anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Atherosclerosis (AS) is a chronic inflammatory disease which gives rise to life-threatening complications like ischemic stroke. Rupture of carotid atherosclerotic plaque is the main cause of ischemic stroke. Emerging evidence has demonstrated that disturbed circadian rhythms could accelerate the progression of atherosclerosis by regulating endothelial function. Moreover, our previous study implicated the circadian gene circadian locomotor output cycles kaput (CLOCK) in the pathogenesis of unstable plaques. In this study, we explored the underlying mechanism that CLOCK mediates endothelial cell autophagy involved in the progression of AS. Circadian and autophagy gene expression was analyzed in the GSE41571 dataset and human carotid atherosclerotic plaque samples. Then we used ox-LDL to treat HUVECs, and analyzed CLOCK and autophagy gene in endothelial cells. Besides that, we comprehensively analyzed in vivo experiments to explore the function of CLOCK in autophagy and atherosclerosis using different staining including HE, MT and IF staining. In the dataset and patient samples, CLOCK expression and autophagy were decreased in the unstable plaque group compared with the stable group. Decreased Beclin1, ATG5, LC3, and CLOCK were also observed in HUVECs under oxidative stress condition which also enhances cell proliferation. In vivo, we also found decreasing level of CLOCK, Beclin1, LC3 and ATG5 in ApoE-/- mice compared with WT mice. Silencing of CLOCK in ApoE-/- mice may further aggravate atherosclerosis including decreased cap thickness and collagens. Our findings implicated that downregulation CLOCK would impair endothelial cell autophagy and accelerate atherosclerotic plaque, which provides a novel strategy for treatment of progression in AS.
Sulfamethoxazole and Trimethoprim is a synthetic antibacterial combination product available in 800 mg sulfamethoxazole and 160 mg trimethoprim Double Strength tablets and 400 mg sulfamethoxazole and 80 mg trimethoprim tablets for oral administration. Each Double Strength tablet contains 800 mg sulfamethoxazole and 160 mg trimethoprim plus magnesium stearate, pregelatinized starch and sodium starch glycolate. Each tablet contains 400 mg sulfamethoxazole and 80 mg trimethoprim plus magnesium stearate, pregelatinized starch, and sodium starch glycolate. Trimethoprim is 2, 4-diamino-5-(3,4,5 trimethoxybenzyl) pyrimidine: the molecular formula is C14H18N4O3. It is a white to light yellow, odorless, bitter compound with a molecular weight of 290.3 and the following structural formula:

Sulfamethoxazole is N1-(5-methyl-3-isoxazolyl) sulfanilamide; the molecular formula is C10H11N3O3S. It is almost white, odorless, tasteless compound with a molecular weight of 253.28 and the following structural formula:
The present invention relates to a composition comprising IgY antibodies against at least two different fungi, the use of the composition for the preparation of a pharmaceutical especially for prophylaxis and/or therapy of all kinds of fungal infections, such as conditions caused by organisms belonging to the  Candida  genus or  Aspergillus  genus, especially of fungi that are less sensitive to antimycotica and a diagnotstic method using the IgY antibodies. Further it relates to immunisation of birds with a combination of at least two different species of fungi to the  Candida  genus or  Aspergillus  genus and a diagnostic method for fungi. It also relates to relates to a novel method for treatment and/or prophylaxis of fungal infections, especially infections by fungi which have lowered sensitivity or resistance to antimycotics. The method is both safe and effective. This is achieved by using IgY directed against fungi, in particular against  Candida  species, which have a lowered sensitivity or resistance against antimycotics. The specific IgY has been obtained by hyper immunising birds with one or several fungi as antigen in order to stimulate the production of immune globulins (IgY) against such fungi. The present invention also relates to a pharmaceutical product from eggs of birds containing immune globulin or a fragment thereof, which can be combined with other preparations, nutritients or pharmaceuticals for simultaneous, separate or sequential use in the prophylaxis or therapy of gastrointestinal infections in newborn infants.
