anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Introduction: Renin and prorenin promote the proliferation of vascular smooth muscle cells (VSMCs) through the (pro)renin receptor, or (P)RR, to promote restenosis occurrence. This study aimed to explore whether prorenin promoted the proliferation of VSMCs in a (P)RR-mediated Ang II-independent manner. Methods: Losartan and PD123319 were used to block the interaction between (P)RR and angiotensin in vitro. Cells were treated with renin, platelet-derived growth factor (PDGF), or RNAi-(P)RR, either jointly or individually. Cell proliferation was measured via Cell Counting Kit-8 (CCK-8) and flow cytometry methods; moreover, real-time polymerase chain reaction (RT-PCR) and Western blot (WB) assays were used to detect the expression of cyclin D1, proliferating cell nuclear antigen (PCNA), (P)RR, NOX1, and phosphatidylinositol 3-kinase (PI3K)/AKT signaling proteins. Immunofluorescence staining was conducted to measure the expression of (P)RR, and the levels of renin, PDGF-BB, inflammatory factors, and oxidative stress were determined by using enzyme-linked immunosorbent assay (ELISA). Moreover, a balloon catheter was used to enlarge the carotid artery of the Sprague Dawley rats. PRO20 was applied to identify angiotensin II (Ang II). The hematoxylin and eosin, RT-PCR, and WB results validated the cell assay results. Results: Renin promoted the proliferation of rat VSMCs by enhancing cell viability and cell cycle protein expression when Ang II was blocked, but silencing (P)RR inhibited this effect. Furthermore, renin enhanced NOX1-mediated oxidative stress and inflammation by activating the extracellular signal-regulated kinase 1/2 (ERK1/2)-AKT pathway in vitro. Similarly, the inhibition of (P)RR resulted in the opposite phenomenon. Importantly, the inhibition of (P)RR inhibited neointimal hyperplasia in vivo after common carotid artery injury by restraining NOX1-mediated oxidative stress through the downregulation of the ERK1/2-AKT pathway. The animal study confirmed these findings. Conclusion: Renin and (P)RR induced VSMC proliferation and neointimal hyperplasia by activating oxidative stress, inflammation, and the ERK1/2-AKT pathway in an Ang II-independent manner.
The invention discloses a method and purpose for constructing a TCM spleen deficiency syndrome AIDS monkey model. Among existing AIDS experimental animals, a monkey resembles to mankind the most. The inventor successfully constructs an HIV infected rhesus monkey TCM spleen deficiency syndrome composite model by two methods respectively. The first method is to carry out gavage with raw rhubarb concentrate to a create spleen deficiency syndrome and then carry out intravenous injection of infected SIV viruses. The second method is to carry out gavage with raw rhubarb concentrate to create the spleen deficiency syndrome after rhesus monkeys is infected with SIV viruses through intravenous injection. Based on the understanding of infection course, pathogenic processes and pathological changes of AIDS viruses in a spleen deficiency syndrome model, research on attack of infected target organs, target tissue and target cells to the immune system, on response of cells of the immune system, on the evolution law of a TCM syndrome, etc., is carried out. The established TCM spleen deficiency syndrome HIV infected monkey composite model in the invention plays an irreplaceable role in studying TCM pathogenesis and evolution of symptomatology of TCM for AIDS and in evaluating drug effects of anti-AIDS TCMs and compounds.
All participants in this clinical study will be dosed on one occasion with BAC TWO. The final dosage will be 80 µg (± 25%).
Participants in Part 1a (age \>= 12 - \<18 years) will receive weight-based etanercept dose up to 50 milligram SC weekly through Week 15. Participants who elect to continue in the study will receive a weight-based guselkumab dose at Weeks 20 and 24, followed by q8w dosing thereafter through Week 48. Participants who are eligible and willing to continue guselkumab treatment, may enter the LTE phase of the study. Part 1b (age \>= 6 - \<12 years) will follow the same dosing and commence after Part 1a data review.
Approximately 220 patients with chronic kidney disease (CKD) and acute NSTEMI, who are scheduled for an urgent coronary angiography (within 72 hours after admission and/or diagnosis of NSTEMI) will be screened for the study. Only patients with acute NSTEMI presumed to be a spontaneous myocardial infarction, related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection (i.e. type 1) are eligible. Written informed consent will be obtained before urgent coronary angiography. Patients with NSTEMI will typically undergo coronary angiography within 72 hours after admission and/or diagnosis of NSTEMI. It is estimated that 70% of these patients will have PCI. Randomization will continue until the 160th patient has had a PCI.
