Epilepsy after pediatric traumatic mind damage (TBI) is connected with low quality of existence. 5 weeks, most TBI mice exhibited spontaneous seizures throughout a 7 d video-EEG documenting period. Entinostat At six months, IL-1Ra-TBI mice got fewer evoked seizures weighed against vehicle settings, coinciding with higher preservation of cortical cells. Results Rat monoclonal to CD4.The 4AM15 monoclonal reacts with the mouse CD4 molecule, a 55 kDa cell surface receptor. It is a member of the lg superfamily, primarily expressed on most thymocytes, a subset of T cells, and weakly on macrophages and dendritic cells. It acts as a coreceptor with the TCR during T cell activation and thymic differentiation by binding MHC classII and associating with the protein tyrosine kinase, lck demonstrate this model's energy to delineate systems root epileptogenesis after pediatric mind damage, and provide proof IL-1 signaling like a mediator of post-traumatic astrogliosis and seizure susceptibility. SIGNIFICANCE Declaration Epilepsy can be a common reason behind morbidity after distressing mind damage in Entinostat early years as a child. However, a restricted knowledge of how epilepsy builds up, particularly in the immature brain, likely contributes to the lack of efficacious treatments. In this preclinical study, we first demonstrate that a mouse model of traumatic injury to the pediatric brain reproduces many neuropathological and seizure-like hallmarks characteristic of epilepsy. Second, we demonstrate that targeting the acute inflammatory response reduces cognitive impairments, the degree of neuropathology, and seizure susceptibility, after pediatric brain injury in mice. These findings provide evidence that inflammatory cytokine signaling is a key process underlying epilepsy development after an acquired brain insult, which represents a feasible therapeutic target Entinostat to improve quality of life for survivors. 0.05,*** 0.001; = 7C10/group). Immunofluorescence staining for ZnT3 mossy fibers, NeuN+ neurons, and DAPI+ nuclei in the injured hippocampus revealed abnormal mossy fiber sprouting at 3 months post-injury (and = 7C10/group. Scale bars: = 0.04; 0.01) and CA1 ( 0.01; 0.001) of vehicle-TBI mice, which was attenuated in rIL-1Ra-TBI mice. = 9C10/group. Scale bar, 200 m. Region-of-interest indicated by dotted white line in (( 0.0001; 0.01) and hippocampus (= 0.03; 0.05; = 0.01). = 5/group; * 0.01, ** 0.01, *** 0.001. Open in a separate window Figure 5. rIL-1Ra treatment attenuates chronic cognitive deficits after pTBI. Mice received either rIL-1Ra or vehicle treatment for 7 d following pTBI or sham surgery, and underwent behavioral assessment at 3 months ( 0.0001). In the hidden platform trials ( 0.0001). Direct comparison of vehicle-TBI and rIL-1Ra-TBI mice revealed a trend toward an effect of treatment (two-way RM ANOVA, = 0.08). However, only vehicle-TBI mice showed a increased latency to locate a hidden platform during subsequent trial days compared with sham controls (= 0.02). On day time 7 of the duty, the probe trial exposed an overall aftereffect of damage (= 0.04), having a priori evaluation uncovering that only vehicle-TBI mice spent less amount of time in the prospective quadrant weighed against their sham settings ( 0.05), indicating a spatial memory deficit that was absent in rIL-1Ra-TBI mice (= 0.01). All mice demonstrated equivalent ability with an accelerating rotarod ( 0.0001) as well as the elevated in addition maze (= 11/group (sham) and 18/group (TBI); * 0.05, *** 0.001. Open up in another window Shape 8. Chronic neuropathology after pTBI. Volumetric evaluation from the dorsal cortex and hippocampus at six months postsurgery by T2-weighted MRI (= 0.02). Hippocampal quantity was unaffected by TBI or medications ( 0.05, color bar indicates value). Region-of-interest quantification of ipsilateral and contralateral corpus callosum fractional anisotropy ideals similarly detected a decrease in TBI mice ( 0.0001, and 0.01), individual of rIL-1Ra treatment. GFAP immunofluorescence staining within the ipsilateral hippocampus (= 0.05, aftereffect of hemisphere; 0.05, aftereffect of treatment). = 8C13/group; * 0.05, ** 0.01, **** 0.0001. Pet model. usage of water and food. The managed cortical impact style of TBI was performed at P21 (1 d; 10 g) in man mice as previously referred to (Pullela et al., 2006; Semple et al., 2015). Pups had been weaned and anesthetized with 1.25% 2,2,2-tribromoethanol in saline (Avertin, Sigma-Aldrich), intraperitoneally at 0.02 ml/g bodyweight (at UCSF; discover Figs. 1C4), or 1.5% isoflurane with a nose cone throughout surgery (at UoM; discover Figs. 5C8). Damage parameters had been 4.5 m/s velocity, 1.73 mm depth, and 150 ms duration (severe) or 4.0 m/s, 1.2 mm depth, and 150 ms duration (moderate). Sham-operated mice underwent similar surgical treatments, without getting the impact. Open up in another window Shape 2. IL-1 response after pTBI. IL-1 proteins was recognized by ELISA across a period program after pTBI, within the ipsilateral cortex (receptor.
Heterochromatin protein 1 (Horsepower1) is a chromatin protein involved in gene silencing. the BRCA1 target promoter during recovery and functions in the activation-repression switch and recovery from BRCA1-mediated transcription in response to DNA damage. INTRODUCTION In eukaryotic cells, DNA is folded along with histone and non-histone chromosomal proteins to form chromatin. Chromatin dynamics play a critical role in the regulation of transcription, replication, DNA repair and cell cycle progression, and the functional state of chromatin is modulated via epigenetic mechanisms. Covalent modifications of histones and DNA play a role in the regulation of 23491-55-6 supplier chromatin structure and dynamics. The regulation of the chromatin-modifying factors that generate or remove covalent histone modifications, including acetylation, methylation, phosphorylation, ubiquitination, small ubiquitin-like modifier (SUMO) proteins (SUMOylation) and DNA methylation, are thought to maintain both chromatin integrity and the correct patterns of gene expression (1C5). One well-characterized histone modification is methylation. The addition and removal of methyl groups has been implicated in both gene activation and repression depending on the site and level of methylation (mono-, di- and trimethylation) (3,6). Specifically, methylation of histone 3 at lysine 9 (H3K9), lysine 20 and lysine 27 has been implicated in transcriptional repression, whereas methylation at lysine 4, lysine 36 and lysine 79 continues to be implicated in transcriptional activation (7,8). H3K9 is present in mono-, di- and trimethylated forms. The histone methyltransferases (HMTs) G9a and SUV39H1 catalyze the methylation of H3K9, circumstances that predominates constitutive heterochromatin (9). Furthermore to chromatin changes and redesigning, the recruitment of nonhistone chromatin proteins is known as very important to the rules of varied DNA-involved procedures, including transcription, replication, DNA restoration and chromosome segregation. For instance, heterochromatin proteins 1 (Horsepower1), a regulatory nonhistone protein, can be recruited to chromatin with the reputation of methylated H3K9 (H3K9me) (10). Horsepower1, that is named following its 23491-55-6 supplier association with 23491-55-6 supplier heterochromatin, features primarily within the maintenance of structural integrity of chromosomes as well as the rules of transcription Rabbit polyclonal to ABHD14B (11). Horsepower1 genes encode chromosomal protein that are extremely conserved from candida to human beings; they connect to chromatin by binding to H3K9me through its conserved N-terminal site, the chromodomain (11). Candida has one Horsepower1 (Swi6) (2). Three paralogs, Horsepower1, Horsepower1 and Horsepower1, are located in mammals and flies, plus they localize to constitutive or facultative heterochromatin and euchromatin (2). Small is known regarding the practical variations among these Horsepower1 proteins. All protein in the Horsepower1 family members are adapters that transmit epigenetic position between histones and DNA, leading to DNA methylation (2). Furthermore, they have an important function in the forming of heterochromatin and gene silencing with a mechanistic connection between heterochromatin framework and transcriptional repression (2C5). The increased loss of Horsepower1 leads to the transcriptional activation from the HIV-1 lengthy terminal repeat (12), and HP1 gene silencing modestly restores tumor necrosis factor- transcription (13). Although the precise mechanisms through which HP1 regulates gene expression are not fully understood, HP1 seems to link DNA and histones through the recruitment of chromatin modifiers. BRCA1 (breast cancer type 1 susceptibility protein) is a tumor suppressor involved in maintaining genomic integrity via its diverse functions in DNA damage signaling, DNA repair and transcription. BRCA1 is also implicated in chromatin structural integrity and dynamics via its interaction with and recruitment of chromatin modifiers, which may repair DNA and lead to transcription via regulation of DNA access (14C16). BRCA1 interacts with histone deacetylases (HDACs), histone acetyl transferases, C-terminal-binding protein and its interacting protein, retinoblastoma protein (Rb), RbAp46/48 and the switch/sucrose non-fermentable complex (14). BRCA1 regulates the transcriptional activity of c-myc, JunB, p53, Rb, estrogen receptor, androgen receptor and ZBRK1 (14). Results from several studies have provided evidence of the involvement of BRCA1 in transcription regulation via control of chromatin structure and dynamics in response to DNA damage. Indeed, BRCA1 can activate and suppress the transcription of genes involved in the control of cell cycle progression, apoptosis and proliferation. This evidence supports its role as a transcriptional coregulator that can respond to DNA damage through the formation of transcriptional activator or repressor complexes with chromatin-modifying proteins such as HDACs, p300, SUMO1 and Brahma-related gene 1 subunits (16,17). In this study, we identified and characterized HP1 as a.
Background Chemoradiotherapy may be the standard of care for patients with oesophageal malignancy unsuitable for surgery due to the presence of co-morbidity or extent of disease, and is a standard treatment option for patients with squamous cell carcinoma of the oesophagus. patients to establish whether the addition of cetuximab to the standard treatment improves overall survival. Methods/Design SCOPE1 is a two arm, open, randomised multicentre Phase II/III trial. Eligible patients will have histologically confirmed carcinoma of the oesophagus and have been chosen to receive definitive chemoradiotherapy by an accredited multidisciplinary team including a specialist Upper GI doctor. 420 patients will be randomised to receive definitive chemoradiotherapy with or without cetuximab using a 1:1 allocation ratio. During Phase II of the study, the trial will assess security (toxicity), activity (failure-free rate) and feasibility (recruitment rate and protocol dose modifications/delays) in 90 patients in the experimental arm. If the Rabbit Polyclonal to DVL3 experimental arm is found to be active, safe, and feasible by the Indie Angiotensin 1/2 (1-9) manufacture Data Monitoring Committee then recruitment will continue into Phase III. This second stage will recruit a further 120 patients into each arm and compare the overall survival of both groups. All patients randomised into Phase II will donate to the Stage III evaluation of overall success. Furthermore to overall success, Stage III of the analysis may also assess toxicity, medical standard of living and cost efficiency. An in Angiotensin 1/2 (1-9) manufacture depth radiotherapy process and quality guarantee procedure continues to be included into this trial. Trial enrollment ISRCTN: ISRCTN47718479 Background World-wide, oesophageal cancers is the 8th most common cancers, responsible for around 482,300 brand-new situations and 406,800 fatalities in 2008 and may be the 5th Angiotensin 1/2 (1-9) manufacture highest in mortality price among tumour sites?. In the united kingdom, there have been 7,966 brand-new situations of oesophageal cancers diagnosed in 2007 which is responsible for around 4% of most cancer fatalities with over 7,600 people dying in 2008?. You can find two primary histological sorts of oesophageal cancers, squamous cell carcinoma (SCC) and adenocarcinoma (AC). Lately there's been an increase within the amounts of adenocarcinomas of the low oesophagus and gastro-oesophageal junction in populations from the , the burkha? as the occurrence of squamous carcinoma provides fallen slightly. In the UK, there has been a 60% increase in oesophageal carcinoma incidence in males over the past 30 years?. Surgery has long been, and remains, the cornerstone for remedy of oesophageal malignancy and is considered for all patients with potentially resectable oesophageal malignancy who are fit for surgery and have no evidence of distant disease. Approximately 23% of patients survive 5 years with the most commonly used surgical treatment strategy?. However, rates of surgical intervention in the UK are as low as 20% of all cases. The most recent figures (for patients diagnosed Angiotensin 1/2 (1-9) manufacture between 2001 and 2006) show that this 5-year survival of all patients with oesophageal malignancy is 10 per cent . Chemoradiotherapy (CRT) in oesophageal malignancy In a pivotal study?, US Intergroup RTOG-8501 randomised 121 patients with squamous cell carcinoma (SCC) or adenocarcinoma (AC) to receive CRT (4 cycles cisplatin and 5-Fluorouracil (5FU), the first 2 cycles given concurrently with 50Gy radiotherapy in 25 fractions) or radiotherapy alone (64Gy in 32 fractions). This trial, together with a subsequent systematic review?, demonstrated a survival superiority of CRT over radiotherapy alone (1-12 months mortality odds ratio 0.61, 95% CI 0.31-0.89, P 0.001), albeit at the expense of increased toxicity. This and other reported studies?[5,7-12] have been predominantly in patients with SCC and have demonstrated a remarkably consistent median survival of 14-18 months and 2 12 months overall survival of 30-40% with CRT. In the UK, most experience has been gained in those patients, both with SCC and AC, deemed unsuitable for surgery due to the presence of co-morbidity or extent of disease?[8,13]. Despite the expected poor prognosis of this patient group, of the 266 individuals who were deemed inoperable at one UK centre between 1995 and 2009, the median survival was 20.6 months (2 and 5 year survival 44% (95% CI: 37, 50%) and 20% (95% CI: 14, 26%) respectively) . With this study 42% of individuals suffered grade 3 and 7% grade 4 toxicities, primarily mucosal and haematological due to the chemotherapy. Rational for standard chemotherapy providers Concurrent CRT regimens have been based upon cisplatin and 5FU. Both have good solitary agent activity in oesophageal malignant disease and are amongst the best radio-sensitisers.
