable and should be discouraged. Stakeholders need to be supportive and more accommodative. Tomorrow belongs to no one and since we might be beneficiaries of the same industry in future, it's only prudent that we change it for the better today.


I need to do a STD (sexual transmitted disease) test on Bali. Could anyone recommend me a good, safe and trustworthy hospital? Does anyones know how long it take to receive the test results? And what the price would be?
SOS internal hospital is probably the best, followed by BIMC (just search for the adresses by google).
Remember that tests for the most serious STD's (hepatitis B and C, HIV) can be false negative for the first three months..
Recommended by my insurance company Europeesche Verzekering. Been there for 3 days after an accident and had to have surgery. People speak reasonable - very good English.


Régal de Bourgogne is a delicious, fresh, triple-cream cheese from Burgundy. It is made with pasteurised or unpasteurised cows' milk.
Garlic, golden raisins that are macerated in eau-de-vie of Mirabelle and Marc de Bourgogne, fines herbes, mustard seeds, pepper, nuts, papaya or cranberries.
It is a small, round, artisan cheese which has been made by Fromagerie Delin in 1996.
If the Régal de Bourgogne cheese is not listed below, select a similar type of cheese from the list below to get a rough idea for the number of calories in Régal de Bourgogne cheese.


Tour merchandise for Foxing's 2016 tour.
Three color screen printed poster on Kraft Chipboard French Paper for Foxing's Spring Tour.
Six color t-shirt design for Foxing. Each of the sloths represents a different member of the band.


text:
package org.apache.jmeter.protocol.http.gui;

import java.awt.BorderLayout;
import java.awt.Component;
import java.awt.FlowLayout;
import java.awt.event.ActionEvent;
import java.awt.event.ActionListener;
import java.io.File;
import java.util.Iterator;

import javax.swing.BorderFactory;
import javax.swing.Box;
import javax.swing.JButton;
import javax.swing.JFileChooser;
import javax.swing.JLabel;
import javax.swing.JPanel;
import javax.swing.JScrollPane;
import javax.swing.JTable;
import javax.swing.ListSelectionModel;
import javax.swing.table.TableCellEditor;

import org.apache.jmeter.gui.util.FileDialoger;
import org.apache.jmeter.gui.util.HeaderAsPropertyRenderer;
import org.apache.jmeter.protocol.http.sampler.HTTPSamplerBase;
import org.apache.jmeter.protocol.http.util.HTTPFileArg;
import org.apache.jmeter.testelement.TestElement;
import org.apache.jmeter.util.JMeterUtils;
import org.apache.jorphan.gui.GuiUtils;
import org.apache.jorphan.gui.ObjectTableModel;
import org.apache.jorphan.reflect.Functor;

/*
 * Note: this class is currently only suitable for use with HTTSamplerBase.
 * If it is required for other classes, then the appropriate configure() and modifyTestElement()
 * method code needs to be written.
 */
/**
 * A GUI panel allowing the user to enter file information for http upload.
 * Used by MultipartUrlConfigGui for use in HTTP Samplers.
 */
public class HTTPFileArgsPanel extends JPanel implements ActionListener {

    private static final long serialVersionUID = 240L;

    /** The title label for this component. */
    private JLabel tableLabel;

    /** The table containing the list of files. */
    private transient JTable table;

    /** The model for the files table. */
    private transient ObjectTableModel tableModel; // only contains HTTPFileArg elements

    /** A button for adding new files to the table. */
    private JButton add;

    /** A button for browsing file system to set path of selected row in table. */
    private JButton browse;

    /** A button for removing files from the table. */
    private JButton delete;

    /** Command for adding a row to the table. */
    private static final String ADD = "add"; // $NON-NLS-1$

    /** Command for browsing filesystem to set path of selected row in table. */
    private static final String BROWSE = "browse"; // $NON-NLS-1$

    /** Command for removing a row from the table. */
    private static final String DELETE = "delete"; // $NON-NLS-1$

    private static final String FILEPATH = "send_file_filename_label"; // $NON-NLS-1$

    /** The parameter name column title of file table. */
    private static final String PARAMNAME = "send_file_param_name_label"; //$NON-NLS-1$

    /** The mime type column title of file table. */
    private static final String MIMETYPE = "send_file_mime_label"; //$NON-NLS-1$

    public HTTPFileArgsPanel() {
        this(""); // required for unit tests
    }

    /**
     * Create a new HTTPFileArgsPanel as an embedded component, using the
     * specified title.
     *
     * @param label
     *  the title for the component.
     */
    public HTTPFileArgsPanel(String label) {
        tableLabel = new JLabel(label);
        init();
    }

    /**
     * Initialize the table model used for the http files table.
     */
    private void initializeTableModel() {
        tableModel = new ObjectTableModel(new String[] {
                FILEPATH, PARAMNAME, MIMETYPE},
            HTTPFileArg.class,
            new Functor[] {
                new Functor("getPath"), //$NON-NLS-1$
                new Functor("getParamName"), //$NON-NLS-1$
                new Functor("getMimeType")}, //$NON-NLS-1$
            new Functor[] {
                new Functor("setPath"), //$NON-NLS-1$
                new Functor("setParamName"), //$NON-NLS-1$
                new Functor("setMimeType")}, //$NON-NLS-1$
            new Class[] {String.class, String.class, String.class});
    }

    public static boolean testFunctors(){
        HTTPFileArgsPanel instance = new HTTPFileArgsPanel(""); //$NON-NLS-1$
        instance.initializeTableModel();
        return instance.tableModel.checkFunctors(null,instance.getClass());
    }

