anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Relapsed/refractory acute lymphoblastic leukemia (R/R ALL) continues to be a major cause of mortality in children worldwide, with around 15% of ALL patients experiencing relapse and approximately 10% eventually dying from the disease. Early identification of R/R ALL in children has posed a longstanding clinical challenge.
METHOD: Genetic analysis of survival outcomes in pediatric patients with ALL from the TARGET-ALL dataset revealed five risk score factors identified through the intersection of differential genes (relapse/non-relapse) from the GSE17703 and GSE6092 databases. A risk score equation was formulated using these factors and validated against prognostic data from 46 ALL cases at our institution. Patients from multiple datasets were stratified into high and low-score groups based on this equation. Protein-protein interaction networks (PPI) were then constructed using the intersecting differential genes from all three datasets to identify hub nodes and predict interacting transcription factors. Additionally, genes related to cell pyroptosis with varying expression across these datasets were screened, and a multifactorial ROC curve (incorporating risk score and differential expression of pyroptosis-related genes) was generated. Furthermore, relationships among variables in the predictive model were depicted using a nomogram, and model efficacy was assessed through decision curve analysis (DCA).
RESULTS: By analyzing the TARGET-ALL, GSE17703, and GSE6092 databases, we developed a prognostic risk assessment model for pediatric ALL incorporating BAG2, EPHA4, FBXO9, SNX10, and WNK1. Validation of this model was conducted using data from 46 pediatric ALL cases obtained from our institution. Following the identification of 27 differentially expressed genes, we constructed a PPI and identified the top 10 hub genes (PTPRC, BTK, LCK, PRKCQ, CD3D, CD27, CD3G, BLNK, RASGRP1, VPREB1). Using this network, we predicted the top 5 transcription factors (HOXB4, MYC, SOX2, E2F1, NANOG). ROC and DCA were conducted on pyroptosis-related genes exhibiting differential expression and risk scores. Subsequently, a nomogram was generated, demonstrating the effectiveness of the risk score in predicting prognosis for pediatric ALL patients.
CONCLUSIONS: We have developed a risk prediction model for pediatric R/R ALL utilizing the genes BAG2, EPHA4, FBXO9, SNX10, and WNK1. This model provides a scientific foundation for early identification of R/R ALL in children.
Patients will receive zunsemetinib by mouth (PO) twice per day (BID) at an assigned dose along with capecitabine (1000 mg/m\^2 PO BID on Days 1-14 an every 21-day cycle). For patients enrolled in phase Ib, capecitabine is dosed on days 2-15 during cycles 1-2. Dose escalation of zunsemetinib will utilize a 3+3 design. A maximum of 3 dose levels of zunsemetinib will be tested, and the two highest dose levels which did not lead to more than 1 of 6 patients with DLT in cycle 1 will be chosen as the RP2D-L1 and RP2D-L2 for Phase II. If only one dose level of zunsemetinib was found tolerable, then only one RP2D will be chosen for Phase II.
Long-term studies in animals have been conducted to evaluate the carcinogenic potential of metoprolol tartrate. In 2-year studies in rats at three oral dosage levels of up to 800 mg/kg/day (41 times, on a mg/m 2 basis, the daily dose of 200 mg for a 60-kg patient), there was no increase in the development of spontaneously occurring benign or malignant neoplasms of any type. The only histologic changes that appeared to be drug related were an increased incidence of generally mild focal accumulation of foamy macrophages in pulmonary alveoli and a slight increase in biliary hyperplasia. In a 21-month study in Swiss albino mice at three oral dosage levels of up to 750 mg/kg/day (18 times, on a mg/m2 basis, the daily dose of 200 mg for a 60-kg patient), benign lung tumors (small adenomas) occurred more frequently in female mice receiving the highest dose than in untreated control animals. There was no increase in malignant or total (benign plus malignant) lung tumors, nor in the overall incidence of tumors or malignant tumors. This 21-month study was repeated in CD-1 mice, and no statistically or biologically significant differences were observed between treated and control mice of either sex for any type of tumor. 

All genotoxicity tests performed on metoprolol tartrate (a dominant lethal study in mice, chromosome studies in somatic cells, a Salmonella/mammalian-microsome mutagenicity test, and a nucleus anomaly test in somatic interphase nuclei) and metoprolol succinate (a Salmonella/mammalian-microsome mutagenicity test) were negative. 

