anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Both extreme temperature events (ETEs) and air pollution affected human health, and their effects were often not independent. Previous studies have provided limited information on the interactions between ETEs and air pollution.
METHODS: We collected data on deaths (non-accidental, cardiovascular, and respiratory) in Zibo City along with daily air pollution and meteorological data from January 2015 to December 2019. Distributed lag non-linear model was used to explore the health effects of ETEs on deaths. Non-parametric binary response model, hierarchical model and joint effect model were used to further explore the interaction between ETEs and air pollution in different seasons. Meanwhile, subgroup analysis by gender and age (≥ 65 years old and < 65 years old) was conducted to identify the vulnerable population.
RESULTS: ETEs increased death risk, especially for cardiovascular and respiratory deaths. Heat waves had a stronger impact than cold spells. Cold spells had a longer lag and fluctuating trend. Heat waves had a short-term impact, followed by a decrease. Females and those aged ≥ 65 were more affected, but subgroup differences were not significant. During ETEs and non-ETEs, there were different effects on deaths with per IQR increase in air pollutant concentrations. Joint effect models revealed that there was a significant interaction between ETEs and air pollution on non-accidental deaths. The interaction between PM2.5 and cold spells was antagonistic in the cold season. In the warm season, the health effects of heat waves and high O3 concentration were enhanced. The relative excess risk due to interaction (RERI) of cold spells and PM2.5 in total population was -0.09 (95 % CI: -0.17, -0.01), and 9 % (95 % CI: 1 %, 17 %) of the total effect was attributable to interaction. Subgroup analysis confirmed the interactions in females and those aged ≥ 65.
CONCLUSIONS: Significant association observed between ETEs and deaths. Females and ≥ 65 age groups were vulnerable. There were interactions between ETEs and air pollution. The effect of PM2.5 on deaths decreased during cold spells, while the effect of O3 increased during heat waves. In addition to improving air quality, it is necessary to further strengthen the prevention and control of ETEs.
The present invention relates to a peptide comprising at least one amino acid sequence selected from the group consisting of the amino acid sequence of SEQ ID NO: 1, the amino acid sequence of SEQ ID NO: 2, the amino acid sequence of SEQ ID NO: 3, and the amino acid sequence of SEQ ID NO: 4, and having prophylactic or therapeutic activity for an inflammatory or autoimmune disease. The present invention also relates to a pharmaceutical or anti-inflammatory composition comprising at least one of the peptides of SEQ ID NOS: 1 to 4 for prophylaxis or therapy of an inflammatory or autoimmune disease. Furthermore, the present invention relates to a use of at least one of the peptides of SEQ ID NOS: 1 to 4 in a therapeutic method for an inflammatory or autoimmune disease or in preparing a therapeutic drug for an inflammatory or autoimmune disease. The peptide comprising any one of the amino acid sequences of SEQ ID NOS: 1 to 4 can significantly inhibit the secretion or expression of inflammatory cytokines such as IL-17, etc. and as such, has a prophylactic or therapeutic activity for an inflammatory or autoimmune disease. Therefore, a composition comprising at least one of the peptides is effective for use in a pharmaceutical composition for prophylaxis or therapy of an inflammatory or autoimmune disease, in a therapeutic method, and in preparing a therapeutic drug, or as an anti-inflammatory composition.
Participants will receive cobimetinib PO daily on Days 1-21 of each 28-day cycle plus venetoclax PO daily on Days 1-28 of each 28-day cycle, at the dose level identified in the safety run-in phase. Treatment will continue until the participant has disease progression, unacceptable toxicity, death, participant or physician decision to withdraw, or pregnancy, whichever occurs first.
This pilot study will investigate the safety and potential benefits of CARA breast positioning by treating 20 patients using the device. Patients will be planned with CARA positioning and standard of care positioning. CARA plans will be evaluated to ensure all treatment planning goals are met and patients will proceed to treatment with CARA positioning. This pilot study will ensure that patients can be safely treated with the CARA and provide us with valuable information from therapists, oncologists and patients about the performance of the current design. This will also inform the direction of design improvements and the production of educational materials for training practitioners in the use of the device. Overall, this will prepare us for a randomized clinical trial of the CARA positioning technique versus current standard of practice to assess whether reduced toxicity can be achieved using the CARA technique.
