anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The design is primarily a randomized control-trial design (2 sessions), comparing the effects excitatory and inhibitory TMS protocols applied to a prefrontal TMS target on reward processing in smokers. Eligible smokers will be invited to attend two experimental sessions over a 1-month period, and asked to abstain from smoking 4 hrs prior to each session. For Sessions A and B, participants will be asked to provide their consent, CO levels and complete the TCQ. Compliance with the 4-hour abstinence period will be defined as breath CO less than 13 ppm. Participants will then be randomly selected to participate in Condition 1a or Condition 1b. All procedures between the two conditions will be identical except for the contrasting TMS protocols (Condition 1a: excitatory protocols, Condition 1b: inhibitory protocols) and the rewards presented in the T-maze task (Condition 1a: monetary rewards, Condition 1b: monetary rewards with cigarette cues). To streamline these studies, the left DLPFC target will be based on conventional DLPFC targeting methods (electrode position F3). For Condition 1a, the protocol administered in Session A and B will be randomized so that participants will either receive 3600 pulses of 10-Hz TMS or 3600 pulses of cTBS. For each session, participants will first engage in one block of T-maze trials (100 trials: Baseline measure). In Condition 1a, participants are told that the reward stimulus indicated 5 cents and that the presentation of the no-reward stimulus indicated the alley was empty (0 cents). Following this block of trials, participants will either receive 10-Hz TMS or cTBS over the predefined DLPFC target (F3), and then asked to complete 3 additional Blocks of the T-maze (300 trials: post-TMS). Immediately after participants complete the T-maze, subjects will be asked to complete the PST and TCQ. At the end of the Session A, participants will complete Session B on a separate day (all procedures identical as Session A). Session A and Session B will be separated by at least 2 days to minimize carryover effects. For Condition 1b, the protocol administered in Session A and B will be randomized so that participants will either receive 600 or 1200 pulses of iTBS. For each session, participants will first engage in one block of T-maze trials (100 trials: Baseline). In Condition 1b, participants are told that the reward stimulus indicated 5 cents and that the presentation of the no-reward stimulus indicated the alley was empty (0 cents). Each reward and no-reward stimulus will be paired with a cigarette cue. Following this block of trials, participants will either receive 600 or 1200 pulses of iTBS over the predefined DLPFC target (electrode F3), and then asked to complete 3 additional Blocks of the T-maze (300 trials: Post-TMS). Immediately after participants complete the T-maze, subjects will be asked to complete the PST and the TCQ. At the end of the Session A, participants will complete Session B on a separate day (all procedures identical as Session A). Session A and Session B will be separated by at least 2 days to minimize carryover effects.
The aims of the current study were to determine the frequencies of specific sleep disturbances in youth with abdominal pain-associated disorders of gut-brain interaction (AP-DGBIs) and to assess relationships with psychological dysfunction. This was a retrospective evaluation of 226 consecutive patients diagnosed with an AP-DGBI. All had undergone a systematic evaluation of gastrointestinal symptoms, the Sleep Disturbance Scale for Children, and the Behavior Assessment System for Children. Disorders of initiation and maintenance of sleep (DIMS; 40%) and disorders of excessive daytime somnolence (DOES; 14%) were each present in more than 10% of the patients. Both DIMS and DOES scores were more likely to be elevated in patients with anxiety and/or depression scores in the at-risk or elevated-risk ranges. Sleep disorders are common in youth with AP-DGBIs and are associated with anxiety and depression, even in those patients with anxiety and depression in the at-risk range.
The aim of this study was to assess the effect of triterpenoids on the development of diabetic nephropathy in an experimental model of diabetes mellitus. For this purpose, a destoned and dehydrated olive oil (DDOO) was used, comparing its effects to a destoned olive oil (DOO). DDOO had a higher triterpenoid content than DOO but an equal content of alcoholic polyphenols. Four study groups (n = 10 animals/group) were formed: healthy rats, diabetic control rats (DRs), and DRs treated orally with 0.5 mL/kg/day of DOO or DDOO for two months. DRs showed impaired renal function (proteinuria, increased serum creatinine, decreased renal creatinine clearance) and morphology (glomerular volume and glomerulosclerosis). These alterations correlated with increased systemic and renal tissue oxidative stress and decreased prostacyclin production. DDOO administration significantly reduced all variables of renal damage, as well as systemic and renal oxidative stress, to a greater extent than the effect produced by DOO. In conclusion, triterpenoid-rich olive oil may prevent kidney damage in experimental diabetes mellitus.
