anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The present invention relates to a traditional Chinese medicine additive for reducing cholesterol of poultry eggs and enhancing production performance and a preparation method thereof, which belongs to the technical field of feed. The present invention is used for solving the problems for enhancing the quality of poultry eggs and disease resistance of poultry and livestock and has the scheme that the traditional Chinese medicine additive is prepared from dandelion, dried ginger, pine needle, pilose asiabell root, etc. by mixing, drying in the sun, pulverization mixing and packaging. The additive is added into poultry feed to have the action of enhancing the appetite and production performance, regulating metabolism of poultry, promoting growth and development of laying hens and reducing the content of cholesterol. The contrast test indicates that the laying rate of laying hens fed with the traditional Chinese medicine additive is enhanced by 2.2% on average, the mortality is reduced by 28% on average, the ratio of eggs to feed is reduced by 8% on average, and the content of cholesterol is reduced by 70% on average. In addition, the additive has the characteristics of no medicine residues, no toxic or side effect, no medicine resistance, etc. and achieves the purpose that egg products have the advantages of environmental protection, nuisance free and health care.
Participants received rituximab (European Union \[EU\] formulation) on days 1 and 15 (dose 1) and a second dose of rituximab (EU formulation) at weeks 24 and 26 (dose 2). Each dose consisted of two 1000 mg intravenous infusions 2 weeks apart.
The WRKYs are a group of plant-specific transcription factors that play important roles in defense responses. In this study, we silenced 2 GmWRKY33B homologous genes using a bean pod mosaic virus (BPMV) vector carrying a single fragment from the conserved region of the GmWRKY33B genes. Silencing GmWRKY33B did not result in morphological changes. However, significantly reduced resistances to Pseudomonas syringae pv. glycinea (Psg) and soybean mosaic virus (SMV) were observed in the GmWRKY33B-silenced plants, indicating a positive role of the GmWRKY33B genes in disease resistance. Kinase assay showed that silencing the GmWRKY33B genes significantly reduced the activation of GmMPK6, but not GmMPK3, in response to flg22 treatment. Reverse transcriptase PCR (RT-PCR) analysis of the genes encoding prenyltransferases (PTs), which are the key enzymes in the biosynthesis of glyceollin, showed that the Psg-induced expression of these genes was significantly reduced in the GmWRKY33B-silenced plants compared with the BPMV-0 empty vector plants, which correlated with the presence of the W-boxes in the promoter regions of these genes. Taken together, our results suggest that GmWRKY33Bs are involved in soybean immunity through regulating the activation of the kinase activity of GmMPK6 as well as through regulating the expression of the key genes encoding the biosynthesis of glyceollins.
Nimesulide, i.e. N-(4-nitro-2-phenoxyphenyl)methane sulfonamide, uses for treatment inflammatory diseases is hard to dissolve in water. The invented water-soluble nimesulide salt consists of the product of reaction of nimesulide with L-lysine and it preferably contains approximately 1 mole of L-lysine per L mole of nimesulide. The salt is prepared by preparing separate hot methanolic solutions containing nimesulide and L-lysine respectively, which are then subsequently placed in contact with each other to obtain a mixture. Preferably aqueous solution of said nimesulide salt is obtained by combining thereof with L-arginine. The invention also concerns a pharmaceutical combination in which the nimesulide and L-lysine are combined with at least one cyclodextrin in the form of a mixture of these compounds, mixture of nimesulide salt and L-lysine with cyclodextrin, a complex of nimesulide-cyclodextrin being mixed with L-lysine or in another way a complex of nimesulide-L-lysine-cyclodextrin.
Bacterial meningitis is still a significant public health concern, with high morbidity and mortality rates. Despite this, it is still a rare event that requires the bacterial invasion of the meninges. However, some predisposing factors can trigger recurrent episodes of meningitis. This study is aimed at determining the clinical characteristics and the molecular epidemiology of episodes of recurrent community-acquired meningitis with and without predisposing factors. For this purpose, we performed a retrospective study of our laboratory database during the period of 2010 to 2020. Additionally, using molecular tools developed in our previous works, the epidemiology of the pathogens causing these episodes was analyzed using cerebrospinal fluid samples, especially in the absence of isolated strains. We observed a total of 1,779 meningitis cases and 230 were caused by Streptococcus pneumoniae. Of those, 16 were recurrent meningitis episodes (16/1,779; 0.9%) from seven patients. Pneumococcus was the main agent responsible in these recurrent episodes and only two episodes were caused by Haemophilus influenzae. The mean age of these patients was 20 years old and three had predisposing factors which could have led to contracting meningitis. The samples presented different pneumococcal serotypes. Most of them were non-vaccine-covered serotypes and antibiotic susceptible strains. Therefore, it was demonstrated how the practical employment of molecular tools, developed for research, when applied in the routine of diagnosis, can provide important information for epidemiological surveillance. Furthermore, it was shown how pneumococcus was the leading cause of recurrent community-acquired meningitis without predisposing factors, suggesting that pneumococcal vaccination may be necessary, even in those groups of individuals considered to be less susceptible.
