anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Patients who will be undergoing elective ventral hernia repair will be potential candidates for this study. Once identified, the surgical team will approach the participant for consent and inclusion in the study. On the day of surgery, the subjects will be assigned to either the Bolus Group (CB) or Continuous Infusion Group (CI) according to a randomly generated assignment procedure. During the procedure, the dose of prophylactic Cefazolin will be given an hour before surgery and will be administered in accordance to group assignment. Subjects in the CB will receive bolus infusions of Cefazolin every 4 hours till the end of surgery. Subjects in the CI group will receive an initial bolus injection of Cefazolin followed by a continuous infusion till the closure of skin incision. Blood samples will be taken during surgery at t=0, 15, 30 and 60 minutes and every hour following till the end of surgery or 6 hours (whichever comes sooner)
<P>PROBLEM TO BE SOLVED: To obtain a pharmaceutical formulation that directly and efficiently delivers a nucleic acid compound such as nucleic acid, gene, etc., to the disease part of an intractable pulmonary diseases such as lung cancer, pulmonary fibrosis, etc., by using a nanoparticle, effectively and continuously develops actions and has high safety.  <P>SOLUTION: The pharmaceutical formulation for transpulmonary administration comprises nanoparticles obtained by sealing a nucleic acid compound such as plasmid, siRNA, etc., acting on target molecules in intractable pulmonary diseases such as lung damage/pulmonary fibrosis, lung cancer, bronchial asthma, etc., in a biocompatible polymer. Consequently, the nucleic acid compound is efficiently introduced organ specifically and disease site specifically into the body. Actions are continuously developed by gradual release of the nucleic acid compound from the insides of the nanoparticles. Possibility to clinical applications is increased due to minimization of influence on the whole body.  <P>COPYRIGHT: (C)2007,JPO&INPIT
The present invention relates to a cosmetic product containing super electrolytic water and a manufacturing method thereof. The method comprises: a step (a) of electrolyzing water to manufacture super electrolytic water having pH 12.5; a step (b) of preparing contents of general cosmetic products; and a step (c) of reacting the super electrolytic water in the step (a) with the cosmetic contents in the step (b). The step (b) is a step for spreading the cosmetic content with 5 mm of a thickness to form a cosmetic membrane, and the step (a) is a step for discharging super electrolytic water having pressure of 20 or more to a micro filter in the size of 0.1 micrometer, thereby filtering heavy metals or the like. The step (c) is to spread the cosmetic contents with 5 mm of a thickness to form a cosmetic membrane, discharges super electrolytic water having pressure of 20 or more to the micro filter in the size of 0.1 micrometer, then strongly injects the super electrolytic water such that the super electrolytic water is contained in the cosmetic contents. The present invention is provided to solve the problems that cosmetics spoils due to bacterial proliferation, efficacy of the cosmetics decreases or expiration dates come down to be short since a user takes out cosmetic products by fingers and thus, bacteria on the user′s hand go into the cosmetic products in a process of using cosmetic products (i.e. creams or the like).
PURPOSE:To obtain a preventive for fish diseases, comprising a water-soluble glucan containing a main chain consisting of beta-1,3-glucoside bond as an active ingredient. CONSTITUTION:A preventive for fish diseases containing a water-soluble polysaccharide glucan comprising a main chain consisting of beta-1,3-glucoside bond and a side chain branched by beta-1,6-glucoside bond. Schizophyllan and scleroglucan may be cited as the glucan. The concentration of the aqueous solution used is 0.01-1%. Administration is carried out by oral administration, intra-abdominal administration (intramuscular injection), immersion, etc., and 3-20mg/kg (weight) is added. The preventive is effective for various bacterial infectious diseases such as vibriosis of young yellowtail, sea bream, bastard halibut, swell fish, sweet fish, carp, tilapia, rainbow trout, eel, etc., pseudotuberculosis, streptococcal infection, nocardiosis, Edwardsiellosis, etc., and viral infectious diseases such as ascites, lymphocystis, KOHAKUSHO, etc.
