anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Ventral hernia repairs in the primary fascial group will be performed similarly except prior to placement of the mesh, the defect will be closed. After the defect size is measured, the mesh will be chosen based upon the unclosed defect size and size will not be adjusted. The hernia defect will be closed as described previously 9,10 with 0-prolene transfascial sutures placed every 1-2 cm. The two caudal-most and cranial-most sutures will be placed. The abdomen will be desufflated and these sutures will be secured. The abdomen will be reinsufflated to 15 mm Hg and the defect progressively closed. Upon completion of fascial closure, the mesh will be placed in the standard fashion as describe above. The lateral overlap will be increased due to the fascial closure.
Gene directed group（PMs）： Voriconazole was intravenously administered 2 times at the loading dose of 4mg/Kg at 12h intervals , followed by maintenance dosing 3mg/Kg at 12h intervals . Voriconazole was oral administered 2 times at the loading dose of 200mg or 100mg（weight\>40Kg or \<40Kg）at 12h intervals , followed by maintenance dosing 100mg . Voriconazole was sequential therapy administered 2 times at the loading dose of 4mg/Kg at 12h intervals , followed by maintenance dosing 100mg.
Glycosylphosphatidylinositol (GPI)-anchored proteins are located at the cell surface by a covalent attachment between protein and GPI embedded in the plasma membrane. This attachment is catalyzed by GPI transamidase comprising five subunits (PIGK, PIGS, PIGT, PIGU, and GPAA1) in the endoplasmic reticulum. Loss of either subunit of GPI transamidase eliminates cell surface localization of GPI-anchored proteins. In humans, pathogenic variants in either subunit of GPI transamidase cause neurodevelopmental disorders. However, how the loss of GPI-anchored proteins triggers neurodevelopmental defects remains largely unclear. Here, we identified a novel homozygous variant of PIGK, NM_005482:c.481A > G,p. (Met161Val), in a Japanese female patient with neurodevelopmental delay, hypotonia, cerebellar atrophy, febrile seizures, hearing loss, growth impairment, dysmorphic facial features, and brachydactyly. The missense variant was found heterozygous in her father, but not in her mother. Zygosity analysis revealed that the homozygous PIGK variant in the patient was caused by paternal isodisomy. Rescue experiments using PIGK-deficient CHO cells revealed that the p.Met161Val variant of PIGK reduced GPI transamidase activity. Rescue experiments using pigk mutant zebrafish confirmed that the p.Met161Val variant compromised PIGK function in tactile-evoked motor response. We also demonstrated that axonal localization of voltage-gated sodium channels and concomitant generation of action potentials were impaired in pigk-deficient neurons in zebrafish, suggesting a link between GPI-anchored proteins and neuronal defects. Taken together, the missense p.Met161Val variant of PIGK is a novel pathogenic variant that causes the neurodevelopmental disorder.
Participants received mycophenolate mofetil (MMF) 0.75 to (-) 1 gram (g), orally (PO), twice daily (BID) from Day 0 through Month 12. Participants also received tacrolimus 0.1-0.15 milligrams per kilogram (mg/kg), PO, BID to reach a target trough dose of 8-10 nanograms per milliliter (ng/mL) from Day 0 through Month 3; the dose was adjusted to reach a target trough level of 7-10 ng/mL in Month 3 and continued through Month 12. Participants also received corticosteroids per center practice.
The principal aim of this study is to extend our evaluation of the PROMETA® Treatment Protocol as a means to improve neurocognitive functioning in recently detoxified alcohol dependent subjects. For many alcohol dependent patients entering treatment, a range of neurocognitive deficits are present that not only had adverse effects on the patient's ability to function and think clearly but these deficits also impair the process of addiction treatment. For example, alcohol dependent subjects typically experience high levels of alcohol craving in the early stages of treatment. The patient is left with the choice of relieving craving by drinking alcohol to provide immediate relief of craving symptoms or abstaining from alcohol to obtain long-term benefits from recovery of the complications from excessive drinking. We have previously shown in open label trials that the PROMETA® Treatment Protocol helps stimulant abusers in the early stages of recovery, have relatively low rates of relapse to stimulant use. It is not clear if the Protocol is effective because of less urges to use stimulants or the ability to resist these urges is improved from a recovery of Neurocognitive functioning. The present proposal extends our previous research by comparing the efficacy of the PROMETA® Treatment Protocol in a double blind placebo controlled trial using a new population of substance abusers (alcohol dependent subjects) and assessing the effects of the PROMETA® Treatment Protocol on neurocognitive functioning, particularly those aspects of functioning that affect the ability to make decisions that have important long-term benefits.