INTRODUCTION: Intestinal barrier dysfunction is a pivotal factor in sepsis progression. The mechanosensitive ion channel Piezo1 is associated with barrier function; however, its role in sepsis-induced intestinal barrier dysfunction remains poorly understood.
METHODS: The application of cecal ligation and puncture (CLP) modeling was performed on both mice of the wild-type (WT) variety and those with Villin-Piezo1flox/flox genetic makeup to assess the barrier function using in vivo FITC-dextran permeability measurements and immunofluorescence microscopy analysis of tight junctions (TJs) and apoptosis levels. In vitro, Caco-2 monolayers were subjected to TNF-α incubation. Moreover, to modulate Piezo1 activation, GsMTx4 was applied to inhibit Piezo1 activation. The barrier function, intracellular calcium levels, and mitochondrial function were monitored using calcium imaging and immunofluorescence techniques.
RESULTS: In the intestinal tissues of CLP-induced septic mice, Piezo1 protein levels were notably elevated compared with those in normal mice. Piezo1 has been implicated in the sepsis-mediated disruption of TJs, apoptosis of intestinal epithelial cells, elevated intestinal mucosal permeability, and systemic inflammation in WT mice, whereas these effects were absent in Villin-Piezo1flox/flox CLP mice. In Caco-2 cells, TNF-α prompted calcium influx, an effect reversed by GsMTx4 treatment. Elevated calcium concentrations are correlated with increased accumulation of reactive oxygen species, diminished mitochondrial membrane potential, and TJ disruption.
CONCLUSIONS: Thus, Piezo1 is a potential contributor to sepsis-induced intestinal barrier dysfunction, influencing apoptosis and TJ modification through calcium influx-mediated mitochondrial dysfunction.
Each subject comes for 2 visits. There is a randomized, double-blind, crossover design so each subject will receive active drug during one visit and placebo during the other.
This arm receives the placebo drug. This medication is taken the night before, 2 hours before surgery, and the night after surgery.
Heart failure tends to deteriorate in colder climates, heightening the risk of major adverse cardiovascular events. Brown adipose tissue (BAT) serves as both a thermogenic organ and an atypical site for triiodothyronine (T3) synthesis in response to cold. This study investigates the potential role of BAT in contributing to abdominal aortic constriction (AAC)-induced pathological cardiac remodeling during cold exposure. In this study, we developed a mouse model of pathological cardiac remodeling using AAC. Physical excision of interscapular BAT (iBATx) was performed during cold exposure, and T3 synthesis levels were measured. Additionally, the impact of uncoupling protein 1 (UCP1) knockout on thermogenic function and pathological cardiac remodeling was investigated. In vitro studies were conducted to assess the effect of T3 on cardiomyocyte hypertrophy induced by phenylephrine (PE). Physical removal of interscapular BAT during cold exposure decreased T3 synthesis and mitigated pathological cardiac remodeling. Conversely, UCP1 knockout eliminated thermogenic function during cold exposure, while preserving BAT integrity increased T3 synthesis and exacerbated pathological cardiac remodeling. In vitro, T3 further aggravated cardiomyocyte hypertrophy caused by PE. These findings underscore the distinct effects of physical and functional BAT ablation on pathological cardiac remodeling, primarily through altering T3 levels rather than thermogenesis in cold environments. This research provides new insights into the differential roles of BAT in cardiac health, particularly under cold exposure conditions.
Omega-3 Fatty Acids (Omega-3) are long poly unsaturated fatty acids that can be found in plants and fish, its refer to a group composed of three type of fatty acids called: Eicosapentaenoic acid (EPA), Alpha-linoleic acid (ALA), and Docosahexaenoic acid (DHA) . The health promoting effect of n-3FA may be due to immune modulating and anti-inflammatory actions . The anti-inflammatory properties of n-3FA are used for treatment of the inflammatory diseases such as irritable bowel syndrome, rheumatoid arthritis, eczema, and psoriasis . Many studies reported a significant reduction in the risk of cancers in breast, prostate, ovaries with supplementation of n-3FA (Larsson et al. 2004) .However, high-doses omega-3 supplements such as 1000 mg/day are widely spread in community pharmacies in Jordan . Currently , community pharmacy around the world are facing the challenge of increased demand for care of uninfected people with Covid -19. Accordingly , the current randomized clinical trial was designed to evaluate the effect of daily 300 mg of omega 3-FA supplements on the immune health status of uninfected people with Covid-19 as a part of as a part of preventive health care .