Colorectal cancer accounts for 8% of all malignant tumors in adults and is considered as a major cause of cancer morbidity and mortality worldwide. Although curative surgical resection is possible in 70-80% of patients at diagnosis, almost half of them will develop local or/and metastatic recurrence and will die of the disease with the liver been the most common site of metastatic spread from CRC.

Combinations of infusional administrated 5-fluorouracil/Leucovorin with irinotecan or oxaliplatin are accepted as the mainstay of first-line treatment and have increase the median overall survival of patients with advanced CRC from 12 months to about 21-22 months. In addition, resection for colorectal metastases (mainly in the liver), has become the standard of care, for patients with limited metastatic disease confounded to the liver and currently remains the only potentially curative therapy Aflibercept, also known as vascular endothelial growth factor (VEGF) Trap, is an angiogenesis inhibitor with a unique mechanism of action. Aflibercept is a recombinant fusion protein that consists of portions of human VEGFR1 and VEGFR2 extracellular domains fused to the Fc portion of human immunoglobulin G1. This fusion protein binds all forms of Vascular Endothelial Growth Factor-A, as well as VEGF-B and placental growth factor, additional angiogenic growth factors that appear to play a role in tumor angiogenesis and inflammation. Aflibercept has been shown to bind VEGF-A, VEGF-B, and placental growth factor (PlGF) with higher affinity than their native receptors. In vitro and in vivo studies have shown that aflibercept can inhibit new vessel growth and tumor vascularization in tumor models.
The invention discloses a traditional Chinese medicine drug granule for treating cervical spondylosis and lumbar spondylosis and a preparation method thereof. The traditional Chinese medicine drug granule is prepared from extract particles and volatile oil clathrate compounds. The extract particles include dry extract powder, diluent and wetting agents. The volatile oil clathrate compounds include volatile oil and clathration materials. The weight ratio of the dry extract powder to the diluent in the extract particles is 1 to 0.3-1.0. The obtained traditional Chinese medicine drug granule is high in percent of pass, small in auxiliary material dosage, high in stability, suitable for transportation and storage in industrial production and capable of being conveniently taken by patients.
Developmental language disorder children who will receive the proposed narrative intervention program. The program will include 24 illustrated story sequences with a minimum of 5 sequences representing the main story elements: characters and setting; problems; internal response; actions; and consequence. Story icons will be designed to represent the main 5 elements to accompany storytelling and act as visual prompts.The narrative intervention program will be applied on the cases groups by a phoniatrician in 24 sessions, 60 minutes in duration, one session per week, for 3 months.
Olmesartan medoxomil 

Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation and renal reabsorption of sodium. Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in vascular smooth muscle. Its action is, therefore, independent of the pathways for angiotensin II synthesis.

An AT2 receptor is found also in many tissues, but this receptor is not known to be associated with cardiovascular homeostasis. Olmesartan has more than a 12,500-fold greater affinity for the AT1 receptor than for the AT2 receptor.

Blockade of the angiotensin II receptor inhibits the negative regulatory feedback of angiotensin II on renin secretion, but the resulting increased plasma renin activity and circulating angiotensin II levels do not overcome the effect of olmesartan on blood pressure.

Hydrochlorothiazide 

Hydrochlorothiazide is a thiazide diuretic. Thiazides affect the renal tubular mechanisms of electrolyte reabsorption, directly increasing excretion of sodium and chloride in approximately equivalent amounts. Indirectly, the diuretic action of hydrochlorothiazide reduces plasma volume, with consequent increases in plasma renin activity, increases in aldosterone secretion, increases in urinary potassium loss, and decreases in serum potassium. The renin-aldosterone link is mediated by angiotensin II, so co-administration of an angiotensin II receptor antagonist tends to reverse the potassium loss associated with these diuretics. The mechanism of the antihypertensive effect of thiazides is not fully understood.