BACKGROUND: Dyslipidemia increases cardiovascular disease risk, the leading cause of death worldwide. Under time-restricted feeding (TRF), wherein food intake is restricted to a consistent window of <12 hours, weight gain, glucose intolerance, inflammation, dyslipidemia, and hypercholesterolemia are all reduced in mice fed an obesogenic diet. LDLR (low-density lipoprotein receptor) mutations are a major cause of familial hypercholesterolemia and early-onset cardiovascular disease.
METHODS: We subjected benchmark preclinical models, mice lacking LDLR-knockout or ApoE knockout to ad libitum feeding of an isocaloric atherogenic diet either ad libitum or 9 hours TRF for up to 13 weeks and assessed disease development, mechanism, and global changes in hepatic gene expression and plasma lipids. In a regression model, a subset of LDLR-knockout mice were ad libitum fed and then subject to TRF.
RESULTS: TRF could significantly attenuate weight gain, hypercholesterolemia, and atherosclerosis in mice lacking the LDLR-knockout mice under experimental conditions of both prevention and regression. In LDLR-knockout mice, increased hepatic expression of genes mediating β-oxidation during fasting is associated with reduced VLDL (very-low-density lipoprotein) secretion and lipid accumulation. Additionally, increased sterol catabolism coupled with fecal loss of cholesterol and bile acids contributes to the atheroprotective effect of TRF. Finally, TRF alone or combined with a cholesterol-free diet can reduce atherosclerosis in LDLR-knockout mice. However, mice lacking ApoE, which is an important protein for hepatic lipoprotein reuptake do not respond to TRF.
CONCLUSIONS: In a preclinical animal model, TRF is effective in both the prevention and regression of atherosclerosis in LDLR knockout mice. The results suggest TRF alone or in combination with a low-cholesterol diet can be a lifestyle intervention for reducing cardiovascular disease risk in humans.
PURPOSE:To obtain an antitumor agent containing an iron-linked type lactoferrin as an active ingredient. CONSTITUTION:An antitumor agent obtained by containing iron-linked type lactoferrin prepared by linking ferric ions in an amount of 1-2 molecules based on 1 molecule lactoferrin separated from milk thereto through chelate bonds as an active ingredient. In order to increase the amount of the linked iron per protein of the lactoferrin, lactoferrin of higher purity without denaturation is preferably used and a separting method utilizing affinity column chromatography immobilizing an antilactoferrin monoclonal antibody is prefer ably applied. Ferric chloride, ferric sulfate, etc., are suitable for the ferric ions. Since the above-mentioned ferric ions are linked through chelate bonds, libera tion will not occur even under acidic condition and the ions reach intestinal tracts in a linked state in the case of administration to human bodies and can be absorbed. The dose thereof is preferably 20-200mg/day/kg.
The application belongs to the technical field of molecular biology, and particularly relates to a preparation method and application of lyase, coding genes, compositions and bacteriostat. A staphylococcal phage lyase PB50 has an amino acid sequence shown in SEQ ID NO. 1. A gene encoding the staphylococcal lyase PB50 of claim 1 having the sequence shown in SEQ ID No. 2. The lyase provided by the application can rapidly lyse staphylococcus, and the heterologous expression of the lyase is strong in solubility and fewer in inclusion bodies.
FIELD: veterinary virology. SUBSTANCE: vaccine consists of two antigenously different strains named "Zakarpatsky" and "Navlya-96" circulating in Russia and in the nearest abroad. Moreover, this vaccine contains theotropine at final concentration 0.06-0.08% which efficiently inactivates the virus by not affecting its immunogenic properties. To decrease the viscosity of vaccine its composition is supplemented with a vaccine emulsifier 139 at final concentration being 0.5-4%. The vaccine is very convenient in application being stable at storage, it enables to obtain 100% protection of vaccinated swines for the whole raising cycle. EFFECT: higher efficiency. 2 ex
Therapeutic uses of liposomes and a lipoprotein particle composition are disclosed. In addition, a lipoprotein particle and a therapeutic lipoprotein particle composition are disclosed. A suspension of small, unilamellar vesicles, composed essentially of lecithin phospholipids with low phase transition temperatures, may be used to treat disease conditions associated with an elevated serum Lp(a) concentration. Treatment continues until a significant drop in serum Lp(a) concentration is observed. A lipoprotein particle, consisting essentially of lecithin phospholipids with low phase transition temperatures and human apoproteins A and C, is also disclosed, as is a therapeutic composition comprising the lipoprotein particles. This composition is also useful in treating disease conditions associated with elevated serum Lp(a) levels, as well as in treating hypertension and acute renal failure.