A pharmaceutical solution comprising 8 wt% buprenorphine and a biocompatible solvent selected from the group consisting of N-methyl-2-pyrrolidone (NMP), dimethyl sulfoxide (DMSO), dimethyl acetamide (DMAC), and a combination thereof, wherein the solution does not comprise a biodegradable polymer. The buprenorphine may be present as a free base or a pharmaceutically acceptable salt form. The solution may further comprise a glycol. The glycol may be polyethylene glycol, propylene glycol or mixtures thereof. The polyethylene glycol may have a molecular weight between 100 and 1000, and may be selected from PEG300 or PEG400. The solution may further comprise 0.01-10 wt% of an antioxidant selected from ascorbic acid, vitamin E, butylated hydroxytoluene (BHT) or butylated hydroxyanisole (BHA). The composition may comprise 0-10 wt% water. The solution may be sterile. The pharmaceutical solution may be for use as a medicament, particularly in the treatment of opioid dependence or pain. The solution is administered via subcutaneous injection to provide a subcutaneous depot having sustained release characteristics.
<P>PROBLEM TO BE SOLVED: To provide devices and methods for preventing formation of scar tissues and/or adhesion subsequent to surgical treatment, an injury, or a wound.  <P>SOLUTION: The invention includes various devices and methods, in which antiproliferative chemical having cytostatic performance is provided between internal tissues solely or with other medicine for preventing formation of scar tissues and/or adhesion during treatment of a wound or other surgical part. The devices for achieving above dosage include permanent implant or biolytic material including antiproliferative chemical such as sirolimus attached to it, but they are not limited to these. The antiproliferative chemical includes antiplatelet agent, antithrombotic agent, or anticoagulant agent, and may be used with other chemical that is not limited to them. The methods for alleviating formation of scar tissues and/or adhesion, or adhesion at an inosculation part are also provided. The antiproliferative chemical having cytostatic performance is dosed for arteriovenous shunt inosculation to a patient of an end-stage renal disease.  <P>COPYRIGHT: (C)2009,JPO&INPIT
A sedative for all the peripheral nerves is prepared by inoculating or infecting organs or tissues of animals such as cows or rabbits with cowpox, removing the organs or tissues 3 to 10 days after inoculation or infection, dispersing them in an aqueous medium, completely removing protein ingredients from the dispersion, and recovering the sedative, which contains no virus protein or lipoid, from the liquid so obtained.  The aqueous medium is physiological saline solution, water, glycerin water, or a mixture thereof, containing carbolic acid.  In the example, a portion of the testicles or skins of animals is removed 4-5 days after inoculation, well-ground and dispersed in a mixture of physiological saline solution, glycerin and carbolic acid.  The dispersion is alternatively frozen at -5 to -10 DEG  C. and thawed at 15-20 DEG C., allowed to stand, the supernatant liquid decanted and proteins removed in stages by (a) heating to 100 DEG  C. for 1 hour (b) adjusting pH to 5 by the addition of hydrochloric acid and (c) filtering through asbestos treated with sodium silicate and magnesium sulphate.  The filtrate from (c) is treated with kaolin at pH 4.5-4.7.  The absorbate containing the virus and sedative is eluted with N/24-N/26 aqueous ammonia and filtered.  The filtrate is adjusted to pH 7.4-7.8 with N/1 acetic acid, concentrated in vacuo, and the sedative precipitated by the addition of a water-miscible organic solvent e.g. acetone or ethylalcohol.  The effective material can be isolated by cataphoresis of the clear liquid obtained after heating and freezing a dispersion of the tissues in saline solution. Active material may also be isolated from urine of infected animals or from a cowpox inoculated hatching egg.