Mechanisms underlying the migraine aura are incompletely understood, which to large extent is related to a lack of models in which cortical spreading depolarization (CSD), the correlate of the aura, occurs spontaneously. Here, we investigated electrophysiological and behavioural CSD features in freely behaving mice expressing mutant CaV2.1 Ca2+ channels, either with the milder R192Q or the severer S218L missense mutation in the α1 subunit, known to cause familial hemiplegic migraine type 1 (FHM1) in patients. Very rarely, spontaneous CSDs were observed in mutant but never in wildtype mice. In homozygous Cacna1aR192Q mice exclusively single-wave CSDs were observed whereas heterozygous Cacna1aS218L mice displayed multiple-wave events, seemingly in line with the more severe clinical phenotype associated with the S218L mutation. Spontaneous CSDs were associated with body stretching, one-directional slow head turning, and rotating movement of the body. Spontaneous CSD events were compared with those induced in a controlled manner using minimally invasive optogenetics. Also in the optogenetic experiments single-wave CSDs were observed in Cacna1aR192Q and Cacna1aS218L mice (whereas the latter also showed multiple-wave events) with movements similar to those observed with spontaneous events. Compared to wildtype mice, FHM1 mutant mice exhibited a reduced threshold and an increased propagation speed for optogenetically induced CSD with a more profound CSD-associated dysfunction, as indicated by a prolonged suppression of transcallosal evoked potentials and a reduction of unilateral forepaw grip performance. When induced during sleep, the optogenetic CSD threshold was particularly lowered, which may explain why spontaneous CSD events predominantly occurred during sleep. In conclusion, our data show that key neurophysiological and behavioural features of optogenetically induced CSDs mimic those of rare spontaneous events in FHM1 R192Q and S218L mutant mice with differences in severity in line with FHM1 clinical phenotypes seen with these mutations.
Percutaneous coronary intervention (PCI) of calcified coronary arteries is associated with poor outcomes. Poorly modified calcified lesion hinders the stent delivery, disrupts drug-carrying polymer, impairs drug elution kinetics and results in under-expanded stent (UES). UES is the most common cause of acute stent thrombosis and in-stent restenosis after PCI of calcified lesions. Angiography has poor sensitivity for recognition and quantification of coronary calcium, thereby mandating the use of intravascular imaging. Intravascular imaging, like intravascular ultrasound and optical coherence tomography, has the potential to accurately identify and quantify the coronary calcium and to guide appropriate modification device before stent placement. Available options for the modification of calcified plaque include modified balloons (cutting balloon, scoring balloon and high-pressure balloon), atherectomy devices (rotational atherectomy and orbital atherectomy) and laser atherectomy. Coronary intravascular lithotripsy (IVL) is the newest addition to the tool box for calcified plaque modification. It produces the acoustic shockwaves, which interact with the coronary calcium to cause multiplanar fractures. These calcium fractures increase the vessel compliance and result in desirable minimum stent areas. Coronary IVL has established its safety and efficacy for calcified lesion in series of Disrupt CAD trials. Its advantages over atherectomy devices include ease of use on workhorse wire, ability to modify deep calcium, no debris embolization causing slow flow or no-flow and minimal thermal injury. It is showing promising results in modification of difficult calcified lesion subsets such as calcified nodule, calcified left main bifurcation lesions and chronic total occlusion. In this review, authors will summarize the mechanism of action for IVL, its role in contemporary practice, evidence available for its use, its advantages over atherectomy devices and its imaging insight in different calcified lesion scenarios.