At the end of their first visit new rheumatology patients will be asked for their interest in joining the Inova biomarker study. If yes, the patient will be consented, blood will be drawn for the Inova biomarkers, and x-rays will be sent for sharp scoring. Patients may decline and will not be part of the Inova study. Patients who decline will continue to receive standard of care treatment henceforth.

Patients in the Inova trial will receive a diagnosis from their doctor and are placed into separate cohorts based upon their diagnosis. The Inova biomarker results of each cohort will be cross-correlated with diagnoses, pre-screening tool results. Baseline disease activity and sharp scores will also be correlation variables.
The invention belongs to the medical field, precisely the pharmaceutical field, and can be used in obstetrics as a milk distribution stimulating medication after childbirth. The purpose of the invention is to increase the pharmatherapeutic activity of the medication and guarantee its qualitative action, without causing side effects to the lactating mother's system. Milk lactation stimulating medication - nasal drops from an active substance oxytocin is a chromatographically pure substance from a natural raw material, which comes from the extract of bovine hypophysis. The drops contain: active substance, natural oxytocine 80 mg., preservatives: nipagin 0.7 g., nipasol 0.3g., or benzalkonium chloride 0.1 g., stabilising substance: sodium acetate x 3H2O 2.2 g, chemically pure acetic acid (0.1 mol/l of concentration) 836.60 ml, isotonising agent: sodium chloride (NaCl) 8.0 g., injection solution up to 1000 ml. Active substance - a natural oxytocin melted in buffering substance, the obtained sodium acetate diluted in the acetic acid and diluting it with the injection solution, isotising with sodium chloride, preserved with nipagin and nipazole, filtered and poured into the bottles. For treatment, 2 drops into the nose are needed before the first breastfeeding of the baby, later increasing the dosage up to 6 drops before each breast-feeding.<IMAGE>
The medicamentous form is an efficient means for the treatment of ulcerous colitis and Crohns' disease. It comprises mesalazine (5-aminosalicylic acid) in micron form, which guarantees the therapeutic effect of the active substance. The problem of wetting the substance during its technological processing is eliminated. The medicamentous form of mesalazine includes supplementary substances - disperser , fillers and mesalazine with particle size under 50 mu, and as binder a combination of two polymers, in wt.%: copolyvidon from 1.1 to 4.4, polyvidon from 2.0 to 5.3 in comparison with the tablet weight. By the method, the tablet core of the medicamentous form is produced when the micronized mesalazine and the supplementary substances are granulated with alcohol-aqueous solution of copolyvidon and polyvidon. 2 claims
The clinician sits at the head of the table with his arms on the table alongside the participant's head but not touching the resting patient who is lying at rest on the table. This position is held for 5 minutes without moving.
Heart failure is a life-threatening cardiovascular disease and characterized by cardiac hypertrophy, inflammation and fibrosis. The traditional Chinese medicine formula Qiangxinyin (QXY) is effective for the treatment of heart failure while the underlying mechanism is not clear. This study aims to identify the active ingredients of QXY and explore its mechanisms protecting against cardiac hypertrophy. We found that QXY significantly protected against isoproterenol (ISO)-induced cardiac hypertrophy and dysfunction in zebrafish. Eight compounds, including benzoylmesaconine (BMA), atractylenolide I (ATL I), icariin (ICA), quercitrin (QUE), psoralen (PRN), kaempferol (KMP), ferulic acid (FA) and protocatechuic acid (PCA) were identified from QXY. PRN, KMP and icaritin (ICT), an active pharmaceutical ingredient of ICA, prevented ISO-induced cardiac hypertrophy and dysfunction in zebrafish. In H9c2 cardiomyocyte treated with ISO, QXY significantly blocked the calcium influx, reduced intracellular lipid peroxidative product MDA, stimulated ATP production and increased mitochondrial membrane potential. QXY also inhibited ISO-induced cardiomyocyte hypertrophy and cytoskeleton reorganization. Mechanistically, QXY enhanced the phosphorylation of Smad family member 2 (SMAD2) and myosin phosphatase target subunit-1 (MYPT1), and suppressed the phosphorylation of myosin light chain (MLC). In conclusion, PRN, KMP and ICA are the main active ingredients of QXY that protect against ISO-induced cardiac hypertrophy and dysfunction largely via the blockage of calcium influx and inhibition of mitochondrial dysfunction as well as cytoskeleton reorganization.
