anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The present trial is split into two successive parts:

* Study Part I is a double-blind, randomized, placebo-controlled study designed to obtain safety, tolerability and pharmacokinetic (PK) data after 14-day multiple oral administrations of once-daily increasing doses of GFT505 (300 and 360 mg) in healthy male subjects. The starting dose of 300 mg/day has been selected on the basis of the results of previous clinical trials and corresponds to the highest dose given in healthy subjects according to a single dose regimen (study GFT505-111-7). A total of 24 male subjects will be included, 12 for each cohort (a cohort corresponding to a dose level). In each cohort, 9 subjects will receive GFT505 and 3 will receive placebo. A Safety Review Committee (SRC) will have a formal meeting after full completion of at least 10 out of 12 subjects of each dose level to review under blinded conditions all safety data and to conclude on the safety and tolerability of a given dose level. Between the first and the second dose level, the SRC will give its agreement on the dose escalation, and at completion of the second level the SRC will define the supra-therapeutic dose to be administered in Study Part II.
* Study Part II will be a parallel group, randomized, placebo-controlled study, with stratification by gender. The study is designed to investigate the potential impact of 14-day multiple oral administrations of once-daily GFT505 on QT/QTc prolongation under conditions of maximal GFT505 exposure, i.e. by administering the expected therapeutic dose of 120 mg/d and a supra-therapeutic dose (defined according to the results of Study Part I), to healthy male and female subjects. A single oral dose of 400 mg moxifloxacin will be used as a positive control in order to document the sensitivity of the experimental conditions. The study treatment administration will be double-blind for placebo and GFT505 and open for moxifloxacin. The ECG readings will be performed under blinded conditions. A preliminary sample size of 128 subjects to have at least 124 evaluable subjects has been fixed by formal justification on a theoretical basis. ECG data collected during Study Part I will support a formal determination using observed data and thus will lead to a final sample size. In all cases, it is anticipated that the sample size could not be less than 124 evaluable subjects. Each gender will represent at least 40% of the study population. Both sub-groups will be balanced between the 4 treatment groups.
The invention relates to genetic engineering field, in particular to eosinophilic lactase BGALA, gene and application thereof. The invention provides a lactase BGALA of eosinophilic Bispora sp.; the amino acid sequence of the lactase BGALA is shown in SEQ ID NO.1; and the invention provides genome and cDNA coding gene bgalA for coding the lactase. The invention obtains an eosinophilic lactase with the most proper pH value of 1.5, which maintains high enzymatic activity in acid environment, has better pH stability and heat stability, and antiprotease hydrolysis. The eosinophilic lactase can effectively hydrolyze the lactose in milk in simulated digestive tract environment. The eosinophilic lactase BGALA with the properties can be used for treating lactose intolerance, diary industry no processing cow milk and whey.
The present research protocol will evaluate clinical effects of two different tDCS protocols: (1) active anodic stimulation over left dorsolateral prefrontal cortex with cathode placed over an extra cephalic area; (2) active cathode placed over the right dorsolateral prefrontal cortex with anode placed over an extra cephalic area. Patients will be clinically evaluated with the Diagnostic and Statistical Manual of Mental Disorders Fourth Edition (DSM-IV) criteria for depression. Symptoms intensity will be rated according to The Hamilton Depression Scale (HAMD -17 items) - main outcome. Patients with scores higher than 16 will be included. Patients with active neurological or severe disorders (such as cancer or auto-imune disorders) will be excluded. The present study is a double-blinded, controlled, randomized trial with 30 patients with depression. The intervention protocol consist in 15 consecutive daily tDCS sessions (skipping the weekend). After meeting eligibility criteria, patients will be randomized (computer generated list) to one of the two intervention groups. We will use a direct current of 2.0 milliamperes (mA) for 30 min. The 35 cm2-rubber electrodes will be wrapped in cotton material, which should be moistened with saline as to reduce impedance. Patients will be clinically assessed at baseline and at end of 6 weeks. Main outcome will be based on HAMD-17 items at a final endpoint of 6-weeks, with secondary outcomes assessing Beck Depression Inventory (21 items) at 6 weeks. Other evaluation scales include Beck Anxiety Inventory, Hamilton Anxiety Scale and Safety and cognitive assessment will be performed with The Montreal Cognitive Assessment, adverse effects scales and clinical evaluation with a trained physician.
