anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Intestinal mucus barrier disruption may occur with chronic inflammatory enteropathies. The lack of studies evaluating mucus health in dogs with chronic colitis arises from inherent challenges with assessment of the intestinal mucus layer. It is therefore unknown if reduced goblet cell (GBC) numbers and/or mucin 2 (MUC2) expression, which are responsible for mucus production and secretion, correlate with inflammation severity in dogs with granulomatous colitis (GC) or lymphocytic-plasmacytic colitis (LPC). It is undetermined if Ki-67 immunoreactivity, which has been evaluated in dogs with small intestinal inflammation, similarly correlates to histologic severity in GC and LPC. Study objectives included comparing Ki-67 immunoreactivity, GBC population and MUC2 expression in dogs with GC, LPC and non-inflamed colon; and exploring the use of ribonucleic acid (RNAscope®) in-situ hybridization (ISH) to evaluate MUC2 expression in canine colon. Formalin-fixed endoscopic colonic biopsies were obtained from 48 dogs over an eight-year period. A blinded pathologist reviewed all biopsies. Dogs were classified into the GC (n=19), LPC (n=19) or no colitis (NC) (n=10) group based on final histopathological diagnosis. Ki-67 immunohistochemistry, Alcian-Blue/PAS staining to highlight GBCs, and RNAscope® ISH using customized canine MUC2-targeted probes were performed. At least five microscopic fields per dog were selected to measure Ki-67 labelling index (KI67%), GBC staining percentage (GBC%) and MUC2 expression (MUC2%) using image analysis software. Spearman's correlation coefficients were used to determine associations between World Small Animal Veterinary Association histologic score (WHS) and measured variables. Linear regression models were used to compare relationships between WHS with KI67%, GBC%, and MUC2%; and between GBC% and MUC2%. Median WHS was highest in dogs with GC. Median KI67% normalised to WHS was highest in the NC group (6.69%; range, 1.70-23.60%). Median GBC% did not correlate with colonic inflammation overall. Median MUC2% normalised to WHS in the NC group (10.02%; range, 3.05-39.09%) was two- and three-fold higher than in the GC and LPC groups respectively. With increased colonic inflammation, despite minimal changes in GBC% overall, MUC2 expression markedly declined in the LPC group (-27.4%; 95%-CI, -49.8, 5.9%) and mildly declined in the GC and NC groups. Granulomatous colitis and LPC likely involve different pathways regulating MUC2 expression. Decreased MUC2 gene expression is observed in dogs with chronic colitis compared to dogs without colonic signs. Changes in MUC2 expression appear influenced by GBC activity rather than quantity in GC and LPC.
1. Technical Result Increase in efficiency of treatment of the diseases caused by bacterial infections.          2. Essence Compounds are presented by the formula wherein if A stands for NH group, then B simultaneously stands for C=O group, or A stands for C=O group then B simultaneously stands for NH group, and the radicals R1, R2, R3, R4, R5, and R6 have the meaning given in the description; a method for its production, a pharmaceutical composition containing the same and its used for treatment of the diseases caused by bacterial infections.          3. Field of Application Medicine.
Jaboticaba peel extract. Patients will ingest 4 capsules/day of jaboticaba (Plinia Cauliflora) peel extract, providing 3.3g of jabuticaba peel extract daily, containing 600mg of phenolic compounds, for one month.
PURPOSE:To obtain a remedy for dysuria, containing aminoalkoxybenzene derivatives including a new compound and salts thereof as principal ingredients, having reducing action on urethratretic tension with low toxicity, capable of selectively reducing urethral resistance without causing hypotensive action and useful for prostatic hypertrophy. CONSTITUTION:A remedy for dysuria obtained by containing a compound expressed by formula I [R<1> is H, hydroxyl, etc.; Q is formula II (R<2> is alkyl, cycloalkyl, etc.; R<3> is H, alkyl, etc.; m is 0, 1 or 2), etc.; n is 2, 3, etc.] and salts thereof as principal ingredients. For example, the compound expressed by formula I is obtained by reacting a compound expressed by formula III (X is halogen) with an amine expressed by formula IV. The compounds expressed by formulas III and IV include new compounds. The compound expressed by formula I is directly administered or contained in an amount of, e.g. 0.1-99.5%, preferably 0.5-90%, in a carrier and administered to animals including humans.