Therefore , this RCT aims to assess whether regular daily dose of regular daily dose of omega 3-FA (300 mg) for 2 months supplementation against COVID-19 infection as a part of preventive treatment protocol in uninfected Jordanian peoples. The investigators hypothesize that the regular dose of omega 3-FA (300 mg) /day for 2 months will significantly change immune responses compared with the control group.
In Part A, subjects with histologically confirmed Cervical Intraepithelial Neoplasia Grade 2 or 3 (CIN2/3) associated with Human Papillomavirus (HPV) 16 or 18, will be allocated to three dose cohorts that are 25µg,75µg and 150µg. In Part B, subjects with histologically confirmed Cervical Intraepithelial Neoplasia Grade 2 or 3 (CIN2/3) associated with Human Papillomavirus (HPV) 16 or 18, will be allocated to 1 or 2 dose levels according to the results of Part A. All subjects will receive a total of three RG002 Injections, administered intramuscularly at assigned dose level, with a dosing frequency of every 2 weeks (D1, D15, and D29).
Although oxidative stress is not the primary aetiology of SCA, oxidative damage could in part account for pathophysiological mechanisms leading to sickle vaso-occlusion, in which anti bande 3 antibodies might play a role. Bande 3 is a protein belonging to red blood cells. These anti bande 3 antibodies are producted when after oxidative damage, a hidden site of bande 3 is revealed. In preliminary data, the Cuban partner of this study showed a significative difference between their level in patients, during steady state and vaso-occlusive crises. Our clinical question is to determine if a decrease of these antibodies, could participate in the occurrence of the crises. Therapeutic strategies aimed to counteract oxidative abnormalities might alleviate this still nowadays unknown mechanisms disease progression.

Band 3 protein which belongs to the anionic interchanger is the main erythrocyte membrane protein, present in about 1.2 x 106 copies per cell. Under certain conditions, band 3 protein modifications in the human erythrocyte membrane surface lead to band 3 aggregates. These modifications are mostly due to oxidative insults that gradually accumulate during red blood cell lifespan. Band 3 clusters on the SS RBCs produce two significant changes: first, these cells acquire an adhesive nature; second, band 3 aggregates are recognized by natural band 3 antibodies. Several studies have shown that band 3 peptides are able to inhibit the adherence of SS RBCs to endothelial cells. This suggests possible participation of band 3 antibodies in the aethiology as well as in the prevention of VOC in SCA. Oxidant damage in RBCs may contribute to the circulatory disorders by affecting their flow properties i.e. their deformability, aggregability and adherence to endothelial cells. Therefore, in parallel of the study of the evaluation of the role of anti bande 3 antibodies in VOC occurrence and severity, the investigators will explore the involvement of oxidative stress on the rheological properties of SSRBCs (deformability and aggregability),
AIM: To explore the potential role of microRNA miR-221-5p on the angiopoietin-1 (Ang-1)/Ang-2/Tie-2 signaling axis after subarachnoid hemorrhage (SAH) in a rat model.
METHODS: Aspects of the rat's behavior were measured using the Kaoutzanis scoring system to test neurological responses. This included feeding behavior, body contraction, motor, and eye-opening responses. Brain sections were studied using transmission electron microscopy and Evans blue extravasation. Levels of Ang-1, Ang-2, and Tie-2 were determined by Western blot, while miR-221-5p was quantified using stem-loop real-time quantitative PCR (RT-qPCR).
RESULTS: The SAH group responded worse to the neurological response test than the sham-operated group. The intercellular space was widened in the SAH group, but not in the sham-operated group. Evans blue dye leaked significantly more into brain tissue cells of the SAH group. Stem-loop qRT-PCR showed elevated miR-221-5p levels. Additionally, Ang-1 and Tie-2 were reduced but Ang-2 expression was increased after SAH. This led to a significant reduction of the Ang-1/Ang-2 ratio in the brain tissue, which was associated with the destruction of the blood-brain barrier.