PURPOSE:To obtain a powdery flavor which suffers less from a loss and deterioration during production and storage and when applied to food, etc., and can give sustained flavor or taste when taken in the mouth by using a powdering base comprising specified substances. CONSTITUTION:A flavor is powdered by using a powdering base comprising a modified starch, a gelatin and thaumatin. In an example, the powdering base, water and optionally an excipient such as dextrin are mixed uniformly with each other to form a solution, the flavor and optionally an eddible oil or fat, etc., are added to this solution, and the resulting mixture is homogenized and dried to form a powder. Examples of the gelatins used include acid-treated gelatin and alkali-treated gelatin. The modified starch/gelatin ratio is desirably 1:10 to 10:1 by weight. When this flavor is applied to food or the like, the amount of the thaumatin used is desirably 0.1-10000ppm based on the food or the like.
Singleton-Merten syndrome (SMS) is a rare immunogenetic disorder affecting multiple systems, characterized by dental dysplasia, aortic calcification, glaucoma, skeletal abnormalities, and psoriasis. Glaucoma, a key feature of both classical and atypical SMS, remains poorly understood in terms of its molecular mechanism caused by DDX58 mutation. This study presented a novel DDX58 variant (c.1649A>C [p.Asp550Ala]) in a family with childhood glaucoma. Functional analysis showed that DDX58 variant caused an increase in IFN-stimulated gene expression and high IFN-β-based type-I IFN. As the trabecular meshwork (TM) is responsible for controlling intraocular pressure (IOP), we examine the effect of IFN-β on TM cells. Our study is the first to demonstrate that IFN-β significantly reduced TM cell viability and function by activating autophagy. In addition, anterior chamber injection of IFN-β remarkably increased IOP level in mice, which can be attenuated by treatments with autophagy inhibitor chloroquine. To uncover the specific mechanism underlying IFN-β-induced autophagy in TM cells, we performed microarray analysis in IFN-β-treated and DDX58 p.Asp550Ala TM cells. It showed that RSAD2 is necessary for IFN-β-induced autophagy. Knockdown of RSAD2 by siRNA significantly decreased autophagy flux induced by IFN-β. Our findings suggest that DDX58 mutation leads to the overproduction of IFN-β, which elevates IOP by modulating autophagy through RSAD2 in TM cells.
Patients receive 6-hydroxymethylacylfulvene (HMAF) IV over 5 minutes on days 1-5. Treatment repeats every 3-4 weeks for at least 2 courses in the absence of disease progression or unacceptable toxicity. Cohorts of 3 patients receive escalating doses of HMAF. The maximum tolerated dose is defined as the dose at which dose limiting toxicity occurs in at least 40% of patients.
BACKGROUND: Patients undergoing open abdominal aortic aneurysm (AAA) repair have a high risk of incisional hernia. Heterogeneity in recommendations regarding prophylactic mesh reinforcement between scientific society guidelines reflects the lack of sufficient data, with the Society for Vascular Surgery making no recommendation on methods for abdominal wall closure. We aimed to synthesize the most current evidence on mesh versus primary suture abdominal wall closure after open AAA repair.
METHODS: A systematic review was conducted on randomized controlled trials (RCTs) comparing mesh reinforcement with primary abdominal wall closure for patients who underwent elective AAA repair with a midline laparotomy incision. Dichotomous and time-to-event data were pooled using random effects models, applying the Mantel-Haenszel or inverse variance statistical method. The revised Cochrane tool and Grades of Recommendation, Assessment, Development, and Evaluation framework were used to assess the risk of bias and certainty of evidence, respectively. Trial sequential analysis assumed alpha = 5% and power = 80%.