Metabolic dysfunction-associated steatotic (fatty) liver disease (MASLD), previously termed non-alcoholic fatty liver disease, is a worldwide epidemic that can lead to hepatic inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The disease is typically a component of the metabolic syndrome that accompanies obesity, and is often overlooked because the liver manifestations are clinically silent until late-stage disease is present (i.e., cirrhosis). Moreover, Asian populations, including Koreans, have a higher fraction of patients who are lean, yet their illness has the same prognosis or worse than those who are obese. Nonetheless, ongoing injury can lead to hepatic inflammation and ballooning of hepatocytes as classic features. Over time, fibrosis develops following activation of hepatic stellate cells, the liver's main fibrogenic cell type. The disease is usually more advanced in patients with type 2 diabetes mellitus, indicating that all diabetic patients should be screened for liver disease. Although there has been substantial progress in clarifying pathways of injury and fibrosis, there no approved therapies yet, but current research seeks to uncover the pathways driving hepatic inflammation and fibrosis, in hopes of identifying new therapeutic targets. Emerging molecular methods, especially single cell sequencing technologies, are revolutionizing our ability to clarify mechanisms underlying MASLD-associated fibrosis and HCC.
Lymphangioleiomyomatosis (LAM) is a rare disease of women that is characterized by a proliferation of abnormal smooth muscle-like cells (LAM cells) in the lungs, which leads to cystic destruction of the lung parenchyma, in the axial lymphatics, resulting in lymphangioleiomyomas, and in abdominal angiomyolipomas, primarily in the kidneys. Lymphangioleiomyomas may cause abdominal distension and compress abdominal organs, producing obstipation, bladder obstruction and neurological deficits. Leakage of chyle may be responsible for ascites and pleural effusions. The lymphangioleiomyomas may change in size during the day. This variation in tumor size may be due to increased chyle formation or alterations in lymphatic flow. These studies however, were not performed with research subjects who were fasting. Our hypothesis is that the ingestion of food increases chyle formation and lymphatic flow, which in turn increases the size of the lymphangioleiomyomas. The aim of this study is to test this hypothesis. We propose to conduct a study in 30 LAM patients who have lymphangioleiomyomas to determine whether the ingestion of food, by increasing chyle formation and lymphatic flow, increases the size of the lymphangioleiomyomas.
Tumour active or tumour diagnostic compound (I), which concentrates in the tumour, is coupled to a compound (II), with at least two phenolic OH groups or at least one aliphatic amino group, where at least 2 OH or at least 1 NH2 groups are substituted with a polyethylene glycol chain whose polymerisation degree, n, is 5-250, and whose terminal OH group is substituted with a 1-12C alkyl ester or ether. Preferably n = 10-200 (100-110) and (I) is a cis-platin compound, tetracycline, steroid, porphin, phthalocyanine or a conventional X-ray contrast agent. (I) is formed by reacting (II) with the polyethylene glycol ester or ether (III) in solution. When (III) has a molecular weight of more than 5000 (especially more than 10,000) it is activated with cyanuric chloride. - (I) may be radio-labelled, especially as Gd-phthalocyanine metal complexes, Dy164 derivatives of e.g. phthalocyanine or radiolabelled diphosphonates for radiotherapy with L131 or L125, or are conjugated to give radio-iodo, radio-bromo or radio-metal ion activated peptides, porphins or phthalocyanines. Highly iodo-substituted compounds especially porphins and tyrosine oligomers, and boric acid esters, luminols, and radiosensitisers especially nitroimidazoles, in the form of polyethylene glycol derivatives, are also claimed.
