anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Not many studies examined genetic determinants of obesity in women. As premenopausal and postmenopausal women appear to have different propensities for fat deposition, genetic loci linked with obesity-related phenotypes might be different by menopausal status. So far, there is no large scale of genetic study deciphering common obesity on women focusing on the interaction between aging and menopause in Taiwan. The investigators propose this study to compare phenotypic profiles of obesity and cardiometabolic factors in a large group of premenopausal and postmenopausal women. The study will examine the contributions of aging and menopausal status to the changes of obesity-related traits, and will evaluate the contribution of genetic susceptibility on body fat deposition among women at different stage of menopause. The investigators plan to recruit two groups of subjects: 600 premenopausal, and 600 postmenopausal women. Each woman will receive anthropometric and blood pressure measurements, fasting blood sampling for lipids, and an optional 75-g oral glucose tolerance test for insulin resistance. Dual energy X-ray absorptiometry will also be used for body composition measurements among the study women if they agree to receive this optional examination. The investigators will collect blood samples for DNA extraction and select several candidate genes to study the associations between susceptible genes and obesity-related traits. The investigators anticipate that the results generated from the study will provide valuable data to a better understanding of the pathogenesis of common obesity during transition from premenopause to postmenopause in women.
The principal pharmacological action of sodium nitroprusside is relaxation of vascular smooth muscle and consequent dilatation of peripheral arteries and veins. Other smooth muscle (e.g., uterus, duodenum) is not affected. Sodium nitroprusside is more active on veins than on arteries, but this selectivity is much less marked than that of nitroglycerin. Dilatation of the veins promotes peripheral pooling of blood and decreases venous return to the heart, thereby reducing left ventricular end diastolic pressure and pulmonary capillary wedge pressure (preload). Arteriolar relaxation reduces systemic vascular resistance, systolic arterial pressure, and mean arterial pressure (afterload). Dilatation of the coronary arteries also occurs.

In association with the decrease in blood pressure, sodium nitroprusside administered intravenously to hypertensive and normotensive patients produces slight increases in heart rate and a variable effect on cardiac output. In hypertensive patients, moderate doses induce renal vasodilatation roughly proportional to the decrease in systemic blood pressure, so there is no appreciable change in renal blood flow or glomerular filtration rate.

In normotensive subjects, acute reduction of mean arterial pressure to 60 to 75 mm Hg by infusion of sodium nitroprusside caused a significant increase in renin activity. In the same study, ten renovascular-hypertensive patients given sodium nitroprusside had significant increases in renin release from the involved kidney at mean arterial pressures of 90 to137 mm Hg.

The hypotensive effect of sodium nitroprusside is seen within a minute or two after the start of an adequate infusion, and it dissipates almost as rapidly after an infusion is discontinued. The effect is augmented by ganglionic blocking agents and inhaled anesthetics.
The susceptibility to autoimmune diseases is conditioned by the association of modest genetic alterations which altogether weaken self-tolerance. The mechanism whereby these genetic interactions modulate T-cell pathogenicity remains largely uncovered. Here, we investigated the epistatic interaction of two interacting proteins involved in T Cell Receptor signaling and which were previously associated with the development of Multiple Sclerosis. To this aim, we used mice expressing an hypomorphic variant of Vav1 (Vav1R63W), combined with a T cell-conditional deletion of Themis. We show that the combined mutations in Vav1 and Themis induce a strong attenuation of the severity of Experimental Autoimmune Encephalomyelitis (EAE), contrasting with the moderate effect of the single mutation in each of those two proteins. This genotype-dependent gradual decrease of EAE severity correlates with decreased quantity of phosphorylated Vav1 in CD4 T cells, establishing that Themis promotes the development of encephalitogenic Tconv response by enhancing Vav1 activity. We also show that the cooperative effect of Themis and Vav1 on EAE severity is independent of regulatory T cells and unrelated to the impact of Themis on thymic selection. Rather, it results from decreased production of pro-inflammatory cytokines (IFN-γ, IL-17, TNF and GM-CSF) and reduced T cell infiltration in the CNS. Together, our results provide a rationale to study combination of related genes, in addition to single gene association, to better understand the genetic bases of human diseases.