Pregabalin group is made up of 20 patients. Patients will receive 150mg/day in two divided does. The patients will be assessed weekly and the dose can be increased to 300mg/day, if the patient does not report any decrease in pain. The following week the dose may be increased to 600mg/day if once again the patient reports no decrease in pain. This is also the maximum permissible does that will be given to the patient. If patient reports any side effects then the dose can be decreased once. The time period of 2 to 5 weeks will be the dose adjustment period. After which the drug maintenance period extends from week 5 to 12. All doses will be given in two divided doses/day.
There is no known antidote for MESNEX.

In a clinical trial, 11 patients received intravenous MESNEX 10 mg/kg to 66 mg/kg per day for 3 to 5 days. Patients also received ifosfamide or cyclophosphamide. Adverse reactions included nausea, vomiting, diarrhea and fever. An increased rate of these adverse reactions has also been found in oxazaphosphorine-treated patients receiving ≥80 mg MESNEX per kg per day intravenously compared with patients receiving lower doses or hydration treatment only.

Postmarketing, administration of 4.5 g to 6.9 g of MESNEX resulted in hypersensitivity reactions including mild hypotension, shortness of breath, asthma exacerbation, rash, and flushing.
BACKGROUND: SGLT2i reduce cardiac hypertrophy, but underlying mechanisms remain unknown. Here we explore a role for serine/threonine kinases (STK) and sodium hydrogen exchanger 1(NHE1) activities in SGLT2i effects on cardiac hypertrophy.
METHODS: Isolated hearts from db/db mice were perfused with 1 µM EMPA, and STK phosphorylation sites were examined using unbiased multiplex analysis to detect the most affected STKs by EMPA. Subsequently, hypertrophy was induced in H9c2 cells with 50 µM phenylephrine (PE), and the role of the most affected STK (p90 ribosomal S6 kinase (RSK)) and NHE1 activity in hypertrophy and the protection by EMPA was evaluated.
RESULTS: In db/db mice hearts, EMPA most markedly reduced STK phosphorylation sites regulated by RSKL1, a member of the RSK family, and by Aurora A and B kinases. GO and KEGG analysis suggested that EMPA inhibits hypertrophy, cell cycle, cell senescence and FOXO pathways, illustrating inhibition of growth pathways. EMPA prevented PE-induced hypertrophy as evaluated by BNP and cell surface area in H9c2 cells. EMPA blocked PE-induced activation of NHE1. The specific NHE1 inhibitor Cariporide also prevented PE-induced hypertrophy without added effect of EMPA. EMPA blocked PE-induced RSK phosphorylation. The RSK inhibitor BIX02565 also suppressed PE-induced hypertrophy without added effect of EMPA. Cariporide mimicked EMPA's effects on PE-treated RSK phosphorylation. BIX02565 decreased PE-induced NHE1 activity, with no further decrease by EMPA.
CONCLUSIONS: RSK inhibition by EMPA appears as a novel direct cardiac target of SGLT2i. Direct cardiac effects of EMPA exert their anti-hypertrophic effect through NHE-inhibition and subsequent RSK pathway inhibition.
PURPOSE:A nail beautifying cosmetic, obtained by incorporating a water-soluble high polymer and water with a nail beautifying cosmetic containing nitrocellulose, resin plasticizer and solvent, safe to nails and having improved separation stability, glass and peeling characteristic without causing double nails and irritation in coating. CONSTITUTION:A nail beautifying cosmetic obtained by incorporating a water- soluble high polymer and with a nail beautifying cosmetic containing nitrocellulose, well-known and conventionally used resin, e.g. alkyd based resin, etc., plasticizer, e.g. dibutyl phthalate, etc., and solvent, e.g. ethyl acetate, etc. The total amount of the water-soluble high polymer and water is 0.5-30%, preferably 1-25% based on the total amount of the nail beautifying cosmetic. The amount of the water-soluble high polymer is within 0.3-20%, preferably 0.5-15% range based on the water. Hydroxyethyl cellulose, hydroxypropyl methyl cellulose, etc., may be used as the water-soluble high polymer. The water and the above-mentioned high polymer form the inner phase of the nail beautifying cosmetic emulsified in the W/O type in the form of an aqueous solution of the water-soluble high polymer.