The characteristics of fibrosis include the abnormal accumulation of extracellular matrix proteins and abnormal tissue repair caused by injury, infection, and inflammation, leading to a significant increase in organ failure and mortality. Effective and precise treatments are urgently needed to halt and reverse the progression of fibrotic diseases. Exosomes are tiny vesicles derived from endosomes, spanning from 40 to 160 nanometers in diameter, which are expelled into the extracellular matrix environment by various cell types. They play a crucial role in facilitating cell-to-cell communication by transporting a variety of cargoes, including proteins, RNA, and DNA. Epithelial cells serve as the primary barrier against diverse external stimuli that precipitate fibrotic diseases. Numerous research suggests that exosomes from epithelial cells have a significant impact on several fibrotic diseases. An in-depth comprehension of the cellular and molecular mechanisms of epithelial cell-derived exosomes in fibrosis holds promise for advancing the exploration of novel diagnostic biomarkers and clinical drug targets. In this review, we expand upon the pathogenic mechanisms of epithelium-derived exosomes and highlight their role in the fibrotic process by inducing inflammation and activating fibroblasts. In addition, we are particularly interested in the bioactive molecules carried by epithelial-derived exosomes and their potential value in the diagnosis and treatment of fibrosis and delineate the clinical utility of exosomes as an emerging therapeutic modality, highlighting their potential application in addressing various medical conditions.
PURPOSE:The titled protein, obtained by labeling a physiologically active protein, having cytotoxicity to L-M cells and capable of causing a hemorrhagic necrotic reaction in Meth A sarcoma cancer cells in vivo and effective for detection and diagnosis of cancerated sites. CONSTITUTION:For example, a physiologically active protein, obtained by the recombinant DNA technique using a DNA having the base sequence expressed by the formula, having cytotoxicity to L-M cells, e.g. human TNF,and capable of causing hemorrhagic reaction in tumorous site on administering to BALB/C mice transplanted with Meth A sarcoma cancer cells is dissolved in a buffer solution, e.g. 0.1mol Na3BO3 at 8.4pH, to give a buffer solution, which is added to a reagent, e.g. Bolton-Hunter reagent, containing radioactive iodine, e.g. <131>I, to carry out the labeling reaction and recover the aimed protein from the reaction solution by column chromatography, etc.
The invention provides a polypeptide, the amino acid sequence of which is shown as SEQ ID No.1, SEQ ID No.2, SEQ ID No.3, SEQ ID No.4, SEQ ID No.5 or SEQ ID No. 6. The invention also provides a polypeptide composition with an anti-tumor effect, the polypeptide composition is fusion of a penetrating peptide and a targeting polypeptide, the amino acid sequence of the penetrating peptide is YGRKRRQRRRR, and the amino acid sequence of the targeting polypeptide is SEQ ID No.3 or SEQ ID No.4. The invention also provides application of the polypeptide composition in preparing a medicament for treating breast cancer. The invention also provides a medicine for treating breast cancer, and the effective components of the medicine comprise the polypeptide composition. The polypeptide composition provided by the invention can block Nur 77/PPARgamma protein interaction, can effectively inhibit proliferation and metastasis of tumor cells, and has an anti-tumor effect.
Participants received loading dose followed by weekly dose of LY3209590 based on the prior randomization basal insulin dose for a period of 32 weeks by subcutaneous injection. Dose titration was done to maintain fasting blood glucose of \<120 mg/dL.
The purpose of the proposed study is to identify effective strategies for implementing lesbian, gay, bisexual, transgender, and queer (LGBTQ)-affirmative CBT (cognitive-behavioral therapy) at LGBTQ community centers across the United States. This study will specifically compare the effectiveness of three implementation strategies: (1) training materials only, (2), training materials and direct training from our expert trainers, and (3) training materials, direct training, and local supervision from a clinical supervisor. The proposed prospective study will utilize a type 3 hybrid implementation-effectiveness trial. This design is used to compare the impact of two or more implementation strategies while also gathering effectiveness data and is recommended when there is already strong evidence for the intervention's effectiveness, strong basis that the implementation strategies are feasible, and strong implementation momentum. Randomization will occur on the center-level, so that MHPs working in the same center will receive one of the three types of training.

