anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Studies in rats at doses of up to 5000 parts per million (ppm) in complete feed (approximately 340 times the maximum recommended human dose, based on surface area) for 30 months showed no evidence of carcinogenesis. In mice, administration of glimepiride for 24 months resulted in an increase in benign pancreatic adenoma formation that was dose-related and was thought to be the result of chronic pancreatic stimulation.

No adenoma formation in mice was observed at a dose of 320 ppm in complete feed, or 46 to 54 mg/kg body weight/day. This is at least 28 times the maximum human recommended dose of 8 mg once daily based on surface area.

Glimepiride was non-mutagenic in a battery of in vitro and in vivo mutagenicity studies (Ames test, somatic cell mutation, chromosomal aberration, unscheduled DNA synthesis, and mouse micronucleus test). 

There was no effect of glimepiride on male mouse fertility in animals exposed up to 2500 mg/kg body weight (>1,500 times the maximum recommended human dose based on surface area). Glimepiride had no effect on the fertility of male and female rats administered up to 4000 mg/kg body weight (approximately 4,000 times the maximum recommended human dose based on surface area).
Local reactions consisting of erythema, itching, swelling, tenderness and sometimes pain may occur at the injection site. These reactions may appear within a few minutes to hours and persist for several days. Local cold applications and oral Antihistamines may be effective treatment. For marked and prolonged local reactions, steroids may be helpful.

Adverse systemic reactions usually occur within minutes and consist primarily of allergic symptoms such as generalized skin erythema, urticaria, pruritus, angioedema, rhinitis, wheezing, laryngeal edema and hypotension. Less commonly, nausea, emesis, abdominal cramps, diarrhea and uterine contractions may occur. Severe reactions may cause shock and loss of consciousness and fatalities have occurred (14).

The treatment of systemic allergic reactions is somewhat dependent upon the symptom complex. Epinephrine hydrochloride 1:1,000 aqueous, in an adult dose of 0.3 - 0.5 mL (or 0.01 mL per kg. for children) administered subcutaneously in the opposite arm is the immediate treatment of choice. A tourniquet should be placed above the site of the injection if the injection was done on the extremities. Antihistamines may offer relief of recurrent urticaria, associated skin reactions and gastrointestinal symptoms. Persistent wheezing may necessitate intravenous aminophylline treatment in addition to inhaled bronchodilators. For profound shock and hypotension, intravenous fluids, vasopressors and oxygen also may be needed. Maintenance of an open airway is critical if upper airway obstruction is present. Corticosteroids may provide benefit if symptoms are prolonged or recurrent. Serious adverse reactions to this product should be reported to MEDWATCH, Food and Drug Administration, 5600 Fishers Lane, Rockville, MD 20852-9782. Telephone (800) 332-1088.
Sepsis is a life-threatening syndrome that can result in multi-organ dysfunction. MicroRNA (miR)-483-3p was previously demonstrated to be upregulated in sepsis patients; however, its specific functions in sepsis-triggered intestinal injury remain unclarified. Human intestinal epithelial NCM460 cell line was stimulated with lipopolysaccharide (LPS) to mimic sepsis-induced intestinal injury in vitro. Terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining was utilized for examining cell apoptosis. Western blotting and real time quantitative polymerase chain reaction (RT-qPCR) were used for detecting molecular protein and RNA levels. LPS-induced cytotoxicity was determined by measuring concentrations of lactate dehydrogenase (LDH), diamine oxidase (DAO) and fatty acid binding protein 2 (FABP2). Luciferase reporter assay was utilized for verifying the interaction between miR-483-3p and homeodomain interacting protein kinase 2 (HIPK2). Inhibiting miR-483-3p alleviates LPS-triggered NCM460 cell apoptosis and cytotoxicity. miR-483-3p targeted HIPK2 in LPS-stimulated NCM460 cells. Knockdown of HIPK2 reversed the above effects mediated by miR-483-3p inhibitor. Inhibiting miR-483-3p ameliorates LPS-triggered apoptosis and cytotoxicity by targeting HIPK2.