Syndromic obesity refers to obesity occurring with additional clinical findings, such as intellectual disability/developmental delay, dysmorphic features, and congenital malformations. PURPOSE OF REVIEW: To present a narrative review regarding the genetic etiology, clinical description, and molecular diagnosis of syndromic obesity, which is a rare condition with high phenotypic variability and genetic heterogeneity. The following syndromes are presented in this review: Prader-Willi, Bardet-Biedl, Pseudohypoparathyroidism, Alström, Smith-Magenis, Cohen, Temple, 1p36 deletion, 16p11.2 microdeletion, Kleefstra, SIM1-related, Börjeson-Forssman-Lehmann, WAGRO, Carpenter, MORM, and MYT1L-related syndromes. RECENT FINDINGS: There are three main groups of mechanisms for syndromic obesity: imprinting, transcriptional activity regulation, and cellular cilia function. For molecular diagnostic, methods of genome-wide investigation should be prioritized over sequencing of panels of syndromic obesity genes. In addition, we present novel syndromic conditions that need further delineation, but evidences suggest they have a higher frequency of obesity. The etiology of syndromic obesity tends to be linked to disrupted neurodevelopment (central) and is associated with a diversity of genes and biological pathways. In the genetic investigation of individuals with syndromic obesity, the possibility that the etiology of the syndromic condition is independent of obesity should be considered. The accurate genetic diagnosis impacts medical management, treatment, and prognosis, and allows proper genetic counseling.
Thiamine Hydrochloride Injection, USP is a sterile solution of thiamine hydrochloride in Water for Injection for intramuscular (IM) or slow intravenous (IV) administration. 

Each mL contains: Thiamine hydrochloride 100 mg; chlorobutanol anhydrous (chloral derivative) 0.5%; monothioglycerol 0.5%; Water for Injection q.s. Sodium hydroxide may have been added for pH adjustment (2.5 to 4.5). 

Thiamine hydrochloride, or vitamin B1, occurs as white crystals or crystalline powder that usually has a slight characteristic odor. 

Freely soluble in water; soluble in glycerin; slightly soluble in alcohol; insoluble in ether and benzene. Thiamine is rapidly destroyed in neutral or alkaline solutions but is stable in the dry state. It is reasonably stable to heat in acid solution. 

The chemical name of thiamine hydrochloride is thiazolium,3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-5-(2-hydroxyethyl)-4- methylchloride, monohydrochloride and it has the following structural formula:
The burden of disease from dementia is a growing global concern as incidence increases exponentially with age and average life expectancy has been increasing around the world. Planning for an aging population requires reliable projections of future dementia prevalence and resource requirements, however, existing population projections are simple and have poor predictive accuracy. The Dementia Population Risk Tool (DemPoRT) will predict incidence of dementia in the population setting using multivariable modeling techniques.

The derivation cohort will consist of elderly Ontario respondents of Canadian Community Health Survey (CCHS) (2001, 2003, 2005, 2007; approximately 19 000 males and 25 000 females). Pre-specified predictors include sociodemographic, general health, behavioral, functional and health condition variables. Incident dementia will be identified through individual linkage of survey respondents to population-level administrative health care databases. Using time of first dementia capture as the primary outcome and death as a competing risk, sex-specific proportional hazards regression models will be estimated. The 2008/2009 CCHS survey be used for validation (approximately 4 600 males and 6 300 females). Overall calibration and discrimination will be assessed as well as calibration within predefined subgroups of importance to clinicians and policy makers.
