anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The study drug dexmedetomidine (PrecedexTM) is supplied as dexmedetomidine HCL 200mcg/vial (100mcg/ml). This will be added to 98 ml 0.9% NaCl to achieve a concentration of 2mcg/ml and infused at 0.2-1mcg/kg/hour from the start of the case. The infusion rate will be commenced at 1mcg/kg/hour in those less than or equal to 65 years of age, and at 0.7mcg/kg/hr in those greater than 65 years of age, and then titrated based on the intraoperative sedation scores (to achieve a Sedation and Agitation scale (SAS) score of less than or equal to 4) and cardiovascular parameters (within 30% of baseline).
Research has shown that when making decisions about treatment with anti-tumor necrosis factor-α (TNFαi) agents, parents of children with inflammatory bowel disease (IBD) experience high levels of decisional conflict. This extreme level of conflict is due to the challenge of considering an effective treatment that has potentially serious side-effects. Elevated levels of decisional conflict have been associated with delays in decision making and failures to implement treatment plans. Given that such delays may lead to worse clinical outcomes, there is an urgent need to improve the decision-making process around TNFαi therapy. The use of structured decision support to help inform and guide parents through this challenging decision may improve the decision-making process. Such structure facilitates high-quality decision making by providing balanced, accurate information, helping individuals clarify what is most important to them, and facilitating conversations between families and healthcare providers. Based the investigators' prior research into the TNFαi decision process, the investigators developed a multi-component decision support intervention designed to improve the TNFαi decision process. This intervention will be tested in a controlled pilot trial designed to assess the acceptability and feasibility of a multi-component intervention and to determine the effect size of the multi-component intervention on both clinical and decision outcomes in children and adolescents with IBD and their parents.
INTRODUCTION: Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), which appeared in 2019, has been classified as critical and non-critical according to clinical signs and symptoms. Critical patients require mechanical ventilation and intensive care unit (ICU) admission, whereas non-critical patients require neither mechanical ventilation nor ICU admission. Several factors have been recently identified as effective factors, including blood cell count, enzymes, blood markers, and underlying diseases. By comparing blood markers, comorbidities, co-infections, and their relationship with mortality, we sought to determine differences between critical and non-critical groups.
METHOD: We used Scopus, PubMed, and Web of Science databases for our systematic search. Inclusion criteria include any report describing the clinical course of COVID-19 patients and showing the association of the COVID-19 clinical courses with blood cells, blood markers, and bacterial co-infection changes. Twenty-one publications were eligible for full-text examination between 2019 to 2021.
RESULT: The standard difference in WBC, lymphocyte, and platelet between the two clinical groups was 0.538, -0.670, and -0.421, respectively. Also, the standard difference between the two clinical groups of CRP, ALT, and AST was 0.482, 0.402, and 0.463, respectively. The odds ratios for hypertension and diabetes were significantly different between the two groups. The prevalence of co-infection also in the critical group is higher.
CONCLUSION: In conclusion, our data suggest that critical patients suffer from a suppressed immune system, and the inflammation level, the risk of organ damage, and co-infections are significantly high in the critical group and suggests the use of bacteriostatic instead of bactericides to treat co-infections.
This study aims to investigate whether miR-29c is involved in regulating transforming growth factor-β (TGF-β) mediated inflammation in diabetic cardiomyopathy (DCM). Our data showed increased inflammation and oxidative stress in diabetic myocardium together with decrease of miR-29c and elevation of TGF-β expression. In vitro experiments, we transfected miR-29c mimic and antagomir into HL-1 cells to explore the effect of miR-29c on inflammation in hyperglycemic conditions. Overexpression of miR-29c down-regulated the elevated TNF-α level, ROS production and NADPH oxidase activity which caused by high glucose. However, above changes were reversed by miR-29c antagomir. Interestingly, TGF-β protein rather than mRNA expression was changed significantly after transfection with miR-29c mimic, indicating that the modulation of TGF-β mediated by miR-29c was at the posttranslational level. Meanwhile, we found that 3'-UTR of TGF-β was the direct target of miR-29c confirmed by dual-luciferase assay. In conclusion, our study revealed that miR-29c could alleviate hyperglycemic-induced inflammation and ROS production via targeting TGF-β in cardiomyocytes, which provides a potential target for the treatment of DCM.
