anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Methods and systems are provided for diagnosing early stages of inflammatory bowel disease (IBD), IBD severity predictions, and the preventions of invasive cancers associated with IBD. Deep learning methods are used for accurate histologic assessment of IBD in one or more target patients. In aspects, IBD associated dysplasia and adenocarcinoma is detected from histopathology data. For example, a deep learning model is modified and trained using a training data set comprising histopathology images to enable Bayesian deep learning. In aspects, the training data set may be labeled based on genetic and immunologic factors. A target patient can be diagnosed as having IBD at a particular severity level based on an output by the deep learned model. Additionally, a care plan for the target patient may be determined, organized, or modified based on the output provided by the deep learned model.
Patients with BRAF fusion or BRAF non-V600 mutation receive trametinib PO QD on days 1-28. Cycles repeat every 28 days in the absence of disease progression or unacceptable toxicity.
Path Pain participants will be receiving 8 weekly therapy session by license clinicians trained in the Path Pain intervention. They will also receive 4, 15-minute phone booster sessions, on a monthly basis after their final therapy session. They will also be invited to monthly group educational sessions. Both intervention and usual care participants will be receiving a pain educational booklet.
Stroke is characterized by high incidence and high rates of recurrence and other endpoint events. Risk assessment is important for secondary prevention of ischemic stroke. To date, no study has been conducted to evaluate the risk of ischemic stroke endpoint events by establishing risk accessment models combining TCM and modern medicine indicators.

The present study aims to develope a risk assessment model of ischemic stroke endpoint events combining multi-dimensional TCM indicators with modern medicine indicators. The proposed study is a registry study based participant survey conducted in 7 hospitals nationwide in China. After obtaining informed consent, a total of 3000 study patients diagnosed with ischemic stroke will be recruited. 1-year follow-ups are carried out on-site in hospitals and by telephone to track endpoint events. Comparative analysis of prevalence of endpoint events and other TCM or modern medicine features in different groups is conducted using frequency analysis and chi-squared tests, and expressed with composition ratios. Comparative analysis of quantitative scores of the scales and related syndromes or symptoms is conducted using rank-sum test. Correlation analysis of endpoint events and TCM or modern medicine factors will be performed using multivariate Cox proportional hazard model.

Participants in the exposed group were treated with QLC, and those in the non-exposed group were not treated with QLC. All participants in two groups received standard treatment without restriction. The intervention course of QLC was 12 weeks. All participants returned for in-person follow-up visits at the 12th week and 24th week. Primary outcome measures included a modified Rankin Scale (mRS), the National Institute of Health Stroke Scale (NIHSS), and the Barthel Index (BI). Secondary outcome measures included TCM syndromes (Qi deficiency syndrome score, blood stasis syndrome score), psychological index (self-rating depression scale, SDS; self-rating anxiety scale, SAS), blood lipid index, blood coagulation index, and homocysteine. Multiple imputations were used for any missing data. Propensity score matching (PSM) was used to deal with any confounding factors (age, gender, scale score, etc.). Rank alignment transformation variance analysis (ART ANOVA) and generalized linear mixed model (GLMM) were introduced to improve the scientific and accuracy of repeated measurement data. All statistical calculations were carried out with R 3.6.1 statistical analysis software.
The present invention relates to a composition for preventing and treating muscular diseases, enhancing muscular function or enhancing motor ability, having as an active ingredient hydrangenol or a  Hydrangea  extract containing same. According to the present invention, the composition of the present invention is a transcription factor for muscle differentiation and development of MyoD and myogenin and enhances muscular function by protecting muscle cells. Increased expression of mTOR and p70S6K proteins increases muscle mass, and AMPK, PGC-1α and SIRT1 activation increases mitochondrial biosynthesis, thereby allowing enhanced endurance. Motor ability can be enhanced by means of increased mitochondrial electron transfer system activity and increased activity of COX and ATG5g1 which are synthetase. Therefore, the hydrangenol or the  Hydrangea  extract containing same which are disclosed in the present specification is derived from a natural product and thus can safely be used without any side effect. The composition thereof can be utilized as drugs, food products, quasi-drugs or cosmetic compositions highly effective in preventing and treating muscular diseases, enhancing muscular function and motor ability.