Chronic obstructive pulmonary disease (COPD) is associated with progressive decline in lung function with resultant chronic respiratory failure. This leads to significant rates of hospitalization, disability, and death. COPD is also associated with sleep disordered breathing and nocturnal hypoventilation, resulting in nocturnal and daytime hypoxemia and hypercapnia. These, in turn, can contribute to fatigue, dyspnea and impaired quality of life. Presence of hypercapnia is associated with a 33% 5-year survival. Nocturnal NPPV can theoretically rest overloaded respiratory muscles, prevent nocturnal hypoventilation, and reset central respiratory drive in patients with hypercapnia. The use of non-invasive positive pressure ventilation (NPPV) in late stage COPD appears logical to change this inexorable course, to alleviate symptoms and to improve quality of life. While NPPV has a definite role in the management of acute hypercapnic respiratory failure, its role in the management of late stage stable COPD is controversial. Multiple studies have shown no survival benefit for nocturnal NPPV in chronic hypercapnic stable COPD patients. The effects on quality of life and dyspnea scores in such patients have been inconsistent. The variable efficacy might have been due to late administration of the intervention in the course of disease, in the presence of advanced hypercapnic respiratory failure. We sought to assess the effect of applying NPPV on indices of health-related quality of life in patients with relative normocapnia. We hypothesized that patients with stable severe COPD have improved quality of life and reduced dyspnea with the use of NPPV.
Oral administration of 25 milligrams of bethanechol taken twice daily for a minimum of 7 days. Total dose taken daily for a minimum of 7 days is 50 mg.
Participants received matching-placebo for up to 3 weeks in Period 1, followed by a washout Period of 1 week, followed by CTN SR tablets starting at a dose of 100 or 200 mg on Day 1. Dose was up titrated up to 800 mg daily dose for up to 3 weeks in Period 2. The dose was decreased based on safety and tolerability based on Investigator's discretion. The most common TDD was 400 mg/day.
Although the negative impact of liver fluke (Fasciola hepatica) infection on production and health in cattle is generally accepted, results of individual research have been variable, ranging from important negative impacts on the animal to minimal or no impact. To add information on the impact of F. hepatica infection in growing cattle, weight gain and liver weight of young experimentally infected animals from seven controlled efficacy studies were analyzed. In each study, fluke naïve animals were inoculated with approximately 450 to 500 F. hepatica encysted metacercariae, blocked on body weight and randomly assigned into one untreated group (controls) and groups which were administered an experimental flukicide when the flukes were 4 weeks old (migrating) and sacrificed 8 weeks thereafter (12 weeks after inoculation). Data of groups which demonstrated >90% reduction of fluke counts following treatment and groups left untreated (total 103 and 47 animals, respectively) were compared. There was a significant (p < 0.0001) negative association between fluke count and weight gain while fluke count and liver weight and fluke count and relative liver weight were positively associated (p < 0.0001). Over the 8-week post-treatment period, flukicide-treated cattle had almost 15% more weight gain than the controls (50.9 kg vs. 44.4 kg; p = 0.0003). Absolute and relative liver weight was significantly (p < 0.0001) lower in flukicide-treated compared to untreated cattle. Overall, this analysis provided evidence of a substantial negative effect of early (migrating) liver fluke infection on the growth of young cattle, likely due to pathology of the liver and associated reduction in its function as the central organ for bioenergy and protein metabolism.
OBJECTIVES: Low plasma folate levels have been reported in patients undergoing hemodialysis and peritoneal dialysis (PD) in clinical studies. However, folate transport has never been mentioned as a factor contributing to low plasma folate levels in patients undergoing PD. The peritoneal equilibrium test (PET) assesses the plasma creatinine level and glucose transport abilities. This study aimed to evaluate the association between plasma folate levels and folate transport during PD based on PET grades.
METHODS: This study recruited 50 patients who underwent PD for ≥3 months and were categorized according to PET grades. Data regarding plasma folate levels and dialysate folate were collected. The primary outcomes were the relationship between the PET grade and plasma folate level and between the PET grade and dialysate-to-plasma folate concentration ratio (D/P folate). Furthermore, the difference in the plasma folate level and D/P folate between men and women was assessed.