The present invention provides polyunsaturated fatty acid compounds having antimalarial and/or neutrophil stimulatory activity. The polyunsaturated fatty acids contain 18-25 carbons and 1-6 double bonds and are characterized in that they have one or two substitutions selected from the group consisting of .beta. oxa, .gamma. oxa, .beta. thia and .gamma. thia. It is also preferred that the polyunsaturated fatty acid compound includes a further substitution selected from the group consisting of hydroxy, hydroperoxy, peroxy, carboxymethyl substitutions or attached to an amino acid. The invention also provides a method of producing an unsaturated oxa substituted fatty acid comprising reacting an unsaturated fatty acid alcohol with a carbene that is inserted in the OH bond of the alcohol. The invention further provides a method of treating inflammation with a composition comprising at least one hydroxy, hydroperoxy or peroxy derivative of a polyunsaturated fatty acid having a C18-24 carbon chain and 1-6 cis or trans double bonds.
Between 3 and 12 month follow-up assessments, a subject was allowed to crossover and undergo a UL procedure if he met crossover inclusion and exclusion criteria. Subjects crossing over will then be followed for 5 years post-treatment. The subject can also be treated by other approved therapies, or receive no treatment at all, which would require participation through 12 months.
The present invention belongs to a medicinal preparation prepared from plant materials, particularly to a liquid medicine for treating tinea and a preparing method thereof. The liquid medicine for treating tinea is formed by soaking pure traditional Chinese medicines including male clove, stemona root, white alum and gallnut into alcohol for several days in a certain proportion, and then, edible acetin is added. The liquid medicine for treating tinea has the advantages of fragrant smell, no toxicity, adhesion, no irritation to skin, no pollution and skin protection (sterilization). Besides, people can feel softly fragrant, cool and smooth when the liquid medicine for treating tinea is applied to the skin. The medicine has one obvious characteristic that people can not be poisoned once eating the medicine by mistake. Therefore, the liquid medicine for treating tinea has no harm to bodies and high safety. The liquid medicine for treating tinea can be used for effectively treating various kinds of tinea corporis, tinea manus and tinea pedis as well as general skin diseases including eczema, turgescence, titillation and the like with conspicuous therapeutic effect.
In this study, patients established on guideline recommended therapy will be implanted with devices and remote monitoring established. Patients will then enter into a 2x2 crossover study of approved drugs during which standard clinical investigations will be undertaken at baseline and maximal therapy on each drug. The cross-over design will provide multiple increases and decreases of drugs known to alter haemodynamics and 6MWT. The study is powered to detect improvement in right ventricular stroke volume measured by MRI from baseline to maximal therapy for each drug. It will then be established if changes in remote monitored measures provide an early indication of clinical efficacy when compared to the MRI, haemodynamics, NTproBNP and 6MWT made at 12-weeks. Remote measurement of haemodynamics during the two periods of de-escalation will inform understanding of physiology and inform clinical practice. The comparison of the two therapeutic strategies in individual patients in one study will facilitate novel clinical study designs and provide evidence for data-driven personalised medicine in the area.
The participants will perform only 6 x 30m sprints. No pre-conditioning exercise will be performed.
PURPOSE: Evidence has suggested that clevidipine may provide faster blood pressure (BP) reduction with less volume than nicardipine in stroke and cardiothoracic surgery patients, but its use in hypertensive crises has not been well established. The primary objective of this study was to compare the treatment success of clevidipine and nicardipine in hypertensive crisis.
METHODS: This was a multicenter, retrospective cohort study including patients who received either clevidipine or nicardipine for treatment of hypertensive crisis. The primary outcome was the time from infusion start to attainment of goal BP, defined as the higher value of the guideline-directed 25% reduction in BP or the physician-ordered goal. Secondary outcomes were the time from infusion start to guideline-directed 25% reduction in BP, drug and total volume intake, the time from order entry to BP goal attainment, the number of BP and heart rate excursions, intensive care unit (ICU) length of stay, and study medication cost.
RESULTS: In total, 182 patients were included in the study (103 receiving nicardipine and 79 receiving clevidipine). Time to goal BP was similar between the groups (35 vs 33 minutes for clevidipine vs nicardipine, respectively; P = 0.37). Time to guideline-directed 25% reduction was also similar (P = 0.42). Volume from study drug was significantly less with clevidipine (222 vs 518 mL; P = 0.01); however, the total volume received in the ICU was similar (3,370 vs 3,383 mL; P = 0.43). Percent time in the goal BP range was similar (43.1% vs 42.3%). The cost of clevidipine was $199.37 per vial (based on the average wholesale price as of June 2023). This cost was 682% higher than that for a bag of nicardipine.