CLL patients complete aerobic based training program on study. Patients then complete all Aim 1 activities again after completion of aerobic based training program.
Subjects classified as HER2 PET/CT negative (cohort B) will receive treatment of physician's choice (TPC) as per the best local clinical practice. Subsequent treatment will be collected and the subject will enter survival follow-up. HER2-PET/CT negative pattern: The dominant part or all of the tumour load lacks significant tracer uptake.
The present invention concerns a compound or the pharmaceutically acceptable salt thereof which has an excellent stearoyl CoA desaturase inhibiting action. The present invention provides a compound of the following formula (I): [wherein, A represents a group of the formula -CONHR1 or a group of the formula -ER2 ( wherein, R1 represents a C1-C6 alkyl group etc. for which it may be substituted independently with 1 to 5 groups selected from substituents a; E represents a 1, 3, 4 oxadiazolyl group, 1, 2, 4-oxadiazolyl group or imidazolyl group and R2 represents a C1-C6 alkyl group etc. for which it may be substituted independently with 1 to 5 groups selected from substituents a etc.); R3 represents a hydrogen atom etc.; R4 represents a hydrogen atom etc.; R5 represents a hydrogen atom etc.; R6 represents a hydrogen atom etc.; R7 represents a hydrogen atom etc.; R8 represents a hydrogen atom, and a halogen atom etc.; Z represents a nitrogen atom etc.; Y represents a nitrogen atom etc.; U represents a single bond, and a methylene group, etc.; V represents a single bond, and a methylene group, etc.; W represents a methylene group, a group of the formula -CH (OH)- etc.; m represents 0 or 1; n represents 0 or 1; substituents a represents a halogen atom, hydroxy group, and a C6-C10 aryl group for which it may be substituted independently with 1 to 5 groups selected from substituents b; substituents b represents a halogen atom, a C1-C6 alkyl group, a halogeno C1-C6 alkyl group, a hydroxyl group etc.] or the pharmaceutically acceptable salt thereof.
Primary liver cancer is the leading cause of cancer worldwide. The majority of primary liver cancers are hepatocellular carcinoma (HCC) and occur in the setting of cirrhosis of the liver. Body fat and systemic inflammation are determinants of HCC risk. Cirrhotic patients with HCC are often treated with locoregional therapies including transarterial chemoembolization (TACE) as a bridge to liver transplantation. Despite this, HCC recurrence rates approach 80%. There is a growing body of evidence to suggest the benefit of exercise in cancer patients. Exercise decreases disease recurrence and improves survival in other primary cancers by altering tumor biology and influencing response to treatment. Although animal models suggest biologic plausibility, whether or not exercise prevents HCC recurrence in cancer patients remains unknown. The overall goal of this proposal is to test the effect of exercise to delay or avert HCC recurrence and gain information regarding the potential molecular mechanisms of HCC tumor inhibition by exercise.
