anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The present invention relates to a composition for prevention or treatment of metabolic disease, fibrotic disease, or muscle disease, comprising Lactobacillus sp. bacteria-derived vesicles. The inventors of the present invention have confirmed that when Lactobacillus sp. bacteria-derived vesicles are administered to an animal model for high-fat diet-induced metabolic disease, high-fat diet-induced metabolic disease is efficiently inhibited, and when Lactobacillus sp. bacteria-derived vesicles are administered to an animal model for choline-deficient L-amino acid-defined high-fat diet-induced non-alcoholic steatohepatitis and fibrotic disease, steatohepatitis and fibrotic disease are effectively inhibited, and when Lactobacillus acidophilus-derived vesicles are administered to muscle cells, the AMPK signals inhibiting metabolic stress-induced apoptosis increases, and thus the Lactobacillus sp. bacteria-derived vesicles according to the present invention may be usefully employed in the development of a medicinal product or a health functional food for prevention, symptom reduction, or treatment of metabolic disease, fibrotic disease, or muscle disease.
BACKGROUND: This study aimed to clarify the population in whom the presence of metabolic dysfunction-associated fatty liver disease (MAFLD) especially contributes to recurrence after liver resection for non-B, non-C hepatocellular carcinoma (NBNC-HCC).
METHODS: Of the 199 patients who underwent liver resection for NBNC-HCC, those who exceeded Milan criteria and with pathologically proven vascular invasion, intrahepatic metastasis, and positive resection margins were excluded, and the remaining 94 were eligible for this study. We explored factors contributing to postoperative recurrence in populations with and without advanced liver fibrosis.
RESULTS: Independent factors contributing to postoperative recurrence in the study population were male sex ( P  = 0.023) and presence of type 2 diabetes (DM) ( P  = 0.006) and advanced liver fibrosis ( P  < 0.001). Factors in cases with advanced liver fibrosis (n = 43) were non-overweight ( P  = 0.02), type 2 DM ( P  = 0.006), and preoperative alpha-fetoprotein level of 8.2 ng/ml or higher ( P  = 0.021). In cases without advanced liver fibrosis (n = 51), only presence of all three MAFLD criteria was related to recurrence.
CONCLUSION: Liver fibrosis is a strong factor contributing to postoperative recurrence of NBNC-HCC, as previously reported. In patients with advanced liver fibrosis, presence of type 2 DM was the only factor associated with recurrence among MAFLD criteria. On the other hand, in patients without advanced liver fibrosis, the combination of all MAFLD criteria, rather than a specific criterion alone, contributed to recurrence. MAFLD criteria were found to have utility as predictors of postoperative recurrence in NBNC-HCC.
BACKGROUND: Lixisenatide, a glucagon-like peptide-1 receptor agonist used for the treatment of diabetes, has shown neuroprotective properties in a mouse model of Parkinson's disease.
METHODS: In this phase 2, double-blind, randomized, placebo-controlled trial, we assessed the effect of lixisenatide on the progression of motor disability in persons with Parkinson's disease. Participants in whom Parkinson's disease was diagnosed less than 3 years earlier, who were receiving a stable dose of medications to treat symptoms, and who did not have motor complications were randomly assigned in a 1:1 ratio to daily subcutaneous lixisenatide or placebo for 12 months, followed by a 2-month washout period. The primary end point was the change from baseline in scores on the Movement Disorder Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) part III (range, 0 to 132, with higher scores indicating greater motor disability), which was assessed in patients in the on-medication state at 12 months. Secondary end points included other MDS-UPDRS subscores at 6, 12, and 14 months and doses of levodopa equivalent.
RESULTS: A total of 156 persons were enrolled, with 78 assigned to each group. MDS-UPDRS part III scores at baseline were approximately 15 in both groups. At 12 months, scores on the MDS-UPDRS part III had changed by -0.04 points (indicating improvement) in the lixisenatide group and 3.04 points (indicating worsening disability) in the placebo group (difference, 3.08; 95% confidence interval, 0.86 to 5.30; P = 0.007). At 14 months, after a 2-month washout period, the mean MDS-UPDRS motor scores in the off-medication state were 17.7 (95% CI, 15.7 to 19.7) with lixisenatide and 20.6 (95% CI, 18.5 to 22.8) with placebo. Other results relative to the secondary end points did not differ substantially between the groups. Nausea occurred in 46% of participants receiving lixisenatide, and vomiting occurred in 13%.