    /**
     * Resize the table columns to appropriate widths.
     *
     * @param table
     *  the table to resize columns for
     */
    private void sizeColumns(JTable table) {
        GuiUtils.fixSize(table.getColumn(PARAMNAME), table);
        GuiUtils.fixSize(table.getColumn(MIMETYPE), table);
    }

    /**
     * Save the GUI data in the HTTPSamplerBase element.
     *
     * @param testElement
     */
    public void modifyTestElement(TestElement testElement) {
        GuiUtils.stopTableEditing(table);
        if (testElement instanceof HTTPSamplerBase) {
            HTTPSamplerBase base = (HTTPSamplerBase) testElement;
            int rows = tableModel.getRowCount();
            @SuppressWarnings("unchecked") // we only put HTTPFileArgs in it
            Iterator<HTTPFileArg> modelData = (Iterator<HTTPFileArg>) tableModel.iterator();
            HTTPFileArg[] files = new HTTPFileArg[rows];
            int row=0;
            while (modelData.hasNext()) {
                HTTPFileArg file = modelData.next();
                files[row++]=file;
            }
            base.setHTTPFiles(files);
        }
    }

    /**
     * A newly created component can be initialized with the contents of a
     * HTTPSamplerBase object by calling this method. The component is responsible for
     * querying the Test Element object for the relevant information to display
     * in its GUI.
     *
     * @param testElement the HTTPSamplerBase to be used to configure the GUI
     */
    public void configure(TestElement testElement) {
        if (testElement instanceof HTTPSamplerBase) {
            HTTPSamplerBase base = (HTTPSamplerBase) testElement;
            tableModel.clearData();
            for(HTTPFileArg file : base.getHTTPFiles()){
                tableModel.addRow(file);
            }
            checkDeleteAndBrowseStatus();
        }
    }

    /**
     * Enable or disable the delete button depending on whether or not there is
     * a row to be deleted.
     */
    private void checkDeleteAndBrowseStatus() {
        // Disable DELETE and BROWSE buttons if there are no rows in
        // the table to delete.
        if (tableModel.getRowCount() == 0) {
            browse.setEnabled(false);
            delete.setEnabled(false);
        } else {
            browse.setEnabled(true);
            delete.setEnabled(true);
        }
    }

    /**
     * Clear all rows from the table.
     */
    public void clear() {
        GuiUtils.stopTableEditing(table);
        tableModel.clearData();
    }

    /**
     * Invoked when an action occurs. This implementation supports the add and
     * delete buttons.
     *
     * @param e
     *  the event that has occurred
     */
    @Override
    public void actionPerformed(ActionEvent e) {
        String action = e.getActionCommand();
        if (action.equals(ADD)) {
            addFile(""); //$NON-NLS-1$
        }
        runCommandOnSelectedFile(action);
    }

    /**
     * runs specified command on currently selected file.
     *
     * @param command specifies which process will be done on selected
     * file. it's coming from action command currently catched by
     * action listener.
     *
     * @see runCommandOnRow
     */
    private void runCommandOnSelectedFile(String command) {
        // If a table cell is being edited, we must cancel the editing before
        // deleting the row
        if (table.isEditing()) {
            TableCellEditor cellEditor = table.getCellEditor(table.getEditingRow(), table.getEditingColumn());
            cellEditor.cancelCellEditing();
        }
        int rowSelected = table.getSelectedRow();
        if (rowSelected >= 0) {
            runCommandOnRow(command, rowSelected);
            tableModel.fireTableDataChanged();
            // Disable DELETE and BROWSE if there are no rows in the table to delete.
            checkDeleteAndBrowseStatus();
            // Table still contains one or more rows, so highlight (select)
            // the appropriate one.
            if (tableModel.getRowCount() != 0) {
                int rowToSelect = rowSelected;
                if (rowSelected >= tableModel.getRowCount()) {
                    rowToSelect = rowSelected - 1;
                }
                table.setRowSelectionInterval(rowToSelect, rowToSelect);
            }
        }
    }

    /**
     * runs specified command on currently selected table row.
     *
     * @param command specifies which process will be done on selected
     * file. it's coming from action command currently catched by
     * action listener.
     *
     * @param rowSelected index of selected row.
     */
    private void runCommandOnRow(String command, int rowSelected) {
        if (DELETE.equals(command)) {
            tableModel.removeRow(rowSelected);
        } else if (BROWSE.equals(command)) {
            String path = browseAndGetFilePath();
            tableModel.setValueAt(path, rowSelected, 0);
        }
    }

    /**
     * Add a new file row to the table.
     */
    private void addFile(String path) {
        // If a table cell is being edited, we should accept the current value
        // and stop the editing before adding a new row.
        GuiUtils.stopTableEditing(table);

        tableModel.addRow(new HTTPFileArg(path));

        // Enable DELETE (which may already be enabled, but it won't hurt)
        delete.setEnabled(true);
        browse.setEnabled(true);

        // Highlight (select) the appropriate row.
        int rowToSelect = tableModel.getRowCount() - 1;
        table.setRowSelectionInterval(rowToSelect, rowToSelect);
    }