Application in the Simulator Group with High Fidelity: Students will be taught cardiopulmonary resuscitation skills with the CPR Simulator. The student and 2 researchers who will practice will remain in the environment, and the student will also be asked to practice.
The investigators anticipate enrolling a total of 40 children between 3 and 18 years of age. Specifically, two groups of children will be recruited; children with unilateral congenital upper-limb reductions (n=20) and age and sex-matched control group of typically developing children (n=20). Considering the effect size from preliminary data and to account for a 10% drop-out rate, a total sample of 40 subjects will provide 80% power to detect a true standardized effect size.

Participants will be asked to attend a total of 3 sessions. Participants will attend an initial measurement session to take a 3D scan of the affected and non-affected upper limbs as well as several anthropometric measurements. During this session, three pictures of the upper limbs will be taken which will also be used to verify the fit the prostheses in a process previously validated by our research team. The research participants will then be asked to come for two testing visits. During the first testing visit (visit 1), participants will be fitted with the prosthesis and required adjustments to improve comfort and avoid pressure point will be performed. After fitting the prosthesis, participants will be given 15 minutes to explore the prosthesis and adjust the tensioner dial to regulate the opening of the fingers to perform the Box and Block Test. After the training and accommodation period, participants will be asked to perform 3 trials of flexion and extension of each wrist with and without the prosthesis and 3 different trials of the Box and Blocks Test for each hand while monitoring neural activity of the primary motor cortex using a fNIRS device. After a period of 20 minutes rest, participants will be asked to perform three trials of a bimanual coordination test using an instrumented tray. The bimanual task will require participants to start from a standard position and then reach forward and grasp (hand-to-tray), transport and place a tray on a ledge (tray transport), and then return the hands to the starting position (hand return). This task will be performed unimanually (3 trials for each hand) and bimanually (3 trials using both hands). Eight weeks after the baseline measurements, participants will be asked to visit our laboratory for a second time and perform the same assessments. Between the testing visits, participants will be encouraged to use the prosthesis for a minimum of 2 hours a day. In addition, an occupational therapy student will perform 3 home visits a week and will direct a training protocol that consists of completing three trials of a series of 6 block building activities for each hand separated by 30 seconds of rest (a total of 18 block building activities per hand). All participants including the control group will perform the same training protocol.
PURPOSE: To compare the efficacy and safety of Holmium laser enucleation of the prostate (HoLEP), Thulium laser enucleation of prostate (ThuLEP) and Thulium fibre laser enucleation of prostate (ThuFLEP) by performing propensity score matched analysis (PSM).
METHODS: We retrospectively analysed the patients who underwent HoLEP (Group 1, n = 696), ThuLEP (Group 2, n = 146) and ThuFLEP (Group 3, n = 193) surgery because of benign prostatic obstruction (BPO). A 1:1:1 HoLEP: ThuLEP: ThuFLEP group matching was performed using PSM analysis. Perioperative, postoperative functional outcomes and complications were analysed and compared.
RESULTS: We observed significant improvement in functional parameters regarding IPSS, Qmax, PVR and quality of life in all groups compared to baseline values at the 1st, 6th and 12th postoperative months. There was no significant difference between different laser types in terms of urge (UUI) and stress urinary incontinence (SUI) at 1st postoperative month. In all three groups, no patient had postoperative SUI or UUI at 6th and 12th postoperative months. In addition, no significant difference was observed between laser types in terms of postoperative complications.
CONCLUSION: HoLEP, ThuLEP and ThuFLEP are safe and effective LEP methods with improvement in functional parameters and low complication rates. Similar results in terms of functional outcomes and complications clearly show that these surgeries are alternatives to each other for the patients with BPO. Experts' opinions, practices and enucleation techniques should also be taken into consideration when choosing a laser for BPO surgery.