1294591 Polymeric carriers for proteins BOEHRINGER MANNHEIM GmbH 17 Feb 1970 [19 Feb 1969] 7538/70 Headings C3G C3H and C3P  Copolymers to which water-insoluble proteins can be bound are derived from (a) acrylamide, (b) ethylene-maleic acid (or anhydride) copolymer and/or (c) maleic acid (or anhydride), and (d) N,N<SP>1</SP>-methylene-bisacrylamide and/or ethylene diacrylate in a weight ratio a : b : c : d of 3 : 0À5-1À5 : 0À05-4 : 0À075-0À9, the weight ratio of a : b+c being not more than 4. (Components (b) and (c) can be present simultaneously or alternatively and, thus, the above weight ratios cover the amounts of (b) and (c) which are to be used when they are present.) The copolymers can be prepared by polymerizing components (a) to (d) in the presence of free radical initiators, e.g. propionio acid nitrile or ammonium persulphate; when the ethylenemaleic acid (or anhydride) copolymer is present, graft polymerization is stated to occur. Polymerization is suitably effected in an aqueous medium which may include a phosphate buffer. The polymer obtained is desirably granulated by forcing through a sieve of the desired mesh size and then washed with water and lyophilized. For fixing of proteins, the dicarboxylic acid residues in the polymer must be in anhydride form; this can be achieved (if not already the case) by heating the lyophilized polymer at 80-120‹ C. in a vacuum or at 160- 220‹ C. at atmospheric pressure. Proteins which can be bound to the copolymer carriers include enzymes, enzyme inhibitors, antigens and anti-bodies. In examples trypsin and calf serum albumin are treated with the copolymers in aqueous medium at pH 5À2.
BACKGROUND: Medullary thyroid carcinoma (MTC) is a rare but aggressive endocrine malignancy that originates from the parafollicular C cells of the thyroid gland. Enhancer RNAs (eRNAs) are non-coding RNAs transcribed from enhancer regions, which are critical regulators of tumorigenesis. However, the roles and regulatory mechanisms of eRNAs in MTC remain poorly understood. This study aims to identify key eRNAs regulating the malignant phenotype of MTC and to uncover transcription factors involved in the regulation of key eRNAs.
METHODS: GSE32662 and GSE114068 were used for the identification of differentially expressed genes, eRNAs, enhancers and enhancer-regulated genes in MTC. Metascape and the transcription factor affinity prediction method were used for gene function enrichment and transcription factor prediction, respectively. qRT-PCR was used to detect gene transcription levels. ChIP-qPCR was used to assess the binding of histone H3 lysine 27 acetylation (H3K27ac)-enriched regions to anti- H3K27ac. RIP-qPCR was used to detect the binding between FOXQ1 and LINC00887. CCK8 and Transwell were performed to measure the proliferation and invasion of MTC cells, respectively. Intracellular reactive oxygen species (ROS) levels were quantified using a ROS assay kit.
RESULTS: Four eRNAs (H1FX-AS1, LINC00887, MCM3AP-AS1 and A1BG-AS1) were screened, among which LINC00887 was the key eRNA promoting the proliferation and invasion of MTC cells. A total of 135 genes controlled by LINC00887-regulated enhancers were identified; among them, BCL2, PRDX1, SFTPD, TPO, GSS, RAD52, ZNF580, and ZFP36L1 were significantly enriched in the "ROS metabolic process" term. As a transcription factor regulating genes enriched in the "ROS metabolic process" term, FOXQ1 could recruit LINC00887. Overexpression of FOXQ1 restored LINC00887 knockdown-induced downregulation of GSS and ZFP36L1 transcription in MTC cells. Additionally, FOXQ1 overexpression counteracted the inhibitory effects of LINC00887 knockdown on the proliferation and invasion of MTC cells and the promotion of intracellular ROS accumulation induced by LINC00887 knockdown.
CONCLUSION: LINC00887 was identified as a key eRNA promoting the malignant phenotype of MTC cells. The involvement of FOXQ1 was essential for LINC00887 to play a pro-tumorigenic role in MTC. Our findings suggest that the FOXQ1/LINC00887 axis is a potential therapeutic target for MTC.
There are no well-validated treatments for functional seizures. While specialist psychotherapy is usually recommended, the evidence for its benefit is qualified, and it can be difficult to obtain. Given the association between hyperventilation and functional seizures we explored an alternative modality, breathing control training, in a multi-site open label pilot trial. Participants with functional seizures over the age of 16 received an hour of breathing training from a respiratory physiotherapist, with a half-hour booster session a month later. Seizure frequency and Nijmegen scores (a measure of hyperventilation) were reported at baseline and follow-up, 3-4 months later. Eighteen subjects were recruited, and 10 completed follow-up. Seven of these 10 had improved seizure frequency, and 3 did not (Wilcoxon signed rank test, p = 0.09), with seizure frequency correlating with Nijmegen score (Spearman's rank correlation = 0.75, p = 0.034). The intervention was well tolerated, with no adverse events reported. These preliminary results support a potentially new approach to treating functional seizures that should prove cost-effective and acceptable, though require confirmation by a randomised controlled trial.