CONCLUSIONS: In participants with early Parkinson's disease, lixisenatide therapy resulted in less progression of motor disability than placebo at 12 months in a phase 2 trial but was associated with gastrointestinal side effects. Longer and larger trials are needed to determine the effects and safety of lixisenatide in persons with Parkinson's disease. (Funded by the French Ministry of Health and others; LIXIPARK ClinicalTrials.gov number, NCT03439943.).
To provide a biological information calculation system which improves the accuracy of assessment. This biological information calculation system is for outputting information about characteristics of carbon dioxide in the blood of a user. The biological information calculation system is provided with an acquisition means, a database, and a generation means. The acquisition means acquires assessment data based on a pulse wave of the user. Classification information generated by using a plurality of training data items is stored in the database in which each of the training data items is obtained from a pair of: input data based on learning pulse waves acquired in advance; and reference data including characteristics of carbon dioxide in the blood associated with the input data. The generation means refers to the database, and generates an assessment result that includes characteristics of the carbon dioxide in the blood with respect to the assessment data.
OBJECTIVES: In the context of musculoskeletal health, the emergence of pre-sarcopenia as a precursor to sarcopenia has garnered attention for its potential insights into early muscle loss. We explored the association between different metabolic phenotypes of obesity, and the incidence of pre-sarcopenia over a 3-year follow-up in a cohort from the Tehran Lipid and Glucose Study (TLGS).
METHODS: In this 3-year longitudinal study, 2257 participants were categorized into four groups based on their BMI and metabolic status: metabolically healthy normal weight (MHNW), metabolically healthy overweight/obese (MHO), metabolically unhealthy normal weight (MUNW), and metabolically unhealthy overweight/obese (MUO). The participants were assessed for various anthropometric and body composition indices including muscle mass determined by bioelectrical impedance analysis (BIA). Blood samples were collected for metabolic indices, and participants underwent measurements for blood pressure. Pre-sarcopenia was defined based on low muscle mass. Statistical analyses included logistic regression and chi-squared tests.
RESULTS: The MUNW group exhibited the highest prevalence of pre-sarcopenia (33.5%), while the MHO group had the lowest (2.8%). Adjusted models revealed that the odds ratio for pre-sarcopenia was higher in the MUNW group (OR = 2.23, P < 0.001), whereas the MHO and MUO groups showed lower odds (OR = 0.11 and 0.13, both P < 0.001). Notably, the association was gender-dependent, with MUNW females having a higher risk even after adjustments (OR = 2.37, P = 0.042).
CONCLUSION: Our findings suggest that metabolic health may play a pivotal role in pre-sarcopenia, emphasizing the need for targeted interventions based on both metabolic and obesity phenotypes.
The identification of moieties and the use of the same for preventing tolerance to bronchodilators are described. More specifically, described is the identification of compositions and methods, which are capable of preventing tolerance to beta 2-adrenergic agonists. The methods and compositions are also useful as analytical tools for functional studies and as combination therapeutic tools. Figure 2 is a graphic representation showing the ability of a representative bronchodilator (salmeterol) used in conjunction with representative effectors (low molecular weight heparin preparations) to prevent tolerance to bronchodilators in a heparin-nonresponsive patient. The first dose of salmeterol caused a marked increase in PD20-methacholine on day 1, showing bronchoprotection. Lesser bronchoprotection was observed after the 3rd-7thdoses of salmeterol (days 2-4), indicating development of tolerance. As shown, tolerance was prevented by inhaled low molecular weight heparin.