The study aims to develop a deep learning based automatic segmentation approach using the UNETR(U-net Transformer) architecture to quantify the volume of individual thigh muscles(27 muscles in 5 groups) for Sarcopenia assessment. By automating the segmentation process, this approach improves the efficiency and accuracy of muscle volume calculation, facilitating a comprehensive understanding of muscle composition and its relationship to Sarcopenia. The study utilized a dataset of 72 whole thigh CT scans from hip fracture patients, annotated by two radiologists. The UNETR model was trained to perform precise voxel-level segmentation and various metrics such as dice score, average symmetric surface distance, volume correlation, relative absolute volume difference and Hausdorff distance were employed to evaluate the model's performance. Additionally, the correlation between Sarcopenia and individual thigh muscle volumes was examined. The proposed model demonstrated superior segmentation performance compared to the baseline model, achieving higher dice scores (DC = 0.84) and lower average symmetric surface distances (ASSD = 1.4191 ± 0.91). The volume correlation between Sarcopenia and individual thigh muscles in the male group. Furthermore, the correlation analysis of grouped thigh muscles also showed negative associations with Sarcopenia in the male participants. This thesis presents a deep learning based automatic segmentation approach for quantifying individual thigh muscle volume in sarcopenia assessment. The results highlights the associations between Sarcopenia and specific individual muscles as well as grouped thigh muscle regions, particularly in males. The proposed method improves the efficiency and accuracy of muscle volume calculation, contributing to a comprehensive evaluation of Sarcopenia. This research enhances our understanding of muscle composition and performance, providing valuable insights for effective interventions in Sarcopenia management.
Table 1 enumerates, for a pool of the three studies in pediatric patients with ADHD, at METADATE CD doses of 20, 40, or 60 mg/day, the incidence of treatment-emergent adverse events. One study was a 3-week placebo-controlled, parallel-group trial, one study was a controlled, crossover trial, and the third study was an open titration trial. The table includes only those events that occurred in 5% or more of patients treated with METADATE CD where the incidence in patients treated with METADATE CD was greater than the incidence in placebo-treated patients. 

The prescriber should be aware that these figures cannot be used to predict the incidence of adverse events in the course of usual medical practice where patient characteristics and other factors differ from those which prevailed in the clinical trials. Similarly, the cited frequencies cannot be compared with figures obtained from other clinical investigations involving different treatments, uses, and investigators. The cited figures, however, do provide the prescribing physician with some basis for estimating the relative contribution of drug and non-drug factors to the adverse event incidence rate in the population studied.
Oral antiviral drugs will be commenced after TACE. That is: Lamivudine 100mg once daily; or Entecavir 0.5mg once daily.
Osteopontin (OPN) is a multi-functional glycoprotein that coordinates the innate immune response, prevents nanocrystal formation in renal tubule fluid, and is a biomarker for kidney injury. OPN expression is markedly increased in cystic epithelial cells of polycystic kidney disease (PKD) kidneys; however, its role in PKD progression remains unclear. We investigated the in vitro effects of recombinant OPN on the proliferation of tubular epithelial cells from PKD and normal human kidneys and in vivo effects of OPN deletion on kidney cyst formation, fibrosis, and mineral metabolism in pcy/pcy mice, a non-orthologous model of autosomal-dominant PKD. In vitro studies revealed that OPN enhanced the proliferation of PKD cells but had no effect on normal kidney cells. Deletion of OPN in pcy/pcy mice significantly reduced kidney cyst burden; however, this was accompanied by increased fibrosis and no change in kidney function. The loss of OPN had no effect on kidney macrophage numbers, cyst epithelial cell proliferation, or apoptosis. Furthermore, there was no difference in kidney mineral deposition or mineral metabolism parameters between pcy/pcy mice with and without OPN expression. Global deletion of OPN reduced kidney cyst burden, while paradoxically exacerbating kidney fibrosis in mice with cystic kidney disease.
Alcohol use disorder has been associated with the development of neurodegenerative diseases, including Alzheimer's disease (AD). However, recent studies demonstrate that moderate alcohol consumption may be protective against dementia and cognitive decline. We examined astrocyte function, low-density lipoprotein (LDL) receptor-related protein 1 (LRP1), and the NF-κB p65 and IKK-α/β signaling pathways in modulating neuroinflammation and amyloid beta (Aβ) deposition. We assessed apolipoprotein E (ApoE) in the brain of APP/PS1 mice using IHC and ELISA in response to low to moderate ethanol exposure (MEE). First, to confirm the intracerebral distribution of ApoE, we co-stained with GFAP, a marker for astrocytes that biosynthesize ApoE. We sought to investigate whether the ethanol-induced upregulation of LRP1 could potentially inhibit the activity of IL-1β and TNF-α induced IKK-α/β towards NF-κB p65, resulting in a reduction of pro-inflammatory cytokines. To evaluate the actual Aβ load in the brains of APP/PS1 mice, we performed with a specific antibody Aβ (Thioflavin S) on both air- and ethanol-exposed groups, subsequently analyzing Aβ levels. We also measured glucose uptake using 18F- fluorodeoxyglucose (FDG)-positron emission tomography (PET). Finally, we investigated whether MEE induced cognitive and memory changes using the Y maze, noble object recognition test, and Morris water maze. Our findings demonstrate that MEE reduced astrocytic glial fibrillary acidic protein (GFAP) and ApoE levels in the cortex and hippocampus in presymptomatic APP/PS1 mice. Interestingly, increased LRP1 protein expression was accompanied by dampening the IKK-α/β-NF-κB p65 pathway, resulting in decreased IL-1β and TNF-α levels in male mice. Notably, female mice show reduced levels of anti-inflammatory cytokines IL-4, and IL-10 without altering IL-1β and TNF-α concentrations. In both males and females, Aβ plaques, a hallmark of AD, were reduced in the cortex and hippocampus of APP/PS1 mice exposed to ethanol starting at pre-symptomatic stage. Consistently, MEE increased FDG-PET-based brain activities and normalized cognitive and memory deficits in the APP/PS1 mice. Our findings suggest that MEE may benefit AD pathology via modulating LRP1 expression, potentially reducing neuroinflammation and attenuating Aβ deposition. Our study implies that reduced astrocyte-derived ApoE and LDL cholesterol levels are critical for attenuating AD pathology.