    /**
     * opens a dialog box to choose a file and returns selected file's
     * path.
     *
     * @return a new File object
     */
    private String browseAndGetFilePath() {
        String path = ""; //$NON-NLS-1$
        JFileChooser chooser = FileDialoger.promptToOpenFile();
        if (chooser != null) {
            File file = chooser.getSelectedFile();
            if (file != null) {
                path = file.getPath();
            }
        }
        return path;
    }

    /**
     * Stop any editing that is currently being done on the table. This will
     * save any changes that have already been made.
     */
    protected void stopTableEditing() {
        GuiUtils.stopTableEditing(table);
    }

    /**
     * Create the main GUI panel which contains the file table.
     *
     * @return the main GUI panel
     */
    private Component makeMainPanel() {
        initializeTableModel();
        table = new JTable(tableModel);
        table.getTableHeader().setDefaultRenderer(new HeaderAsPropertyRenderer());
        table.setSelectionMode(ListSelectionModel.SINGLE_SELECTION);
        return makeScrollPane(table);
    }

    /**
     * Create a panel containing the title label for the table.
     *
     * @return a panel containing the title label
     */
    private Component makeLabelPanel() {
        JPanel labelPanel = new JPanel(new FlowLayout(FlowLayout.CENTER));
        labelPanel.add(tableLabel);
        return labelPanel;
    }

    /**
     * Create a panel containing the add and delete buttons.
     *
     * @return a GUI panel containing the buttons
     */
    private JPanel makeButtonPanel() {
        add = new JButton(JMeterUtils.getResString("add")); // $NON-NLS-1$
        add.setActionCommand(ADD);
        add.setEnabled(true);

        browse = new JButton(JMeterUtils.getResString("browse")); // $NON-NLS-1$
        browse.setActionCommand(BROWSE);

        delete = new JButton(JMeterUtils.getResString("delete")); // $NON-NLS-1$
        delete.setActionCommand(DELETE);

        checkDeleteAndBrowseStatus();

        JPanel buttonPanel = new JPanel();
        buttonPanel.setBorder(BorderFactory.createEmptyBorder(0, 10, 0, 10));
        add.addActionListener(this);
        browse.addActionListener(this);
        delete.addActionListener(this);
        buttonPanel.add(add);
        buttonPanel.add(browse);
        buttonPanel.add(delete);
        return buttonPanel;
    }

    /**
     * Initialize the components and layout of this component.
     */
    private void init() {
        JPanel p = this;

        p.setLayout(new BorderLayout());

        p.add(makeLabelPanel(), BorderLayout.NORTH);
        p.add(makeMainPanel(), BorderLayout.CENTER);
        // Force a minimum table height of 70 pixels
        p.add(Box.createVerticalStrut(70), BorderLayout.WEST);
        p.add(makeButtonPanel(), BorderLayout.SOUTH);

        table.revalidate();
        sizeColumns(table);
    }

    private JScrollPane makeScrollPane(Component comp) {
        JScrollPane pane = new JScrollPane(comp);
        pane.setPreferredSize(pane.getMinimumSize());
        return pane;
    }
}

redpajama_set_name: RedPajamaGithub


The new Matrix TF50 folding treadmill has a commercial grade belt and deck combination, a modern ergonomic design, and thoughtful engineering to provide a smooth, consistent, comfortable workout experience. Features a 3.25 chp motor, aluminum side rails, and welded steel frame for years of maintenance free use. 20″ x 60″ running surface fits users of any size comfortably. Folds up more vertical than most treadmills on the market for easier storage.
Choice of three different consoles to help keep you motivated and entertained. The Matrix TF50 has a gym-quality movement and feel. Wifi connectivity for use with ViaFit app and other online tracking programs, as well as entertainment apps and web browser capabilities which are available on some consoles.


text:
Q: I need to extract Data from a single line of json-data which is inbetween two variables (Powershell) I need to extract Data from a single line of json-data which is inbetween two variables (Powershell)
my Variables:
in front of Data:
DeviceAddresses":[{"Id":
after Data:
,"
I tried this, but there needs to be some error because of all the special characters I'm using:
$devicepattern = {DeviceAddresses":[{"Id":{.*?},"}
#$deviceid = [regex]::match($changeduserdata, $devicepattern).Groups[1].Value
#$deviceid

A: As you've found, some character literals can't be used as-is in a regex pattern because they carry special meaning - we call these meta-characters.
In order to match the corresponding character literal in an input string, we need to escape it with \ -

*

*to match a literal (, we use the escape sequence \(,

*for a literal }, we use \}, and so on...

Fortunately, you don't need to know or remember which ones are meta-characters or escapable sequences - we can use Regex.Escape() to escape all the special character literals in a given pattern string:
$prefix = [regex]::Escape('DeviceAddresses":[{"Id":')
$capture = '(.*?)'
$suffix = [regex]::Escape(',"')
$devicePattern = "${prefix}${capture}${suffix}"

You also don't need to call [regex]::Match directly, PowerShell will populate the automatic $Matches variable with match groups whenever a scalar -match succeeds:
if($changeduserdata -match $devicePattern){
  $deviceid = $Matches[1]
} else {
  Write-Error 'DeviceID not found'
}

For reference, the following ASCII literals needs to be escaped in .NET's regex grammar:
$ ( ) * + . ? [ \ ^ { |

Additionally, # and   (regular space character) needs to be escaped and a number of other whitespace characters have to be translated to their respective escape sequences to make patterns safe for use with the IgnorePatternWhitespace option (this is not applicable to your current scenario):
\u0009 => '\t'   # Tab
\u000A => '\n'   # Line Feed
\u000C => '\f'   # Form Feed
\u000D => '\r'   # Carriage Return

... all of which Regex.Escape() takes into account for you :)

A: To complement Mathias R. Jessen's helpful answer:
Generally, note that JSON data is much easier to work with - and processed more robustly - if you parse it into objects whose properties you can access - see the bottom section.
As for your regex attempt:

*

*Note: The following also applies to all PowerShell-native regex features, such as the -match, -replace, and -split operators, the switch statement, and the Select-String cmdlet.