The dosage of disopyramide (as the phosphate) must be individualized for each patient on the basis of response and tolerance. The usual adult dosage of disopyramide is 400 to 800 mg (calculated as the disopyramide base) per day given in divided doses. The recommended dosage for most adults is 600 mg/day given in divided doses (150 mg every 6 hours). For patients whose body weight is less than 110 pounds (50 kg), the recommended dosage is 400 mg/day given in divided doses (100 mg every 6 hours). In the event of increased anticholinergic side effects, plasma levels of disopyramide should be monitored and the dose of the drug adjusted accordingly. A reduction of the dose by one third, from the recommended 600 mg/day to 400 mg/day, would be reasonable, without changing the dosing interval.

For patients with cardiomyopathy or possible cardiac decompensation, a loading dose, as discussed below, should not be given, and initial dosage should be limited to 100 mg every 6 to 8 hours. Subsequent dosage adjustments should be made gradually, with close monitoring for the possible development of hypotension and/or congestive heart failure (see WARNINGS).

For patients with moderate renal insufficiency (creatinine clearance greater than 40 mL/min) or hepatic insufficiency, the recommended dosage is 400 mg/day given in divided doses (100 mg every 6 hours).

For patients with severe renal insufficiency (Ccr 40 mL/min or less), the recommended dosage regimen of disopyramide is 100 mg at intervals shown in the table below, with or without an initial loading dose of 150 mg.

For patients in whom rapid control of ventricular arrhythmia is essential, an initial loading dose of 300 mg disopyramide (200 mg for patients whose body weight is less than 110 pounds) is recommended, followed by the appropriate maintenance dosage. Therapeutic effects are usually attained 30 minutes to 3 hours after administration of a 300 mg loading dose. If there is no response or evidence of toxicity within 6 hours of the loading dose, 200 mg of disopyramide every 6 hours may be prescribed instead of the usual 150 mg. If there is no response to this dosage within 48 hours, either disopyramide should then be discontinued or the physician should consider hospitalizing the patient for careful monitoring while subsequent disopyramide doses of 250 mg or 300 mg every 6 hours are given. A limited number of patients with severe refractory ventricular tachycardia have tolerated daily doses of disopyramide up to 1600 mg per day (400 mg every 6 hours), resulting in disopyramide plasma levels up to 9 mcg/mL. If such treatment is warranted, it is essential that patients be hospitalized for close evaluation and continuous monitoring.
Tauopathies are age-associated neurodegenerative diseases whose mechanistic underpinnings remain elusive, partially due to a lack of appropriate human models. Here, we engineered human induced pluripotent stem cell (hiPSC)-derived neuronal lines to express 4R Tau and 4R Tau carrying the P301S MAPT mutation when differentiated into neurons. 4R-P301S neurons display progressive Tau inclusions upon seeding with Tau fibrils and recapitulate features of tauopathy phenotypes including shared transcriptomic signatures, autophagic body accumulation, and reduced neuronal activity. A CRISPRi screen of genes associated with Tau pathobiology identified over 500 genetic modifiers of seeding-induced Tau propagation, including retromer VPS29 and genes in the UFMylation cascade. In progressive supranuclear palsy (PSP) and Alzheimer's Disease (AD) brains, the UFMylation cascade is altered in neurofibrillary-tangle-bearing neurons. Inhibiting the UFMylation cascade in vitro and in vivo suppressed seeding-induced Tau propagation. This model provides a robust platform to identify novel therapeutic strategies for 4R tauopathy.
The intervention activities are the same as those described in Arm 1. However, in this study arm, the intervention activities will start 6 months later than those in Arm 1. This arm will serve as a controlled comparison during those initial 6 months.
It was based on exercises for strengthening the hip adductor muscles associated with a bridge using a small exercise ball (two sets of 15 repetitions with seven seconds in isometry), strengthening the hamstrings with ankle weights in prone position, bilateral hip flexor strengthening in supine position with ankle weights, bilateral shoulder flexor strengthening with dumbbells, bilateral shoulder extensor strengthening with dumbbells, bilateral shoulder abductor strengthening with dumbbells, and bilateral serratus anterior muscle strengthening with dumbbells (all exercises, except the first, performed in three sets of 10 repetitions). Considering a 15-second interval between repetitions and a one-minute break between sets, totaling 30 minutes. The progression of each patient occurred through load progression.