RESULTS: The plasma folate level and the D/P folate significantly differed among the 4 PET groups (both P < .001). PET grade was significantly negatively correlated with plasma folate levels (r = -0.56, P < .001) and positively correlated with D/P folate (r = 0.686, P < .001). In subgroup analysis, neither the plasma folate level nor the D/P folate significantly differed between men and women.
CONCLUSIONS: Our study provides clinical evidence that the PET grade is associated with the plasma folate level and D/P folate, regardless of sex. Larger cohort studies are warranted to assess the importance of folate supplementation during PD based on PET grades.
A polypeptide of molecular weight about 20,000 and having protease inhibitory properties, is prepared in a partially purified state from an aqueous suspension of powdered defatted peanuts by treating with acid at pH3-5 and/or alkali at pH 9-10, and removing the precipitate, treating the supernatant with an ion-exchange resin or by heating to 70-80 DEG  C. and removing the precipitate, dialysing the resulting solution, and then precipitating the partially purified product with a water-miscible organic liquid (e.g. ethanol).  This product may be purified to the homogeneous polypeptide by re-solution in water, precipitation with ammonium sulphate to 44% concentration, followed by re-solution, passage over diethylamino ethanol at pH5, and then at pH 7.5, and dialysis and lyophilization to give the purified polypeptide.  The product has anti-esterase and antiprotease activity against trypsin and chymotrypsin and also inhibits the fibrinolytic activity of plasmin; it has an electrophoretic mobility of 0.8 x 10-5 cms.2/sec./volt in pH 8.0 Michaelis buffer, an isoelectric point of pH 6.75, a sedimentation velocity of 0.82 Svedburg units, contains no tryptophan and a large amount of cysteine.  An amino acid analysis is given.ALSO:A protease inhibitor which is a homogenous polypeptide (see Div. C3) is prepared in a partially purified state by removal of unwanted proteins from an aqueous suspension of ground defatted peanuts, by (i) treating with acid at pH 3 to 5 and/or alkali at pH 9 to 10 and removing the precipitate; (2) treating the supernatant with an ion exchange resin or heating it to 70 DEG  to 80 DEG C, and removing the resulting precipitate; (3) dialysing the so-treated solution; (4) addition of a water-miscible organic liquid (e.g. ethanol) to precipitate the partially purified product.  This product may be purified to the polypeptide by dissolving it in water and re-precipitating by addition of saturated aqueous ammonium sulphate to a final concentration of 44%, followed by re-solution and passage over diethylaminoethyl-cellulose, first at pH 5, then again at pH 7.5, with final dialysis and lyophilisation of the solution emerging. Pharmaceutical compositions contain the purified polypeptide with a suitable carrier, and may be administered internally or externally as injectable preparations, solutions, tablets, drops, suppositories, powders, aerosols, pomades or callyria, a unit dosage preferably containing 200,000 to 2,000,000 inhibitory units (1 unit inhibits 1 S.T. unit of trypsin).  The polypeptide has inhibitory effects on the esterase and protease properties of trypsin, chymotrypsin and plasmin, and may be used to treat fibrinolytic conditions and pancreatitis.
Methods for identifying subjects having, or at risk for developing, osteoarthritis or other cartilage degenerative conditions by measuring levels of expression of F-spondin are provided. Assays, kits and methods for determining and assaying the presence of F-spondin in individual patients are disclosed. Oligonucleotide probes and primers for use in the assays, kits and methods are described. Assays and methods are disclosed for identifying candidate compounds that modulate F-spondin levels of expression and/or function or for determining and evaluating an individual's response to drugs and therapeutic agents, are provided. The invention further relates to the modulation of F-spondin, particularly the inhibition of F-spondin, for increasing or stimulating bone formation and/or growth and mediating the alleviation of bone disease, disorders or conditions. The use of F-spondin, an active fragment thereof, or a modulator thereof for enhancing cartilage repair or preventing or treating cartilage degeneration, degenerative diseases or arthritic conditions is also provided.