Within the domain of cardiovascular diseases, arrhythmia is one of the leading anomalies causing sudden deaths. These anomalies, including arrhythmia, are detectable through the electrocardiogram, a pivotal component in the analysis of heart diseases. However, conventional methods like electrocardiography encounter challenges such as subjective analysis and limited monitoring duration. In this work, a novel hybrid model, AttBiLFNet, was proposed for precise arrhythmia detection in ECG signals, including imbalanced class distributions. AttBiLFNet integrates a Bidirectional Long Short-Term Memory (BiLSTM) network with a convolutional neural network (CNN) and incorporates an attention mechanism using the focal loss function. This architecture is capable of autonomously extracting features by harnessing BiLSTM's bidirectional information flow, which proves advantageous in capturing long-range dependencies. The attention mechanism enhances the model's focus on pertinent segments of the input sequence, which is particularly beneficial in class imbalance classification scenarios where minority class samples tend to be overshadowed. The focal loss function effectively addresses the impact of class imbalance, thereby improving overall classification performance. The proposed AttBiLFNet model achieved 99.55% accuracy and 98.52% precision. Moreover, performance metrics such as MF1, K score, and sensitivity were calculated, and the model was compared with various methods in the literature. Empirical evidence showed that AttBiLFNet outperformed other methods in terms of both accuracy and computational efficiency. The introduced model serves as a reliable tool for the timely identification of arrhythmias.
Increasing rates of child neurodevelopmental vulnerability are a significant public health challenge. The adverse effect of socioeconomic adversity on offspring cognition may be mediated through elevated prenatal maternal systemic inflammation, but the role of modifiable antecedents such as maternal nutrition has not yet been clarified. This study aimed to examine (1) whether prenatal factors, with an emphasis on maternal nutrition, were associated with prenatal maternal systemic inflammation at 28 weeks' gestation, including the metabolomic marker glycoprotein acetyls (GlycA); (2) the extent to which the association between prenatal maternal nutrition and child cognition and language at age two years was mediated by elevated maternal inflammation in pregnancy; (3) the extent to which the associations between prenatal socioeconomic adversity and child neurodevelopment were mediated through prenatal maternal nutrition and GlycA levels. We used a prospective population-derived pre-birth longitudinal cohort study, the Barwon Infant Study (Barwon region of Victoria, Australia), where 1074 mother-child pairs were recruited by 28 weeks' gestation using an unselected sampling frame. Exposures included prenatal factors such as maternal diet measured by a validated food frequency questionnaire at 28 weeks' gestation and dietary patterns determined by principal component analysis. The main outcome measures were maternal inflammatory biomarkers (GlycA and hsCRP levels) at 28 weeks' gestation, and offspring Bayley-III cognition and language scores at age two years. Results showed that the 'modern wholefoods' and 'processed' maternal dietary patterns were independently associated with reduced and elevated maternal inflammation respectively (GlycA or hsCRP p < 0.001), and also with higher and reduced offspring Bayley-III scores respectively (cognition p ≤ 0.004, language p ≤ 0.009). Associations between dietary patterns and offspring cognition and language were partially mediated by higher maternal GlycA (indirect effect: cognition p ≤ 0.036, language p ≤ 0.05), but were less evident for hsCRP. The maternal dietary patterns mediated 22 % of the association between socioeconomic adversity (lower maternal education and/or lower household income vs otherwise) and poorer offspring cognition (indirect effect p = 0.001). Variation in prenatal GlycA levels that were independent of these dietary measures appeared less important. In conclusion, modifiable prenatal maternal dietary patterns were associated with adverse child neurocognitive outcomes through their effect on maternal inflammation (GlycA). Maternal diet may partially explain the association between socioeconomic adversity and child neurocognitive vulnerability. Maternal diet-by-inflammation pathways are an attractive target for future intervention studies.