Outcomes include mental health providers' changes in demonstrated skills in providing LGBTQ-affirmative CBT from baseline to 4-, 8-, 12-, and 24-months post-baseline. This study will also investigate determinants of successful implementation of LGBTQ-affirmative CBT and examine the impact of the implementation strategies on client mental health.
The invention provides a method for predicting the susceptibility of a patient suffering from a cancer or a myeloid-mediated disease to immunotherapy. Furthermore, the invention provides a method for treating a patient suffering from a cancer or a myeloid-mediated disease with immunotherapy. In accordance with these embodiments, the inventive method includes assaying myeloid cells obtained from the patient prior to treatment for the expression of CXCR3. The invention also provides a genetically engineered myeloid cell (GEMy) in which the expression of CXCR3 is modulated (up- or down-regulated). The invention further provides a composition comprising the inventive GEMy and a pharmaceutically acceptable carrier. The invention also provides a method for treating a patient in need of immunotherapy comprising administering the inventive composition to a patient.
Molecular testing for HPV with partial genotyping for types 16/18, with referral of the HPV16/18-positive group for diagnostic evaluation, and secondary randomisation of women testing positive for other oncogenic HPV infection (not 16/18), to either image-read cytology screening or dual-stained (DS) cytology testing with p16/Ki67 - the "HPV arm". Screening performed 5 yearly.
Immunometabolism has been unveiled in the last decade to play a major role in controlling macrophage metabolism and inflammation. There has been a constant effort to understand the immunomodulating properties of regulated metabolites during inflammation with the aim of controlling and re-wiring aberrant macrophages in inflammatory diseases. M-CSF and GM-CSF-differentiated macrophages play a key role in mounting successful innate immune responses. When a resolution phase is not achieved however, GM-CSF macrophages contribute substantially more towards an adverse inflammatory milieu than M-CSF macrophages, consequently driving disease progression. Whether there are specific immunometabolites that determine the homoeostatic or inflammatory nature of M-CSF and GM-CSF-differentiated macrophages is still unknown. As such, we performed metabolomics analysis on LPS and IL-4-stimulated M-CSF and GM-CSF-differentiated human macrophages to identify differentially accumulating metabolites. Adenine was distinguished as a metabolite significantly higher in M-CSF-differentiated macrophages after both LPS or IL-4 stimulation. Human macrophages treated with adenine before LPS stimulation showed a reduction in inflammatory gene expression, cytokine secretion and surface marker expression. Adenine caused macrophages to become more quiescent by lowering glycolysis and OXPHOS which resulted in reduced ATP production. Moreover, typical metabolite changes seen during LPS-induced macrophage metabolic reprogramming were absent in the presence of adenine. Phosphorylation of metabolic signalling proteins AMPK, p38 MAPK and AKT were not responsible for the suppressed metabolic activity of adenine-treated macrophages. Altogether, in this study we highlight the immunomodulating capacity of adenine in human macrophages and its function in driving cellular quiescence.
The present invention relates to a self-microemulsifying system, preferably comprising active pharmaceutical ingredient, and a medicine prepared therefrom. This invention also relates to a process for preparing a solid self-microemulsifying system. In addition, it relates to a use of the self-microemulsifying system and a use of microcrystalline cellulose in admixture with the self-microemulsifying system. Specifically it describes a process for preparing a self-microemulsifying system comprising dispersing microcrystalline cellulose in a solvent, wherein the solvent further contains a viscosity enhancer, mixing the solvent with a self-microemulsifying system and spray drying the obtained mixture. In addition It provides the process comprising mixing a solid support and self-microemulsifying system to form a primary mixture and further granulating said primary mixture with a solution or suspension of a granulation binder. Both processes remarkably enhance processability of the solid self-microemulsifying system. Product and medicine obtainable by said processes are also provided.
Patients receive nivolumab SC on day 1 of each cycle. Cycles repeat every 28 days in clinic for 2 cycles, then at home by a HHNP for 4 cycles, followed by either in-clinic or at-home administration for up to 1 year in the absence of disease progression or unacceptable toxicity. Patients receive in-home visits by a home health nurse and undergo remote patient monitoring including vital sign measurements and condition-specific symptom assessments throughout study.