Obesity is a recognized public health epidemic with a prevalence that continues to increase dramatically in nearly all populations, impeding progress in reducing incidence rates of cardiovascular disease. Over the past decade, obesity science has evolved to improve knowledge of its multifactorial causes, identifying important biological causes and sociological determinants of obesity. Treatments for obesity have also continued to develop, with more evidence-based programs for lifestyle modification, new pharmacotherapies, and robust data to support bariatric surgery. Despite these advancements, there continues to be a substantial gap between the scientific evidence and the implementation of research into clinical practice for effective obesity management. Addressing barriers to obesity science implementation requires adopting feasible methodologies and targeting multiple levels (eg, clinician, community, system, policy) to facilitate the delivery of obesity-targeted therapies and maximize the effectiveness of guideline-driven care to at-need patient populations. This scientific statement (1) describes strategies shown to be effective or promising for enhancing translation and clinical application of obesity-based research; (2) identifies key gaps in the implementation of obesity science into clinical practice; and (3) provides guidance and resources for health care professionals, health care systems, and other stakeholders to promote broader implementation and uptake of obesity science for improved population-level obesity management. In addition, advances in implementation science that hold promise to bridge the know-do gap in obesity prevention and treatment are discussed. Last, this scientific statement highlights implications for health research policy and future research to improve patient care models and optimize the delivery and sustainability of equitable obesity-related care.
BACKGROUND: There is growing evidence indicating immune inflammation is a key factor in the progression of chronic obstructive pulmonary disease (COPD). Immune checkpoints (ICs) are crucial targets for modulating the functional activation and differentiation of immune cells, particularly in relation to immune inflammation and the regulation of T cell activation and exhaustion. However, the precise mechanisms of ICs in COPD remain understood.
METHODS: COPD datasets were obtained from the Gene Expression Omnibus (GEO) and analyzed using GEO2R and Limma to identify differentially expressed genes. LASSO regression was then applied to screen ICs closely associated with COPD. Finally, target genes were selected based on gene expression profiles. Gene ontology (GO), immune infiltration analysis, and gene set enrichment analysis (GSEA) were utilized to assess the relationship between IC genes (ICGs) and immune cells. Subsequently, tobacco-exposed mice, anti-Tim3-treated mice, and HAVCR2-knockout mice were generated, with flow cytometry being used to confirm the results.
RESULTS: Through the analysis of GSE38974 and LASSO regression, five ICGs were identified. Subsequent validation using GSE20257 and GSE76925 confirmed these findings. Gene expression profiling highlighted HAVCR2 as having the strongest correlation with COPD. Further investigation through immune infiltration analysis, GO, and GSEA indicated a link between HAVCR2 and CD8+ T cells in COPD. Flow cytometry experiments demonstrated high Tim3 expression in CD8+ T cells of mice exposed to tobacco, promoting Tc1 and inhibiting Tc17, thus affecting CD8+ Tem activation and CD8+ Tcm formation, leading to an immune imbalance within CD8+ T cells.
CONCLUSION: Prolonged exposure to tobacco upregulates Tim3 in CD8+ T cells, triggering its regulatory effects on Tc1/Tc17. Knocking out HAVCR2 further upregulated the expression of CD8+ Tem while suppressing the expression of CD8+ Tcm, indicating that Tim3 plays a role in the activation and differentiation of CD8+ T cells in the context of tobacco exposure.
<P>PROBLEM TO BE SOLVED: To provide a safe and easily combinable skin irritation ameliorating agent excellent in amelioration of skin irritation without affecting the functions or form of preparation and an external preparation for skin.  <P>SOLUTION: The external preparation for skin contains p-hydroxybenzoic acid and/or 2,4-dihydroxybenzoic acid, and further a skin irritation causative substance [such as retinol and its derivatives (e.g. retinyl acetate and retinyl palmitate) and an oily pharmaceutical components such as a UV absorbing agent (e.g. octyl methoxycinnamate)]. The irritation ameliorating agent is composed of p-hydroxybenzoic acid and/or 2,4-dihydroxybenzoic acid.  <P>COPYRIGHT: (C)2008,JPO&INPIT