Myostatin (MSTN) is really a potent bad regulator of skeletal muscle tissue growth. in improving MSTN-inhibitory strength of truncated types of MSTNpro protein, and MBP-fused pig MSTNpro comprising amino INCB018424 acidity residues 42C175 is enough to maintain the entire MSTN-inhibitory capacity. Intro Myostatin (MSTN) can be a member from the changing growth element- (TGF-) superfamily and adversely regulates skeletal muscle tissue growth and advancement with little influence on additional tissues [1C3]. Much like INCB018424 additional TGF- relative protein, MSTN can be translated like a precursor proteins (preproMSTN) comprising a signal series, an N-terminal propeptide site (MSTNpro) along with a C-terminal adult (energetic) domain [2, 4]. Upon entering into the endoplasmic reticulum, signal peptide is removed from preproMSTN, then proMSTN forms a disulfide-linked homodimer and is proteolytically processed at a conserved Arg-Arg-X-Arg site by the furin family of proprotein convertases to generate MSTNpro and mature MSTN [5, 6]. After the cleavage, two MSTNpros make a non-covalent complex formation with disulfide-linked homodimer of mature MSTN in a latent/inactive state to suppress MSTN binding to its receptor [6C8]. Administration or overexpression of MSTNpro has been shown to enhance skeletal muscle growth in laboratory animal species [4, 5, 9C14], supporting the inhibitory role of MSTNpro on MSTN activity. Activation of MSTN from the latent state involves cleavage of MSTNpro by members of the bone morphogenetic proteins-1/tolloid (BMP-1/TLD) of metalloproteinases [4, 15]. The administration of wild type MSTNPro had no effect on skeletal muscle growth, while the administration of metalloproteinase-resistant mutant form of MSTNPro significantly enhanced skeletal muscle growth in mice , supporting the role of the metalloproteinase-cleavage site of MSTNpro on MSTN activity regulation. According to a study , a region INCB018424 of human MSTNpro containing amino acid residues 42C115 was critical for MSTN inhibition. Similarly, a region of human MSTNpro containing residues 42C99 fully suppressed MSTN activity in co-transfection experiments , and a synthetic mouse MSTNpro peptide covering residues 45C68 was effective in suppressing MSTN activity . We have also shown that maltose binding protein (MBP)-fused flatfish MSTN1pro region consisting of residues 45C100 had the same MSTN inhibitory potency as the MBP-fused full sequence flatfish MSTN1pro . These studies together suggest that partial sequences of MSTNpro would be sufficient to maintain the full MSTN-inhibitory capacity. In a previous study, we have successfully produced bioactive metalloproteinase-resistant mutant form of pig MSTNpro in  in an effort to examine the potential of MSTNpro to improve skeletal muscle growth of meat-producing animals. Since molecular size is a factor affecting the production yield in the expression system , the determination of MSTN-inhibitory domain of pig MSTMpro would contribute to enhancing the production yield of MSTNpro-type proteins having an equivalent potency to the full sequence MSTNpro. LPP antibody Thus, the objective of this study was to express and purify various truncated forms of pig MSTNpro to examine their MSTN-inhibitory capacities in an INCB018424 effort to investigate the region of pig MSTNpro critical for MSTN inhibition, as well as the minimum region possessing the full capacity for MSTN inhibition. Similar to previous studies, current results showed that inhibition of MSTN did not require full sequence of pig MSTNpro.It was also observed that MBP-fusion enhanced MSTN-inhibitory potency of truncated forms of MSTNpro proteins. Materials and strategies Construction of manifestation vectors Building of plasmid including complete cDNA series of pig MSTNpro with mutation in the BMP-1/TLD proteolytic site (GenBank Accession No. "type":"entrez-nucleotide","attrs":"text message":"KT932616″,"term_id":"1009295983″,"term_text message":"KT932616″KT932616) was reported previously , which plasmid was utilized like a template in creating four truncated types of pig MSTNpro cDNAs. The four truncated types of pig MSTNpro had been called Pro42-218, Pro42-175, Pro42-115, and Pro42-98, pursuing their beginning and closing positions within the series. The DNA sequences of the aforementioned truncated types of pig MSTNpro are located from GenBank Accession No. "type":"entrez-nucleotide","attrs":"text message":"KT932617″,"term_id":"1009295985″,"term_text message":"KT932617″KT932617, "type":"entrez-nucleotide","attrs":"text message":"KT932618″,"term_id":"1009295987″,"term_text message":"KT932618″KT932618, "type":"entrez-nucleotide","attrs":"text message":"KT932619″,"term_id":"1009295989″,"term_text message":"KT932619″KT932619, and "type":"entrez-nucleotide","attrs":"text message":"KT932620″,"term_id":"1009295991″,"term_text message":"KT932620″KT932620, respectively. The amino acidity sequences from the truncated pig MSTNpro proteins are available in Fig 1. For Gibson set up cloning from the inserts in to the XmnI site of manifestation vector (New Britain Biolab, MA, USA), PCR was.
The purpose of this study was to assess multifactorial -cell responses to metabolic perturbations in primary rat and human islets. mTORC1-dependent manner. Nutrient activation of mTORC1 upregulated the expression of adipose differentiation related protein (ADRP), known to stabilize lipid droplets. Rat islet size and new DNA synthesis also increased under nutrient overload. Insulin secretion into the culture medium increased continuously over a Perindopril Erbumine (Aceon) 4-day period without any significant difference between glucose (10 mM) alone and the combination of glucose (10 mM) and FFAs (240 M). Insulin content and insulin biosynthesis, however, were significantly reduced under the combination of nutrients compared with glucose alone. Elevated nutrients also stimulated lipid droplet formation in human islets in an mTORC1-dependent manner. Unlike rat islets, however, human islets did not increase in size under nutrient overload despite a normal response to nutrients in releasing insulin. The different responses of islet cell growth under nutrient overload appear to impact insulin biosynthesis and storage differently in rat and human islets. strong class="kwd-title" Keywords: lipid droplets, mTORC1, ADRP, rapamycin, nutrient overload, human islets, time lapse studies, insulin Introduction Type 2 diabetes mellitus (T2DM) is usually characterized by insulin resistance and defects Perindopril Erbumine (Aceon) in -cell function, growth, and survival. Chronic nutrient overload associated with obesity is implicated in both insulin resistance and -cell defects. Adaptive responses of -cells under conditions of insulin resistance and nutrient overload, including lipid accumulation and -cell mass growth, have been widely observed in numerous experimental models.1-5 However, the specific molecular mechanisms by which nutrients promote lipid accumulation and -cell mass expansion and the causal relationship between these adaptive responses and -cell defects are not clearly understood. Furthermore, metabolic and morphological changes of Perindopril Erbumine (Aceon) human islets under nutrient overload are poorly comprehended, despite their potential impact on understanding the etiology of T2DM. The storage of TG in lipid droplets requires the activation of the two pathways: TG biosynthesis through the esterification pathway6 and expression of lipid droplet-associated proteins that stabilize lipid droplets by preventing FLJ13165 lipolysis. Lipid droplets contain neutral lipids (TG, cholesterol ester) in the primary, surrounded by way of a phospholipid monolayer along with a layer of specific protein.7 These lipid droplet-associated proteins are designated because the PAT proteins [perilipin, adipophilin/adipose differentiation related protein (ADRP), TIP47 as well as other related proteins], which play structural and functional assignments in cellular lipid fat burning capacity.8 Both perilipin and ADRP have already been within the rat and individual islets.9,10 The expansion of -cell mass continues to be seen in genetically modified obese rodents,4,11 regular mice fed a high-fat diet5,12 and mice infused with elevated degrees of glucose or FFAs.13,14 The upsurge in -cell mass connected with insulin resistance and nutrient overload continues to be widely accepted to correlate with hypersecretion of insulin, providing a compensatory mechanism to overcome insulin resistance. Nevertheless, recent evidence an upsurge in -cell mass under circumstances like a chronic fat rich diet or 60% pancreatectomy had not been connected with a matching improvement of -cell function12,15-17 shows that a rise in -cell mass isn't generally correlated with improved -cell function. The causal romantic relationship between -cell mass extension and -cell function under nutritional overload, therefore, continues to be to become elucidated. Under chronic nutritional overload, rodent -cells go through quality metabolic adaptations including lipid deposition and -cell mass extension. We suggest that mammalian focus on of rapamycin complicated 1 (mTORC1), a conserved serine/threonine kinase that features as a nutritional sensor, is certainly a common mediator that regulates both replies. mTORC1 may integrate indicators from growth elements and nutrition to regulate proteins translation, DNA synthesis, cell size, and proliferation.18-23 Two prominent downstream goals of mTORC1 will be the 70-kDa ribosomal proteins S6 kinase (S6K1) and eukaryotic initiation aspect 4E-binding proteins 1 (4EBP1), which regulate proteins translation.20,24 The mTORC1 signaling pathway has been implicated as a link between nutrient excess and development of both obesity and insulin resistance.25,26 Recent evidence indicates that mTORC1 signaling is also implicated in -cell regenerative processes.27-30 Furthermore, the present study suggests that mTORC1 plays a pivotal role in lipid accumulation in -cells. Preservation of -cell function and mass under chronic nutrient overload is definitely of great interest like a potential strategy for restorative treatment for type 2 diabetes. To this end, we analyzed the complex -cell metabolic reactions to nutrient overload in rat and human being islets using a combination of microscopy Perindopril Erbumine (Aceon) and biochemical methods. We statement that mTORC1 takes on a central part in lipid build up as well as rat islet cell growth,.
We evaluated the function from the inositol 1,4,5-triphosphate (IP3) receptor-mediated Ca2+ discharge in the positive inotropic ramifications of -adrenergic arousal using a book, potent, selective membrane-permeable blocker of IP3 receptor, xestospongin C. the concentration-response curve for phenylephrine. On the other hand, xestospongin C didn't have an effect on the concentration-response curve for phenylephrine obtained in the presence of ryanodine (1?M). On the other hand, xestospongin C affected neither basal contractions nor the positive inotropic effects of a high extracellular Ca2+ concentration (3.2?mM) or that of isoprenaline (1 and 10?nM). These results suggest that the IP3-mediated increase in Ca2+ release is involved in the positive inotropic effects of -adrenergic activation in the guinea-pig cardiac muscle mass. sp., has recently been shown to be a membrane-permeable blocker of IP3-mediated Ca2+ release (Gafni sp. (Kobayashi em et al /em ., 317366-82-8 supplier 1998). Cyclopiazonic acid and xestospongin C were dissolved in dimethylsulphoxide and ethanol, respectively. Statistics The numerical data were expressed as means.e.mean. Differences 317366-82-8 supplier between mean values were evaluated by paired Student's em t /em -test and, where appropriate, analysis of variance (ANOVA) followed by the Bonferroni test. A probability of less than 0.05 was 317366-82-8 supplier taken as a statistically significant difference. Results The effects of xestospongin C on pressure oscillations in saponin-skinned muscle tissue In saponin-skinned guinea-pig papillary muscle mass, pressure oscillations were observed in pCa2+ 6.5 solution (Figure 1a), and the addition of IP3 (100?pM to 100?M) augmented the pressure oscillation in dose-dependent manner (Physique 1a,b), as has been reported by Nosek em et al /em . (1986). Using these pressure oscillations in saponin-skinned fibre, we examined the pharmacology of xestospongin C on cardiac SR functions. Open in a separate window Physique 1 Effects of IP3 (1?pMC100?M) around the pressure oscillations in saponin-skinned muscle tissue. Force oscillations were introduced by low-EGTA (0.05?mM) and pCa2+ 6.5 solution. (a) Common trace of effect of IP3. (b) Summarized data of (a). The area of the pressure oscillations during 1?min was used for the quantitative assessment of effects of IP3. * em P /em 0.05, ** em P /em 0.01 vs the basal force oscillations. The basal spontaneous pressure oscillations were completely inhibited by 1?M ryanodine (Physique 2a) or by 30?M cyclopiazonic acid, a SR Ca2+ -ATPase inhibitor (data not shown), suggesting that this force oscillations were induced by the rhythmic Ca2+ release from your SR. The pressure oscillations stimulated by 100?M IP3 were also abolished by 30?M cyclopiazonic acid. On the other hand, the basal pressure oscillations were not changed by 3?M xestospongin C. However, in the presence of xestospongin C, IP3 failed to enhance the pressure oscillations (Physique 2c). These results are PRMT8 summarized in Physique 2d. Open in a separate window Physique 2 Effects of xestospongin C (Xe-C, 3?M) around the pressure oscillations in saponin-skinned muscle tissue. (a) Common trace of effects of 1?M ryanodine around the force oscillations. (b) Common trace of 100?M IP3-induced potentiation of oscillations and the effects of addition of cyclopiazonic acid (CPA, 30?M). (c) Common trace of the effect of 100?M IP3 in the presence of 3?M xestospongin C. (d) Summarized data of (b) and (c). The numbers of the experiments is proven near each column. ** em P /em 0.01 vs the basal force oscillations. # em P /em 0.05, ## em P /em 0.01 vs the outcomes obtained in the current presence of IP3. The consequences of xestospongin C in unchanged muscles The use of 3?M xestospongin C had zero influence on the peak force of contraction in regular PSS (Amount 3a). A rise in extracellular Ca2+ focus ([Ca2+]o) from 1.6 to 3.2?mM increased the top drive. Xestospongin C (3?M) didn't have an effect on the positive inotropic aftereffect of the elevation in [Ca2+]o (Amount 3a,b). Open up in another window Amount 3 Ramifications of 3?M xestospongin C (Xe-C) over the force of contractions in 1.6 and 3.2?mM [Ca2+]o. (a) Usual tracings from the drive. (b) Summarized data ( em n /em =4). Each column represents the means.e.mean. Beliefs obtained in regular PSS at 0.5?Hz were taken seeing that 100%. Positive inotropic results had been also elicited by 1?nM isoprenaline in the current presence of 1?M phentolamine.
It is popular that (PG) has various pharmacological results such as for example anti-aging and anti-inflammation. DKK-1 inhibited hair regrowth, and PG remove dramatically reversed the result of DKK-1 on individual hair organ lifestyle. PG remove antagonizes DKK-1-induced catagen-like adjustments, in part, with the legislation of apoptosis-related gene appearance in HFs. These results recommended that PG remove may reduce hair thinning despite the existence of DKK-1, a solid catagen inducer via apoptosis. (12,13) confirmed that DKK-1 is certainly secreted from hDPCs in response to DHT which it promotes the regression of HFs by preventing Wnt/-catenin signaling and by inhibiting the development of ORS keratinocytes and triggering apoptotic cell loss of life. The reviews also discovered that, although DKK-1 treatment quickly HKI-272 transformed the anti-apoptotic proteins Bcl-2, DKK-1 marketed the pro-apoptotic protein Bax in a dose-dependent manner in ORS keratinocytes. (PG) has a wide range of pharmacological effects including anti-inflammatory (14,15), antioxidant (16), anticancer FLJ23184 (17) and anti-aging (18C22) effects as well as the promotion of hair growth (23,24). PG contains many other ingredients such as sugars, proteins and lipids besides ginsenosides. Ginsenosides are a unique component of ginseng that is found only in ginseng, while sugars and proteins are common components of other plants. Also, numerous studies have indicated that this pharmacological effect of ginseng is derived from ginsenosides (25,26). Recently, the authors reported that PG extract, which is a ginsenoside-enriched PG extract made using the repeated fractionalizing method, significantly enhanced the proliferation of hDPCs, potassium channel-opening activity, and HKI-272 human HF growth via a mechanism similar to that of minoxidil (27). Usually, ginsenosides of commercial PG extract are 3C6%, but a ginsenoside-enriched PG extract are concentrated up to 20% using the preparation method used. The major ginsenosides detected in the ginsenoside-enriched PG extract were Rb1, Rb2, Rc, Rd, Re HKI-272 and Rg1. One of them, ginsenoside Re showed the highest level among the six ginsenosides and its content was approximately 6.23% (w/w) (27). In the current study, the authors investigated the inhibitory effect of ginsenoside-enriched PG extract on DKK-1-induced apoptosis in HFs in addition to the underlying mechanism of action. Materials and methods The planning of PG remove The authors executed tests utilizing the same examples as PG remove, which had hair regrowth effect inside our prior studies (27). The main of PG was extracted from Geumsan Ginseng Marketplace (Geumsan-gun, Korea). The dried out and crushed root base of PG (300 g) had been extracted with 70% aqueous ethanol at 50C for 8 h. The ingredients had been filtered and focused under decreased pressure at 60C. The residue was dissolved with 100% ethanol and do it again purification and vacuum distillation. Components Minoxidil, MTT and dimethyl sulfoxide had been bought from Sigma-Aldrich; Merck KGaA (Darmstadt, Germany). Individual DKK-1 was bought from R&D Systems, Inc. (Minneapolis, MN, USA). Isolation and civilizations of individual ORS keratinocytes Non-balding head specimens were extracted from sufferers undergoing locks transplantation medical procedures (IRB:DKUH 2013-08-012-001). The medical moral committee from the Dankook Medical University (Section of Dermatology, Cheonan, Korea) accepted every one of the defined studies, and up to date created consent was extracted from the sufferers. HFs had been isolated and cultured with the previously defined technique, with minor adjustments (28). Cultured ORS keratinocytes of early passing were useful for the tests and were preserved at 37C within a humidified atmosphere with 5% CO2. MTT assay Cell viability was motivated using an MTT assay which was performed by way of a small modification of the technique defined by Philpott (29). Quickly, ORS keratinocytes had been seeded in a thickness of 2104 cells/well into 96-well plates and had been cultured for 24 h. Ahead of treatment, the cells had been cultured for 24 h in a rise supplement-free moderate. The cells had been after that treated with PG extract HKI-272 and DKK-1 for 24 h. The examples were evaluated by calculating absorbance at 540 nm using a Synergy? 2 Multi-Detection Microplate Audience (BioTek Equipment, Inc., Winooski, VT, USA). The cell viability prices were calculated in the optical thickness readings and so are symbolized as percentages from the control worth (neglected cells). Change transcription-quantitative polymerase string reaction The full total RNA was isolated using TRIzol? reagent (Invitrogen; Thermo Fisher Scientific, Inc., Waltham, MA, USA), and 2 Cell Loss of life Detection package, Fluorescein, Roche Diagnostics GmbH, Mannheim, Germany) was utilized based on the manufacturer's process to judge apoptotic cells. Quickly, ORS keratinocytes at 2104 cells/200 lifestyle of whole individual head HFs. Minoxidil (MNX) and automobile served as negative and positive handles, respectively. HFs treated with PG remove grew longer compared to the harmful control HFs at.