Bladder cancer (BC) is a crisis to human health. It is necessary to understand the molecular mechanisms of the development and progression of BC to determine treatment options. Publicly available expression data were obtained from TCGA and GEO databases to spot differentially expressed genes (DEGs) between cancer and normal bladder tissues. Weighted co-expression networks were constructed, and Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. Associations in hub genes, immune infiltration, and immune therapy were evaluated separately. Protein-protein interaction (PPI) networks for the genes identified in the normal and tumor groups were launched. 3461 DEGs in the TCGA dataset and 1069 DEGs in the GSE dataset were identified, including 87 overlapping genes between cancer and normal bladder groups. Hub genes in the tumor group were mainly enriched for cell proliferation, while hub genes in the normal group were related to the synthesis and secretion of neurotransmitters. Based on survival analysis, CDH19, RELN, PLP1, and TRIB3 were considerably associated with prognosis (P < 0.05). CDH19, RELN, PLP1, and TRIB3 may play important roles in the development of BC and are potential biomarkers in therapy and prognosis.
Synchronized ferroptosis contributes to nephron loss in acute kidney injury (AKI). However, the propagation signals and the underlying mechanisms of the synchronized ferroptosis for renal tubular injury remain unresolved. Here we report that platelet-activating factor (PAF) and PAF-like phospholipids (PAF-LPLs) mediated synchronized ferroptosis and contributed to AKI. The emergence of PAF and PAF-LPLs in ferroptosis caused the instability of biomembranes and signaled the cell death of neighboring cells. This cascade could be suppressed by PAF-acetylhydrolase (II) (PAFAH2) or by addition of antibodies against PAF. Genetic knockout or pharmacological inhibition of PAFAH2 increased PAF production, augmented synchronized ferroptosis and exacerbated ischemia/reperfusion (I/R)-induced AKI. Notably, intravenous administration of wild-type PAFAH2 protein, but not its enzymatically inactive mutants, prevented synchronized tubular cell death, nephron loss and AKI. Our findings offer an insight into the mechanisms of synchronized ferroptosis and suggest a possibility for the preventive intervention of AKI.
Water-soluble bad-tasting drugs and vitamins are put into chewable tablet form wherein the drugs and vitamins have a pleasant taste and are readily available upon ingestion. A water solution or water-alcohol solution of the bad-tasting substance is absorbed into rice endosperm using about enough solution for complete hydration or slightly less, followed by drying. Precooked rice endosperm can also be used. The drugs include phenothiazine tranquilizers and barbiturates and the vitamins include thiamin, niacinamide and pyridoxine. The water-soluble substance may constitute up to 60 percent of the finished product, with the rice endosperms, which may be previously comminuted, making up the balance. The pleasant tasting chewable tablets contain the bad tasting substance with the bad taste masked, conventional chewable tablet base constituents for the tableting of the rice endosperm-drug particles being combined with the treated rice endosperms.
PURPOSE:To easily obtain at a low cost the title material mild in digestion and absorption, having high antiobesity by binding a sucrose fatty acid ester to a starch to effect specifying the amylose occupancy rate in the starch by said sucrose fatty acid ester. CONSTITUTION:(A) 2-20 pts.wt. of an ester compound from sucrose and pref. a 14-22C fatty acid (e.g. sucrose caprylate) is brought into contact with (B) 100 pts.wt. of a starch prepared from rice, wheat, potatoes etc., in the presence of (C) 5-500 pts.wt. of water, thus giving the objective material >=10% (pref. 40-95%) in the amylose occupancy rate in the starch by said sucrose fatty acid ester.
BACKGROUND: Depression remains one of the most prevalent psychiatric disorders, with many patients not responding adequately to available treatments. Electroacupuncture (EA), a nonpharmacologic therapy, holds great promise for alleviating depressive symptoms. In this study, RNA sequencing (RNA-Seq) was used to identify genome-wide alterations in the hippocampus of rats after chronic unpredictable mild stress (CUMS) and EA treatments to further elucidate the mechanism by which EA ameliorates depression to provide a basis for the clinical application of EA in stress-related diseases.