*Mathias' answer uses [regex]::Escape() to escape the parts of the regex pattern to be used verbatim by the regex engine.

*

*This is unequivocally the best approach if those verbatim parts aren't known in advance - e.g., when provided via a variable or expression, or passed as an argument.

*However, in a regex pattern that is specified as a string literal it is often easier to individually \-escape the regex metacharacters, i.e. those characters that would otherwise have special meaning to the regex engine.

*

*The list of characters that need escaping is (it can be inferred from the .NET Regular-Expression Quick Reference):

*

*\ ( ) | . * + ? ^ $ [ {

*If you enable the IgnorePatternWhiteSpace option (which you can do inline with
(?x), at the start of a pattern), you'll additionally have to \-escape:

*

*#

*significant whitespace characters (those you actually want matched) specified verbatim (e.g., ' ', or via string interpolation,"`t"); this does not apply to those specified via escape sequences (e.g., \t or \n).

Therefore, the solution could be simplified to:
# Sample JSON
$changeduserdata = '{"DeviceAddresses":[{"Id": 42,"More": "stuff"}]}'

# Note how [ and { are \-escaped
$deviceId = if ($changeduserdata -match 'DeviceAddresses":\[\{"Id":(.*?),"') {
  $Matches[1]
}

Using ConvertFrom-Json to properly parse JSON into objects is both more robust and more convenient, as it allows property access (dot notation) to extract the value of interest:
# Sample JSON
$changeduserdata = '{"DeviceAddresses":[{"Id": 42,"More": "stuff"}]}'

# Convert to an object ([pscustomobject]) and drill down to the property
# of interest; note that the value of .DeviceAddresses is an *array* ([...]).
$deviceId = (ConvertFrom-Json $changeduserdata).DeviceAddresses[0].Id  # -> 42


Akira wants to create an awesome design tool for Linux that could compete with the likes of Figma, Sketch and Adobe XD. They need your help to achieve this goal. [Read more...] about Akira: The Linux Design Tool We've Always Wanted?


text:
Winter Park Complexes
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StayWinterPark Guest Guide App
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ABOUT STAYWINTERPARK
You are here: Home / Blog / Winter Park News / Top 12 Restaurant of the Month – The Tabernash Tavern
Winter Park News
Top 12 Restaurant of the Month – The Tabernash Tavern
Continuing my monthly review of the top restaurants in the valley, this month my wife and I chose The Tabernash Tavern. For those unfamiliar with the valley, this restaurant is "Located in beautiful lower downtown Tabernash", and I can attest that indeed it is located in Tabernash! (6 miles outside of Winter Park). I'm not so sure about the rest of the location details obviously written tongue-in-cheek, but if great food and a cozy ambience are what you're looking for, The Tavern is a real treat.
The reputation is borne of the Head Chef, Al Sapien, who formerly ran the Ranch House Restaurant at Devils Thumb, The Shed and then the Untamed Steakhouse in Winter Park, and has established such a following that it's kind of like a "if you open it, they will come" scenario. Well, it opened in June 2008 and I noticed that the Tavern has a Facebook page with 623 fans! That's quite a fan base.
It's definitely advisable to make a reservation ahead of time. In so doing, we were taken straight to our table in the main (front) part of the restaurant which is the place to be. With dark-stained wooden (cedar I think) walls, cathedral ceiling and spot lighting, the dining area has a very warm feel to it, and all around is an eclectic mix of old cooking utensils, skis, sleds, tankards, cans, posters and other items no doubt collected over the years.
Al's menu often changes, so don't necessarily rely on what's in the Menu Guide, or the telephone book if you're into advanced menu selections. What he does however (which also applies to the wine list) is to present a variety of International choices, drawn from past experience and travels abroad. After Thai curry mussels for appetizer, which were sublime, we had the Steak Mazatlan – very tasty and very filling by the way– and the Paella which was absolutely outstanding. A bottle of Benton-Lane Oregon Pinot Noir was the perfect accompaniment and it was somewhat disappointing we didn't have room for dessert as the choices were more than tempting. Perhaps we'll just go for beer, apps and a dessert next time.
All in all, a very nice evening out. Al has recently opened an Italian restaurant in Winter Park – called Aleberto's for some reason – which is where I think we're heading next month.
Verdict: highly recommended.
February 19, 2010 /1 Comment/by stevep
Love the Tabernash Tavern! And don't worry, the desserts are fantastic too!
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Winter Park Resort Hosts Annual NASTAR Championships March 25-28, 2010 Intrawest – the latest!