Seeks: To mimic, in an animal model of alcoholism, the protective phenotype against alcohol consumption observed in humans carrying a fast alcohol dehydrogenase (ADH1B*2) and an inactive aldehyde dehydrogenase (ALDH2*2). important public health problems in the Western world (Rehm allele (Thomasson allele (Mizoi allele is likely a brief increase in arterial blood acetaldehyde. Since individuals carrying both protecting genes are digital abstainers (Chen BJ5183 stress to create a plasmid including the recombinant adenoviral genome. The infections had been propagated in HEK-293 cells, purified in two consecutive CsCl gradients, and dialyzed for 24?h against 10?mM TrisCHCl, 2?mM MgCl2 and 5% sucrose (storage space buffer). Total viral contaminants had been approximated by absorbance at 260?nm (Mittereder manifestation of rADH47His and asALDH2 in hepatic cells. H4-II-E-C3 cells had been from ATCC and cultivated as indicated for HEK-293 cells. The tradition moderate was supplemented with 10% equine serum and 5% fetal bovine serum. Transduction of H4-II-E-C3 cells with adenoviral vectors The rat hepatoma cells had been plated on 6-well plates at 2??106 cells/well and transduced with different volumes (0C1000?l) of the crude HEK-293 cell lysate containing AdVCADH/asALDH2 vector. Seventy-two hours following the transduction, GCN5L the cells had been gathered, lysed in 1% Triton X-100 with 0.33?mM dithiothreitol (DTT), centrifuged at 20,800for 20?min in 4C and examples of the supernatant were collected. Total proteins concentrations within the examples had been determined utilizing the Bio-Rad Proteins Assay package. Assay of ADH and ALDH2 actions The experience of ADH and ALDH2 had been determined spectrophotometrically from the dimension of absorbance (340?nm) of nicotinamide adenine dinucleotide reduced (NADH) generated from NAD+. The ADH activity was assessed as reported previously and was indicated as nanomoles of NADH each and every minute per milligram of proteins (Rivera-Meza for 20?min in 4C, as well as the supernatant was collected. The ADH and ALDH activity within the examples had been assessed by duplicate in 10 and 5?l of supernatant respectively, mainly because described previously. ADH and ALDH actions had been indicated as micromoles of NADH each and every minute per gram of cells. Statistical analyses Data had been indicated as means??SE. Statistical variations had been analyzed by Student's administration from the AdV-ADH/asALDH2 vector Influence on the voluntary ethanol intake of alcohol-dependent pets Rats from the high alcohol-drinking UChB range had been rendered alcoholic beverages dependent by a short 60-day time amount of voluntary ethanol intake (24?h/day time) where pets reached a voluntary ethanol consumption of 6C7?g ethanol/kg/day time (see also Ocaranza didn't affect ethanol intake. The daily drinking water usage in pets getting the AdVCADH/asALDH2 vector had not been not the same as that of pets that received the control vector (data not really shown). Dedication of bloodstream acetaldehyde amounts After completing the voluntary ethanol usage period, ethanol was eliminated and the pets had been allowed a 7-day time amount of abstinence. Thereafter, arterial acetaldehyde amounts had been measured at differing times following a administration of the dosage of ethanol (1?g/kg, we.p.). Shape?4 indicates that upon ethanol administration, rats treated using the AdVCADH/asALDH2 vector displayed elevated degrees of bloodstream acetaldehyde having a maximum at 5C10?min after ethanol administration that was 400% (results elicited from the administration from the AdV-ADH/asALDH2 vector on ethanol usage and bloodstream acetaldehyde amounts were found to become in keeping with the adjustments measured LY 2874455 within the liver organ actions of ADH and ALDH2 enzymes. Shape?5A demonstrates liver organ ADH activity LY 2874455 in pets transduced using the AdV-ADH/asALDH2 vector was 176% (aftereffect of the antisense RNA against manifestation was substantially lower weighed against the result of rADH47His. Upon the administration of the moderate dosage of ethanol (1?g/kg, we.p.), the pets treated with AdVCADH/asALDH2 demonstrated a designated elevation within the arterial acetaldehyde amounts reaching a maximum at 5C10?min post-injection, that was 5-fold greater than that detected within the control pets. Since bloodstream acetaldehyde amounts reflect the total amount between its hepatic era by ADH and its own degradation by ALDH, the kinetics of bloodstream acetaldehyde amounts within the pets treated with AdVCADH/asALDH2 are in keeping with the adjustments detected within the comparative ADH and ALDH liver organ activities. Therefore, the original LY 2874455 burst of bloodstream acetaldehyde (2.5C10?min) after ethanol administration may likely be because of the large activity of the fast rADH47His, even though.
Background In the present study, extracts ready through the leaves of Roxb. and human being PBLs. The anti-HIV activity can be mediated through inhibition of HIV-1 protease activity. Both components didn't disturb the integrity of monolayer shaped by intestinal epithelial Caco-2 cells. The components when examined up to 100?g/ml didn't significantly decrease the viability of and anti-HIV activity and initial safety profile from the components prepared through the leaves of Roxb. (Anacardiaceae) is recognized as Tintidika in Sanskrit vocabulary, broadly distributed in Nepal, North India, Bhutan and Sri Lanka in the altitudinal selection of 700C1100?m . It really is documented in Ayurvedic pharmacopoeia as having restorative uses for Vta vikra, the problems linked to neurological disorders including anxiousness, sleeping disorders, epilepsy, and arthritis rheumatoid . In Nepal, fruits of are also utilized for human usage and decoction of fruits or stem bark utilized to treatment dysentery [17,18]. Bark draw out is used externally on wounds and little twigs are utilized for cleaning tooth . In a few tribal areas, infusions of leaves received in cholera . Phytochemicals like gallic acidity, some flavones viz., rutin, Urapidil hydrochloride myricetin, quercetin, myricitrin, quercitrin, kampferol plus some glycosides (isorhamnetin-3–L-arabinoside) have already been isolated through the vegetable [16,21]. The existing research was undertaken to judge anti-HIV property from the aqueous and 50% ethanolic components ready from leaves of using assays. Further, pre-clinical protection profile of the components regarding viability of sp., epithelial cell monolayer integrity and secretion of pro-inflammatory cytokines by genital keratinocytes continues to be studied. Methods Assortment of vegetable material Refreshing leaves (1?kg) from the crazy vegetable were collected in-may 2008 from Khairna, Nainital, India (Accession Number-NBRH16) and specimen continues to be submitted to Herbarium of Country wide Botanical Study Institute (NBRI), Lucknow, India. The vegetable material was collected and identified by Dr. A. K. S. Rawat, who is a taxonomist/botanist, Pharmacognosy Department, NBRI, Lucknow. The leaves were air and shade dried, grinded and strained through a mesh (size 30, mesh opening 0.5?mm). Preparation of 50% ethanolic and aqueous extracts To prepare 50% ethanolic extract, leaves powder (100 gm) was charged in a percolator, treated with ethanol: water (500?ml, 1:1?v/v) and left overnight at 25-30C. The percolate (300?ml) was drained and the marc extracted thrice by cold percolation, each time with 500?ml of ethanol: water (1:1?v/v) and the combined percolate (1200?ml) was evaporated at 40-45C under vacuum to concentrate the extract up to 80?ml. The concentrated 50% ethanolic extract was lyophilized at ?20 to ?40C to afford 8-10% dried extract. To prepare aqueous extract, leaves powder (100 gm) was Urapidil hydrochloride treated with 500?ml of MilliQ water at 65-75C for 6C8?h. The hot water extract was filtered through Whatman filter paper number 1 1. The marc was extracted thrice, each time with 500?ml of water at 60-75C. The combined filtrate (1200?ml) was distilled at 45-50C under vacuum to Urapidil hydrochloride afford concentrated aqueous extract up to 70?ml. The extract was subsequently, lyophilized at Rabbit Polyclonal to 5-HT-2C ?20 to ?40C to afford 9-11% dried extract. Both aqueous and 50% ethanolic extracts were characterized by High Performance Liquid Chromatography (HPLC), wherein 20?l of the respective extract (1?mg/ml) was resolved by C18 column (Cap cell Pak C18, Phenomenex, CA, USA) using an isocratic acetonitrile and water supplemented with 10?mM formic acid (35:65; v/v), at a flow rate of 0.4?ml/min. The elution profile was monitored at 280?nm. Cell maintenance and HIV Anti-HIV assays were performed using TZM-bl [recombinant HeLa cell line expressing high levels of CD4, HIV-1 co-receptors CCR5 & CXCR4 with -galactosidase and luciferase reporter genes under HIV-1 long terminal repeat (LTR) promoter] and CEM-GFP [a CD4+ T-lymphocytic reporter cell line expressing green fluorescent protein (GFP) under Urapidil hydrochloride HIV-1 LTR promoter] reporter cells. Urapidil hydrochloride TZM-bl cells were maintained in Dulbecco's modified Eagles medium (DMEM; Sigma-Aldrich Inc., St..
This study targeted at acquiring knowledge around the hypoglycemic mechanisms of sodium metavanadate (SMV) showed that this liver glucokinase and muscle hexokinase activities increased rapidly after oral SMV was given, and that the blood glucose level was correlated closely with the activities of the two enzymes but not with the insulin level; which indicated that SMV could improve the altered glucose phosphorylation in diabetic mice independently of stimulating insulin secretion. the mice were given the test 133865-89-1 supplier solutions ( em P /em 0.05) (Table ?(Table11 and Table ?Table22). Table 1 Liver glucokinase activity level of each group (mIU/min/mg protein) thead align="center" Time (week)DM hr / Control hr / DV ( em n /em =9)D ( em n /em =9)CV ( em n /em =6)C ( em n /em =6) /thead 01.290.641.330.88#24.563.9524.874.77?115.361.57*1.040.45#26.454.0225.302.38?214.652.16*1.460.57#25.693.1823.943.86?316.491.54*1.180.66#24.094.6925.714.48?415.532.26*1.550.73#26.193.5424.013.81?516.011.76*1.320.75#25.023.4126.454.55? Open in a separate windows * em P /em 0.01 vs DV (0 week) # em P /em 0.05 em P /em 0.05 ? em P /em 0.05 Table 2 Muscle hexokinase activity level of each group (mIU/min/mg protein) thead align="center" Time (week)DM hr / Control hr / DV ( em n /em =9)D ( em n /em =9)CV ( em n /em =6)C ( em n /em =6) /thead 01.930.502.060.69#27.025.5926.826.05?118.621.71*1.860.53#28.174.7925.915.81?217.933.49*1.920.86#26.425.8727.314.51?318.842.58*2.551.15#28.085.7026.875.57?419.253.25*1.730.89#26.926.3228.074.78?518.832.83*2.711.94#27.384.8627.456.35? Open in a separate windows * em P /em 0.01 vs DV (0 week) # em P /em 0.05 em P /em 0.05 ? em P /em 0.05 Effects of SMV on blood glucose level in the experimental mice After being given the SMV solution for one week, the blood glucose of the DV group decreased obviously ( em P /em 0.01), and remained so in the 5 weeks SMV was given towards the DV group. As the blood glucose degrees of CV, C and D groupings were not considerably transformed ( em P /em 0.05) (Desk BTLA ?(Desk33). Desk 3 Blood sugar degree of each group (mmol/L) thead align="middle" Period (week)DM hr / Control hr / DV ( em n /em =9)D ( em n /em =9)CV ( em n /em =6)C ( em n /em =6) /thead 018.771.2818.741.21#5.770.335.910.44?18.940.94*19.962.01#6.010.175.370.38?29.830.22*17.491.47#5.480.356.070.18?37.920.71*18.381.02#5.920.235.450.49?48.091.07*19.150.91#6.270.315.640.26?59.470.93*18.311.84#5.380.515.690.36? Open up in another home window * em P /em 0.01 vs DV (0 week) # em P /em 0.05 133865-89-1 supplier em P /em 0.05 ? em P /em 0.05 Ramifications of SMV on insulin level within the experimental mice In the complete period, the insulin degree of the DV, D and C groups weren't significantly changed ( 133865-89-1 supplier em P /em 0.05), as the insulin degree of the CV group was obviously decreased after SMV was presented with to it for just one week ( em P /em 0.01) (Desk ?(Desk44). Desk 4 Insulin degree of each group (mU/L) thead align="middle" Period (week)DM hr / Control hr / DV ( em n /em =9)D ( em n /em =9)CV ( em n /em =6)C ( em n /em =6) /thead 06.330.86*5.930.95#29.411.7429.781.87?16.321.28*6.350.83#24.482.2528.531.46?26.310.66*6.010.62#23.842.1329.452.35?37.261.02*6.111.19#24.111.9829.080.97?45.980.79*7.210.76#23.921.7628.461.02?55.490.94*6.321.08#24.610.8529.812.33? Open up in another home window * em P /em 0.05 # em P /em 0.05 em P /em 0.01 vs CV (0 week) ? em P /em 0.05 DISCUSSION Glucose phosphorylation may be the first rung on the ladder of glucose metabolism in cell. The task is normally catalyzed by glucokinase within the liver organ and by hexokinase in various other organs or tissue like muscles. Inside our research, SMV got remarkable hypoglycemic results and could certainly enhance the actions of glucokinase and hexokinase, although it got no influence on bloodstream insulin in diabetic mice. Relationship analysis demonstrated that there is obvious negative relationship between the blood sugar level and glucokinase activity ( em r /em =?0.887, em P /em 0.0001) and hexokinase activity ( em r /em =?0.868, em P /em 0.0001), which meant there is obvious positive relationship between the lower of blood sugar and boost of glucokinase and hexokinase 133865-89-1 supplier actions. Recently some research got the same outcomes that many kinds of vanadate could enhance the activities of glucokinase and hexokinase (Carla et al., 2003; Satish et al., 2002; Lucia et al., 2002). Gupta et al., (1999) gave sodium orthovanadate (0.6 mg/ml) to alloxan diabetic rats; after 21 days, the activities of the significantly decreased hexokinase isozymes were restored to almost control levels, and using insulin alone also yielded the same result (Gupta et al., 1999). Some recent investigations on molecule level have exhibited that vanadate can not only impact insulin receptor level, but can also impact the post-insulin-receptor level. This may possibly provide us some evidence how SMV causes the above-mentioned effects around the glucokinase activity and hexokinase activity. One of the major effects of vanadate on insulin receptor level is that it can inhibit the action of the protein tyrosine phosphatase (PTPase). For example, vanadate can cause the phosphorylated phosphofructokinase.