RESULTS: Five RCTs were included reporting a total of 487 patients (260 in the mesh group and 227 in the primary suture group). Patients who had mesh closure had statistically significantly lower odds of developing incisional hernia after open AAA repair than those with primary suture closure (odds ratio (OR) 0.20, 95% confidence interval (CI) 0.09-0.43). Time-to-event analysis confirmed that the hazard of incisional hernia was statistically significantly lower in patients who had mesh closure (P < 0.05). Meta-analysis found statistically significantly lower odds of reoperation for incisional hernia in the mesh group (OR 0.23, 95% CI 0.06-0.93), but there was no statistically significant difference in wound infection (risk difference 0.02, 95% CI -0.03-0.08). The overall risk of bias was low in one study, high in 2 studies, "some concerns" in 2 studies for incisional hernia and reoperation for incisional hernia, and high in all studies reporting wound infection. The certainty of evidence was judged to be low for all outcomes. Trial sequential analysis confirmed a benefit of mesh reinforcement in reducing the risk of incisional hernia.
CONCLUSIONS: Meta-analysis of the highest-level data demonstrated a benefit of prophylactic mesh reinforcement, with trial sequential analysis confirming no additional RCTs required. This provides compelling evidence to support the use of mesh for midline laparotomy closure in patients undergoing open AAA repair.
Bedaquiline: 400 mg once daily for 2 weeks followed by 200 mg 3 times per week for 22 weeks Pretomanid: 200mg once daily for 24 weeks Moxifloxacin: 400 mg once daily for 24 weeks Linezolid: 600mg daily for 16 weeks then 300mg daily (or 600mg x3/wk) for the remaining 8 weeks or earlier when moderately tolerated Drug: Bedaquiline Bedaquiline is a diarylquinoline class antimicrobial which blocks the proton pump for ATP synthase of mycobacteria. This in turn blocks the ATP production required for cellular energy production and leading to cell death.
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.

Clinical and laboratory evidence of exacerbations of hepatitis have occurred after discontinuation of treatment with adefovir dipivoxil.

Adverse reactions to adefovir dipivoxil identified from placebo-controlled and open label studies include the following: asthenia, headache, abdominal pain, diarrhea, nausea, dyspepsia, flatulence, increased creatinine, and hypophosphatemia.

The incidence of these adverse reactions in studies 437 and 438, where 522 patients with chronic hepatitis B and compensated liver disease received double-blind treatment with adefovir dipivoxil (N=294) or placebo (N=228) for 48 weeks is presented in Table 2. Patients who received open-label adefovir dipivoxil for up to 240 weeks in Study 438 reported adverse reactions similar in nature and severity to those reported in the first 48 weeks.

No patients treated with adefovir dipivoxil developed a confirmed serum creatinine increase greater than or equal to 0.5 mg/dL from baseline or a confirmed phosphorus decrease to 2 mg/dL or less by Week 48. By Week 96, 2% of adefovir dipivoxil-treated patients, by Kaplan-Meier estimate, had increases in serum creatinine greater than or equal to 0.5 mg/dL from baseline (no placebo-controlled results were available for comparison beyond Week 48). For patients who chose to continue adefovir dipivoxil for up to 240 weeks in Study 438, 4 of 125 patients (3%) had a confirmed increase of 0.5 mg/dL from baseline. The creatinine elevation resolved in 1 patient who permanently discontinued treatment and remained stable in 3 patients who continued treatment. For 65 patients who chose to continue adefovir dipivoxil for up to 240 weeks in Study 437, 6 had a confirmed increase in serum creatinine of greater than or equal to 0.5 mg/dL from baseline with 2 patients discontinuing from the study due to the elevated serum creatinine concentration. See Adverse Reactions (6.2) for changes in serum creatinine in patients with underlying renal insufficiency at baseline.
This study consists of an initial dose escalation followed by an expansion cohort. Dose escalation of guadecitabine starts from 30 mg/m\^2 given SC on days 1-5 every 28 days in combination with fixed dose of nivolumab at 240 mg given IV on days 8 and 22 every 28 days. Dose escalation will continue until the maximum tolerated dose is reached or all planned doses are administered.