In this study, students of the Bible will find a detailed, systematic yet innovative and classical approach to the interpretation and exposition of this Psalm. Dr. Taylor has succeeded in journeying with the psalmist in the period before this contemporary era (BCE) creating a seamless connection with Jesus as the Good Shepherd and relating the events to Caribbean realities. He observes how the Psalmist's testimony of the goodness of God leads people to pay tribute to God for specific blessings experienced. He also challenges the reader to both ask God for blessings and acknowledge God for the blessings received. A tribute to God must stand on its own and become a part of the believer's spirituality as he relates to God.
"At many significant stages of the birthing and development of the Jamaican nation, the Rev. William Edwards has been eye-witness or participant, distant enough to give an angle which would not be found in the official records of some institutions... This book is an important and timely addition to the Jamaican and Caribbean ecclesiastical history as it chronicles the journey of an eye-witness, a pioneer, a candid and gifted story-teller. It offers a perspective on the history of important national and regional institutions such as Calabar High School, the Jamaica Baptist Union and the Bible Society of the West Indies. It is also a personal story told with the candor, which has always been a hallmark of Pastor Eddie."


text:
Patrick Colquhoun
Biography of Patrick Colquhoun
Patrick Colquhoun (1745-1820) was a colonial merchant in Glasgow. Born in Dumbarton, he served an apprenticeship as a sixteen-year-old in Virginia in North America. Likely working in a tobacco store, on his return to Glasgow he became one of the city's famous 'Tobacco Lords'. He had multiple commercial interests and was also a co-partner in the Glasgow-West India firm, Colquhoun & Ritchie, that traded with Jamaica and Antigua. As such, his wealth was derived from transatlantic slavery and its commerce.
In 1782 he built Kelvingrove House - in what is now Kelvingrove Park - as his residence. Colquhoun was Lord Provost of Glasgow, 1782-1784 and founder and the first Chairman of Britain's oldest Chamber of Commerce in Glasgow in 1783. He was an honorary graduate of the University (1797) and the Colquhoun Lectureship in Business History is named for him. He moved to London in 1789 where he became a magistrate and published pamphlets on policing and other social issues of the day.
Born 14 March 1745.
Died 25 April 1820.
University Link: Honorary Graduate
Occupation categories: merchants
NNAF Reference: GB/NNAF/P129829
View Major Archive Collection Record
Search for this person in the DNB
Record last updated: 1st Jul 2019
Honorary Graduate
Lectureships:
Colquhoun Lectureship in Business History


text:
Q: Launch meteor with a shell script I have no trouble starting my meteor server from the terminal window.  But surely I can do this from a shell script that I make with Automator.  This is what I do in the terminal window:
cd myAppName
meteor

For the the automator shell script, I change the directory differently:
cd /Users/myName/myAppName

... and that seems to work fine.  But the next line gives a "meteor --command not found" message.  I read somewhere that the shell that automator runs doesn't have access to the Environment variables that the terminal window uses.  That must be the problem.  So how do I run meteor from the shell script?

A: Try setting the PATH variable from inside your script. It should include the directory path to your meteor executable.
It should be something like:
export PATH=$PATH:/opt/meteor/bin/meteor

After that meteor should launch. If meteor starts launching but it fails then you're missing more environment variables inside your script and you must export them as you did with the PATH.
To know which environment variables you have in your shell type this:
set


Probe into US banks' Greek debt dealings | City A.M.
GOLDMAN Sachs is among Wall Street banks being investigated for helping Greece mask its alarming financial woes, US Federal Reserve boss Ben Bernanke revealed yesterday.
Bernanke said the Fed and the US Securities and Exchange Commission were "interested" in complex derivative deals arranged by the big banks for the previous Greek government.
Goldman Sachs is already being looked at by the European Union for a currency swap dating to 2001 that apparently allowed Greece to hide the bloating of its public deficit and national borrowing.
Earlier this week, Goldman Sachs co-chairman Gerald Corrigan insisted the structures put in place for Greece were "consistent" with regulations at the time. Other banks being examined are thought to include Morgan Stanley and JPMorgan.
The US authorities will particularly scrutinise Goldman's sale of $15bn (£9.8bn) of Greek gilts nine years ago after a loan-turned-currency swap.
The transaction, described as "just an ordinary swap" by then finance minister Yannos Papantoniou, did not legally have to be disclosed but allowed Athens to disguise the extent of its budget shortfall at a point when it had just joined the euro.
The news could hardly come at a worse time for Greece, which will need to refinance more than €8bn (£7.1bn) of debt in April and May.