PURPOSE:To obtain FGAG useful as a remedy for disseminated intravascular coagulation having specific physical and chemical properties, strong anticoagulating action and high safety, by extracting Holothurian with an alkali and then carrying out digestive extraction with a protease. CONSTITUTION:Holothurian is extracted with an alkali and subjected to digestive extraction with a protease to produce FGAG potassium salt having the following properties. Molecular weight: 55,000+ or -25,000 (polyacrylamide electrophoresis). Properties of substance: white amorphous powder. Decomposition point: 225-230 deg.C. Distinction of basicity, neutrality and acidity. pH6.5-7.5 at 1% aqueous solution. Solubility: soluble in water and insoluble in organic solvents such as ethanol, acetone, etc. Specific angle of rotation: [alpha]D<19>=-61--65 deg.C (C=1%). Color reaction: as shown in table I. Composition analysis: as shown in table II, etc.
Carcinogenicity, mutagenicity, and impairment of fertility studies with VYXEOS (daunorubicin and cytarabine) liposome for injection have not been conducted.

Carcinogenicity and mutagenicity studies have been conducted with daunorubicin. Published literature reported data that suggest daunorubicin (5 mg/kg) could be tumorigenic in rats at 0.68 times the recommended human dose on an mg/m2 basis. A high incidence of mammary tumors was observed about 120 days after a single intravenous dose of 12.5 mg/kg daunorubicin in rats (about 1.7 times the recommended human dose on an mg/m2 basis). A carcinogenic evaluation of daunorubicin by the IARC Working Group classified daunorubicin as a possible human carcinogen based on sufficient evidence in animals and inadequate data in humans. Daunorubicin was mutagenic in in vitro tests (Ames assay, V79 hamster cell assay), and clastogenic in in vitro (CCRF-CEM human lymphoblasts) and in in vivo (SCE assay in mouse bone marrow) tests.

Daunorubicin intravenous doses of 0.25 mg/kg/day (about 0.12 times the recommended human dose on a mg/m2 basis) in male dogs caused testicular atrophy and total aplasia of spermatocytes in the seminiferous tubules.

Cytarabine was mutagenic in in vitro tests and was clastogenic in vitro (chromosome aberrations and SCE in human leukocytes) and in vivo (chromosome aberrations and SCE assay in rodent bone marrow, mouse micronucleus assay). Cytarabine caused the transformation of hamster embryo cells and rat H43 cells in vitro.

No studies assessing the impact of cytarabine on fertility are available in the literature. Cytarabine was clastogenic to meiotic cells; a dose-dependent increase in sperm-head abnormalities and chromosomal aberrations occurred in mice given IP cytarabine.
Tinnitus is the phantom auditory perception of sound in the absence of an external or internal acoustic stimulus. It is a frequent problem which can interfere significantly with the ability to lead a normal life. One significant modulator of tinnitus is stress. Tinnitus has been shown to be generated in the brain, as a result of functional reorganization of auditory neural pathways and the central auditory system. Repetitive transcranial magnetic stimulation (rTMS) is also effective in treatment of tinnitus with moderate effect size. Pilot data were positive for low-frequency rTMS applied to the temporal and temporoparietal areas. Continuous theta burst stimulation (cTBS) is a new protocol of rTMS with a possible superior effect in contrast to low-frequency rTMS. Also anatomical neuronavigation might increase the efficacy of rTMS due to exact targeting of the primary auditory cortex. Thus, the aim of this study is the evaluation of the clinical efficacy of neuronavigated left-sided cTBS in chronic tinnitus in a randomised sham-controlled two-arm design.
INTRODUCTION: Evidence shows that resistance training (RT) reduces lymphoedema in patients with breast cancer-related lymphoedema (BRCL), making it a safe and efficient intervention. However, it is uncertain if RT is safe and effective in patients at risk of developing BRCL. This systematic review (SR) protocol aims to describe all methodological aspects in order to evaluate the short-, medium- and long-term effects of RT on the prevention of BCRL.