Idiopathic pulmonary fibrosis (IPF) is a chronic pulmonary fibrosis disease that is fatal. Mesenchymal stem cells (MSCs)-secreted exosomes (exos) have been linked to improving PF. Moreover, exosomal microRNAs (miRs) can control the growth of numerous diseases, including lung disorders. Our bioinformatics analysis showed that miR-30b was downregulated in tissue samples from surgical remnants of biopsies or lungs explanted from patients with IPF who underwent pulmonary transplantation. This suggests that miR-30b plays an important role in both the pathogenesis and treatment of IPF. Herein, this research was designed to ascertain the mechanism of MSCs-exos-packaged miR-30b in alleviating PF. The serum was harvested from idiopathic PF (IPF) patients with interstitial pneumonia caused by dermatomyositis and the MLE12 lung epithelial cell fibrosis model was built with TGF-β1 (10 ng/mL), followed by miR-30b expression determination. TGF-β1-stimulated MLE12 cells were co-incubated with exos from MSCs with or without Spred2 or Runx1 overexpression, followed by measurement of cell viability and apoptosis. After establishing the IPF mouse model with bleomycin and injecting exos and/or silencing and overexpressing adenovirus vectors, fibrosis evaluation was conducted. In mice and cells, the expression of TGF-β1, TNF-α, and IL-1β was tested via ELISA, and the levels of E-cad, ZO-1, α-SMA, and collagen type I via western blot analysis. The promoters of miR-30b, Runx1, and Spred2 were investigated. miR-30b was downregulated in the serum of IPF patients and TGF-β1-stimulated MLE12 cells. Mechanistically, miR-30b inhibited Spred2 transcription by negatively targeting Runx1. MSCs-exos or MSCs-exo-miR-30b decreased the apoptosis, inflammation, and fibrosis while increasing their viability in TGF-β1-stimulated MLE12 cells, which was annulled by overexpressing Runx1 or Spred2. Exo-miR-30b decreased Runx1 expression to downregulate Spred2, reducing fibrosis and inflammation in IPF mice. Our results indicated that MSCs-exos-encapsulated miR-30b had a potential function to inhibit PF and part of its function may be achieved by targeting RUNX1 to reduce the Spred2 transcription level. Moreover, this work offered evidence and therapeutic targets for therapeutic strategies for managing clinical PF in patients.
BACKGROUND: Hepatoblastoma and HCC are the most common malignant hepatocellular tumors seen in children. The aim of this study was to develop a liquid biopsy test for circulating tumor cells (CTCs) for these tumors that would be less invasive and provide real-time information about tumor response to therapy.
METHODS: For this test, we utilized indocyanine green (ICG), a far-red fluorescent dye used clinically to identify malignant liver cells during surgery. We assessed ICG accumulation in cell lines using fluorescence microscopy and flow cytometry. For our CTC test, we developed a panel of liver tumor-specific markers, including ICG, Glypican-3, and DAPI, and tested it with cell lines and noncancer control blood samples. We then used this panel to analyze whole-blood samples for CTC burden with a cohort of 15 patients with hepatoblastoma and HCC and correlated with patient characteristics and outcomes.
RESULTS: We showed that ICG accumulation is specific to liver cancer cells, compared to nonmalignant liver cells, non-liver solid tumor cells, and other nonmalignant cells, and can be used to identify liver tumor cells in a mixed population of cells. Experiments with the ICG/Glypican-3/DAPI panel showed that it specifically tagged malignant liver cells. Using patient samples, we found that CTC burden from sequential blood samples from the same patients mirrored the patients' responses to therapy.
CONCLUSIONS: Our novel ICG-based liquid biopsy test for CTCs can be used to specifically detect and quantify CTCs in the blood of pediatric patients with liver cancer.
Atherosclerosis, an immunoinflammatory disease of medium and large arteries, is associated with life-threatening clinical events, such as acute coronary syndromes and stroke. Chronic inflammation and impaired lipoprotein metabolism are considered to be among the leading causes of atherosclerosis, while numerous risk factors, including arterial hypertension, diabetes mellitus, obesity, and aging, can contribute to the development of the disease. In recent years, emerging evidence has underlined the key role of mitochondrial dysfunction in the pathogenesis of atherosclerosis. Mitochondrial dysfunction is believed to result in an increase in reactive oxygen species, leading to oxidative stress, chronic inflammation, and intracellular lipid deposition, all of which can contribute to the pathogenesis of atherosclerosis. Critical cells, including endothelial cells, vascular smooth muscle cells, and macrophages, play an important role in atherosclerosis. Mitochondrial function is also involved in maintaining the normal function of these cells. To better understand the relationship between mitochondrial dysfunction and atherosclerosis, this review summarizes the findings of recent studies and discusses the role of mitochondrial dysfunction in the risk factors and critical cells of atherosclerosis. FACTS: OPEN QUESTIONS.