BACKGROUD: It is widely acknowledged that Metformin (MET), an established medication for managing type 2 diabetes, possesses diverse pharmacological effects. This study aims to investigate the protective effects of MET against Nω-Nitro-L-arginine methyl ester (L-NAME)-induced preeclampsia (PE).
METHODS: Sprague Dawley (SD) rats were exposed to 200 mg/kg L-NAME with or without prior MET treatment. Histopathological analysis was performed using Hematoxylin and Eosin staining. Serum levels of inflammatory, antiangiogenic, and angiogenic factors were quantified using ELISA kits. Immunohistochemistry (IHC) staining was employed to observe NLRP3 and IL-1β expressions in placental tissues. Western blot and Quantitative Real-Time PCR (q-PCR) analyses were conducted to assess protein and mRNA expressions of NLRP3, caspase-1, ASC, and IL-1β.
RESULTS: We found that MET could mitigate placental histopathological deterioration and improve pregnancy outcomes in L-NAME-induced PE rat models. MET not only suppressed L-NAME-induced elevation of antiangiogenic factors but also stimulated the production of pro-angiogenic factors. Additionally, MET treatment reversed the excessive inflammatory response induced by L-NAME. Furthermore, MET inhibited the activation of the NLRP3 inflammasome triggered by L-NAME, evidenced by the downregulation of NLRP3 expression, caspase-1, and IL-1β.
CONCLUSIONS: MET demonstrates a protective effect against L-NAME-induced PE rats, potentially mediated through inhibition of the inflammatory response, downregulation of NLRP3 inflammasome expression in the placenta, and regulation of the balance between anti-angiogenic and pro-angiogenic factors.
INTRODUCTION: Excessive maternal gestational weight gain (GWG) is strongly correlated with childhood obesity, yet how excess maternal weight gain and gestational diabetes mellitus (GDM) interact to affect early childhood obesity is poorly understood. The purpose of this study was to investigate whether overall and trimester-specific maternal GWG and GDM were associated with obesity in offspring by age 6 years.
METHODS: A cohort of 10,335 maternal-child dyads was established from electronic health records. Maternal weights at conception and delivery were estimated from weight trajectory fits using functional principal components analysis. Kaplan-Meier curves and Cox regression, together with generalized raking, examined time-to-childhood-obesity.
RESULTS: Obesity diagnosed prior to age 6 years was estimated at 19.7% (95% CI: 18.3, 21.1). Maternal weight gain during pregnancy was a strong predictor of early childhood obesity (p < 0.0001). The occurrence of early childhood obesity was lower among mothers with GDM compared with those without diabetes (adjusted hazard ratio = 0.58, p = 0.014). There was no interaction between maternal weight gain and GDM (p = 0.55). Higher weight gain during the first trimester was associated with lower risk of early childhood obesity (p = 0.0002) whereas higher weight gain during the second and third trimesters was associated with higher risk (p < 0.0001).
DISCUSSION: Results indicated total and trimester-specific maternal weight gain was a strong predictor of early childhood obesity, though obesity risk by age 6 was lower for children of mothers with GDM. Additional research is needed to elucidate underlying mechanisms directly related to trimester-specific weight gain and GDM that impede or protect against obesity prevalence during early childhood.