No evidence of impaired fertility due to metoprolol tartrate was observed in a study performed in rats at doses up to 22 times, on a mg/m 2 basis, the daily dose of 200 mg in a 60-kg patient.
This is a 6-month study enrolling persons with HIV with no known history of heart disease. Participants will be screened for early signs of heart failure using cardiac ultrasound (cardiac transthoracic echocardiography or cardiac TTE). Those participants who have early changes in the structure and function of the heart and may be at future risk for heart failure will be enrolled into the study. Additional imaging of the heart will occur using cardiac magnetic resonance imaging (cardiac MRI). Following baseline studies, participants will either receive a medication called sacubitril/valsartan or placebo for 6 months. Sacubitril/valsartan in an FDA approved medication currently being used for heart failure with reduced ejection fraction in the general population, and we are evaluating whether this medication could be useful to reduce HIV-related heart failure with preserved ejection fraction. Sacubitril/valsartan is an oral medication taken twice daily that may block aldosterone hormone and increase natriuretic peptide hormone. Overall, this study aims to investigate the effect of sacubitril/valsartan on measures of heart disease related to inflammation, structure and function of the heart muscle in HIV using cardiac TTE and cardiac MRI imaging as well as blood markers of heart failure and inflammation.
Chronic obstructive pulmonary disease (COPD) is a disease characterized by chronic respiratory symptoms due to inflammatory and destructive changes of the lung leading to progressive airflow obstruction. Fragility fractures associated with osteoporosis are among major comorbidities and have significant impacts on quality of life and prognosis of patients with COPD. Evidence suggests that both decreased bone mineral density (BMD) and impaired bone quality contribute to bone fragility and resultant fractures in COPD. Although various clinical risk factors of osteoporosis have been described, mechanisms of COPD-associated osteoporosis are still largely unknown. In addition, its specific treatment has not been established, either. Previous studies have suggested involvement of low BMI and sarcopenia in the pathogenesis of COPD-associated osteoporosis. In this narrative review, we will propose critical roles of vitamin D deficiency and inflammation, both of which are often present in COPD and may underlie the development of osteosarcopenia and impaired bone quality, ultimately causing fractures in COPD patients.
Methods are disclosed for preparing core-shell polymers of poly-γ-glutamic acid. The final products of the present invention are useful as drug delivery systems, for gene therapy, magnetic resonance imaging as well as in encapsulation technology. A method of forming a poly-γ-glutamic acid (PGA) useful in the formation of core shell polymers is disclosed. According to the method a PGA is prepared by fermentation with a suitable microorganism, capable of producing PGA in a suitable fermentation medium, under conditions and time appropriate for the microorganism used. The resulting culture medium is treated with centrifugation, to separate the cells from the PGA. Acetone is used to treat the resulting cell-free liquid to obtain the PGA from the fermentation medium. The obtained PGA is purified by dialysis and freeze drying the PGA. A method of forming a core shell polymer of a poly-γ-glutamic acid (PGA) is also disclosed. The core is formed by partially amidating a poly-γ-glutamic acid (PGA) by reaction with a diamino compound to at least partially cross-link the PGA. The outer shell of the core shell polymer is formed from a hydrophilic or a hydrophobic polymer.
INTRODUCTION: The presence of hypoxic-ischemic brain damage (HIBD) in neonates triggers a strong neuroinflammatory reaction. Pyroptosis, a programmed cell death mechanism associated with inflammation, plays a crucial role in HIBD. Pyruvate kinase M2 (PKM2) plays a significant role in connecting metabolic processes and inflammatory responses, but whether it affects hippocampus pyroptosis in HIBD is unclear. The aim of this study is to elucidate the role of PKM2 in HIBD and to propose a novel therapeutic approach for neonatal ischemic-hypoxic encephalopathy.