PURPOSE: To obtain an ultraviolet absorbing agent composed of 5,6- dehydrokawain, exhibiting excellent absorbing action in both ultraviolet A and B regions and having high safety and to prepare a cosmetic containing the absorbing agent and having excellent effect to protect the skin from ultraviolet rays. CONSTITUTION: This ultraviolet absorbing agent is composed of 5,6- dehydrokawain expressed by the formula and extracted from the bark of spice bush belonging to the family Lauraceae. The extraction is carried out e.g. by adding 1-20 pts. of a polar solvent to 1 pt. of the bark of spice bush, extracting at room temperature or by heating at a temperature near the boiling point of the solvent and purifying the product. This cosmetic is prepared by compounding 0.01-10wt.% of the ultraviolet absorbing agent as an active component based on the total cosmetic. It can be used as a foundation cosmetic to be applied to the skin (e.g. cream, milky lotion and face lotion), a make-up cosmetic (e.g. eye color, cheek color, foundation and under-makeup), etc.
The invention relates to biotechnology and, in particular, can be used in the pharmaceutical industry for preparing a drug for treating a B-cell disorder, depleting B-cells or slowing the development of a pathological condition associated with B-cell abnormalities. A bispecific antibody specifically binding to CD3 and CD19 comprises two chains connected by disulphide bonds. Each chain contains light and heavy chain variable domains of antibodies against CD3 and CD19, linker sequences, an immunoglobulin IgG hinge region and an immunoglobulin IgG Fc domain constant region. The antibody is produced with the aid of recombinant DNA technology using a nucleic acid that codes for the antibody and/or using a vector containing said nucleic acid, which are introduced into a host cell. A method of producing the antibody includes at least cultivating a host cell and isolating the target product. A method of purifying the antibody includes at least a chromatography stage. The antibody is used to treat a B-cell disorder, deplete B-cells or slow the development of a pathological condition associated with B-cell abnormalities. A corresponding pharmaceutical composition contains said antibody and a pharmaceutically acceptable carrier. A method of treating disorders includes administering to a patient in need thereof a therapeutically effective amount of the antibody. The invention provides for more convenient anti-CD3*CD19 therapy as a result of an anti-CD3*CD19 antibody with an increased half-life and an enhanced cytotoxic effect, which has high bioavailability even when administered subcutaneously.
Dysregulation of the gut microbiota and their metabolites is involved in the pathogenic process of intestinal diseases, and several pieces of evidence within the current literature have also highlighted a possible connection between the gut microbiota and the unfolding of inflammatory pathologies of the joints. This dysregulation is defined as the "gut-joint axis" and is based on the joint-gut interaction. It is widely recognized that the microbiota of the gut produce a variety of compounds, including enzymes, short-chain fatty acids, and metabolites. As a consequence, these proinflammatory compounds that bacteria produce, such as that of lipopolysaccharide, move from the "leaky gut" to the bloodstream, thereby leading to systemic inflammation which then reaches the joints, with consequences such as osteoarthritis, rheumatoid arthritis, and spondylarthritis. In this state-of-the-art research, the authors describe the connections between gut dysbiosis and osteoarthritis, rheumatoid arthritis, and spondylarthritis. Moreover, the diagnostic tools, outcome measures, and treatment options are elucidated. There is accumulating proof suggesting that the microbiota of the gut play an important part not only in immune-mediated, metabolic, and neurological illnesses but also in inflammatory joints. According to the authors, future studies should concentrate on developing innovative microbiota-targeted treatments and their effects on joint pathology as well as on organizing screening protocols to predict the onset of inflammatory joint disease based on gut dysbiosis.
BACKGROUND: Inflammation is the common pathogenesis of coronary atherosclerosis disease (CAD) and rheumatoid arthritis (RA). Although it is established that RA increases the risk of CAD, the underlining mechanism remained indefinite. This study seeks to explore the molecular mechanisms of RA linked CAD and identify potential target gene for early prediction of CAD in RA patients.