Chemical characterization of fine fractions of particulate matter. Atmospheric pollutants analytical methods development and validation. Application of multivariate statistical methods (PCA, DFA, CA, APCS, TTFA, CMB, DFA etc… for the source apportionment. Black carbon, Organic carbon and Water Soluble Organic Carbon studies both in PM segregated samples and PM10, PM2,5 and PM1 samples, collected in urban and remote areas. Indoor air quality: physical-chemical characterization of fine fractions of particulate matter. NOx and VOCs photocatalytic degradation assisted by nanocrystalline TiO2.


The HELIX 7 CHIRP SI GPS G2N fish finder features CHIRP Side Imaging, CHIRP Down Imaging, CHIRP Digital Sonar, ethernet networking capability, BluetoothⓇconnectivity, one-of-a-kind AutoChartⓇLive and the new Humminbird Basemap cartogrophy built-in. The 7", ultra-wide display gives you ample room to view screens side-by-side with detailed cartography screens.
The HELIX 7 CHIRP DI GPS G2N fish finder features CHIRP Down Imaging, CHIRP Digital Sonar, ethernet networking capability, BluetoothⓇconnectivity, one-of-a-kind AutoChartⓇLive and the new Humminbird Basemap cartogrophy built-in. The 7", ultra-wide display gives you ample room to view screens side-by-side with detailed cartography screens.
The HELIX 10 CHIRP DI GPS G2N features a large 10.1" display with LED backlight, CHIRP Down Imaging and CHIRP Digital Sonar. Includes GPS chartplotting with built-in Bluetooth, Ethernet networking capabilities, AutoChart Live with depth, vegetation and bottom hardness mapping, and unit cover. Humminbird Basemap cartography built-in.