The present invention relates to a competitive antagonist antibody that specifically binds to AMHR-II, said antibody comprising (a) a heavy chain, wherein the variable domain comprises H-CDR1 having the sequence shown in SEQ ID No. 3; H-CDR2 having a sequence as shown in SEQ ID NO. 4; and H-CDR3 having the sequence shown in SEQ ID NO. 5; and (b) a light chain, wherein the variable domain comprises at least a CDR selected from the group consisting of: L-CDR1 having a sequence shown in SEQ ID NO. 8, L-CDR2 having a sequence shown in SEQ ID NO. 9; and an L-CDR3 having the sequence shown in SEQ ID NO. 10. The invention also contemplates nucleic acid sequences encoding the antibodies, vectors comprising the nucleic acid sequences, host cells comprising the nucleic acid sequences or vectors, immunoconjugates comprising the antibodies, pharmaceutical compositions comprising the antibodies or immunoconjugates, and uses of the antibodies, cells or compositions as pharmaceuticals.
MCT8 deficiency (that is also known as Allan-Herndon-Dudley syndrome) is a rare X-linked inherited disorder of brain development that causes severe intellectual disability and problems with movement. This condition, which occurs almost exclusively in males, disrupts development from before birth. There is no sucking reflex and the child has marked hypotonia. Developmentally, unlike normal infants, affected males are unable to turn over from belly to back. Individuals with identical mutations have identical phenotypes and all individuals, regardless of the phenotype have severe neuropsychological impairment. Diagnosis is confirmed by demonstration of a mutation in the MCT8 gene (1,2).

MCT8-specific thyroid hormone cell-membrane transporter deficiency is characterized by severe cognitive deficiency, infantile hypotonia, diminished muscle mass and generalized muscle weakness, progressive spastic quadriplegia, joint contractures, and dystonic and/or athetoid movement with characteristic paroxysms or kinesigenic dyskinesias. Seizures occur in about 25% of cases. Most affected males never sit or walk independently or lose these abilities over time; most never speak or have severely dysarthric speech (1). Brain MRI obtained in the first few years of life shows transient delayed myelination, which improves by age four years (3). Although psychomotor findings observed in affected males do not occur in heterozygous females, the latter often have thyroid test abnormalities intermediate between affected and normal individuals.
1. Technical Result Increase in efficiency of treatment, reduction of side-effects, providing the stable remission and cure.          2. Essence A chemical agent 5-carbarnoyl-5H-dibenz (b,f) azepin, its derivatives and analogues are used for treating bronchial asthma, bronchospastic syndrome and diseases with such a syndrome.          3. Field of Application Medicine, therapy.
Dose-related weight gain was seen with rosiglitazone alone and rosiglitazone together with other hypoglycemic agents (see Table 6). No overall change in median weight was observed with AVANDAMET in drug-naïve patients. The mechanism of weight gain with rosiglitazone is unclear but probably involves a combination of fluid retention and fat accumulation. 

In a 4- to 6-year, monotherapy, comparative trial (ADOPT) in patients recently diagnosed with type 2 diabetes not previously treated with antidiabetic medication, the median weight change (25th, 75th percentiles) from baseline at 4 years was 3.5 kg (0.0, 8.1) for rosiglitazone, 2.0 kg (-1.0, 4.8) for glyburide, and -2.4 kg (-5.4, 0.5) for metformin.

In postmarketing experience with rosiglitazone alone or in combination with other hypoglycemic agents, there have been rare reports of unusually rapid increases in weight and increases in excess of that generally observed in clinical trials. Patients who experience such increases should be assessed for fluid accumulation and volume-related events such as excessive edema and congestive heart failure [see Boxed Warning].
It is recommended that efavirenz be taken on an empty stomach, preferably at bedtime. Table 1 describes the recommended dose of efavirenz for pediatric patients 3 months of age or older and weighing between 3.5 kg and 40 kg [see Clinical Pharmacology (12.3)]. The recommended dosage of efavirenz for pediatric patients weighing 40 kg or greater is 600 mg once daily. For pediatric patients who cannot swallow capsules, the capsule contents can be administered with a small amount of food or infant formula using the capsule sprinkle method of administration . 

  


aCapsules can be administered intact or as sprinkles [see Dosage and Administration (2.4)].

bTablets must not be crushed