METHODS: In this study, we employed neonatal 7-day-old Sprague Dawley rats to establish a model of HIBD using the Rice-Vannucci surgical technique and a hypoxia device. To inhibit the elevation of PKM2, we utilized the PKM2 inhibitor shikonin. The rats were categorized into four groups: Sham, Shikonin, HIBD, and Shikonin + HIBD. Behavioral tests, hematoxylin eosin staining, immunofluorescence staining, ELISA (IL-1β, IL-18), and LDH were conducted in each group to evaluate neurological function, hippocampal damage, the occurrence of neuronal pyroptosis, and the neuroinflammation. Western blot was used to assess the expression levels of PKM2, NLRP3, Caspase-1, Cleaved Caspase-1, GSDMD, GSDMDN, and IL-1β.
RESULTS: The expression of PKM2 elevated in hippocampal tissues of the HIBD model and the localization of PKM2 in the hippocampus was activated in neurons instead of microglia during the HIBD. Meanwhile, the inhibition of PKM2 improved the behavioral test scores and the body weight of rats, the neuronal damage in the CA1 region of hippocampal tissue was also attenuated. In addition, inhibiting PKM2 alleviated neuronal pyroptosis by decreasing the expression of PKM2, NLRP3, Caspase-1, Cleaved Caspase-1, GSDMD, GSDMDN. Furthermore, serum levels of LDH and inflammatory factors IL-1β and IL-18 decrease with PKM2 inhibition.
CONCLUSIONS: Based on these findings, we can conclude that PKM2 plays a crucial role in regulating hippocampal neuronal pyroptosis of HIBD rats via NLRP3/Caspase-1/GSDMD pathway. Therefore, inhibiting PKM2 could be a promising therapeutic strategy for the treatment of neonatal ischemic-hypoxic encephalopathy.
A composition of a compound represented by FIG. 1 for use in substance-assisted therapy. A method of changing neurotransmission, by administering a pharmaceutically effective amount of a compound of FIG. 1 to a mammal, interacting with serotonin 5-HT2A receptors in the mammal, in particular also human beings, and inducing psychoactive effects. A method of treating a patient having adverse reactions to psychedelics by administering a desoxyscaline derivative to the patient, and avoiding adverse effects present with psychedelics. A method of changing neurotransmission of an individual, by administering a desoxyscaline derivative, and changing neurotransmission in the individual.
The present invention belongs to the field of traditional Chinese medicine and pharmacy and relates to specific medicine for curing tuberculosis by traditional Chinese medicine. The medicine can effectively solve the defects of the existing anti-tuberculosis medicine, operation, etc. The medicine is mainly characterized in that the medicine uses prepared aconite roots with the functions of supplementing fire and invigorating yang as main medicine. Different from a traditional therapy, the medicine comprises the prepared aconite roots plus silkworms, stemona roots and processed urine deposits which are processed into fine powder which is sieved with a sieve of 60 meshes. Then, the powder is placed in a container without air leakage. The medicine is mainly used for curing tubercle bacillus infected diseases of bone tuberculosis, scrofula, phthisis, intestinal tuberculosis, renal tuberculosis, etc. and non-tuberculous mycobacterium diseases, such as lymphadenitis, etc.
PURPOSE: A method for preparing an antiserum for treatment of canine distemper virus containing inoculating Newcastle disease virus of birds into a live dog, taking a blood sample and then separating antiserum is provided. Whereby, the antiserum has almost no adverse effects and is simple in application. CONSTITUTION: Newcastle disease virus of birds is intravenously injected to a live dog with an intravenous catheter. A sufficient amount of blood is taken therefrom though the jugular vein after 11 to 12hr. Antiserum is then separated. The Newcastle disease virus uses B-1 type, Lasota stain.
BACKGROUND: Comprehensive healthcare for patients with gender dysphoria includes access to gender-affirming hormone therapy. It may cause cutaneous and adnexal side effects, which often affect quality of life, are underdiagnosed, and do not receive timely treatment. The literature on this subject is scarce. The main objective was to identify skin manifestations secondary to hormone treatment in adults with gender dysphoria.
METHODS: Observational, descriptive, cross-sectional study. A search was performed in the database of patients with gender dysphoria older than 18 years treated at the dermatology and/or endocrinology outpatient clinic of the Hospital de San José de Bogotá in the period 2015-2021. Medical records of patients on hormone therapy with skin manifestations were selected, while patients using other medications as possible triggers were excluded.