This study aimed to explore the underlying mechanism of neddylation in macrophage polarization during sepsis. A mouse model of sepsis was established by cecal ligation and puncture (CLP). ELISA and Flow cytometry were performed to analyze the generation of pro-inflammatory factors and M1/M2 macrophage polarization, respectively. Western blotting was applied to detect NEDD8-mediated neddylation and glycolysis-related proteins. ECAR method was used to analyze the glycolysis level. HE staining was applied to detect the lung injury. The bacterial load in peritoneal cavity and peripheral blood was determined by counting the colony-forming units. The results showed the upregulated neddylation, M1 polarization and glycolysis of macrophage in patients with sepsis and CLP-challenged mice. NEDD8-mediated Cullin1 neddylation promoted M1 polarization and glycolysis to accelerate inflammation via NF-κB p65 pathway in E.coli-treated Raw264.7 cells. MLN4924 treatment alleviated sepsis by inhibiting neddylation to prevent M1 polarization in CLP-challenged mice. In summary, this study demonstrated that upregulation of NEDD8-mediated Cullin1 neddylation promotes glycolysis and M1 polarization of macrophage via NF-κB p65 pathway, accelerating inflammation in sepsis.
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To reduce the development of drug-resistant bacteria and maintain the effectiveness of Vancomycin Hydrochloride for Oral Solution and other antibacterial drugs, Vancomycin Hydrochloride for Oral Solution should be used only to treat or prevent infections that are proven or strongly suspected to be caused by bacteria.

This preparation for the treatment of colitis is for oral use only and is not systemically absorbed. Vancomycin Hydrochloride for Oral Solution must be given orally for treatment of staphylococcal enterocolitis and antibiotic-associated pseudomembranous colitis caused by Clostridium difficile. Orally administered Vancomycin Hydrochloride for Oral Solution is not effective for other types of infection.   


Parenteral administration of vancomycin is not effective for treatment of staphylococcal enterocolitis and antibiotic-associated pseudomembranous colitis caused by C. difficile. If parenteral vancomycin therapy is desired, use an intravenous preparation of vancomycin and consult the package insert accompanying that preparation.
Cancer cachexia causes skeletal muscle atrophy, impacting the treatment and prognosis of patients with advanced cancer, but no treatment has yet been established to control cancer cachexia. We demonstrated that transcutaneous application of carbon dioxide (CO2) could improve local blood flow and reduce skeletal muscle atrophy in a fracture model. However, the effects of transcutaneous application of CO2 in cancer-bearing conditions are not yet known. In this study, we calculated fat-free body mass (FFM), defined as the skeletal muscle mass, and evaluated the expression of muscle atrophy markers and uncoupling protein markers as well as the cross-sectional area (CSA) to investigate whether transcutaneous application of CO2 to skeletal muscle could suppress skeletal muscle atrophy in cancer-bearing mice. Human oral squamous cell carcinoma was transplanted subcutaneously into the upper dorsal region of nude mice, and 1 week later, CO2 gas was applied to the legs twice a week for 4 weeks and FFM was calculated by bioimpedance spectroscopy. After the experiment concluded, the quadriceps were extracted, and muscle atrophy markers (muscle atrophy F-box protein (MAFbx), muscle RING-finger protein 1 (MuRF-1)) and uncoupling protein markers (uncoupling protein 2 (UCP2) and uncoupling protein 3 (UCP3)) were evaluated by real-time polymerase chain reaction and immunohistochemical staining, and CSA by hematoxylin and eosin staining. The CO2-treated group exhibited significant mRNA and protein expression inhibition of the four markers. Furthermore, immunohistochemical staining showed decreased MAFbx, MuRF-1, UCP2, and UCP3 in the CO2-treated group. In fact, the CSA in hematoxylin and eosin staining and the FFM revealed significant suppression of skeletal muscle atrophy in the CO2-treated group. We suggest that transcutaneous application of CO2 to skeletal muscle suppresses skeletal muscle atrophy in a mouse model of oral squamous cell carcinoma.