CONCLUSION: The data indicate that miR-221-5p might regulate blood-brain barrier dysfunction through the Ang-1/Ang-2/Tie-2 signaling axis, suggesting that it should be further investigated as a potential novel biomarker.
The aim of this study is to investigate the outcome of patients with colorectal liver metastases (CLM) undergoing multiple minor hepatectomies (MMH) instead of major hepatectomies (MH). Indeed, the performance of MMH versus MH in patients with CLM is object of debate. For this purpose, the databases at two independent institutions were retrospectively reviewed. To control for confounding variable distributions, a propensity score-matched analysis 1:1 was performed, and the nearest neighbor-matching method with caliper distance of 0.01 was used. Among 554 patients, 110 patients undergoing MMH and 110 undergoing MH were matched. They were similar in baseline characteristics, comorbidities, features of the primary tumors, and CLM. Primary outcomes were short- and long-term outcome.
The proposed work should help move toward the long-term goal of selection of antihypertensive drug therapy based on a patient's genetic make-up. Hypertension (HTN) is the most common chronic disease for which drugs are prescribed, and the most prevalent risk factor for heart attack, stroke, renal failure and heart failure. Responses to antihypertensive drug therapy exhibit considerable interpatient variability, contributing to poor rates of HTN control (currently 34% in the US), and frequent nonadherence and dropout from therapy. We propose to identify genetic predictors of the antihypertensive and adverse metabolic responses to two preferred and pharmacodynamically contrasting drugs, a beta-blocker (atenolol) and a thiazide diuretic (hydrochlorothiazide) given initially as monotherapy, and subsequently in combination, to 800 individuals with uncomplicated hypertension. High quality phenotype data, including both home and ambulatory measures of blood pressure (BP) response, and lipid and insulin sensitivity measures of adverse metabolic responses will be related to genetic variation through two approaches. First, testing 7 single nucleotide polymorphisms (SNPs) in each of 70 candidate genes, we will examine the influence of these genes' variation on responses to beta-blockers and diuretics (Specific Aim 1). This will include assessment of genetic associations with: antihypertensive responses to monotherapy (Aim 1a), addition of a second drug to monotherapy (Aim 1b), and combination therapy (Aim 1c); and adverse metabolic responses to mono and combination therapy (Aim 1d). This candidate gene approach will be supplemented by discovery of novel genes involved in variable BP and metabolic responses to beta-blockers and diuretics through testing of 20,000 putative functional SNPs that span the human genome (Specific Aim 2). As in Aim 1, Aim 2 will include testing for associations with antihypertensive and adverse metabolic responses to monotherapy and combination therapy. The proposed research will substantially increase our understanding of the pharmacogenetics of mono- and combination antihypertensive drug therapy. It will also lead to creation of data sets and samples that can be used by others in the field, through deposit of data to PharmGKB, and creation of immortalized cell lines from all study participants to share data and biological samples with other researchers. The proposed research is significant because genetically-targeted antihypertensive therapy could lead to dramatically higher response rates and fewer adverse effects than the usual trial-and-error approach. This would likely lead to higher rates of HTN control, less need for polypharmacy, reduced health care costs, and improved outcomes.
Insulin will be initiated utilizing clinical standards using trimester-specific weight-based dosing criteria, including both basal and prandial insulins for up to a total of 4 daily injections. Consistent with clinical practice, some people may be managed with a single dose of intermediate- or long-acting insulin at night to treat isolated fasting hyperglycemia, while others may require additional treatment of postprandial hyperglycemia with shorter-acting insulin. The sites' insulin formularies include rapid- (Novolog and Humalog), intermediate- (Humulin N, Novolin N, and NPH), and long-acting insulins (Detemir and Lantus).
<P>PROBLEM TO BE SOLVED: To provide muscle cells and the use of the muscle cells in cardiac repair.  <P>SOLUTION: Muscle cells and methods for using the muscle cells are provided. In one embodiment, the invention provides transplantable skeletal muscle cell compositions and their methods of use. In one embodiment, the muscle cells can be transplanted into patients having disorders characterized by insufficient cardiac function, (e.g., congestive heart failure), in a subject by administering the skeletal myoblasts to the subject. The muscle cells can be autologous, allogeneic, or xenogeneic to the recipient.  <P>COPYRIGHT: (C)2011,JPO&INPIT
Patients on DAPT for at least 6 months will be tested for platelet function testing with the P2Y12 VerifyNow assay at baseline. The patients will then undergo at least a 2-week course of Trimetazidine 35 mg/q12h, followed thereafter by platelet function testing.