RESULTS: In total, 85 patients were included, with a predominance of young transgender men (average age was 27 ± 9 years) in whom the main manifestation was acne (87%), followed by androgenetic alopecia and acanthosis nigricans. Transgender women presented more acne, androgenetic alopecia, hypertrichosis, seborrheic dermatitis, and melasma. The majority received treatment, mainly topical therapies. More than half of the patients were treated by the endocrinology and dermatology services.
CONCLUSIONS: Skin manifestations in patients with gender dysphoria on hormone therapy are frequent, so they should be known and taken into account in the multidisciplinary approach to these patients, which should involve dermatologists. This is the first Colombian and Latin American study focused on documenting skin manifestations in patients with gender dysphoria undergoing hormone therapy.
These participants receive information about high blood pressure and medications. They will complete a mid-assessment at 3-months and a post-assessment at 6-months.
AVALIDE can cause fetal harm when administered to a pregnant woman. Use of drugs that act on the renin-angiotensin system during the second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death. Resulting oligohydramnios can be associated with fetal lung hypoplasia and skeletal deformations. Potential neonatal adverse effects include skull hypoplasia, anuria, hypotension, renal failure, and death. When pregnancy is detected, discontinue AVALIDE as soon as possible [see Use in Specific Populations (8.1)].

Thiazides cross the placenta and use of thiazides during pregnancy is associated with a risk of fetal or neonatal jaundice, thrombocytopenia, and possibly other adverse reactions that have occurred in adults.
The present invention relates to an apparatus and a method for generating disease onset information based on a time-dependent correlation using a polygenic risk score. According to the present invention, in generating disease onset information including onset prediction information, a group-specific PRS model is designed with respect to gene mutations respectively included in groups classified using preprocessed genome data and checkup result data. Individual checkup result values by disease correlation factor included in the checkup result data are input to a time-dependent correlation calculation model in which a polygenic risk score calculated using the PRS model is applied as a covariate. As a result, a time point-specific correlation magnitude is calculated between independent and dependent variables to be input to a COX model and selected as a time-series characteristic variable. While applying the at least one time-series characteristic variable calculated with respect to the checkup result data, COX regression analysis is performed for each group with respect to the checkup result data related to the disease correlation factors of multiple applied persons to calculate the amount of change in risk degree using the value of difference in the degree of disease onset risk by group. Onset prediction information is generated in this manner, and thus relatively more accurate disease onset information can be provided with time flow reflected.
The population of the study will consist of mothers of premature infants receiving care and treatment in the neonatal intensive care units where the study is planned to be conducted between November 15, 2023 and June 01, 2024. Since there is no similar study in the literature, the sample size of the study will be determined as a result of the post-hoc power analysis performed after the pre-application in all groups. Premature infants and their mothers sampled in the study will be assigned to the intervention and control groups by randomization with the stratified block method according to the gestation week, gender and birth weight of the infants. Block randomization will be done by creating 6 blocks consisting of 4 letters. Block randomization will be done by an academic independent of the research. The group with which the study will start will be determined by lottery by the independent academic and the participants will be assigned to the intervention and control groups with randomization envelopes. Mother Descriptive Information Form, Infant Descriptive Information and Follow-up Form, Preparation for Discharge from the Neonatal Intensive Care Unit and Home Care Scale, Neonatal Intensive Care Unit Parental Stress Scale, Problem Solving Skills Assessment Form, Ankara Developmental Screening Inventory, and Process Evaluation Form will be used for data collection. The research will be carried out in three stages; (1) creating the content of the follow-up program, (2) designing the web page, (3) implementing the program with mothers. The implementation of the program based on the Empowerment Model will be implemented in 3 stages: preparation of the premature infant hospitalized in the neonatal intensive care unit for discharge from the hospital, transition to home and home care.
BACKGROUND AND AIMS: We aimed to identify serum metabolites associated with mucosal and transmural inflammation in paediatric Crohn disease [pCD].