PROBLEM TO BE SOLVED: To obtain a new peptide compound having a single L-asparaginly-L- prolyl-L-asparaginyl-L-alanine (NPNA) turn structure as an immunoreactive site with antimalarial serum and useful for malaria diagnosing materials, malaria vaccines, etc. SOLUTION: This peptide compound has a tetrapeptide having β-turn structure by hydrogen bond produced between a carbonyl group present on the side chain of the first L-asparagine residue of tetrapeptide having a sequence of NPNA and the second amino group of L-alanine as an immunoreactive site with antimalarial serum. The peptide compound is e.g. a peptide of the formula GIGNPNAGIG. The peptide is obtained also by any synthetic method among organic chemical synthetic method, biochemical synthetic method, etc. In the case of the organic chemical synthetic method, the peptide is obtained by dividing the above peptide compound into several parts, separately synthesizing these parts and binding these parts.
Tumour samples from 30 participants with HNSCC that undergone curative surgery will be used to establish patient-derived xenografts (PDXs). These tumours will also undergo exome sequencing. This will provide a biobank of PDX models with available genomic information for future research projects. Another 30 participants with recurrent or metastatic HNSCC (RMHNSCC) will be recruited to this study. PDX models will be developed from these patient tumours, followed by genomic sequencing. PDX models are developed by transplanting small tumour pieces into immunocompromised mice. These mice are then treated with different available drugs for RMHNSCC at the discretion of their medical oncologist. These mice will be then followed up to examine the tumour response to treatments. When studied in clinic, PDX models have shown high correlation with patient response to the treatment. The PDX drug testing results will be provided to the treating medical oncologist to guide care at the oncologists discretion. Investigators' hope is that improved chemotherapy responses are observed with this strategy.
Disclosed are a CD3-targeting antibody, a bispecific antibody and the use thereof. The CD3-targeting antibody comprises a light chain variable region (VL) and a heavy chain variable region (VH). The VL has the amino acid sequence as shown in SEQ ID NO: 56 or a mutation thereof. The VH has mutations on the amino acid sequence as shown in SEQ ID NO: 42, and the mutations occur at one or more of the sites of amino acid residues selected from positions 30, 73, 76, 78, 93 and 94. The bispecific antibody comprises a first protein functional region and a second protein functional region, wherein the first protein functional region comprises the CD3-targeting antibody as described above. The CD3-targeting antibody reduces the toxicity caused by cytokine release syndrome, and the bispecific antibody prepared therefrom is stable and has the ability to bind to T cells, and also reduces the difficulty of producing.
Patients with (a) history of SNAS (coexistence of typical cutaneous and gastrointestinal symptoms); (b) positive Ni-patch test; (c) clinical improvement of at least 70% from baseline after 4 weeks of low-Ni diet; (d) positivity of a double-blind placebo-controlled oral Ni challenge (DBPCO). Exclusion criteria include (a) age \< 18 years and \>65 years; (b) other organic gastrointestinal diseases, such as peptic ulcer, inflammatory bowel diseases, celiac disease, gastrointestinal infections, and small intestinal bacterial overgrowth; (c) diabetes mellitus; (d) hepatic, renal or cardiac dysfunction; (e) thyroid disease or tumour; (f) concomitant treatment with steroids and/or antihistamines in the previous 4 weeks; (g) pregnancy and lactation; (h) smoking, abuse of alcohol, coffee, tea, and cola intake, and (i) inability to give written informed consent.