MATERIALS AND METHODS: The study utilized five raw datasets: GSE55235, GSE55457, GSE12021 for RA patients, and GSE42148 and GSE20680 for CAD patients. Gene Set Enrichment Analysis (GSEA) was used to investigate common signaling pathways associated with RA and CAD. Then, weighted gene co-expression network analysis (WGCNA) was performed on RA and CAD training datasets to identify gene modules related to single-sample GSEA (ssGSEA) scores. Overlapping module genes and differentially expressed genes (DEGs) were considered as co-susceptible genes for both diseases. Three hub genes were screened using a protein-protein interaction (PPI) network analysis via Cytoscape plug-ins. The signaling pathways, immune infiltration, and transcription factors associated with these hub genes were analyzed to explore the underlying mechanism connecting both diseases. Immunohistochemistry and qRT-PCR were conducted to validate the expression of the key candidate gene, PPARG, in macrophages of synovial tissue and arterial walls from RA and CAD patients.
RESULTS: The study found that Fc-gamma receptor-mediated endocytosis is a common signaling pathway for both RA and CAD. A total of 25 genes were screened by WGCNA and DEGs, which are involved in inflammation-related ligand-receptor interactions, cytoskeleton, and endocytosis signaling pathways. The principal component analysis(PCA) and support vector machine (SVM) and receiver-operator characteristic (ROC) analysis demonstrate that 25 DEGs can effectively distinguish RA and CAD groups from normal groups. Three hub genes TUBB2A, FKBP5, and PPARG were further identified by the Cytoscape software. Both FKBP5 and PPARG were downregulated in synovial tissue of RA and upregulated in the peripheral blood of CAD patients and differential mRNAexpreesion between normal and disease groups in both diseases were validated by qRT-PCR.Association of PPARG with monocyte was demonstrated across both training and validation datasets in CAD. PPARG expression is observed in control synovial epithelial cells and foamy macrophages of arterial walls, but was decreased in synovial epithelium of RA patients. Its expression in foamy macrophages of atherosclerotic vascular walls exhibits a positive correlation (r = 0.6276, p = 0.0002) with CD68.
CONCLUSION: Our findings suggest that PPARG may serve as a potentially predictive marker for CAD in RA patients, which provides new insights into the molecular mechanism underling RA linked CAD.
Cellular senescence is an important factor leading to pulmonary fibrosis. Deficiency of 8-oxoguanine DNA glycosylase (OGG1) in mice leads to alleviation of bleomycin (BLM)-induced mouse pulmonary fibrosis, and inhibition of the OGG1 enzyme reduces the epithelial mesenchymal transition (EMT) in lung cells. In the present study, we find decreased expression of OGG1 in aged mice and BLM-induced cell senescence. In addition, a decrease in OGG1 expression results in cell senescence, such as increases in the percentage of SA-β-gal-positive cells, and in the p21 and p-H2AX protein levels in response to BLM in lung cells. Furthermore, OGG1 promotes cell transformation in A549 cells in the presence of BLM. We also find that OGG1 siRNA impedes cell cycle progression and inhibits the levels of telomerase reverse transcriptase (TERT) and LaminB1 in BLM-treated lung cells. The increase in OGG1 expression results in the opposite phenomenon. The mRNA levels of senescence-associated secretory phenotype (SASP) components, including IL-1α, IL-1β, IL-6, IL-8, CXCL1/CXCL2, and MMP-3, in the absence of OGG1 are obviously increased in A549 cells treated with BLM. Interestingly, we demonstrate that OGG1 binds to p53 to inhibit the activation of p53 and that silencing of p53 reverses the inhibition of OGG1 on senescence in lung cells. Additionally, the augmented cell senescence is shown in vivo in OGG1-deficient mice. Overall, we provide direct evidence in vivo and in vitro that OGG1 plays an important role in protecting tissue cells against aging associated with the p53 pathway.
Improved clay, comprising a clayey phyllosilicate (having equidistant layers at 1.5-1.6nm, a cation exchange capacity of 170-1700m eq. per 100g and equidistant redn. of the layers to 1.2-1.4nm by heating to 490deg.C) combined with 0.005-0.5 wt parts of magnesium hydroxide per part of clay, i.e. contg. about 5-33% of magnesium hydroxide, and having an X-ray spectrum where the characteristics of magnesium hydroxide are not present, is new.  The acid addn. salts of the clay with carbonic, citric, tartaric, phosphoric and silicic acids are also claimed.