MATERIALS AND METHODS: Throughout 2024, randomised clinical trials (RCTs) will be identified in electronic databases MEDLINE/PubMed, Embase, Cochrane Central Register of Controlled Trials, PEDro and LILACS. Only studies in English, Spanish and Portuguese will be included. Grey literature and clinical trial registration will also be reviewed. The primary outcome will be the occurrence of lymphoedema and quality of life. Second, pain intensity, upper limb function, range of movement, grip strength and adverse events will be considered. The individual studies' risk of bias will be evaluated using the Cochrane Risk of Bias 2.0 tool. Pairwise meta-analyses using a frequentist approach and random effects model will be conducted. The Grading of Recommendations Assessment, Development and Evaluation system will be used to evaluate the certainty of the evidence.
ETHICS AND DISSEMINATION: This protocol does not require the approval of an ethics committee, as it is a secondary study. The results will be disseminated through peer-reviewed publications.
PROSPERO REGISTRATION NUMBER: CRD42023455720.
FIELD: biotechnology. SUBSTANCE: bacteria were cultured at 35-37 C for 14 days under continuous aeration on one of the following liquid nutrient media of the following composition, wt.-%: enzymatic pepton, 2.0-3.0; magnesium sulfate, 0.1-0.15, and water, the balance; or dry skimmed milk, 2.0-3.0; sodium chloride, 0.4-0.5; and water, the balance, pH = 7.3 ± 0.2. Sowing is carried out with mother culture or cultural fluid of one of the preceding generations heated at 80 C for 20 min and taken at amount 1-2% of medium volume to be sown. Spore suspension obtained from cultural fluid is used as bacterial preparation that can be stored without lyophilic drying. EFFECT: simplified method, decreased cost. 1 tbl
About 50% of patients undergoing cardiac surgery require red blood cell (RBC) transfusion. Given the limited blood supply and harms of transfusion, evidence-based blood conservation strategies are a priority. There is one such simple conservation technique called Retrograde autologous priming (RAP), in which the patient's own blood, rather than crystalloid fluid, is used to prime the heart-lung machine. Ultimately, it minimizes the loss of RBCs during surgery. Despite evidence of RAP reducing incidence of RBC transfusions by 40% and RBC units transfused by 38% in small randomized trials, it is not routinely used due to the uncertainty about overall benefit and potential harms. Routine RAP may be beneficial, but this needs to be confirmed in a large pragmatic randomized trial. Therefore, the goal of this vanguard trial is to assess the feasibility of a full-scale multi-centre randomized cluster crossover trial to determine whether an institutional policy of routine RAP reduces the number of RBC units transfused up to 72 hours after cardiac surgery compared to crystalloid priming. This will include 4 sites that will test the two policies in an alternating sequence during 12 periods of 4 weeks, with an expected volume of 4500 cardiac surgery patients. If the adherence to both polices is \>=90%, a full trial will be conducted. The findings of this study have the potential to improve the outcomes of tens of thousands of patients around the world and will provide the basis for cardiac practice guidelines.
Inflammaging, a pro-inflammatory status that characterizes aging and primarily involving macrophages, is a master driver of age-related diseases. Mineralocorticoid receptor (MR) activation in macrophages critically regulates inflammatory and fibrotic processes. However, macrophage-specific mechanisms and the role of the macrophage MR for the regulation of inflammation and fibrotic remodeling in the aging heart have not yet been elucidated. Transcriptome profiling of cardiac macrophages from male/female young (4 months-old), middle (12 months-old) and old (18 and 24 months-old) mice revealed that myeloid cell-restricted MR deficiency prevents macrophage differentiation toward a pro-inflammatory phenotype. Pathway enrichment analysis showed that several biological processes related to inflammation and cell metabolism were modulated by the MR in aged macrophages. Further, transcriptome analysis of aged cardiac fibroblasts revealed that macrophage MR deficiency reduced the activation of pathways related to inflammation and upregulation of ZBTB16, a transcription factor involved in fibrosis. Phenotypic characterization of macrophages showed a progressive replacement of the TIMD4+MHC-IIneg/low macrophage population by TIMD4+MHC-IIint/high and TIMD4-MHC-IIint/high macrophages in the aging heart. By integrating cell sorting and transwell experiments with TIMD4+/TIMD4-macrophages and fibroblasts from old MRflox/MRLysMCre hearts, we showed that the inflammatory crosstalk between TIMD4- macrophages and fibroblasts may imply the macrophage MR and the release of mitochondrial superoxide anions. Macrophage MR deficiency reduced the expansion of the TIMD4- macrophage population and the emergence of fibrotic niches in the aging heart, thereby protecting against cardiac inflammation, fibrosis, and dysfunction. This study highlights the MR as an important mediator of cardiac macrophage inflammaging and age-related fibrotic remodeling.