Metastatic colorectal cancer continues to have a high fatality rate, with approximately only 14% of patients surviving more than 5 years. To improve the survival rate of these patients, the development of new therapeutic drugs is a priority. In this study, we investigated the effects of Oroxylin A on the metastasis of human colorectal cancer cells and its potential molecular mechanism. This study utilised CCK8 assay, transwell assay, flow cytometry, western blot analysis, molecular docking, HE staining, immunofluorescence staining, and xenograft models. The proliferation, migration, and invasion of colon cancer cells were effectively suppressed by Oroxylin A in a dose-dependent manner. Oroxylin A has the potential to inhibit the process of epithelial‒mesenchymal transition (EMT) by upregulating the expression of E-cadherin, a marker associated with epithelial cells, while downregulating the levels of N-cadherin, Snail, vimentin, and slug, which are markers associated with mesenchymal cells. In addition, 200 mg/kg of Oroxylin A inhibited the growth of colorectal tumours. Molecular docking technology revealed that Oroxylin A can bind to TGFβ and inhibit the activation of the TGFβ-smad signalling pathway. The overexpression of TGFβ weakened the inhibitory effect of Oroxylin A on the proliferation, migration, and invasion of human colorectal cancer cells, as well as the promoting effect on apoptosis. Oroxylin A inhibited the activation of the TGF-smad signalling pathway and the EMT process, thereby suppressing the migration and invasion of human colorectal cancer cells.
PURPOSE:To provide a drug containine humulong or lupulone obtained by extracting hop with a specific solvent as active component, capable of lowering the blood sugar level, and useful as an antidiabetic agent having low side effects. CONSTITUTION:The agent contains humulone or lupulone as active components. The components can be prepared as follows. The granules of hop are extracted with an alcohol, the extract is evaporated to dryness, and the residue is extracted with ether. The extract is treated in similar manner successively with alcohol and n-hexane, and the residue is dissolved in alcohol. Alcoholic lead acetate is added to the solution, the precipitate is filtered and dissolved in alcohol, the solution is made acidic with hydrochloric acid, filtered, and the filtrate is extracted with petroleum ether to obtain humulone. The filtrate obtained after the addition of the alcoholic lead acetate is concentrated, washed with saline water, and extracted with petroleum ether to obtain lupulone. The agent can be administered orally without causing hypoglycemic phenomenon.
Participants will engage in concentration meditation for 40 minutes every day for a week while recording heart rate. They will focus on the sensations around the belly.
INTRODUCTION: During the last decades, the pathogenesis of cold agglutinin disease (CAD) has been well elucidated and shown to be complex. Several documented or investigational therapies have been made available. This development has resulted in major therapeutic advances, but also in challenges in choice of therapy.
AREAS COVERED: In this review, we address each step in pathogenesis: bone marrow clonal lymphoproliferation, composition and effects of monoclonal cold agglutinin, non-complement mediated erythrocyte agglutination, complement-dependent hemolysis, and other effects of complement activation. We also discuss the heterogeneous clinical features and their relation to specific steps in pathogenesis, in particular with respect to the impact of complement involvement. CAD can be classified into three clinical phenotypes with consequences for established treatments as well as development of new therapies. Some promising future treatment approaches - beyond chemoimmunotherapy and complement inhibition - are reviewed.
EXPERT OPINION: The patient's individual clinical profile regarding complement involvement and hemolytic versus non-hemolytic features is important for the choice of treatment. Further development of treatment approaches is encouraged, and some candidate drugs are promising irrespective of clinical phenotype. Patients with CAD requiring therapy should be considered for inclusion in clinical trials.