The BJP leader also said that the issue is linked to India's rich culture, heritage and history.
Delhi: The Ram temple should be built in Ayodhya through mutual consent, and is not a "communal or religious" issue, Union Minister Nitin Gadkari said Tuesday.
The senior BJP leader also said that the issue is linked to India's rich culture, heritage and history.
"Ayodhya issue is not a communal issue and is not religious as well. Lord Rama is symbol of our history, culture and heritage. It has been proven that temple was there. If Ram temple cannot be built at birth place in Hindustan then where should it be? Crores of people's sentiments and desire is that Ram temple should be built there," Gadkari said at a conclave by Aaj Tak news channel.
The minister said this sentiment was earlier also in Bharatiya Janata Party (BJP) agenda and remains at present as well.
"There are three ways for it – matter is in court, it can be through mutual consent or by any decision in Parliament through 2/3rd majority. But I believe it should happen through mutual consent. our fabric is 'sarvadharma sambhav'. it should be based on this," Gadkari, who holds several key portfolios in the Cabinet, said.
He said even large number of people in Muslim community are in favour of settling the issue.
"The matter is in (the) Supreme Court … they have the right to decide. I personally feel that the matter reached court as it was not solved at political level. If court tries to find out a way then it can find out a way……mutual consent is the way out and it can be solved," the minister said.
On assembly election results of the three states in the Hindi heartland, Gadkari said winning or losing is part of democracy.
"Anything can happen in cricket and politics," he said, adding that while vote percentage margin was negligible in one state election, anti-incumbency factors were there in others, but BJP will look into all aspects and reform it.
Rejecting that these results in any way would impact the Lok Sabha results, Gadkari said his party was confident of a being victor in 2019 with a reasonable and comfortable margin.
He said: "Development" was the main agenda of the Modi government and it had done unparallel work in last 4.5 years, which has no match to the work done in the past 50 years.
In reply to a query that he was being viewed as a consensus candidate for the post of PM, Gadkari said party was doing tremendous work under Prime Minister Narendra Modi, and neither there is any such possibility nor any aspiration.
On Rafale, he said, the Supreme Court has already given verdict on it that it was a transparent deal but Congress was not ready to accept this clear judgement.
He further added that the Rafale deal will not be an election issue.
In reply to a query, he said, Shiv Sena-BJP relations were good as it is based on on Hindutva and there are no ideological differences.
"BJP wants alliance. our CM is working towards it. It is up to them (Shiv Sena) if they want ruling alliance or opposition, they have to decide. Our feeling is this alliance will be in the interest of Maharashtra and BJP," he said.
The minister also said that announcements to not to contest elections by senior leaders like Sushma Swaraj and Uma Bharti should not be linked to election prospects.
He also urged media to portray anything in totality and urged them to caution exercise when it comes to national interest, citing how the US media did not show bodies during 9/11 attack, while a section of Indian media during the Bombay attacks showed operations by security forces benefitting terrorists.


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neu.2019.6480.pdf (723.65 kB)
Delineating astrocytic cytokine responses in a human stem cell model of neural trauma.
posted on 2020-01-15, 16:48 authored by Eric Peter Thelin, Claire E Hall, Giulia E Tyzack, Arvid Frostell, Susan Giorgi-Coll, Aftab Alam, Keri LH Carpenter, Jamie Mitchell, Tamara Tajsic, Peter J Hutchinson, Rickie Patani, Adel Helmy
Neuroinflammation has been shown to mediate the pathophysiological response following traumatic brain injury (TBI). Accumulating evidence implicates astrocytes as key immune cells within the central nervous system (CNS), displaying both pro- and anti-inflammatory properties. The aim of this study was to investigate how in vitro human astrocyte cultures respond to cytokines across a concentration range that approximates the aftermath of human TBI. To this end, enriched cultures of human induced pluripotent stem cells (iPSC)-derived astrocytes were exposed to interleukin-1β (IL-1β) (1-10,000pg/ml), IL-4 (1-10,000pg/ml), IL-6 (100-1,000,000pg/ml), IL-10 (1-10,000pg/ml) and tumor necrosis factor-alpha (TNF) (1-10,000 pg/ml). Following 1, 24, 48 and 72hours, cultures were fixed and immunolabeled, and the secretome/supernatant was analyzed at 24, 48 and 72h using a human cytokine/chemokine 39-plex Luminex assay. Data was compared to previous in vitro studies of neuronal cultures and clinical TBI studies. The secretome revealed concentration-, time- and/or both concentration and time-dependent production of downstream cytokines (29, 21 and 17 cytokines, respectively p<0.05). IL-1β exposure generated the most profound downstream response (27 cytokines), IL-6 and TNF had intermediate responses (13 and 11 cytokines, respectively), while IL-4 and IL-10 only led to weak responses over time or in escalating concentration (8 and 8 cytokines, respectively). Notably, expression of IL-1β, IL-6 and TNF cytokine receptor mRNA was higher in astrocyte cultures in comparison to neuronal cultures. Several secreted cytokines had temporal trajectories, which corresponded to those seen in the aftermath of human TBI. In summary, iPSC-derived astrocyte cultures exposed to cytokine concentrations reflecting those in TBI generate an increased downstream cytokine production, particularly IL-1β. Although more work is needed to better understand how different cells in the CNS respond to the neuroinflammatory milieu after TBI, our data shows that iPSC-derived astrocytes represent a tractable model to study cytokine stimulation in a cell type-specific manner.
IN VITRO STUDIESINFLAMMATIONSECONDARY INSULTSTEM CELLSTRAUMATIC BRAIN INJURYIL-10IL-1βIL-4IL-6TBITNFcytokine exposurehuman iPSC-derived astrocytesin vitroPatani - secNeurology & Neurosurgery1103 Clinical Sciences1109 Neurosciences