CONCLUSION: Time to goal BP was similar for clevidipine and nicardipine in this population. Any decreases in medication-associated volume with clevidipine were no longer evident when all volume sources were considered. These results show that clevidipine may not provide meaningful benefit in this heterogenous population. The difference in cost does not seem justified given the lack of improvement in clinically relevant outcomes.
The present invention relates to an anti-thrombosis composition containing a Teleogryllus emma extract as an active ingredient. More specifically, the present invention relates to a pharmaceutical composition and a health functional food for preventing or treating/alleviating thrombosis through blood coagulation suppression, wherein the pharmaceutical composition or the health functional food contains an extract of Teleogryllus emma which is a Korean native cricket as an active ingredient. As proved through examples of the present specification, the Teleogryllus emma extract as an active ingredient of the pharmaceutical composition and the health functional food for preventing or treating thrombosis according to the present invention exhibits a strong anti-thrombosis activity by suppressing a thrombosis generation-related enzyme and a blood coagulation factor, and at the same time does not exhibit a cythemolysis activity to human red blood cells. Also, the Teleogryllus emma extract has excellent thermal stability, and does not exhibit a loss in an effect of suppressing a thrombosis generation-related enzyme and a blood coagulation factor even in a pH 2 acidity condition and plasma, and thus is expected to be able to be used to prevent and treat thrombosis such as ischemic stroke and hemorrhagic stroke through the improvement of blood circulation. The active ingredient has an effect of being processed in various forms such as an extract, a powder, a pill, a tablet, and the like to be taken anytime. Thus, the present invention is very useful in the pharmaceutical industry and the food industry.
The study design will be a single-center, randomized, placebo-controlled, cross-over trial. After informed consent has been obtained, 18 eligible subjects with pancreatic insufficient cystic fibrosis will be enrolled in the study. Participants will take part in two 4 week study sessions, each separated by a 4 week washout period. One session will involve treatment with placebo and the other two sessions will provide treatment with approximately 25mg and 35 mg of DHA/kg of body weight. The patients will be assigned to each of the treatment sessions in random order, as described above. The DHA source will be provided by Martek Biosciences Corporation, Columbia, MD, USA in the form of a chewable capsule containing 200 mg of DHA. The placebos will be identical to the DHA supplement but will not contain the active ingredient, DHA. Subjects will be instructed to take the study capsules in addition to their normal doses of pancreatic enzymes with meals and to maintain their usual diets. Blood, urine, and exhaled breath condensate samples will be collected at baseline and after completion of each of the study periods. Patients will be screened and enrolled when they present to clinic for their routine check-up. The subjects have routine blood work at their annual check-ups, and when possible will have an additional tube of blood saved for the baseline fatty acid profiles so as to avoid unnecessary blood draws. Following each study period, blood draw, urine collection, and exhaled breath condensate (EBC) will be collected at the Vanderbilt Clinical Research Center. The patients will also be given the supply of DHA and placebo (for the entire study) at time of enrollment. The order in which they take the supplement or the placebo will be determined using a randomization table.
The invention relates to of 2 thienyloxiacetic acide derivatives, espesially to the obtaining of acides of 5-[2-(benzenessilphonylamine)ethyl]- or 5-[2-(4-chlorbenzenesulphonylamine)ethyl]-2 thienyloxiacetics which may be used in medicine for the treatment of thrombotic sickness.The purpose is the creation of new substances with an increasing activity from indicated class. The synthesis is done by the oxidation, for example, of acide amine N-[2-[2-(5-(2-hydroxi)-ethoxi)-thienyl]-ethyl]-benzenesulphone with silock oxide in water-alkaline medium. The amide is dissolved in KOH or NaOH solution with a concentration of 0,5-4n, preferential 2n, oxidizes with 2-16 equivalents of silveroxide at the temperature of 75-85°C during 2-3 hours. Silver oxide initial is obtained preliminarily by dissolving AgNO3 in distilled water and is added equimolar cantities of NaOH. The product with special destination is separated in free form or in shape of salt pharmaceutical useful. The new compounds are a little toxic and 4 times more active than dazoxiben, the beginning of antithrombotic action observing at 1 mg/kg and attains the maximum level of 5 mg/kg against 20 mg/kg.Tab.: 2
Subjects will receive Neulasta subcutaneously every 2 weeks for 12 weeks (6 doses). In addition, the following test will be done: Mixed Meal Tolerance Test (MMTT), Hemoglobin A1C (HbA1c) blood test, and Human Leukocyte Antigen (HLA) DNA Test.