text:
Q: Combining shape objects to create a composite i have a program i have to do where i have to take individual shape objects and combine them to create a final car shape. we are given premade shapes such as front tire, back tire, body, windshield, and roof and supposed to combine them into one car shape. the code already given to me is the following:
CompositeShape shape = new CompositeShape();

  final double WIDTH = 60;
  Rectangle2D.Double body
     = new Rectangle2D.Double(0, WIDTH / 6,
        WIDTH, WIDTH / 6);
  Ellipse2D.Double frontTire
     = new Ellipse2D.Double(WIDTH / 6, WIDTH / 3,
        WIDTH / 6, WIDTH / 6);
  Ellipse2D.Double rearTire
     = new Ellipse2D.Double(WIDTH * 2 / 3, WIDTH / 3,
        WIDTH / 6, WIDTH / 6);
  shape.add(body);
  shape.add(frontTire);
  shape.add(rearTire);

now, i have to create the compositeShape class which is where the combining takes place, but im not sure what to do in the add(Shape) method. we were also told that we were supposed to use a pathiterator method, but we werent really taught about pathiterator or what we are supposed to do with it. Im not asking for someone to tell me what exactly to code, just some helpful starter points.
the first thing that came to my mind was something like this:
public class CompositeShape implements Shape  {
    Graphics2D g2;
    public void add(Shape shape){
        g2.draw(shape);
    }

but it doesnt work because i cant instantiate a new graphics object and i get a null pointer exception. after that, im pretty much stumped as to what to do. any help would be greatly appreciated. thanks!

A: Probably, instead of drawing the Shape inside the add() method, you're just supposed to store the added Shape for drawing later. You could do that by giving CompositeShape some kind of collection to hold Shapes that are added, and that's all I'd put in the add() method. Beyond that, it would depend what other behavior CompositeShape is supposed to have. If you have to be able to draw a CompositeShape, then you'll probably be given an Graphics object to draw on. You won't have to create your own. Then drawing a CompositeShape would be drawing all of the Shapes that it contains.

A: java.awt.geom.Area can combine multiple shapes with methods add, subtract, exclusiveOr, and intersect. It's a ready-made class for CompositeShape.
It seems extremely weird that you've been asked to recreate it as "CompositeShape", because Area already does what you want.
The solution could be as simple as
class CompositeShape extends java.awt.geom.Area {}
and you're done.
Or, the fact that you've been given a hint about PathIterator, it might be that you're being encouraged to manage the added shapes in a list manually, then implement all the methods of the Shape interface in terms of iterating over the other shapes.
E.g., getBounds() needs to return the rectangular bounds of the shape, so get the rectangular bounds of the first, then use Rectangle.union to join it with the bounds of the others.
And for getPathIterator(), return a new inner class implementing PathIterator that will iterate over all the shapes in your collection, and iterate the path segments of each of their getPathIterator methods, returning each path segment.
It all sounds unnecessary in practice, since the needed class already exists. I think you should get clarification on what is wanted. Good luck.

To clarify what I said about the implementation of getPathIterator, return something like this. I didn't test this. This assumes your list is called shapes.
public PathIterator getPathIterator(final AffineTransform at, final double flatness) {
    return new PathIterator() {
        private PathIterator currentPathIterator;
        private Iterator<Shape> shapeIterator = shapes.iterator();
        { nextShape(); }

        private void nextShape() {
            if (shapeIterator.hasNext()) {
                currentPathIterator = shapeIterator.next().getPathIterator(at, flatness);
            } else {
                currentPathIterator = null;
            }
        }

        public int getWindingRule() {
            return WIND_NON_ZERO;
        }

        public boolean isDone() {
            for (;;) {
                if (currentPathIterator == null) return true;
                if (!currentPathIterator.isDone()) return false;
                nextShape();
            }
        }

        public void next() {
            currentPathIterator.next();
        }

        public int currentSegment(float[] coords) {
            return currentPathIterator.currentSegment(coords);
        }

        public int currentSegment(double[] coords) {
            return currentPathIterator.currentSegment(coords);
        }
    };
}

redpajama_set_name: RedPajamaStackExchange


U.S. regulation of chemicals and contaminants in personal care products and cosmetics is falling. Falling therefore behind the rest of the world. That's according to an EWG analysis and first of all, more than 40 nations are better then the USA.
This list is as a result ranging from major industrialized economies like the United Kingdom and Germany. As well as to developing states like Cambodia and Vietnam. All have therefore enacted regulations. Given that and as a result, regulations are targeted toward the safety and ingredients in our cosmetics and personal care products.
Most noteworthy, some of these nations have restricted or completely banned more than 1,400 chemicals from cosmetic products.
Therefore and by contrast, the U.S. Food and Drug Administration has banned or restricted only NINE chemicals for safety reasons.
Source: EWG, from the EU, ASEAN,MERCOSUR, Japan, Australia, South Korea and Canada.
So regulators in some nations subject formaldehyde. It's first of all, a known carcinogen. As well as chemicals that release formaldehyde, to tight restrictions. But similar restrictions are not placed on formaldehyde and formaldehyde releasers. Those therefore used in cosmetics and other personal care products sold in the U.S.
In addition, Parabens are regulated in Japan. As well as the EU and the Southeast Asian nations. All where officials have set maximum concentration standards. In the EU and Southeast Asian nations, some parabens that EWG found in U.S. products (isobutyl and isopropyl parabens). They are not permitted in any cosmetic product.
Beginning in July 2020, the use of PFOA, that's one of the thousands of fluorinated compounds (known as PFAS). It will be restricted in cosmetics and other personal care products sold in the EU. But there are no such restrictions on this carcinogen in the U.S. So therefore EWG found 13 PFAS compounds in nearly 200 cosmetics. Also and other personal care products.
So the FDA has banned the use of triclosan. A chemical which disrupts the hormone system. This was originally in antiseptic wash products like liquid hand soaps. Although not in other consumer products. By contrast, more than 40 other nations restrict the amount of triclosan in consumer products.
This chemical, linked to reproductive and neurological harm. It is restricted in nail products in Europe and Southeast Asian nations. However and most noteworthy can be used at any level in cosmetics sold in the U.S.
Many of these toxic chemicals and contaminants are also consequently being phased out of the store-brand products offered by U.S. retailers. That's even though they are still legal in this country. They are consequently: CVS Health, Target, Rite Aid and Walgreens. All have publicly committed to restricting or banning many of these chemicals. Consequently from their own cosmetic brands in coming years.
Federal cosmetics law was put in place in 1938 for personal care products. In addition, it has not kept up with the changes to the industry. As a result, even though some retailers and other countries have. There are efforts in the current Congress to modernize the lax regulation. You know, and as a result keep pace with the international community.
So this demand is for the reason that Sens. Dianne Feinstein (D-Calif.) and Susan Collins (R-Maine) have introduced legislation.
So this legislation is to therefore give the FDA more power. Power to as result review and, if needed, regulate or even ban chemicals of concern.
However it seems like, states are as a result, not waiting for Congress to act. Thereby and because two California state legislators have introduced legislation.
Legislation to consequently ban 20 of the worst chemicals and contaminants. Those cosmetics that are known as OUR PERSONAL CARE PRODUCTS.
Consequently, a Connecticut state senator has introduced legislation to subject U.S. cosmetics to the same standards. Standards likewise as those adopted by the EU. So we would therefore get Legislation Would Therefore Ban These "Toxic Twenty" Chemicals in Cosmetics Sold in California.
So finally and most noteworthy, please see details on these chemicals. Furthermore their uses and consequently their health effects here.
The Environmental Working Group is a nonprofit, non-partisan organization. One that therefore empowers people to live healthier lives in a healthier environment. Even more and through research, advocacy and unique education tools. Therefore and hence, EWG drives consumer choice and civic action.
VIDEO: Finally, Chemicals like formaldehyde, asbestos and lead acetate have no place in our personal care products.
That's because we demand #BeautyMadeBetter.