Beta-lactam antibiotics are widely used in the intensive care unit due to their favorable effectiveness and safety profiles. Beta-lactams given to patients with sepsis must be delivered as soon as possible after infection recognition (early), treat the suspected organism (appropriate), and be administered at a dose that eradicates the infection (adequate). Early and appropriate antibiotic delivery occurs in >90% of patients, but less than half of patients with sepsis achieve adequate antibiotic exposure. This project aimed to address this quality gap and improve beta-lactam adequacy using the Define, Measure, Analyze, Improve, and Control Lean Six Sigma quality improvement framework. A multidisciplinary steering committee was formed, which completed a stakeholder analysis to define the gap in practice. An Ishikawa cause and effect (Fishbone) diagram was used to identify the root causes and an impact/effort grid facilitated prioritization of interventions. An intervention that included bundled education with the use of therapeutic drug monitoring (TDM; i.e. drug-level testing) was projected to have the highest impact relative to the amount of effort and selected to address beta-lactam inadequacy in the critically ill. The education and TDM intervention were deployed through a Plan, Do, Study, Act cycle. In the 3 months after "go-live," 54 episodes of beta-lactam TDM occurred in 41 unique intensive care unit patients. The primary quality metric of beta-lactam adequacy was achieved in 94% of individuals after the intervention. Ninety-four percent of clinicians gauged the education provided as sufficient. The primary counterbalance of antimicrobial days of therapy, a core antimicrobial stewardship metric, was unchanged over time (favorable result; P = .73). Application of the Define, Measure, Analyze, Improve, and Control Lean Six Sigma quality improvement framework effectively improved beta-lactam adequacy in critically ill patients. The approach taken in this quality improvement project is widely generalizable to other drugs, drug classes, or settings to increase the adequacy of drug exposure.
INTRODUCTION: Numerous studies have linked deficits in Theory of Mind (ToM) with language problems. We aimed to explore the similarities and differences between children's patterns of performance on a ToM task that requires minimal linguistic skill and a pragmatic inference task that relies on both ToM and language. We assessed variability in pragmatic inference skills and ToM across populations of children (8-14 years) displaying varying cognitive profiles. We further compared the sensitivity of ToM versus pragmatic ability to core language skills, memory and executive functioning (EF).
METHOD: ToM was tested using the Social Attribution Task (SAT-MC-II). Pragmatic ability was assessed in an implicature comprehension task. Receptive vocabulary, grammar comprehension, short-term and working memory (STM and WM) capacity and EF were measured using Hungarian adaptations of standard tasks and tests developed by the authors' lab. In addition to typically developing (TD) children (n = 33), we included children with neurodevelopmental disorders where ToM and/or language abilities are vulnerable: autism spectrum disorder (ASD, n = 26), attention deficit hyperactivity disorder (ADHD, n = 25) and developmental language disorder (DLD, n = 18).
RESULTS: Results revealed a significant but only moderate positive correlation between pragmatic inference and ToM indicating that the two abilities are related but distinct. The ASD group showed impairments in both ToM and pragmatic inference ability but no significant deficit was observed in ADHD or DLD relative to TD children in either skill. However, while SAT-MC-II results were only affected by verbal WM and vocabulary measures, pragmatic performance was associated with STM, verbal WM, EF, grammatical skills and vocabulary.
CONCLUSION: Our findings indicate that disentangling the contributions of different cognitive skills to ToM tasks may help clarify the role of ToM in language skills and identify distinct patterns of ToM and pragmatic skills in developmental disorders.
BACKGROUND: The mitochondrial unfolded protein response (UPRmt) is an evolutionarily conserved mitochondrial response that is critical for maintaining mitochondrial and energetic homeostasis under cellular stress after tissue injury and disease. Here, we ask whether UPRmt may be a potential therapeutic target for ischemic stroke.
METHODS: We performed the middle cerebral artery occlusion and oxygen-glucose deprivation models to mimic ischemic stroke in vivo and in vitro, respectively. Oligomycin and meclizine were used to trigger the UPRmt. We used 2,3,5-triphenyltetrazolium chloride staining, behavioral tests, and Nissl staining to evaluate cerebral injury in vivo. The Cell Counting Kit-8 assay and the Calcein AM Assay Kit were conducted to test cerebral injury in vitro.
RESULTS: Inducing UPRmt with oligomycin protected neuronal cultures against oxygen-glucose deprivation. UPRmt could also be triggered with meclizine, and this Food and Drug Administration-approved drug also protected neurons against oxygen-glucose deprivation. Blocking UPRmt with siRNA against activating transcription factor 5 eliminated the neuroprotective effects of meclizine. In a mouse model of focal cerebral ischemia, pretreatment with meclizine was able to induce UPRmt in vivo, which reduced infarction and improved neurological outcomes.