10.1 Mechanism of Action

Diclofenac has analgesic, anti-inflammatory, and antipyretic properties. The mechanism of action of diclofenac, like that of other NSAIDs, is not completely understood but involves inhibition of cyclooxygenase (COX-1 and COX-2). Diclofenac is a potent inhibitor of prostaglandin synthesis in vitro. Diclofenac concentrations reached during therapy have produced in vivo effects. Prostaglandins sensitive afferent nerves and potentiate the action of bradykinin in inducing pain in animal models. Prostaglandins are mediators of inflammation. Because diclofenac is an inhibitor of prostaglandin synthesis, its mode of action may be due to a decrease of prostaglandins in peripheral tissues.

10.2 Pharmacokinetics

Diclofenac is more than 99% bound to human serum proteins, primarily to albumin. Diclofenac diffuses into and out of the synovial fluid. Diffusion into the joint occurs when plasma levels are higher than those in the synovial fluid, after which the process reverses and synovial fluid levels are higher than plasma levels. It is not known whether diffusion into the joint plays a role in the effectiveness of diclofenac. Five diclofenac metabolites have been identified in human plasma and urine. The metabolites include 4’-hydroxy-, 5-hydroxy-, 3/hydroxy-, 4’,5-dihydroxy- and 3’-hydroxy-4’-methoxy diclofenac. Diclofenac is eliminated through metabolism and subsequent urinary and biliary excretion of the glucuronide and the sulfate conjugates of the metabolites.
PROBLEM TO BE SOLVED: To obtain the subject tablets having such hardness as to be extrudable from a PTP package by processing by a specific means only the surface layer of tablets formed under low-pressure compression and comprising a noncrystallized saccharide. SOLUTION: The tablets are obtained by infiltrating water into the surface layer of tablets formed by low-pressure compression of a noncrystallized saccharide to convert the surface layer to a crystalline saccharide and effect binding solidification. The compression pressure is pref. 0.01-0.5 ton/cm<2> . The noncrystallized saccharide to be used is afforded using the corresponding crystalline saccharide as raw material which is e.g. lactose, glucose, maltose, mannitol, refined sugar. The tablets of the present invention can be used as a medicine or food formulated, as appropriate, with any kind of medicinal additive(s) or food additive(s).
This invention relates generally to medical devices, such as stents, for delivering a biologically active material to a desired location within the body of a patient. In particular, the invention relates generally to a medical device for delivering a biologically active material to a surface of a body lumen. More particularly, the invention is directed to a medical device comprising two opposing end sections, each having a surface, and a middle portion. The middle portion comprises a plurality of struts and the two opposing end sections comprises non-structural elements. The end sections of the surface either ( 1 ) contain a greater amount of a biologically active material per unit length of the surface or ( 2 ) have a greater capacity per unit length to contain such material than the middle section of the surface by having a greater surface area per unit length of the surface than the middle section or having a greater affinity for the biologically active material per unit length of the surface than the middle section. The struts and the non-structural elements comprise biologically active materials. The invention is also directed to a method for delivering the biologically active material to the body tissue of a patient by inserting this medical device into the body of the patient. Still further, the invention is directed to a method of treating a body lumen surface by preventing or treating restenosis or hyperplasia, using the system of the invention. Still further, the invention is directed to a stent having a sidewall which comprises a middle section, a first end section and a second end section. The stent also comprises a band comprising a biologically active material. The band is connected to the first end section and/or second end section of the stent.
Exposing the skin to UV radiation interferes with the induction of the T-cell mediated immune response, including both delayed (DHS) and contact (CHS) hyper-sensitivity immune responses initiated at non-irradiated sites. The present inventors have discovered that DNA is at least one of the targets for UV-induced hypersensitivity, and demonstrate that the application of DNA repair enzymes can reverse the damaging effects of UV irradiation on both the DHS and CHS response. The usefulness of the invention in this regard was tested using a model immunosuppression system in mice. In these studies, mice were first exposed to UV radiation and then liposomes were used to deliver a dimer-specific excision repair enzyme to their epidermis in situ. The application of liposomal T4 endonuclease V encapsulated to the UV-irradiated skin both decreased the number of cyclobutane pyrimidine dimers in the epidermis and prevented suppression of both delayed and contact hypersensitivity responses. Moreover, the formation of suppressor lymphoid cells was inhibited. These studies illustrate that the delivery of lesion-specific DNA repair enzymes to living skin after UV irradiation is an effective tool for restoring immune function and suggest that this approach may be broadly applicable to preventing other alterations caused by DNA damage, including preventing or reversing viral activation (e.g., herpes virus activation), oncogene expression, or autoimmune episodes.