The etiology of many neurological and neuromuscular disorders is largely unknown. Contributions likely come from both inherited and environmental factors. Amyotrophic lateral sclerosis ("ALS") is a prototypical example. In 5-10% of cases, genetic mutations exert a strong enough influence on disease development that the syndrome is transmitted in a clearly Mendelian fashion. Investigations in these "familial" ALS cases have identified more than 20 causative disease genes. Intensive study of these genes has helped identify several key cellular pathways as important for disease, not only in cases with obvious gene mutations, but even in the 90% of ALS cases that appear to be "sporadic." Further insights have come from investigating blood biomarkers in ALS such as gene and protein expression and lymphocyte profiling. It is hoped that further genetic and biomarker analysis will identify additional genetic risk factors or biomarkers to better understand the disease and improve therapeutic development. These advances can be applied not just to ALS but to the broad range of neurological and neuromuscular diseases, including Charcot Marie Tooth neuropathy, the muscular dystrophies, epilepsies, Parkinson's disease, and Alzheimer's disease.
Cellular phenotype and function are altered in different microenvironments. For targeted therapies it is important to understand site-specific cellular adaptations. Juvenile idiopathic arthritis (JIA) is characterized by autoimmune joint inflammation, with frequent inadequate treatment responses. To comprehensively assess the inflammatory immune landscape, we designed a 37-parameter spectral flow cytometry panel delineating mononuclear cells from JIA synovial fluid (SF) of autoimmune inflamed joints, compared to JIA and healthy control blood. Synovial monocytes and NK cells (CD56bright) lack Fc-receptor CD16, suggesting antibody-mediated targeting may be ineffective. B cells and DCs, both in small frequencies in SF, undergo maturation with high 4-1BB, CD71, CD39 expression, supporting T-cell activation. SF effector and regulatory T cells were highly active with newly described co-receptor combinations that may alter function, and suggestion of metabolic reprogramming via CD71, TNFR2, and PD-1. Most SF effector phenotypes, as well as an identified CD4-Foxp3+ T-cell population, were restricted to the inflamed joint, yet specific SF-predominant CD4+ Foxp3+ Treg subpopulations were increased in blood of active but not inactive JIA, suggesting possible recirculation and loss of immunoregulation at distal sites. This first comprehensive dataset of the site-specific inflammatory landscape at protein level will inform functional studies and the development of targeted therapeutics to restore immunoregulatory balance and achieve remission in JIA.
Hyperphosphatemia is a common feature in patients with impaired kidney function and is associated with increased risk of cardiovascular disease. This phenomenon extends to the general population, whereby elevations of serum phosphate within the normal range increase risk; however, the mechanism by which this occurs is multifaceted, and many aspects are poorly understood. Less than 1% of total body phosphate is found in the circulation and extracellular space, and its regulation involves multiple organ cross talk and hormones to coordinate absorption from the small intestine and excretion by the kidneys. For phosphate to be regulated, it must be sensed. While mostly enigmatic, various phosphate sensors have been elucidated in recent years. Phosphate in the circulation can be buffered, either through regulated exchange between extracellular and cellular spaces or through chelation by circulating proteins (ie, fetuin-A) to form calciprotein particles, which in themselves serve a function for bulk mineral transport and signaling. Either through direct signaling or through mediators like hormones, calciprotein particles, or calcifying extracellular vesicles, phosphate can induce various cardiovascular disease pathologies: most notably, ectopic cardiovascular calcification but also left ventricular hypertrophy, as well as bone and kidney diseases, which then propagate phosphate dysregulation further. Therapies targeting phosphate have mostly focused on intestinal binding, of which appreciation and understanding of paracellular transport has greatly advanced the field. However, pharmacotherapies that target cardiovascular consequences of phosphate directly, such as vascular calcification, are still an area of great unmet medical need.