Yesterday I chose to keep my mouth shut although I had to basically keep repeating to myself to keep my mouth shut. It was difficult but I did it. I'm unsure why sometimes we just blab whatever comes into our heads.
I need to remember the proverbs you have posted here.


Abd. pain, nausea, There are many possibilities for the cause or causes of your problem. Make an appointment to see your doctor for a complete exam to find out what is wrong.
Is it possible to have strong prgncy symptoms — sore breasts, cramps/twinges, lower backache, bloating/gas, vivid dreams - before a positive test?
This month I'm having pms symptoms of cramps, backache and sore breasts 14 days before expected period. What is causing this? Virgin. Scared.
Period a week late. Backache, cramps, sore breast, and spotting. Took 2 HPT and were neg. And I'm NOT stressed either. What could it be?
Last period was July 15-19 I've been having cramps, pain sometimes on my right side, nausea, tender breasts, back pain, bloating. Could I be pregnant?
I am not due for my period for another 2 weeks and I have cramps, bloating, tender breasts, and black discharge, but no blood at all. What is this?
In the last 7 weeks I've had a abdominal bloating backaches irregular periods black blood blood clots vaginal bleeding nauseous so sore breast?
Torn meniscus, week after, I have a sore calf and cramps in my calf & thigh, and my leg is swollen, is this normal? Are these symptoms of blood clot?
Missed period, Period like cramps on and off, sore breast and back pain. What's wrong?


text:
Carriera
Cresce tra le file della Pro Patria, con la quale debutta in Serie A a 19 anni.

Dopo due tornei con i bustocchi nel massimo campionato si trasferisce all'Atalanta dove disputa una stagione al termine della quale passa alla Lazio.

Nella capitale non disputa nemmeno una partita. Torna così alla Pro Patria, nel frattempo scesa in Serie C, contribuendo al ritorno della squadra nel campionato cadetto.

Termina la carriera dopo quattro campionati a Busto Arsizio.

Palmarès

Club

Competizioni nazionali

Lazio: 1958

Pro Patria: 1959-1960

Bibliografia

Collegamenti esterni

redpajama_set_name: RedPajamaWikipedia


text:
Q: How to mount a broken usb that just can be detected with 'dmesg' (with terminal) but not shows the /dev/usb file Loading with Rufus a Windows-Image in a USB, it was damaged, ceasing to be recognized by the system. Neither windows nor ubuntu can detect it. I've tried using Windows disk partition editor, the Rufus software itself, KDE partition (I'm using KDE Neon)... and nothing, none of these attempts have worked.
Finally I've been able to detect something with the terminal thanks to this post. Basically it uses sudo lsusb for listing the devices. In my terminal I can see the broken usb in the penultimate line:
Bus 002 Device 001: ID 1d6b:0003 Linux Foundation 3.0 root hub
Bus 001 Device 005: ID 0eef:c0aa D-WAV Scientific Co., Ltd eGalaxTouch EXC3104-1324-07.00.00
Bus 001 Device 004: ID 0cf3:e007 Qualcomm Atheros Communications
Bus 001 Device 003: ID 0bda:5696 Realtek Semiconductor Corp. Integrated_Webcam_HD
Bus 001 Device 015: ID 046d:c534 Logitech, Inc. Unifying Receiver
Bus 001 Device 019: ID 1f75:0817 Innostor Technology Corporation USB 2.0
Bus 001 Device 001: ID 1d6b:0002 Linux Foundation 2.0 root hub

But then, when it's time to use dmesg I can't see the /dev/ assignment:
[12020.461164] usb 1-1: new high-speed USB device number 20 using xhci_hcd
[12020.610146] usb 1-1: New USB device found, idVendor=1f75, idProduct=0817, bcdDevice= 0.01
[12020.610159] usb 1-1: New USB device strings: Mfr=1, Product=2, SerialNumber=3
[12020.610165] usb 1-1: Product: USB 2.0
[12020.610168] usb 1-1: Manufacturer: innostor
[12020.610172] usb 1-1: SerialNumber: 0012343171372180
[12022.483384] usb 1-1: can't set config #1, error -71

And because of this when the post talks about mounting the filesystem I don't know exactly what to do. I've tried this with the given information by dmesg. A new file call hiddev0 has appeared in /dev/usb/ then I've tried to mount it in /media/usb-drive (with sudo mount /dev/usb/hiddev0 /media/usb-drive/) but the answer is
mount: /media/usb-drive: /dev/usb/hiddev0 is not a block device.
Thanks in advance.
More helpful information.
Running usb-devices:
T:  Bus=01 Lev=01 Prnt=01 Port=00 Cnt=01 Dev#= 20 Spd=480 MxCh= 0
D:  Ver= 2.00 Cls=00(>ifc ) Sub=00 Prot=00 MxPS=64 #Cfgs=  1
P:  Vendor=1f75 ProdID=0817 Rev=00.01
S:  Manufacturer=innostor
S:  Product=USB 2.0
S:  SerialNumber=0012343171372180
C:  #Ifs= 0 Cfg#= 0 Atr= MxPwr=
cat: '/sys/bus/usb/devices/usb1/1-1/1-*:?.*/bInterfaceNumber': No such file or directory
cat: '/sys/bus/usb/devices/usb1/1-1/1-*:?.*/bAlternateSetting': No such file or directory
cat: '/sys/bus/usb/devices/usb1/1-1/1-*:?.*/bNumEndpoints': No such file or directory
cat: '/sys/bus/usb/devices/usb1/1-1/1-*:?.*/bInterfaceClass': No such file or directory
cat: '/sys/bus/usb/devices/usb1/1-1/1-*:?.*/bInterfaceSubClass': No such file or directory
cat: '/sys/bus/usb/devices/usb1/1-1/1-*:?.*/bInterfaceProtocol': No such file or directory
/usr/bin/usb-devices: 76: printf: (none): expected numeric value
I:  If#=0x Alt= 0 #EPs= 0 Cls=() Sub= Prot= Driver=

A: Given the information you have provided, it looks like there is a problem with the firmware.
As you mentioned, lsusb command is listing your device, thereby it is detecting it. But when you run the command lsblk, it does not detect your usb as a block device.
I'm not an expert with this, but it looks like the problem could be with the firmware and the driver associated with it.
Finally, nowadays, USBs have become extremely cheap. You can find USBs with 32GB storage for less than 10.


Should you be wandering around the streets of Copenhagen, Denmark, in the month of May 1999, in the old part of town they call indre byen (inner city), you would certainly go by Rundtårnet (the Round Tower), and turning a corner would find yourself on Krystalgade.
And going down that street a ways you would pass Kobenhavns Hovedbibliotek (Copenhagen Head Library), and in their windowns you would see large-format pages of original comic book art by various Danish artists, part of an exhibition displayed inside.
And hey, look, you might also notice that several windows were filled with original art from ARMAGEDDONQUEST. Suddenly interested, you would peer inside through the glass to see that there was an entire AQ Room in there: drawings on the walls (and floor), and a sofa with a complete set of the AQ Trilogy to read in comfort.
This is Det Kulørte Bibliotek (the Colored Library), the Comic Book department of Kobenhavns Hovedbibliotek. That's right, the Danish headquarters of public literacy and culture pushes comic books, and has a specialized library department just for that purpose.
Actually, there is a wealth of good stuff to push: the European comics scene--especially the French--is very vital and grandoise; American comics have had a power renaissance that hasn't topped out yet; Japanese manga is emerging as an unique pop-art form; etc. So the Danes treat comic books seriously, considering them to be just as literate and respectable an art form as "real" books, or music, or movies, and therefore have them available in libraries.
Det Kulørte Bibliotek bought four sets of my own AQ Trilogy last year, upon the apparently enthusiastic reccomendations of some young library assistants who had read AQ. The department librarian, Inge Kandil, informs me however that the books are hard to get a hold of because they are always checked out.
Inge is herself also enthusiastic about AQ, and because I live in Copenhagen wanted to include AQ and me in an exhibition of "local author/artists", with an emphasis upon the coming "New Millenium".
Being a cultural center, the library regularly holds udstillinger (exhibitions) featuring news-or-noteworthy graphic literature, presentations of original drawings by guest artists, essays and analysis of works and creators, stuff like that.
I was, of course, flattered, honored, etc, to be invited to represent ARMAGEDDONQUEST in such an exhibition, and gladly assembled the material. Most of the artwork I contributed is displayed here in the AQ Gallery of this Home Page, but also an entire 12-page Tazio story (published in Sirius' Crypt of Dawn #2 as a teaser to the AQ Trilogy).
The Exhibition will be on display throughout the month of May 1999.