1. Anacidity (diagnosis)—Pentagastrin is indicated as a diagnostic aid for evaluation of gastric acid secretory function. It is effective in testing for anacidity (achlorhydria) in patients with suspected pernicious anemia, atrophic gastritis, or gastric carcinoma. It is also effective in determining the reduction in acid output after operations for peptic ulcer, such as vagotomy or gastric resection.
  2. Hypersecretory conditions, gastric (diagnosis)—Pentagastrin is indicated as a diagnostic aid in testing for gastric hypersecretion in patients with suspected duodenal ulcer or postoperative stomal ulcer, and for the diagnosis of Zollinger-Ellison tumor
Hepatocellular carcinoma (HCC) is a highly aggressive malignant tumor with limited treatment options and poor prognosis. In this study, we reveal the pivotal role of Stratifin (SFN), also recognized as 14-3-3σ, in driving HCC progression. Our investigation underscores a substantial upregulation of SFN within HCC tissues, manifesting a significant association with worse prognostic outcomes among HCC patients. In vitro and in vivo experiments reveal that SFN overexpression significantly amplifies proliferation, mitigates sorafenib-induced effects on HCC cells, and enhances tumorigenesis. While SFN silencing exerts converse effects on HCC progression. Additionally, we unveil a critical interaction between SFN and AKT, where SFN boosts AKT kinase activity by disrupting the binding of PHLPP2 and AKT, thereby intensifying the malignant progression of HCC cells. In conclusion, this study identifies the oncogenic role of SFN and elucidates the regulatory mechanism of the SFN/AKT axis in HCC, which may provide valuable insights into the mechanisms of HCC progression and potential targets for therapeutic intervention.
There has been increasing interest in the field of human microbiome, considering its impact on health and diseases. The gastrointestinal tract represents the most heavily inhabited organ with microorganisms, counting 10 times the total number of human cells; for this reason, the gut microbiome has recently been referred as a proper organ. Intestinal microbial composition is unique for each individual and it is influenced by numerous factors, of which delivery mode is an important one with gestational age of the newborn, type of feeding and intrapartum or neonatal antibiotic therapy. Recent reports suggest that dysbiosis secondary to delivery mode affects the subsequent regulation of immune response and may be associated with several pathologic conditions, for example allergic diseases or obesity. Moreover, gut microbiome seems to impact on neurodevelopment during first six months of life. Bifidobacteria is the most represented group of intestinal microbiota in the newborn, followed by Enterobacteria, and it plays an important role in the infant gut. This includes the fundamental function performed by Bifidobacterium bifidum: it supplies the nutritional material to the rest of the microbial community, particularly Bifidobacterium breve and Bifidobacterium longum infantis that are the other typical bifidobacteria of the newborn. It is a powerful metabolizer of the intestinal mucus and the HMOs (Human Milk Oligosaccharides) present in breast milk. Thanks to its exocitable enzymes, the degradative catabolism occurs in the intestinal environment. Thus, B. bifidum favour the increase in intestinal richness and biodiversity (9), which correlates with the host's state of health. However, bifidobacteria is reduced in infants born by cesarean delivery.

Aim of the study is to assess if the Bifidobacterium Bifidum PRL2010 supplementation effectively ameliorat bifidocentric dysbiosis due to the delivery mode and we want to confirm this by analyzing fecal microbiota in caesarean birth infants.
BACKGROUND: Novel biomarkers can quantify both kidney tubule function, including proximal tubule reabsorptive (urine α-1 microglobulin (uα1m)) and tubule protein synthesis capacities (urine uromodulin (uUMOD)), and tubular injury (urine neutrophil gelatinase-associated lipocalin (uNGAL)). In a blood pressure trial, we reported that lower reabsorptive and synthetic protein capacity at times of health predicted future risk of acute kidney injury (AKI), but most AKI was related to hemodynamic causes in this trial. Associations between tubular function and injury and future AKI related to other causes is unknown.