Disclosed is a site specific microcapsule delivery system and microcapsules for delivering one or more active agents to a preselected site. The system includes a catheter and microcapsules. A preferred embodiment of the catheter includes an inner inflatable balloon having an outer perforated delivery balloon concentrically disposed thereon. The microcapsule preferably comprises a water dissolvable core, and at least one outer protective shell. In a preferred embodiment, the core comprises phosphorous 31 and the outer shell comprises PGLA or other water soluble material. Neutron beam activation of the core produces phosphorous 32, for emitting therapeutic radiation to the treatment site. The outer protective shell dissipates over time, and, following a predetermined delivery period, the outer shell is removed and the central core dissipates to leave only biologically compatible break down products.
Cardiovascular disease (CVD) is highly prevalent in patients suffering from chronic kidney disease (CKD). The risk of patients with CKD developing CVD is manifested already in the early stages of CKD development. The impact of declined kidney function on increased cardiovascular risk and the underlying mechanisms are complex and multifactorial. This review discusses the impact of (a) traditional cardiovascular risk factors such as smoking, dyslipidemia, diabetes, and hypertension as well as (b) CKD-specific pathophysiological and molecular mechanisms associated with an increased cardiovascular risk. The latter include uremic toxins, post-translational modifications and uremic lipids, innate immune cell activation and inflammation, oxidative stress, endothelial cell dysfunction, increased coagulation and altered platelet responses, vascular calcification, renin-angiotensin-aldosterone-system (RAAS) and sympathetic activation, as well as anemia. Unraveling the complex interplay of different risk factors, especially in the context of patient subcohorts, will help to find new therapeutic approaches in order to reduce the increased cardiovascular risk in this vulnerable patient cohort.
PROBLEM TO BE SOLVED: To stably obtain the subject compound excellent in stability with the passage of time and useful for external preparation, etc., having effectiveness. SOLUTION: A plant extract having pH >=2 and <4 is extracted from a plant of the family Rutaceae, preferably e.g. a plant of the genus Pilocarpus with water or hot water. Then, pH of the extract is adjusted by using a cation exchange chromatography and the extract is concentrated so as to become preferably 8-20wt.%, further preferably 8-16wt.% as solid content. The insoluble part of the resultant concentrate is removed by adding >=40%, preferably 50-80% methanol to the concentrate. Then, an alkalizing agent (e.g. NaHCO3 or KOH) is added to the extract to adjust pH of the extract to >=4 and <7.
In this cross-over study, each patient receives subcutaneous and intravenous metoclopramide, with a randomized order of administration. During each perfusion phases, metoclopramide is administrated with continuous flow, doses being increased every two days, first from 10 to 20 and then from 20 to 30 mg/d. In order to guarantee plasmatic balance during route change, the first dose of the second phase is extended for three days. Metoclopramide plasmatic concentration is measured at inclusion and at the end of each dose administration, with a total of 7 dosages.

Principal purpose of this research is to clarify subcutaneous bioavailability of metoclopramide. For this meaning, the mean difference between all subcutaneous and intravenous concentration ratios is compared. Secondary purposes consist of: calculating metoclopramide subcutaneous bioavailability for each study dose (10, 20 and 30 mg/d); describing dose-bioavailability relation for subcutaneous metoclopramide; comparing dose-concentration relationship of intravenous and subcutaneous metoclopramide; studying local tolerance by checking all inflammatory signs surrounding injection site; evaluating clinical efficacy by comparing between the two groups the number of vomiting episodes, use of Serotonin receptor antagonists and the nausea scores on a 11-level numerical scale.

Eighteen patients have to be analysed at least. For each patient not having completed the study, one more will be included in order to reach the eighteen necessary patients. Therefore, it is expected to include twenty-four patients. Included population characteristics will be described. A three-dimensional analysis with period, subject and dose is performed to determine metoclopramide absolute bioavailability. For secondary criteria, dose-concentration relation is analysed with a four-dimensional analysis; dose-bioavailability and dose-concentration relations are described by linear and log-linear regression. For principal purpose, only results of patients having completed the study are part of this aforementioned analyse.