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US box office hits $11bn in 2015
DECEMBER 29 UPDATE: Combined grosses reached $11bn in North America on Tuesday according to Rentrak, powered by Star Wars: The Force Awakens and Jurassic World. This was the first time Hollywood achieved the feat – at least when unadjusted for inflation.
The result overtook 2013's $10.92bn even though the number of tickets sold in North America was relatively light. As of Sunday that figure stood at 1.306bn – 18th in the all-time roster.
This illustrates the draw of alternative forms of entertainment as well as the superhero powers of inflation that have sent the average ticket price for the past 12 months in North America to $8.34 and saw 2015 over the finish line as the highest of all time.
However when adjusted for inflation, Hollywood has already crossed the $11bn mark nine times since 1980. 2002 ranks as the biggest year of modern times on $12.08bn in real terms – see box below.
HOLLYWOOD'S $11BN YEARS SINCE 1980, ADJUSTED FOR INFLATION
2013 – $10.92bn equates to $11.13bn
2010 – $10.57bn equates to $11.5bn
2007 – $9.66bn equates to $11.06bn
The Force Awakens has reached $571.4m and could overtake Jurassic World on $652.3m to become the biggest release of the year by January 1. Insiders estimate Hollywood's collective annual haul could rise to $11.1bn.
Universal and Disney dominated North American box office this year with seven of the top 10 and approximately 21% and 20% market share, respectively. Universal enjoyed a record $6.8bn worldwide take this year, which illustrates what it takes to go toe-to-toe with Disney.
Few studios or films came close to the top 10, representing Hollywood's version of the decline of the middle class.
TOP 10 NORTH AMERICAN HITS OF 2015
Jurassic World (Universal) $652.3m
Star Wars: The Force Awakens (Buena Vista) $571.4m*
Avengers: Age Of Ultron (Buena Vista) $459m
Inside Out (Buena Vista) $356.5m
Furious 7 (Universal) $353m
Minions (Universal) $336m
The Hunger Games: Mockingjay – Part 2 (Lionsgate) $264.6m
The Martian (Fox) $224.9m
Cinderella (Buena Vista) $201.2m
Spectre (Sony Pictures) $196.2m.
* still in release


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Anton Kazantsev (born August 26, 1986) is a Kazakhstani professional ice hockey defenceman. He is currently playing with the Yermak Angarsk of the Supreme Hockey League (VHL). Kazantsev previously played for Barys Astana of the Kontinental Hockey League (KHL).

International
He participated at the 2010 IIHF World Championship as a member of the Kazakhstan men's national ice hockey team.

Kazantsev was named to the Kazakhstan men's national ice hockey team for competition at the 2014 IIHF World Championship.

Career statistics

References

External links

Living people
Barys Nur-Sultan players
Kazakhstani ice hockey defencemen
Kazakhstani people of Russian descent
Saryarka Karagandy players
1986 births
Asian Games gold medalists for Kazakhstan
Medalists at the 2017 Asian Winter Games
Asian Games medalists in ice hockey
Ice hockey players at the 2017 Asian Winter Games
People from Kostanay Region