INTRODUCTION: Rapid genomic sequencing (rGS) in critically ill infants with suspected genetic disorders has high diagnostic and clinical utility. However, rGS has primarily been available at large referral centres with the resources and expertise to offer state-of-the-art genomic care. Critically ill infants from racial and ethnic minority and/or low-income populations disproportionately receive care in safety-net and/or community settings lacking access to state-of-the-art genomic care, contributing to unacceptable health equity gaps. VIrtual GenOme CenteR is a 'proof-of-concept' implementation science study of an innovative delivery model for genomic care in safety-net neonatal intensive care units (NICUs).
METHODS AND ANALYSIS: We developed a virtual genome centre at a referral centre to remotely support safety-net NICU sites predominantly serving racial and ethnic minority and/or low-income populations and have limited to no access to rGS. Neonatal providers at each site receive basic education about genomic medicine from the study team and identify eligible infants. The study team enrols eligible infants (goal n of 250) and their parents and follows families for 12 months. Enrolled infants receive rGS, the study team creates clinical interpretive reports to guide neonatal providers on interpreting results, and neonatal providers return results to families. Data is collected via (1) medical record abstraction, (2) surveys, interviews and focus groups with neonatal providers and (3) surveys and interviews with families. We aim to examine comprehensive implementation outcomes based on the Proctor Implementation Framework using a mixed methods approach.
ETHICS AND DISSEMINATION: This study is approved by the institutional review board of Boston Children's Hospital (IRB-P00040496) and participating sites. Participating families are required to provide electronic written informed consent and neonatal provider consent is implied through the completion of surveys. The results will be disseminated via peer-reviewed publications and data will be made accessible per National Institutes of Health (NIH) policies.
TRIAL REGISTRATION NUMBER: NCT05205356/clinicaltrials.gov.
The release of paused RNA polymerase II (RNAPII) from promoter-proximal regions is tightly controlled to ensure proper regulation of gene expression. The elongation factor PTEF-b is known to release paused RNAPII via phosphorylation of the RNAPII C-terminal domain by its cyclin-dependent kinase component, CDK9. However, the signal and stress-specific roles of the various RNAPII-associated macromolecular complexes containing PTEF-b/CDK9 are not yet clear. Here, we identify and characterize the CDK9 complex required for transcriptional response to hypoxia. Contrary to previous reports, our data indicate that a CDK9 complex containing BRD4 but not AFF1/4 is essential for this hypoxic stress response. We demonstrate that BRD4 bromodomains (BET) are dispensable for the release of paused RNAPII at hypoxia-activated genes and that BET inhibition by JQ1 is insufficient to impair hypoxic gene response. Mechanistically, we demonstrate that the C-terminal region of BRD4 is required for Polymerase-Associated Factor-1 Complex (PAF1C) recruitment to establish an elongation-competent RNAPII complex at hypoxia-responsive genes. PAF1C disruption using a small-molecule inhibitor (iPAF1C) impairs hypoxia-induced, BRD4-mediated RNAPII release. Together, our results provide insight into potentially targetable mechanisms that control the hypoxia-responsive transcriptional elongation.
In courses 1-3, patients receive doxorubicin hydrochloride (30 mg/m2) IV over 15 minutes, vincristine sulfate (1.5 mg/m2 (maximum dose 2 mg)) IV, and methotrexate intrathecally (age-adjusted dosing) (IT) on day 1 and oral prednisone (40 mg/m2/day) three times daily and oral mercaptopurine (225 mg/m2) once daily on days 1-5. In courses 4 and 5, patients receive doxorubicin (30 mg/m2), vincristine sulfate (1.5 mg/m2 (Maximum dose 2 mg)), prednisone (120 mg/m2/day), and mercaptopurine (225 mg/m2) as in courses 1-3. In courses 6-15, patients receive vincristine sulfate (1.5 mg/m2), prednisone (120 mg/m2/day), and mercaptopurine (225 mg/m2) as in courses 1-3 and methotrexate (60 mg/m2) IV on day 1. Treatment repeats every 21 days for up to 15 courses in the absence of disease progression or unacceptable toxicity.