CONCLUSIONS: These findings suggest that the UPRmt is important in maintaining the survival of neurons facing ischemic/hypoxic stress. The UPRmt mechanism may provide a new therapeutic avenue for ischemic stroke.
Schistosomiasis remains the most devastating neglected tropical disease, affecting over 240 million people world-wide. The disease is caused by the eggs laid by mature female worms that are trapped in host's tissues, resulting in chronic Th2 driven fibrogranulmatous pathology. Although the disease can be treated with a relatively inexpensive drug, praziquantel (PZQ), re-infections remain a major problem in endemic areas. There is a need for new therapeutic drugs and alternative drug treatments for schistosomiasis. The current study hypothesized that cysteinyl leukotrienes (cysLTs) could mediate fibroproliferative pathology during schistosomiasis. Cysteinyl leukotrienes (cysLTs) are potent lipid mediators that are known to be key players in inflammatory diseases, such as asthma and allergic rhinitis. The present study aimed to investigate the role of cysLTR1 during experimental acute and chronic schistosomiasis using cysLTR1-/- mice, as well as the use of cysLTR1 inhibitor (Montelukast) to assess immune responses during chronic Schistosoma mansoni infection. Mice deficient of cysLTR1 and littermate control mice were infected with either high or low dose of Schistosoma mansoni to achieve chronic or acute schistosomiasis, respectively. Hepatic granulomatous inflammation, hepatic fibrosis and IL-4 production in the liver was significantly reduced in mice lacking cysLTR1 during chronic schistosomiasis, while reduced liver pathology was observed during acute schistosomiasis. Pharmacological blockade of cysLTR1 using montelukast in combination with PZQ reduced hepatic inflammation and parasite egg burden in chronically infected mice. Combination therapy led to the expansion of Tregs in chronically infected mice. We show that the disruption of cysLTR1 is dispensable for host survival during schistosomiasis, suggesting an important role cysLTR1 may play during early immunity against schistosomiasis. Our findings revealed that the combination of montelukast and PZQ could be a potential prophylactic treatment for chronic schistosomiasis by reducing fibrogranulomatous pathology in mice. In conclusion, the present study demonstrated that cysLTR1 is a potential target for host-directed therapy to ameliorate fibrogranulomatous pathology in the liver during chronic and acute schistosomiasis in mice.
The antibiotic regimens will be according to the local hospital's antibiotic guideline for cholangitis (e.g. dosage form, dosage, frequency)and/or the national SWAB guideline in the Netherlands. In the experimental group, duration of ABT after adequate drainage will be 1 day. The duration will be 4 days and can be extended to 7 days in case of gram-negative bacteraemia, according to the national SWAB guideline regarding gram-negative sepsis.
The growing prevalence of obesity in older adults including many older Veterans, has become a major concern in the US already strained health care system in general and in the VA in particular. In older adults, obesity exacerbates the age-related decline in physical function resulting in frailty, decrease in quality of life, loss of independence, and increase in nursing home admissions. The investigators' group demonstrated that weight loss from lifestyle therapy improves physical function and ameliorates frailty but the improvement was modest at best and most obese older adults remained frail. More importantly, there are concerns that the weight-loss induced loss of muscle and bone mass could worsen underlying age-related sarcopenia and osteopenia in the subset of frail obese elderly. Metformin, a biguanide, is a widely available drug used as first line treatment of type 2 diabetes. Animal studies suggest that metformin improves health span and increases lifespan, hence may represent a novel intervention for frailty. Because metformin reduces cellular senescence and senescence-associated phenotype (SASP), it is believed to retard accelerated aging most especially in older adults with obesity. The objective is to conduct a head-head comparative efficacy, placebo controlled, randomized controlled trial to test the hypothesis that lifestyle therapy + metformin for six months will be more effective than lifestyle therapy alone or metformin alone in improving physical function and preventing the weight loss-induced reduction in muscle and bone mass in obese (BMI \> 30 kg/m2) older (age 65 years) Veterans with physical frailty.
Capsule vancomycin 125 mg x 4 times daily p.o. for 7-14 days followed by Rectal bacteriotherapy with 200 ml suspension of a fixed mixture of bacterial strains administrated with a rectal catheter.