redpajama_set_name: RedPajamaWikipedia


Dr. Debiao Li, Biomedical Imaging Research Institute, Cedars-Sinai Medical Center, PACT Suite 800, 8700 Beverly Boulevard, Los Angeles, California 90048.
In recent years, noninvasive imaging has shown the ability to identify patients with high-risk coronary artery atherosclerotic plaques that could cause future cardiovascular events. Noncontrast computed tomography (CT) can readily detect calcification because of its high attenuation, and the coronary calcium score has been shown to be a predictor of coronary events (1). With coronary CT angiography, which allows assessment of coronary artery stenosis and noncalcified plaque, adverse plaque characteristics, including positive remodeling and low-attenuation plaque, have been shown to add to stenosis in coronary event prediction (2). Investigators have shown that total and noncalcified plaque burden quantified by coronary CT angiography substantially improves discrimination of hemodynamically significant lesions determined by fractional flow reserve over stenosis grading (3). Cardiac magnetic resonance (MR) has been used to assess coronary lumen (4), vessel wall morphology (5), and important markers of high-risk plaques including positive remodeling (6), intraplaque hemorrhage (7,8), and vascular inflammation (8,9). Positron emission tomography (PET) is a sensitive imaging technology that can assess biological processes in atherosclerosis. Using hybrid PET/CT scanners, with CT providing the registered anatomic background information and attenuation correction, coronary plaque inflammation has been detected by 18F-fluorodeoxyglucose uptake (10,11). Vascular microcalcification detected by 18F-sodium fluoride uptake has been shown to identify and localize ruptured and high-risk coronary plaques (12,13).
Recently, systems that combine PET and MR have become available that allow for simultaneous PET and MR image acquisitions. MR requires no ionizing radiation and produces high spatial and temporal resolution images with excellent soft tissue contrast. In addition, information describing respiratory and cardiac motion obtained from MR data (14) can be used to reduce motion artifacts in PET data. In a feasibility study described in this issue of iJACC, Robson et al. (15) demonstrate that PET/MR can detect inflammation and microcalcification activity in the coronary arteries at a low radiation dose. A focal increase in 18F-fluorodeoxyglucose and 18F-sodium fluoride uptake was clearly observed in multiple patients with coronary artery disease.
Given the small size of the coronary arteries and coronary artery plaques and their movement with cardiac and respiratory motion, coronary imaging with PET/MR presents multiple technical challenges. In the current study by Robson et al. (15), several of these challenges have been successfully addressed. An important problem presented by PET/MR of the coronary arteries is how to perform the attenuation correction that is essential to quantitation of the PET signal. The work of Robson et al. (15) describes a major technical innovation with the use of free-breathing, golden-angle radial MR acquisition (16) for PET attention correction. This approach performed better than standard end-expiration, breath-held, spoiled gradient-echo acquisition (17). This improvement would be expected because breath-held imaging position does not reflect accurately the average imaging position during free-breathing PET acquisitions. Golden-angle radial acquisition is also known to provide robust image reconstructions in the presence of patient motion. Robson et al. (15) also observed that by increasing the number of iterations for PET reconstruction, the target-to-background-ratio and standard uptake value for the coronary lesions are enhanced.
The positive initial experience of Robson et al. (15) in using PET/MR to detect coronary artery plaque biology is highly encouraging and provides valuable technical considerations on which future studies will build. However, there are certain limitations of the approach used, some of which are mentioned in the article. Although the current study by Robson et al. (15) appeared to alleviate respiratory artifacts by using the free-breathing approach, it did not apply cardiac gating to account for coronary artery motion during heartbeat. For attenuation correction, only 2 tissue types—soft tissue and background air—were included. More tissue types, such as fat, lung, and bone, may improve the accuracy in quantifying tracer activity (18). A direct comparison of PET/MR with PET/CT using the same radiotracer will be useful to evaluate the accuracy of the attenuation map (19). In addition, only 3 and 6 iterations in PET reconstruction were compared. It is not clear whether a number of iterations >6 will further increase target-to-background-ratio and standard uptake value of the coronary lesions.
The excellent work by Robson et al. (15) demonstrates that it is feasible to detect disease activity of coronary artery atherosclerosis such as inflammation and microcalcification by using hybrid PET/MR. MR offers potential advantages over CT, such as better soft tissue contrast and functional evaluation of the heart. PET/MR is associated with reduced radiation dose as compared with PET/CT, thus making longitudinal studies to evaluate the response to lifestyle interventions or medical therapy more feasible. In the future, large studies with comparisons with PET/CT will be needed. More advanced attenuation correction approaches including more tissues types and optimized MR image acquisition and tissue segmentation methods should be explored. Another major technical improvement may be possible by taking advantage of the respiratory and cardiac motion information available from the MR data for both MR and PET motion correction, PET attention correction, and partial volume correction, which could improve hotspot detection. Promising results have been obtained through rigid-body motion correction in PET/MR neurologic applications (20).
The work of Robson et al. (15) provides early evidence that PET/MR has the potential to examine multiple markers of coronary plaque biology. The approach will likely become a useful tool for research into understanding the processes underlying the development and progression of high-risk plaques. However, given the expense of PET/MR systems, determining whether PET/MR imaging of the coronary arteries has the potential to become a valuable clinical tool for identification of patients at highest risk for cardiac events and for guiding their management will require further investigation.
(2015) Automated quantitative plaque burden from coronary CT angiography noninvasively predicts hemodynamic significance by using fractional flow reserve in intermediate coronary lesions. Radiology 276:408–415.
(2013) Characterization of coronary atherosclerosis by magnetic resonance imaging. Circulation 128:1244–1255.
(2009) Positive remodeling of the coronary arteries detected by magnetic resonance imaging in an asymptomatic population: MESA (Multi-Ethnic Study of Atherosclerosis). J Am Coll Cardiol 53:1708–1715.
(2012) Coronary arterial 18F-FDG uptake by fusion of PET and coronary CT angiography at sites of percutaneous stenting for acute myocardial infarction and stable coronary artery disease. J Nucl Med 53:575–583.
(2016) Vision 20/20: magnetic resonance imaging-guided attenuation correction in PET/MRI: challenges, solutions, and opportunities. Med Phys 43:1130–1155.
(2012) PET/MRI for neurologic applications. J Nucl Med 53:1916–1925.
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The hip is where the femur (thigh bone) meets the pelvis in a ball and socket joint. The hip can undergo degenerative changes due to arthritis, and surgery may be necessary to relieve pain from the condition. There are many surgical options to treat hip pain due to arthritis, including total replacement of the hip joint, and more.


A vet in your pocket!
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This app is great for times where you are not 100% sure you need to go to a vet .


Not enough Halitosis Dentists to choose from?
Halitosis, or more normally referred to as 'bad breath' can result from poor dental health habits and may be a sign of other health problems. Bad breath and halitosis is made worse by the types of foods you eat. It can result from poor dental health habits and may be a sign of other health problems. Are you looking for halitosis treatment in Arlington? Or trying to find an Arlington dentist who treats halitosis? These dentists in Arlington are able to provide Arlington halitosis treatment or can refer you to other dentists who can help with treatment of halitosis in Arlington or help for treating bad breath.


A guy takes all the clothes he's wearing to give to a homeless couple living under the bridge.
A utility worker escaped without injury when an electrical wire fell and struck wet ground following overnight raining.
TOO CLOSE FOR COMFORT! A state trooper walking on the side of the road in Idaho had a close call when a driver spun off the road and slid right in front of him. No one was hurt in the crash.
Two naughty puppies play in a flower pot in a backyard, making a mess. Breeds are Cavalier and Bichon Frise.
Emotional outburst of a man sentenced to serve up to 65 years in prison for torturing a child.
Baby girl makes a funny laugh then a unique crawl using her hands as two cats run around. Dad says "You're almost walking." Cats Persian and Himalayan.
Snowbarder attempts a back flip and fails.
Soccer players trying to get a ball stuck in a tree during a game.
A man pulling a small suitcase crosses train tracks just as a train is pulling up to the intersection. The man is nearly run over but seems not to react.
Dashcam footage shows a police officer dodging an out of control car on the freeway.
Dashcam footage shows a police officer guiding a motorist off the railway line seconds before a diesel train crashes into his car.
A car crosses railroad tracks and a split second later a train passes behind it narrowly missing the car.
A cyclist crosses train tracks in front of an oncoming train. The engineer brakes the train slowing it down a bit so the cyclist escapes unhurt.