BACKGROUND: Posterior urethral valves (PUV) represents a heterogenous spectrum in which guidelines for management are lacking particularly for those patients facing end-stage kidney disease and transplant. In this study we aim to 1) evaluate our long term PUV pediatric transplant outcomes compared to those without lower urinary tract dysfunction and 2) assess our PUV cohort for trends in bladder management and evaluate outcomes to inform development of institutional guidelines.
MATERIALS AND METHODS: A retrospective cohort analysis of all patients with a diagnosis of PUV who underwent kidney transplant from 2000 to 2023 was completed. A matched cohort of patients without lower urinary tract dysfunction was identified for comparison of graft function. Charts of PUV patients were reviewed for both sociodemographic and clinical variables. Patients were classified by bladder management at the time of transplantation into three separate groups for analysis: voiding, clean intermittent catheterization, and incontinent diversion. Primary outcomes of interest were eGFR, graft failure, and UTIs post-transplant.
RESULTS: 45 patients met inclusion criteria. 69% were on dialysis prior to transplant. 51% of grafts were from a deceased donor. Bladder management consisted of voiding (62%), CIC (4 via urethra, 10 via channel) (31%), and incontinent diversion (7%). 20% underwent augmentation cystoplasty (5 = ureter, 2 = gastric, 1 = colon, and 1 = ileum) prior to or at the time of transplant. Median follow up duration was 5.4 years (3.0, 10.8). Patients on CIC had higher rates of UTI; however, we found no significant difference in graft function outcomes (eGFR, graft failure) between bladder management groups or year of transplant. VUR in the transplant kidney was associated with vesicostomy (p = 0.028). 2 of 2 gastric augments developed malignancy, one of which was cause of death. Graft failure rate was 22% in both the PUV group and matched cohort, with median interval times to failure of 6.7 years and 3.7 years, respectively (p = 0.71). There were no differences in eGFR at follow-up time points between the PUV and matched cohort.
CONCLUSIONS: Patients with PUV represent a spectrum of disease with heterogeneous management before and after kidney transplant. Overall, graft function outcomes were similar when compared to matched cohort without lower urinary tract dysfunction. Patients on CIC had higher rates of UTI but without impact on graft function. Gastric augmentation cystoplasty should be avoided given risk for malignancy. Guidelines to standardize evaluation and management would be helpful for patient care and outcomes.
The study is based on data from morbidly obese patients who fulfilled the criteria for bariatric surgery during 2016-2018 at the Department of Surgery, University Hospital Ostrava, Czech Republic. Patients with age above 18 years, BMI \> 35-40 kg/m2, and associated with at least one of the complications including hypertension, diabetes, and failure of the current therapies to relieve the symptoms were included in the study. Patients included in the current study do not have a history of excessive alcohol consumption, use of hepatotoxic drugs, infectious liver diseases (i.e. hepatitis A, B, C), and genetic hemochromatosis. A total of 72 patients including n = 26 during 2016, n = 26 during 2017, and n = 20 during 2018 who qualified for bariatric surgeries were included in this observational study. Data related to patients' gender, age (years), weight (kg), height (cm), and associated co-morbidities like diabetes and hypertension were recorded before surgery. BMI (kg/m2), biochemical parameters including triglycerides profile (mmol/L), platelet count (number/L), Gamma glutamyl-transferase (international units - IU/L), albumin concentration (g/L), Alanine amino-transferases (units/L), Aspartate aminotransferases (international units - IU/L), were evaluated following standard procedures. Platelet count, triglycerides, and enzymes were determined using standard procedures.

The biochemical results were compared to the corresponding paired values before surgery and after surgery. The current study was designed to prospectively investigate the effect of bariatric surgeries among non-alcoholic obese individuals from 2016-2018 and one year follow up on liver biochemistry, BMI, non-alcoholic fatty liver disease (NAFLD) fibrosis score, Fibrosis 4 (FIB 4) Index, and Fatty Liver Index (FLI).