The invention relates to an externally used medicament for treating psoriasis and a preparation method thereof, which is used for solving the problem that psoriasis is difficult to cure. The invention has the technical scheme that the medicament is prepared from the following raw materials in weight: 16-19% of Chinese honey locust leaves, 20-26% of sesame leaves, 15-18% of pepper tree leaves and 16-18% of caltrop seedlings. The medicament is the result of a formulation handed down from ancestors and clinic experience for many years, the four medicinal materials are carefully selected through long-time clinic practices, and the content of each medicinal material is determined. The medicament is pulverized, mixed with water into a paste and coated to affected parts. Psoriasis can be cured after three courses of treatment in general, the cure rate can reach 80%, the effective rate reaches 97%, and psoriasis does not recur. Each medicinal material of the medicament is natural plant stems and leaves. The medicament has the advantages of simple treatment method, low treatment cost, no pain during treatment, no any toxic or side effect and the like.
To serve as an observational reference group, they (n=15) will continue their urate-lowering agents for 12 months. Randomization is stratified based on the urinary urate excretion rate (≤5.5% vs. \>5.5%).
Chronic kidney disease (CKD) has emerged as one of the leading noncommunicable diseases affecting >10% of the population worldwide. Bone and mineral disorders are a common complication among patients with CKD resulting in a poor life quality, high fracture risk, increased morbidity and cardiovascular mortality. According to Kidney Disease: Improving Global Outcomes, renal osteodystrophy refers to changes in bone morphology found in bone biopsy, whereas CKD-mineral and bone disorder (CKD-MBD) defines a complex of disturbances including biochemical and hormonal alterations, disorders of bone and mineral metabolism and extraskeletal calcification. As a result, the management of CKD-MBD should focus on the aforementioned parameters, including the treatment of hyperphosphatemia, hypocalcemia, abnormal PTH and vitamin D levels. Regarding the bone fragility fractures, osteoporosis and renal osteodystrophy, which constitute the bone component of CKD-MBD, anti-osteoporotic agents constitute the mainstay of treatment. However, a thorough elucidation of the CKD-MBD pathogenesis is crucial for the ideal personalized treatment approach. In this paper, we review the pathology and management of CKD-MBD based on the current literature with special attention to recent advances.
FIELD: veterinary medicine.SUBSTANCE: group of inventions relates to the field of veterinary medicine, it can be used to obtain a vaccine for the prevention of infectious pathologies in turkeys, ducks and geese caused by the bacteria Riemerella anatipestifer, Pasteurella multocida, Salmonella typhimurium, Salmonella infantis, Salmonella enteritidis. Polyvalent inactivated vaccine against riemerellosis, pasteurellosis and salmonellosis of turkeys, ducks and geese contains the following components per 1 cm3of the drug: inactivated protective antigen of the Riemerella anatipestifer strain No. 549-ARRIEVM (All-Russian Research Institute of Experimental Veterinary Medicine)- 2 billion microbial cells, inactivated protective antigen of the R. anatipestifer strain No. 566-ARRIEVM- 2 billion microbial cells, inactivated protective antigen of the R. anatipestifer strain No. 571-ARRIEVM - 2 billion microbial cells, inactivated protective antigen of the Pasteurella multocida strain No. 367-ARRIEVM - 2 billion microbial cells, inactivated protective antigen of the Salmonella enteritidis strain No. 162-ARRIEVM - 1 billion microbial cells, inactivated protective antigen of the Salmonella typhimurium strain No. 178-ARRIEVM - 1 billion microbial cells, inactivated protective antigen of the Salmonella infantis strain No. 1827-ARRIEVM - 1 billion microbial cells, as well as pharmaceutically acceptable target additives. The group of inventions also relates to the method for preparing this vaccine.EFFECT: use of this group of inventions makes it possible to prepare a vaccine against riemerellosis, pasteurellosis and salmonellosis of turkeys, ducks and geese, based on a balanced antigenic composition containing the most common serotypes of bacteria Riemerella anatipestifer, Pasteurella multocida, Salmonella spp. on the territory of the Russian Federation, ensuring the creation of long-term and intense immunity in vaccinated poultry.7 cl, 10 tbl, 19 ex
Volunteers from this group will have bonded buttons on vestibular surfaces of elements 1.4, 1.5 and 1.6. Then they will use Sensodyne Repair \& Protect for home oral care for 30 days. In this time period, the buttons will be respectively debonded at 7 (1.4), 15 (1.5) and 30 (1.6) days after the bonding procedures, in order to be evaluated at SEM.