Foamable compositions are disclosed. The compositions contain one or more active ingredients combined with a foaming agent and optionally one or more surface tension adjusting agents. The foaming agent may comprise, for instance, a derivatized dimethicone. The surface tension adjusting agent, on the other hand, comprises a chemical species that either increases or decreases the surface tension of the composition within a desired range so that the composition is readily foamable. In this manner, active ingredients can be incorporated into the compositions that are typically hard to foam. Such ingredients include cleaning solvents and various skin care agents. Of particular advantage, foamable compositions can be formulated in accordance with the present disclosure that contain relatively small amounts of water such as less than about 20 percent by weight, such as less than about 10 percent by weight. In other embodiments, the composition can be completely anhydrous.
Left atrial or left atrial appendage thrombosis (LAT) is contraindicated for cardiac ablation (CA) or cardioversion (CV) of atrial fibrillation (AF). This study was aimed to compare the frequency of LAT detected by transesophageal echocardiography (TEE) before CA or CV in patients with AF treated with direct oral anticoagulants (DOACs) or vitamin K antagonists (VKAs). We searched PubMed, Scopus, Web of Science, and Cochran Library databases from inception through July 13, 2023 to select studies reporting data on LAT identification before CA or CV using TEE in patients with AF treated with DOACs or VKAs. Pooled odds ratios (ORs) with 95% confidence interval were calculated with a random-effects model. Studies retrieved were 50 (38 observational), 29 on CA, 15 on CV, and 6 on both procedures (17,096 patients on DOACs and 13,666 on VKAs). The overall prevalence of LAT was smaller in DOACs than in VKAs, with an OR of 0.66 (0.52 to 0.84), confirmed at sensitivity analysis and in most subgroups. This finding was consistent for the 3 most reported DOACs: the pooled OR for LAT was 0.68 (0.50 to 0.90) in apixaban, 0.67 (0.51 to 0.88) in dabigatran, 0.61 (0.43 to 0.89) in rivaroxaban, and 1.10 (0.74 to 1.64) in edoxaban (not significant). In conclusion, in this large meta-analysis in patients with AF, the prevalence of LAT by TEE evaluation performed before CV or CA appears lower in those treated with DOACs than in those on VKAs. Additional research may help in better understanding differences between these classes of anticoagulant drugs in the setting of protection against AF-related left atrial thrombotic formation.
The use of rattan root extract (funcus effusns) as a medicament to combat albuminuria is claimed. No side-effects are observed and the condition may be cured in ca 3 days. The extract may be formulated in a potable fluid, esp. red wine. The formulation is prepd. by boiling 600g dried rattan roots in 21/2 l. red wine till such time as half the liq. has evaporated.
The specific gamma ray constant for Tc99m is 5.4 microcoulombs/kg-MBq-hr (0.78R/mCi-hr) at 1cm. The first half value layer is 0.017cm of lead (Pb). Relative attenuation of the radiation emitted by this radionuclide results from the interposition of various thicknesses of Pb. The corresponding attenuation is shown in Table 2. To facilitate control of the radiation exposure from MBq (mCi) amounts of this radionuclide, a 0.25 cm thickness of Pb will attenuate the radiation by a factor of 1,000.

To correct for the physical decay of this radionuclide, the fractions that remain at selected time intervals after the time of calibration are shown in Table 3.
The non-dedicated (NON-DED) set comprised a ventilator for MPV (PB560) using a single active tubing with an exhalation valve. A custom-made arm support and plastic mouthpiece were used.