MATERIALS AND METHODS: We performed a case-control study in REGARDS, a population-based cohort study, among participants who provided urine at the baseline visit. We matched each septic AKI case by age, sex, race, and time from baseline to hospital admission 1 : 1 to a participant with sepsis who did not develop AKI (controls). Using conditional logistic regression, we evaluated the associations of uα1m, uUMOD, urine ammonium, and uNGAL with septic AKI.
RESULTS: Mean age was 69 ± 8 years, 44% were female, and 39% were Black participants. Median baseline eGFR among cases and controls was 73 (55, 90) and 82 (65, 92) mL/min/1.73m2, and median albuminuria was 19 (8, 87) vs. 9 (5, 22) mg/g, respectively. No independent associations were observed between the tubule function or injury markers and subsequent risk of septic AKI once models were adjusted for baseline albuminuria, estimated glomerular filtration rate, and other risk factors.
CONCLUSION: Among community participants, tubule function and injury markers at times of health were not independently associated with future risk of septic AKI.
Subject will receive the standard dose (0.9mg/kg) of IV rt-PA. This IV dose will be discontinued at 40 minutes. The subject will immediately receive an IV bolus of 135mcg/kg eptifibatide followed by an IV infusion of 0.75 mcg/kg/min eptifibatide for 2 hours. Five out of six subjects will be in this group.
Functional pelvic floor muscle training will be started with 3 exercises (toe tap, bridge and clamshall exercises), each exercise will be performed with 1 set and 30 repetitions. In every 2-week control, the number of exercises will be increased by one. Cat-cow exercise will be added at 3-4th weeks, squats will be added at 5-6th weeks, and lunges will be added at 7-8th weeks.
Erythropoietin was administered at 150 units/kg subcutaneously every day. If patients stopped responding, they were subsequently treated with Erythropoietin (150 units/kg) and filgrastim and then Erythropoietin (300 units/kg) and filgrastim.
After established on a gluten free and casein free diet for at least 6 weeks, participants received double blind, placebo controlled challenges containing gluten, casein, gluten+casein, or placebo in a random order. Data was collected on behavioral and physiologic responses relative to the challenges. Children remained on the gluten free and casein free diet throughout this period.
The alarming rise in pediatric obesity over the past few decades has been associated with an increase in the occurrence of impaired glucose tolerance and inflammation in children and adolescents. These conditions are part of the "metabolic syndrome", and children with risk factors such as these are much more likely to develop cardiovascular disease or diabetes as adults compared with their lean peers. Within the last few years there has been a growing body of evidence that optimizing vitamin D (vit D) status may alleviate these obesity-associated complications. Further, there is also research that shows that the better the vit D status of overweight individuals, the more favorably they respond to dieting by losing more body fat. The prevalence of vit D deficiency/insufficiency in the North American population has been classified as an "epidemic" by experts in the field and obese teens are considered at an even greater risk for deficiency because they tend to store vit D in their fat stores which is not readily mobilized for use by the body. The investigators' project will study the effects of optimizing the vit D status of obese adolescents on markers of glucose metabolism and inflammation. Obese teens attending an established adolescent weight loss clinic will be supplemented with high-dose vit D for 6 months (mos) which will be administered concurrently with their standard medical care and treatment. At baseline, 3 mos and 6 mos the investigators will measure vit D status, serum markers of insulin sensitivity and glucose metabolism; serum markers of inflammation; and body weight/height and waist circumference. At baseline and 6 mos only the investigators also measure body composition (percent body fat by dual-energy x-ray absorptiometry) and confounding lifestyle factors known to affect vit D, glucose metabolism or inflammation (e.g., nutrient intake, physical activity, sun exposure, pubertal stage). Results gleaned from this study will help to advance the prevention and treatment of obesity-related complications and have the potential to lead to significant reductions in healthcare costs and co-morbidities.