This is a double-blind, double-dummy, randomized, 4-period cross-over, placebo- and positive-controlled, Phase I study. This means neither the study doctor nor the participants know in which treatment session you will receive which active medication or matching placebo. Every participant will receive 4 treatment sessions (Treatments A, B, C and D) in a different order. The order in which you receive the treatment sessions is determined by chance, like tossing a coin. The purpose of the study is to evaluate the effect of TMC435 on the results of electrocardiograms (electric recording of the heart). Two dose regimens of TMC435 will be tested, ie, 150 mg once daily (the dose that will be given to patients) and 350 mg once daily (a dose higher than the one that will be given to patients), administered for 7 days. A single dose of 400 mg moxifloxacin will be used as a positive control to assess trial sensitivity. The trial population will consist of 60 healthy volunteers of which approximately 18 will be females. In each treatment, dummy capsules will be added in order to have the same number of capsules in each treatment. Treatment A will consist of 150 mg TMC435 once daily for 7 days (2 capsules of TMC435 and 2 capsules placebo on days 1-7, 1 placebo tablet for moxifloxacin on Day 7). Treatment B will consist of 350 mg TMC435 once daily for 7 days (4 capsules of TMC435 on Days 1-7, 1 placebo tablet for moxifloxacin on Day 7). Treatment C will consist of 400 mg moxifloxacin on Day 7 (4 capsules of placebo for TMC435 on Days 1-7, 1 moxifloxacin tablet on Day 7). In Treatment D only placebo will be given (4 capsules of placebo for TMC435 on Days 1-7, 1 placebo tablet for moxifloxacin on Day 7). There will be a washout period of at least 10 days between subsequent treatments. A pharmacogenomic blood sample (DNA sample, blood sample from which your genetic information can be analyzed) will be collected from all volunteers and will be analyzed upon observation of irregular electrocardiogram during the study. The purpose is to see if irregularities in the electrocardiogram can be linked to genetic variants. DNA samples may also be analyzed for additional genes related to pharmacokinetics (what the body does with the drug), pharmacodynamics (what the drug does to your body) or safety and tolerability of TMC435 during the study, as necessary. Two oral doses of TMC435 (150 or 350 mg) or placebo will be given once daily for 7 consecutive days. A single dose of moxifloxacin 400 mg will be administered orally on Day 7 in one of the treatment sessions only.
Procedure for obtaining uretan derivatives. Consists in cultivating a subculture of one of the races of estreptomyces sp x-14667 nrrl 11336 (atc 31551), streptomyces sp x-14573 nrrl 11337 (atcc 31552) and streptomyces sp x-14575 nrri 11338 (atcc 31553) in a carbohydrate solution aqueous, containing a nitrogen nutrient, under submerged aerobic conditions; then the product obtained is isolated. The reaction is effected at a temperature comprised between 20 and 35 c and a neutral ph. Antibacterial agents, promoters of growth in ruminants and monogastric animals. Treatment of swine disseneration. (Machine-translation by Google Translate, not legally binding)
Participants in this arm will undergo tACS at a frequency 2 Hz above their IAPF during stimulation session 1. They will undergo tACS at a frequency 2 Hz below their IAPF during stimulation session 2.
Myocardial ischaemia-reperfusion injury (MIRI) caused by the treatment of acute myocardial infarction (AMI) is the primary cause of severe ventricular remodelling, heart failure (HF), and high mortality. In recent studies, research on the role of necroptosis in MIRI has focused on cardiomyocytes, but new biomarkers and immunocyte mechanisms of necroptosis are rarely studied. In the present study, weighted gene co-expression network analysis (WGCNA) algorithms were used to establish a weighted gene co-expression network, and Casp1, Hpse, Myd88, Ripk1, and Tpm3 were identified as biological markers of necroptosis using least absolute shrinkage, selection operator (LASSO) regression and support vector machine (SVM) feature selection algorithms. The role and discriminatory power of these five genes in MIRI had never been studied. Single-cell and cell-talk analyses showed that hub genes of necroptosis were focused on macrophages, which mediate the functions of monocytes, fibroblasts, haematopoietic stem cells, and cardiomyocytes, primarily through the TNF/TNFRSF1A interaction. The polarisation and functional activation of macrophages were affected by the MIF signalling network (MIF CD74/CXCR4 and MIF CD74/CD44) of other cells. The results of the immune infiltration assay showed that the five genes involved in necroptosis were significantly related to the infiltration and functional activity of M2 macrophages. TWS-119 is predicted to be a molecular drug that targets key MIRI genes. A mouse model was established to confirm the expression of five hub genes, and ventricular remodelling increased with time after ischaemia-reperfusion injury (IRI). Therefore, Casp1, Hpse, Myd88, Ripk1, and Tpm3 may be key genes regulating necroptosis and polarisation in macrophages, and causing ventricular remodelling.