The proposed research is part of strategies to manipulate postprandial glycemia and generate weight-control-related benefits, such as promoting satiation. Literature has shown pre-loading caloric nutrients can change postprandial glycemia, but the mechanism is unclear. The investigators hypothesize that a small number of nutrients released in the small intestine can initiate physiological changes and develop feedback control to delay gastric emptying, leading to the delay in digestion of glycemic carbohydrates and the consequent moderate glycemic responses. The investigators propose to use potatoes as the testing glycemic carbohydrates, and the pre-load foods are green vegetables. The investigators will be testing the optimal preload time to achieve the highest control of glycemic response as well as the strongest effect in satiety induction. In addition, green vegetables will be consumed with or without a preload fat enhancer (canola oil) to investigate the mechanism behind significant preload compositions. Healthy adults will be instructed to eat the leafy vegetables first (with or without canola oil), followed by the potato foods (i.e., mashed potatoes). The measurement is the gastric emptying time, blood sugar concentration, insulin, and an appetite-related gut hormone GLP-1. In order to monitor gastric emptying using a non-invasive approach, a popular breath test used in children and a hydrogen breath test will be used to present the change of gastric emptying and the level of gut fermentation.

Results will demonstrate the mechanism of the impact of pre-loading nutrients on the digestion of glycemic carbohydrates. The goal is to eliminate the negative influence of glycemic carbohydrate consumption. Instead, to generate health benefits from dietary carbohydrates.
In pediatric patients with hemolytic uremic syndrome (HUS), cardiac involvement and autonomic nervous system function can be evaluated by a non-invasive method called heart rate variability (HRV). This study aims to evaluate heart rate variability and electrocardiography findings in patients with HUS by comparing a healthy group. Patients who are diagnosed with HUS at a university hospital from December 2020 to June 2022 are screened by electrocardiography (ECG), echocardiography, and 24-h Holter ECG. A healthy control group, compatible in age and gender with the patient group, was selected from healthy subjects. HRV parameters, laboratory values, and ECG findings were analyzed and compared with the healthy group and each other. There were 25 patients with HUS and 51 participants in the healthy control group. Statistically significant differences were found in some HRV parameters: standard deviation of normal to normal intervals, the mean of the 5-min RR interval standard deviations, the standard deviation of 5-min RR interval means, the triangular interpolation of normal to normal interval, and very-low-frequency power. HUS patients had impaired and declined HRV values compared to the healthy group. There was a significant decrease in the PR distance, while a significant increase in the corrected QT and QT dispersion values was detected in the electrocardiographic findings of the patient group. HRV values impaired as renal failure parameters increased.  Conclusion: Patients with HUS may have autonomic nervous system dysfunction. HRV measurement is a non-invasive method that can evaluate this. It can be thought that there may be an increased risk of cardiovascular events and arrhythmias in some patients with HUS. ECG should be also considered to detect arrhythmia. What is Known: • Hemolytic uremic syndrome (HUS) primarily effects the hematologic parameters and kidney. • Secondary cardiomyopathy with hypertension and renal failure could be observed in these patients. • Rhythm problems are not expected primarily in these patients. • There is very limited data in evaluating autonomic function and arrhythmia risk for these patients. What is New: • Patients with HUS may have autonomic nervous system dysfunction. • HRV measurement is a non-invasive method that can evaluate this. • Cardiovascular events and arrhythmias due to the deterioration of the balance between the sympathetic and parasympathetic systems could manifest in patients with HUS. • An ECG and screening patients for cardiac events, and monitoring them closely should be considered.
This project proposes to test the effect of immersion in a tilted virtual reality on verticality representation in hemisphere stroke patients showing lateropulsion and in healthy participants. The idea is to use the virtual reality as a tool to recalibrate the internal reference of verticality (contralesionally biased) in stroke patients and to experimentally create a bias in verticality perception of healthy participants, then to investigate how this modulation of the internal model of verticality might affect the erect posture. The investigators hypothesize that, in stroke patients, the recalibration of the verticality perception might ameliorate their lateropulsion, whereas in healthy participants, the experimental verticality bias introduced might induce a transient experimental lateropulsion. A transmodal modulation of the verticality perception, both on PV and VV, would imply a modulation by the virtual reality not only at the level of perception but also at the internal model of verticality, advocating for a powerful effect of this technology. The analysis of a post-effect (on verticality perception) that would continue after the intervention (immersion in the virtual titled room) would be a supplementary argument advocating for its clinical use in rehabilitation of post-stroke lateropulsion. To judge the effect of the immersion in tilted virtual reality, the following measures will be considered: (a) PV perception, (b) VV perception, (c) body orientation measured by inertial captors, and (d) weight-bearing asymmetry in erect posture assessed by posturography.