METHODS: The sucrose preference test (SPT), open field test (OFT), and forced swimming test (FST) were used to investigate the ability of EA at Baihui (GV20) and Taichong acupoints (LR3) to improve depression-like behavior in rats subjected to CUMS. Subsequently, RNA-Seq analysis revealed transcriptomic profiles of the hippocampus of rats subjected to CUMS in which EA ameliorated depressive behavior. Finally, the expression profiles of major differentially expressed genes were tested by real-time quantitative polymerase chain reaction (qRT-PCR) to determine the accuracy of the RNA-Seq results.
RESULTS: Rats subjected to CUMS exhibited depressive-like behaviors, such as decreased sucrose consumption in the SPT (p < .001), decreased time in the central area of the OFT (p < .001), and increased immobility in the FST (p < .01). Importantly, rats subjected to CUMS and treated with EA showed increased sucrose consumption (p < .001), increased time spent in the central area of the OFT (p < .001) and decreased immobility in the FST (p < .01). Sixty-three genes that were differentially expressed following CUMS were altered by EA; most of these were associated with immune pathways. Compared with those in the control group, the expression levels of Colla2 (p < .001), Col3a1 (p < .001), Psmb9 (p < .01), and Tap1 (p < .01) in the hippocampus of rats subjected to CUMS were lower. The changes in the expression of these genes were reversed by EA treatment.
CONCLUSION: EA at GV20 and LR3 attenuated CUMS-induced depression-like behaviors by regulating the expression of specific genes such as Colla2, Col3a1, Psmb9, and Tap1.
PROBLEM TO BE SOLVED: To ameliorate the chronic damage, swellable wound, etc., accompanied with the exudation (oozing, leaking, etc.) of body fluid by supplying polyvalent metals (zinc, manganese, copper, selenium, etc.) exclusive of magnesium. SOLUTION: This bandage product for the chronic damage accompanied with the body fluid contains a calcium alginate base agent combined with the alginate of at least one of the polyvalent metals exclusive of the magnesium. The alginate of the polyvalent metals is produced from the sodium alginate extruded through a die arranged within a flocculating bath for the chloride soln. of the polyvalent metals. The alginate of the polyvalent metals is combined with the calcium alginate base agent by means of a textile fabric technique.
There have been postmarketing reports of fatal and non-fatal hepatic failure in patients taking ULORIC, although the reports contain insufficient information necessary to establish the probable cause. During randomized controlled studies, transaminase elevations greater than three times the upper limit of normal (ULN) were observed (AST: 2%, 2%, and ALT: 3%, 2% in ULORIC and allopurinol-treated patients, respectively). No dose-effect relationship for these transaminase elevations was noted [see Clinical Pharmacology (12.3)].

Obtain a liver test panel (serum alanine aminotransferase [ALT], aspartate aminotransferase [AST], alkaline phosphatase, and total bilirubin) as a baseline before initiating ULORIC.

Measure liver tests promptly in patients who report symptoms that may indicate liver injury, including fatigue, anorexia, right upper abdominal discomfort, dark urine or jaundice. In this clinical context, if the patient is found to have abnormal liver tests (ALT greater than three times the upper limit of the reference range), ULORIC treatment should be interrupted and investigation done to establish the probable cause. ULORIC should not be restarted in these patients without another explanation for the liver test abnormalities.

Patients who have serum ALT greater than three times the reference range with serum total bilirubin greater than two times the reference range without alternative etiologies are at risk for severe drug-induced liver injury and should not be restarted on ULORIC. For patients with lesser elevations of serum ALT or bilirubin and with an alternate probable cause, treatment with ULORIC can be used with caution.
Patients receive brentuximab vedotin 1.5mg/kgIV over 30 minutes on days 1 and 8; ifosfamide IV over 24 hours and carboplatin IV over 1 hour on day 2; and etoposide IV over 1 hour on days 1-3. Treatment repeats every 21 days for 2 courses in the absence of disease progression or unacceptable toxicity. Patients planning to go on to consolidative HDT and ASCT may undergo PBSC mobilization following the 2nd course of study therapy at the discretion of the treating physician.