text:
Book Review: The Martian Chronicles
January 18, 2017 Wendy Van Camp	4 Comments
Book Name: The Martian Chronicles
Author: Ray Bradbury
First Published: 1950
Ray Bradbury was an American fantasy, science fiction, and mystery fiction writer. He was known for his dystopian novel Fahrenheit 451 and for the science fiction and horror stories gathered together in The Martian Chronicles and The Illustrated Man. Many of Bradbury's works have been adapted into television and films and he has left his stamp on the science fiction and fantasy genres.
Bradbury was born in the mid-west, but his family moved back and forth between Waukegan, Illinios and Tucson, Arizona for most of his formative years. When Bradbury was fourteen, his family settled in Los Angeles, California and he remained in the Southern California area for much of his life. Bradbury was a reader and writer throughout his youth. He claimed that he was inspired by Edgar Rice Burroughs' John Carter of Mars series and wrote a fanfiction based on those tales at the age of twelve. He credits this series as the inspiration for The Martian Chronicles and notes that he likely would never have written about Mars at all if it was not for his love of the Burroughs' series.
Bradbury cited H.G. Wells and Jules Verne as his biggest science fiction influences, followed by Robert A. Heinlein, Arthur C. Clarke, Theodore Sturgeon, and A. E. van Vogt. As Bradbury matured, he drew more from the style and works of Alexander Pope and poet John Donne. When later asked about the lyrical nature of his prose, Bradbury replied that it came, "From reading so much poetry every day of my life. My favorite writers have been those who've said things well." He also has said, "If you're reluctant to weep, you won't live a full and complete life."
Bradbury did not attend college. Instead, he sold newspapers once he graduated from high school and spent much of his time reading. "Libraries raised me. I don't believe in colleges and universities. I believe in libraries because most students don't have any money. When I graduated from high school, it was during the Depression and we had no money. I couldn't go to college, so I went to the library three days a week for 10 years." Bradbury wrote Fahrenheit 451 at the UCLA's Powell Library where he rented a typewriter in one of their study rooms. The rental rate for completing the entire novel was around ten dollars since the rental of the manual typewriter was ten cents per half hour. He preferred to write on a typewriter instead of computers because that was what he was used to.
Ray Bradbury lived at home until the age of twenty-seven when he married his sweetheart, Marguerite McClure. They had four children together. He was an active member of Los Angeles Science Fiction Society where he made his first connections in the writing community of Los Angeles. From these connections, he began to meet publishers and gained a following for his work that now spans the globe. Bradbury is credited with writing 27 novels and over 600 short stories. More than eight million copies of his works, published in over 36 languages, have been sold around the world.
In his later years, Ray Bradbury became a well sought out speaker at literary events in the Southern California area. He never obtained a driver's license and did not enjoy travel. It was well known on the speaker circuit, if you wanted Ray Bradbury to speak at your event, you should arrange to have a driver come and get him. I regret that I did not take the opportunity to meet Mr. Bradbury in person before he passed away in December of 2011. He was a favorite on the literary speaker's circuit in Southern California and I personally know many writers that consider him to be an inspiration.
"Science is no more than an investigation of a miracle we can never explain, and art is an interpretation of that miracle." – Ray Bradbury, The Martian Chronicles
The Martian Chronicles is a collection of short stories based on the colonization of the planet Mars by people fleeing from an atomic devastated Earth. There is conflict between the aboriginal Martians and the colonists as they adjust to life on the new world. The stories are tied together by short vignettes, creating a loose novel in three parts.
The first third of the book tells of the first attempts by humans to land and explore on Mars. The native Martians endeavor to prevent them from returning. In the fourth story _And the Moon be Still as Bright, it is discovered that the Martians have been decimated by a plague brought by the humans, much the way that the American natives were brought down by European disease by the conquistadors. This sets the stage for the second part of the book when the humans colonize the deserted planet and set about making it into a second Earth. The final part of the book occurs after a global nuclear war on Earth cuts off contact between the two worlds. The few surviving humans that remain on Mars become the new Martians and the circle of life continues.
My first exposure to The Martian Chronicles was during the 1980s when the mini-series starring Rock Hudson came out in 1980. Hudson played one of the colonists from the fourth Martian expedition who later returned with his family to colonize Mars. I have never forgotten the scene when Hudson playing Col. John Wilder takes his children to a Martian canal and points at their reflection in the water. "There are the Martians." He tells them. One day there will be humans to do this and not all that far in the future.
I have always loved the ERB series, John Carter of Mars, and between the two, a love for stories about the red planet has grown in me. After The Martian Chronicles mini-series, I made a point to seek out the original book. While I enjoyed the written stories, I think that in this case, I prefer the mini-series, although Ray Bradbury himself thought it boring! You can still see all three episodes today on YouTube. ONE TWO THREE
The science behind the stories is sorely outdated. Back when Bradbury wrote the stories, it was believed that Mars had more atmosphere and it would be more hospitable to human life. Today, we know that living on Mars will be much more difficult than simply getting there and setting up homes. We will need to combat a rampant CO2 atmosphere, low gravity and live without the protection of a magnetic planetary field. Still, this is a classic science fiction tale and several of the stories in the collection are well worth reading. My personal favorites are: "Rocket Summer", "Ylla", "-And The Moon Be Still As Bright", "The Off Season", and "The Million-Year Picnic."
book reportbook reviewbooksmarsray bradburysci-fiscience fiction
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4 thoughts on "Book Review: The Martian Chronicles"
Hannah Fearless says:
I loved this book. So amazing. Such original ideas.
Wendy Van Camp says:
It is certainly a classic. 🙂 One that I think anyone who loves science fiction should read.
Tim Kimber says:
Love this review. Great background, and I never knew about the mini-series (watching it now!)
I wrote a short take on it too, over here, if you're interested: https://rightplacerighttim.com/2017/04/20/the-martian-chronicles-ray-bradbury-book-review/
Thanks Tim. I will check out your review too. 🙂

redpajama_set_name: RedPajamaCommonCrawl


text:
Monthly Review Press
MR (Castilian)
Climate & Capitalism
Money on the Left
Contact/Submission
Recent Articles Archive
Monthly Review Essays
Israeli Left Archive
By Reuven Kaminer (Posted Feb 03, 2007)
Israel, LebanonCommentary
Nostalgic? Curious? Historian?
We would like to take this occasion to present to you and your friends our new Web site data base:
ISRAELI-LEFT-ARCHIVE.ORG
The Web site is built around collections of historical documents from various important sections of the Israeli left and peace forces: Women in Black and other sections of the women's peace movement; SIAH (New Israeli Left); the Committee for Solidarity with Bir Zeit University; the Committee against the War in Lebanon; Matzpen (Israeli Socialist Organization) and other groups that grew out of Matzpen such as La'kam, Ma'avak; Avanguard and others; SHASI (Israeli Socialist Left); Yesh Gvul; Twenty-First Year; Dai La'kibush (Down with the Occupation); and others.
The data base of close to 5,000 different documents includes periodicals, position papers, press clippings, organizational texts such as invitations and minutes, etc. The material covers roughly the period of the seventies and the eighties of the previous century.
Of course, the overwhelming majority of the texts are in Hebrew, but there are many documents in English created by different groups.
Come on in and look around. There is great material for research and reference. The sight might have nostalgic value if you were around and active during the period. We would be pleased to hear any comments or criticism.
For more information, please contact shmarmel@hotmail.com or rkaminer@netvision.net.il.
Reuven Kaminer is a writer, political analyst, and veteran activist of the Left in Israel. Read his blog at <reuvenkaminer.com>. He is the author of "The Politics of Protest – The Israeli Peace Movement and the Palestinian Intifada" and innumerable other articles in Hebrew and English. He is one of the founders and editors of "Ha'gada Ha'Smolit" [The Left Bank], a leading news and commentary website in the country: hagada.org.il. Kaminer was a founding member of various protest formations such as SIAH (the New Israeli Left), the Israeli Committee for Solidarity with Bir Zeit University, and the Committee against the War in Lebanon and "Dai L'kibush" [End the Occupation]. Kaminer — along with the late Eliezer Feiler, Yael Lotan, and Latif Dori — was one of the defendants in a historic court case in 1987-1990, when the four were tried for having met with the PLO in Romania. For more information, visit a special archive of the Israeli radical Left of the seventies and the eighties: israeli-left-archive.org. He is now a member of the Control Commission of the Democratic Front for Peace and Equality and the local left-leaning branch of Peace Now in Jerusalem. He is proud that Matan Kaminer, his grandson, is one of the Israeli refuseniks who went to prison for refusing to serve in the Israeli army of occupation. The nicest compliment that he ever heard was the comment of a youngster, previously unknown to him, outside the Jaffa Military Court during the refuseniks trial, who told him that some people say that he is the grandfather of all the refuseniks.
It's Not My Fault
Freedom Fight: An interview with Milenko Srećković
Also by Reuven Kaminer
Intervention in the Name of Stability by Reuven Kaminer May 10, 2011
The Constantly Widening Gap between Words and Deeds by Reuven Kaminer June 07, 2009
On the Concept "Totalitarianism" and Its Role in Current Political Discourse by Reuven Kaminer August 15, 2007
Israeli Left Archive by Reuven Kaminer February 03, 2007
Extractivism in the Anthropocene
John Bellamy Foster
Late Imperialism and the Expropriation of the Earth.
End of Cold War Illusions
Harry Magdoff
In this reprint of the February 1994 "Notes from the Editors," former MR editors Harry Magdoff and Paul M. Sweezy ask: "The United States could not have won a more decisive victory in the Cold War. Why, then, does it continue to act as though the Cold War is still on?"
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This is something you don't see every day.
According to Recent Study, Montana Tied For "Worst Drivers" in the U.S.
CarInsuranceComparison.com has updated its driving statistics with new data and have once again determined the "Worst Drivers by State." Montana tied South Carolina with THE worst drivers in the country. Find out why.
Join Mothers Against Drunk Driving for a community discussion about the drunk driving epidemic in Montana at the Bozeman Public Library on Monday, August 4 from 6 - 8 pm.
16-year-old Ethan Couch caused a crash which took the lives of four people. At the time of the crash, Couch was 3 times over the legal blood alcohol limit for an adult at .24. His sentence - 10 years probation without a single day in jail. My thoughts at the bottom of the post.
An Arkansas woman is facing charges of public intoxication and disorderly conduct after allegedly crashing her car into a mobile home and attempting to make a pantless escape on a child's battery-powered toy truck.


text: ASP.NET IUT Project

redpajama_set_name: RedPajamaGithub


text:
Corazon narrates her struggles with post-partum stress – Nairobi News
Socialite Corazon Kwamboka has spoken about her battle with post-partum stress two months after welcoming their son with fitness enthusiast Frankie Kiarie aka Frankie JustGymIt.
Corazon shared her struggles with her fans on Instagram, saying that after the birth of her baby she found herself extremely emotional to the point that she would get agitated by every little thing happening around her.
"I had my baby in August, no one tells you how hard it's going to be, it was the best moment in my life but it was also the toughest moments for me. I found myself crying for no reason, banging doors and throwing myself on the floor, every small thing would trigger me to go nuts, like if the food did not have enough salt," she said.
World Mental Health Day. Before this day is over I would like to share a short story. I had my baby in August, no one tells you how hard it's going to be, it was the best moment in my life but it was also the toughest moments for me. I found myself crying for no reason, banging doors and throwing myself on the floor, every small thing would trigger me to go nuts, like if the food did not have enough salt. I had such a hard time, Frankie tried, I mean he really tried to make it easier but I was just pushing him away. One day I started driving in the middle of the night with my baby strapped on his seat. That's when I realized I was endangering myself and my baby and I needed help. I had been embarrassed to ask for help, embarrassed to admit that I was having a hard time, it took a huge toll on me trying to deal with it alone. I guess what I'm trying to say is it's okay to be stressed or to have blues. Surround yourself with people who love and support you and don't push them away, and when you feel you can't take it anymore, it's okay to seek help. We are just humans too. Share with me your hardest moments adjusting as moms. Let's give one another some kind and encouraging words. Love and light to all moms
A post shared by Lilythegenie (@corazon_kwamboka) on Oct 10, 2020 at 12:02pm PDT
Corazon said that Frankie tried to help her during that difficult phase but she pushed him away.
"I had such a hard time, Frankie tried, I mean he really tried to make it easier, but I was just pushing him away," she said.
She further revealed that she was too ashamed to ask for help from anyone and ended up trying to deal with everything herself, which only worsened the situation.
"I had been embarrassed to ask for help, embarrassed to admit that I was having a hard time, it took a huge toll on me trying to deal with it alone. I guess what I'm trying to say is it's okay to be stressed or to have blues," she said.
Corazon advised women going through post-partum depression to surround themselves with people who love them and to seek help when things get too tough.
"Surround yourself with people who love and support you and don't push them away, and when you feel you can't take it any more, it's okay to seek help. We are just humans too," she said.
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NewsZetu.com-Breaking news, international news, Business news, Sports news > Gossip > Corazon narrates her struggles with post-partum stress – Nairobi News


Most of all, having fun as you set the groundwork for your future!
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If you have recently graduated and your MPI student membership is about to expire, you can take advantage of this special program.