METHODS: In all, 56 pCD patients were included through a pre-planned sub-study of the multicentre, prospective, ImageKids cohort, designed to develop the Paediatric Inflammatory Crohn magnetic resonance enterography [MRE] Index [PICMI]. Children were included throughout their disease course when undergoing ileocolonoscopy and MRE and were followed for 18 months, when MRE was repeated. Serum metabolites were identified using liquid chromatography/mass spectroscopy. Outcomes included: PICMI, the simple endoscopic score [SES], faecal calprotectin [FCP], and C-reactive protein [CRP], to assess transmural, mucosal, and systemic inflammation, respectively. Random forest models were built by outcome. Maximum relevance minimum redundancy [mRMR] feature selection with a j-fold cross-validation scheme identified the best subset of features and hyperparameter settings.
RESULTS: Tryptophan and glutarylcarnitine were the top common mRMR metabolites linked to pCD inflammation. Random forest models established that amino acids and amines were among the most influential metabolites for predicting transmural and mucosal inflammation. Predictive models performed well, each with an area under the curve [AUC] > 70%. In addition, serum metabolites linked with pCD inflammation mainly related to perturbations in the citrate cycle [TCA cycle], aminoacyl-tRNA biosynthesis, tryptophan metabolism, butanoate metabolism, and tyrosine metabolism.
CONCLUSIONS: We extend on recent studies, observing differences in serum metabolites between healthy controls and Crohn disease patients, and suggest various associations of serum metabolites with transmural and mucosal inflammation. These metabolites could improve the understanding of pCD pathogenesis and assessment of disease severity.
Type 2 diabetes (T2D) is potentially linked to disordered tryptophan metabolism that attributes to the intricate interplay among diet, gut microbiota, and host physiology. However, underlying mechanisms are substantially unknown. Comparing the gut microbiome and metabolome differences in mice fed a normal diet (ND) and high-fat diet (HFD), we uncover that the gut microbiota-dependent tryptophan metabolite 5-hydroxyindole-3-acetic acid (5-HIAA) is present at lower concentrations in mice with versus without insulin resistance. We further demonstrate that the microbial transformation of tryptophan into 5-HIAA is mediated by Burkholderia spp. Additionally, we show that the administration of 5-HIAA improves glucose intolerance and obesity in HFD-fed mice, while preserving hepatic insulin sensitivity. Mechanistically, 5-HIAA promotes hepatic insulin signaling by directly activating AhR, which stimulates TSC2 transcription and thus inhibits mTORC1 signaling. Moreover, T2D patients exhibit decreased fecal levels of 5-HIAA. Our findings identify a noncanonical pathway of microbially producing 5-HIAA from tryptophan and indicate that 5-HIAA might alleviate the pathogenesis of T2D.
The number of midlife women transitioning into menopause is substantial, with more than 1 million women in the United States entering menopause each year. Vasomotor symptoms (VMS), mood and sleep disturbances, and sexual problems are common during the menopause transition yet often go untreated. Menopausal hormone therapy is the most effective treatment of VMS, and the benefits typically outweigh the risks for women without contraindications who are younger than 60 years or within 10 years from menopause onset. For women who cannot or choose not to use hormone therapy, nonhormone prescription options exist to treat VMS. Many of these therapies have secondary benefits beyond VMS relief. For example, whereas paroxetine is Food and Drug Administration approved to treat VMS, it can also help with depressive and anxiety symptoms. The aim of this paper is to summarize prescription treatments of VMS and their secondary benefits for other common symptoms experienced by midlife women. The tools presented will help clinicians caring for midlife women provide individualized, comprehensive care with the goal of improving their quality of life during the menopause transition and beyond.
Subcutaneous injections of Mepolizumab 100 mg once per month for 16 weeks. A total of 4 injections.
The invention discloses a compound Chinese herbal medicine for controlling Zoothamnium penaei nov. sp. and a preparation method thereof. The compound Chinese herbal medicine for controlling Zoothamnium penaei nov. sp. comprises seven Chinese herbal medicines, and the seven Chinese herbal medicines comprise rheum officinale, sophora flavescens, phellodendron, Chinese gall, melia azedarach and sweet wormwood with a ratio of 24 :13:18:12:9:18:25. The preparation method comprises the specific steps: (1) first-time decocting for extracting; (2) second-time decocting; (3) double-effect concentration; and (4) spray drying. The method is simple and easily understandable, the compound Chinese herbal medicine is prepared by employing high-pressure decocting, double-effect vacuum concentration and spray drying, and the drug effect and the palatability are substantially improved.