Nerves throughout the luminal gastrointestinal (GI) tract express neuronal nitric oxide synthase (nNOS), which generates nitric oxide (NO), a key neurotransmitter in the regulation of GI motility. Several co-factors are known to be important for nNOS activity, including nicotinamide adenine dinucleotide phosphate hydrogen (NADPH), calcium, and tetrahydrobiopterin (BH4). The homodimeric conformation of all 3 isoforms of nitric oxide synthase (NOS) is regulated by BH4. In the absence of BH4, uncoupling of NO production occurs and leads to super oxide production, resulting in further impaired nNOS bioactivity.

CNSA-001 is a new chemical entity that is an endogenous, naturally occurring precursor of BH4 via the pterin salvage pathway. Oral administration of CNSA-001 will result in increases in both intracellular and circulating BH4 concentrations. Increased BH4 concentration is hypothesized to improve nNOS function resulting in a positive effect on gastric accommodation and emptying.
The gene encoding an alpha-galactosidase from guar seed has been isolated and identified. It has been expressed in yeasts, e.g. $i(Saccharomyces), $i(Kluyveromyces) and $i(Hansenula), in bacteria, e.g. $i(Bacillus), and in plants, e.g. $i(Nicotiana). The resulting alpha-galactosidase is able to decrease the galactose content of galactomannans such as guar gum by splitting off 1-6 linked alpha-D-galactopyranosyl units attached to a main chain of 1-4 linked beta-mannopyranosyl units. Thus a commercially feasible process becomes available for producing alpha-galactosidases suitable for providing galactomannans having improved properties, which can meet the increasing demand for good quality polysaccharides. It has further been demonstrated that other alphagalactosidases, which show a positive immunological cross-reaction with an antibody raised against the alpha-galactosidase from guar, are also effective in decreasing the galactose content of galactomannans such as guar.
Taletrectinib 600mg will be given po daily every day within 2 hours of meals on days 1-21, on a 21-day cycle. Study drug will be given until intolerance, consent withdrawal, progression per RECIST 1.1, or death (i.e., no maximum number of cycles).
Robotic-assisted gait training （RAGT）is an effective alternative to treadmill therapy with partial body weight in intense gait rehabilitation after some neuropathy. The investigators use LokoHelp for training, which is provided to the feet and the patient actively controls the knee and hip joints. The participants of RAGT treatment group receive 30 min conventional rehabilitation and 30 min robotic-assisted gait training daily for 8 weeks.
Sepsis is an important factor for trauma related death, especially the refractory septic shock, which has a mortality rate exceeding 50%. The treatment of sepsis is a medical problem that needs to be solved urgently. The role and status of extracorporeal membrane oxygenation (ECMO) in the treatment of cardiopulmonary failure has become more and more prominent, and its role in the treatment of sepsis in children and infants has gained remarkable achievements. However, its role in adult sepsis remains controversial, with current reports showing varied outcomes for ECMO in adult sepsis treatment. ECMO application can potentially cause renal impairment, and renal impairment can affect the outcomes of ECMO treatment in turn. Studies have shown that adjunctive renal replacement therapy during non-ECMO treatment of septic shock can improve the prognosis, and whether the combination with renal replacement therapy in the early stage of ECMO treatment can effectively improve the treatment outcome still needs to be confirmed by multicenter and prospective studies. Based on this, this article reviews the relevant research on the application of ECMO combined with renal replacement therapy in the treatment of sepsis after war trauma, aiming to provide clinical reference for the treatment of sepsis after war trauma.