Thandie is known for roles such as Linda in The Pursuit of Happyness, Nyah Nordoff-Hall in Mission: Impossible II and Christine in Crash, for which she received a number of awards including a BAFTA Award for Best Actress in a Supporting Role. Thandie Newton bra size & body measurements are listed below.
Ranked #48 in Stuff magazine's 102 Sexiest Women in the World" in 2002!


text:
require "database_loader"

namespace :db do
  namespace :sql do
    namespace :load do
      DatabaseLoader.schemas.each do |schema|
        desc "Load SQL statements in #{schema}"
        task schema do
          DatabaseLoader.types.each do |type|
            Rake::Task["db:sql:load:#{schema}:#{type}"].invoke
          end
        end
        namespace schema do
          DatabaseLoader.types.each do |type|
            desc "Load SQL #{type.to_s.singularize} statements in #{schema}"
            task type => :environment do
              DatabaseLoader.connect_as(schema) do |connection_config|
                DatabaseLoader.enable_dbms_output
                DatabaseLoader.files(schema, type, ENV['NAME']).each do |file|
                  puts "* #{file.type}/#{file.name} ".ljust(80, "-")
                  file.username = connection_config[:username]
                  file.statements.each do |statement|
                    puts "  #{statement.excerpt}"
                    begin
                      statement.execute
                      DatabaseLoader.dbms_output do |line|
                        puts "! DBMS_OUTPUT: #{line}"
                      end
                    rescue => e
                      $stderr.puts e.message
                    end
                  end
                end
                DatabaseLoader.invalid_objects.each do |h|
                  puts "! #{h['name']} #{h['type']} #{h['status']}"
                end
                DatabaseLoader.errors.each do |h|
                  puts "! #{h['name']} #{h['type']} #{h['attribute']} at line #{h['line']}: #{h['text']}"
                end
              end
            end
          end
        end
      end
    end

    namespace :dump do
      DatabaseLoader.schemas.each do |schema|
        desc "Dump SQL statements in #{schema}"
        task schema do
          DatabaseLoader.types.each do |type|
            Rake::Task["db:sql:dump:#{schema}:#{type}"].invoke
          end
        end
        namespace schema do
          DatabaseLoader.types.each do |type|
            desc "Dump SQL #{type.to_s.singularize} statements in #{schema}"
            task type => :environment do
              connection_config = ActiveRecord::Base.connection.raw_connection.instance_variable_get("@config").symbolize_keys
              DatabaseLoader.files(schema, type, ENV['NAME']).each do |file|
                file.username = connection_config[:username]
                puts "-- #{file.type}/#{file.name} ".ljust(80, "-")
                puts file.to_s
                puts
              end
            end
          end
        end
      end
    end

    namespace :package do
      DatabaseLoader.schemas.each do |schema|
        desc "Package SQL files for remote installation in #{schema}. rake db:sql:package:#{schema} NAME=CM0000072322 COMMIT=master."
        task schema => :environment do
          unless ENV['NAME'].present?
            STDERR.puts "You have to specify NAME environment"
          end
          if ENV['COMMIT']
            files = `git diff --diff-filter=ACM --name-only #{ENV['COMMIT']} ./db/sql/#{schema}`.strip.split(/\n/).sort
          else
            files = `find ./db/sql/#{schema} -type f`.strip.split("\n").sort
          end
          connection_config = ActiveRecord::Base.connection.raw_connection.instance_variable_get("@config").symbolize_keys
          pkg_name = ENV['NAME']
          pkg_dir = File.join(DatabaseLoader.package_path, connection_config[:username].to_s.downcase)
          # Package SQL files
          mkdir_p(File.join(pkg_dir, pkg_name))
          Dir[File.join(pkg_dir, pkg_name) + "/*/"].each do |dir|
            rm_rf(dir)
          end
          DatabaseLoader.types.each do |type|
            DatabaseLoader.files(schema, type, "*").each do |file|
              next unless files.any? { |f| f.include?(file.name) }
              file.username = connection_config[:username]
              puts "-- #{file.type}/#{file.name} ".ljust(80, "-")
              sql = file.to_s
              sql += "\nEXIT\n" # tell sqlplus to exit
              # puts sql
              FileUtils.mkdir_p(File.join(pkg_dir, pkg_name, file.type.to_s))
              File.open(File.join(pkg_dir, pkg_name, file.type.to_s, file.name), "wb") { |f| f.write sql }
            end
          end
          # Generate shell script
          sh_content = DatabaseLoader::Template.new(File.read(DatabaseLoader.template_path)).render({
            "cm_number" => pkg_name.gsub(/[^\d]/, ''),
            "application" => connection_config[:username]
          })
          File.open(File.join(pkg_dir, pkg_name, "#{pkg_name}.sh"), "wb") { |f| f.write(sh_content) }
          # Generate summary
          if ENV['COMMIT']
            File.open(File.join(pkg_dir, pkg_name, "#{pkg_name}.txt"), "wb") do |f|
              f.write(`git diff --stat #{ENV['COMMIT']} ./db/sql/#{schema}`)
            end
            File.open(File.join(pkg_dir, pkg_name, "#{pkg_name}.diff"), "wb") do |f|
              f.write(`git diff #{ENV['COMMIT']} ./db/sql/#{schema}`)
            end
          end
          # Try to open the folder for manual reviewing
          system `open #{File.join(pkg_dir, pkg_name)}`
          # Cleanup & compress
          puts "Press return key to continue"; STDIN.getc
          Dir.chdir(pkg_dir)
          sh "tar cf #{pkg_name}.tar #{pkg_name}"
          ### print
          puts
          # puts "# export TWO_TASK=..."
          puts "Instructions for #{pkg_name}:"
          puts "$ tar vxf #{pkg_name}.tar"
          puts "$ cd #{pkg_name}"
          puts "$ sh #{pkg_name}.sh <#{connection_config[:username]}_user> <#{connection_config[:username]}_pwd> <#{schema}_user> <#{schema}_pwd>"
        end
      end
    end
  end
end


text:
Print Column: The Ugly, Nasty, Awful Heitkamp Political Machine
October 17, 2018 | by Rob Port
MINOT, N.D.—This week Sen. Heidi Heitkamp's campaign attempted to dunk on its opponent, Congressman Kevin Cramer, with a print ad accusing him of being insensitive.
It very quickly turned into a self own.
The ad was shaped in the form of an open letter from sexual assault survivors to Cramer responding to some of his comments related to the controversy around Supreme Court Justice Brett Kavanaugh, but some of the named women didn't give their permission to be used in the ad.
Thirteen women named in the ad are now on the record saying they didn't want to be named.
In a Facebook post, one of them said she isn't even a sexual assault survivor.
Another woman said privately she didn't learn of her inclusion in the ad until she got a call from father who, in turn, had been getting calls from friends and family thinking she'd been raped or assaulted.
It's an awful situation. One would expect someone, like Heitkamp, who has vociferously touted her record on sexual assault would be more careful in how the names of sexual assault survivors are used.
Sadly, sticking it to Cramer seems to have won out over the senator's better judgment.
Rush Limbaugh Changed My Life
Heidi Heitkamp Still Has Over $4.5 Million in Her Senate Campaign, and How She's Been Spending It Will Raise Some Eyebrows
Is It Back to Business as Usual With China?


text:
Congratulations Lizzie!
by Emma Mead | Aug 25, 2014 | Criminal Law, Driving Offences, Lizzie McLaughlin
CONGRATULATIONS LIZZIE! It is with very mixed feelings today that we farewell our beloved Lizzie McLaughlin. Lizzie has made the bold move to go to the Bar. Lizzie will commence her work as a barrister in September. We look forward to being amongst the first to brief...
School's back – don't get caught!
by Burke & Mead | Jul 16, 2014 | Commercial Law, Driving Offences, Lizzie McLaughlin
School has gone back this week in NSW which means speed limits around your local school are now back down to 40 km/h on school days between 8am and 9.30am and 2.30pm and 4pm. In the 2012/2013 financial year, NSW drivers paid $142.9 million dollars to the government...
Penalty for Setting Cyclist Traps
by Burke & Mead | Jul 7, 2014 | Criminal Charges Courts & Police, Criminal Law, Emma Mead, Kara Greiner, Lizzie McLaughlin, Matthew Harper, Michael Burke, Personal Injury
The front cover of today's Newcastle Herald reported that people have been setting 'booby traps' for cyclists on the Fernleigh Track. Some of the hazards that have been reported to the police include scattering thumb tacks on the Track and stringing layers of cling...
Judge Paul Muscat: Teenage Sex Laws are 'Draconian'
by Burke & Mead | Jun 13, 2014 | Criminal Charges Courts & Police, Criminal Law, Kara Greiner, Lizzie McLaughlin, Matthew Harper, Michael Burke
South Australian Judge Paul Muscat has allowed a child sex offender to avoid a conviction on sentence determining that the laws on consensual teenage sex are 'draconian' and need to change. Judge Paul Muscat was faced with the following facts on sentence: 1. The...
Release Me! New Bail Act in NSW
by Burke & Mead | May 12, 2014 | Criminal Charges Courts & Police, Criminal Law, Kara Greiner, Lizzie McLaughlin, Matthew Harper, Michael Burke
If you know someone who is in custody because they have been refused bail, they might like to get some legal advice about whether or not the commencement of the new Bail Act will help them get bail. The new Bail Act, which will commence operation in NSW on 20 May...
The Right to Infer Guilt
With the controversial new right to silence laws under the Evidence Amendment (Evidence of Silence) Bill being assented to on the 25th March 2013, the focus is now turning to the obligations these amendments impose on those being questioned or interviewed. The new...