The experimental group will have a CPM applied in the PACU immediately post-op and it will be utilized while the patient is awake in bed for 2 hours on and 2 hours off, when not mobilizing with Physical Therapy (PT). The experimental group will also have traditional PT, including sessions 1 to 3 times a week.
This study aimed to investigate whether the different pharmaceutical forms of HMB show distinct bioavailability and pharmacokinetic profile in humans. A counterbalanced crossover open-label study was conducted. 20 male and female participants were recruited, of which 18 met the inclusion criteria and 16 enrolled in the study. All participants visited the laboratory on 3 different occasions, 5-7 days apart to receive one of the following treatments: 1) 1 g of HMB-FA, or 2) HMB-Ca (equivalent of 1 g of HMB) in capsules, or 3) HMB-Ca (equivalent of 1 g of HMB) dissolved in water. The order of treatments was counterbalanced to control for carryover and order effects using a 3-by-6 (treatment-by-participant) Latin square table (www.statpages.info/latinsq.html). To randomly allocate participants to treatment sequences, participants were recruited in blocks of 6, each containing 3 males and 3 females so that sexes were counterbalanced too. The allocation sequence within each block was defined using a random sequence generator (www.random.org). Blood samples were collected before HBM ingestion and 15, 30, 45, 60, 90, 120, 180, 240, 360 and 720 minutes after HMB ingestion. Urine samples were collected before HMB ingestion (midstream sample) and 24 hours post ingestion (24h total urine). A standardised breakfast was provided to all participants 1h before treatment ingestion. A standardised snack was given to all participants 4 hours after treatment ingestion, and a standardised meal was given 6 hours after treatment ingestion. Water ingestion was standardised in the first 360 minutes after ingestion. In the last 6 hours of the protocol, the participants were dismissed from the lab and returned for the 720 post-ingestion blood collection. They consumed food and water ad-libitum. HMB concentrations were determined in urine and plasma samples by LC/MS using tandem electrospray ionization (ESI). The following pharmacokinetic parameters were calculated: Time to peak, maximum concentration, area under the curve, half-life time and slope of the incremental phase. Plasma and urine HMB concentrations were compared between treatments across time with a 2-factor mixed models analysis. Fixed factors were treatment and time, and participants were the random factor. All pairwise comparisons were adjusted with the Tukey-Kraemer correction. AUC, relative bioavailability, Cmax and Tmax were compared between treatments with repeated measures one-way ANOVA with post-hoc tests adjusted for multiple comparisons using the Bonferroni correction.
Patients follow our usual workflow as outlined in the Traditional Pathway. In addition, patients are provided both Emmi education programs and IVR follow-up as previously outlined. These patients are also scheduled for a 3 month follow-up.
Expansion of cytotoxic T lymphocytes (CTLs) is a crucial step in almost all cancer immunotherapeutic methods. Current techniques for expansion of tumor-reactive CTLs present major limitations. The present invention comprises a novel method to effectively produce and expand tumor-activated CTLs using high-voltage pulsed electric fields. Tumor cells were subjected to high-frequency irreversible electroporation (HFIRE) with various electric field magnitudes and pulse widths, or irreversible electroporation (IRE). The treated tumor cells were subsequently cocultured with CD 8+ cytotoxic T cells along with antigen-presenting cells. Tumor- activated CTLs can be produced and expanded when exposed to treated tumor cells. The activated CTLs produced with the present invention could be used for clinical applications with the goal of targeting and eliminating tumors.
A surgical system including an implantable medical device having a size and shape. The surgical device having a substrate and a coating that covers at least a portion of the substrate. The coating including collagen, glycerin and a hemostatic agent. The substrate including a first piece and a second piece that is joined with the first piece. The first piece and the second piece forming a pocket having a cavity and an opening that is in communication with the cavity. The device being pre-formed such that a size and shape of the cavity conforms to the size and shape of the implantable medical device.