The continuous variables were expressed as mean ± standard deviation and median (interquartile range) in case of normal and non-normal distribution, respectively. The Shapiro-Wilk test was used to test for normal distribution. The within-patient changes in clinical parameters (continuous or ordinal variables) from baseline to 1-year after bariatric surgery were compared using the Wilcoxon matched-pairs signed-rank tests for ordinal variables and continuous variables when the change was not normal or using the paired Student's t-test otherwise. The statistical testing was done at the two-tailed α level of 0.05. The data were analyzed using GraphPad Prism Version 8.0.2 (GraphPad Software, Inc., USA).
Use caution when administering fosphenytoin sodium injection because of the risk of dosing errors [see Warnings and Precautions (5.1)].    
Phenytoin Sodium Equivalents (PE)    
The dose, concentration, and infusion rate of fosphenytoin sodium injection should always be expressed as phenytoin sodium equivalents (PE). There is no need to perform molecular weight-based adjustments when converting between fosphenytoin and phenytoin sodium doses. Fosphenytoin sodium injection should always be prescribed and dispensed in phenytoin sodium equivalent units (PE). The amount and concentration of fosphenytoin is always expressed in terms of mg of phenytoin sodium equivalents (mg PE).   
Concentration of 50 mg PE/mL    
Do not confuse the concentration of fosphenytoin sodium injection with the total amount of drug in the vial.   
Errors, including fatal overdoses, have occurred when the concentration of the vial (50 mg PE/mL) was misinterpreted to mean that the total content of the vial was 50 mg PE. These errors have resulted in two-or ten-fold overdoses of fosphenytoin sodium injection since each of the vials actually contains a total of 100 mg PE (2 mL vial) or 500 mg PE (10 mL vial). Ensure the appropriate volume of fosphenytoin sodium injection is withdrawn from the vial when preparing the dose for administration. Attention to these details may prevent some fosphenytoin sodium injection medication errors from occurring.
PROBLEM TO BE SOLVED: To obtain a sound hair agent capable of bringing the hair healthy, preventing hair damages and curing damaged hair, having effects to bring the hair to be beautiful and healthy inherent to the hair and safe to human bodies by bringing the agent to contain a rice preparation. SOLUTION: This sound hair agent contains a rice preparation. The rice preparation is made of rice as a raw material, e.g. a product from pulverized rice, a rice extract and rice processed with an enzyme and/or malt, a product processed with the enzyme and/or malt before, simultaneously or after the extraction in extraction-treating rice, an alcohol fermentation and/or organic acid fermentation product from the rice extract or the product of rice treated with enzyme and/or malt and the like are cited. The sound hair agent is produced, e.g. by using the rice preparation itself, or the rice processed by compression, filtration and the like and adding additives depending on its use. The content of the rice preparation in the whole weight of the sound hair agent is preferably 0.01-90 wt.%, more preferably 1-70 wt.% and further preferably 3-50 wt.%.
Patients with acute myeloid leukemia treated with intensive chemotherapy. From 2009 to 2011, any patient received antifungal (anti-aspergillosis) prophylaxis.
Move with HaRT is a 12-session, weekly, manualized mental health intervention led by trained paraprofessionals. It is delivered in groups of 8-12 individuals and includes breathwork, yoga poses, guided meditations, and discussions aligned with weekly themes. Group discussions include topics such as noticing how we feel in our bodies, recognizing and allowing all emotions, practicing self-acceptance, and developing deeper connections with others with whom we feel safe.
Kidney toxicity was observed in animals who received casimersen [see Use in Specific Populations (8.4) and Nonclinical Toxicology (13.2)]. Although kidney toxicity was not observed in the clinical studies with AMONDYS 45, kidney toxicity, including potentially fatal glomerulonephritis, has been observed after administration of some antisense oligonucleotides. Kidney function should be monitored in patients taking AMONDYS 45. Because of the effect of reduced skeletal muscle mass on creatinine measurements, creatinine may not be a reliable measure of kidney function in DMD patients. Serum cystatin C, urine dipstick, and urine protein-to-creatinine ratio should be measured before starting AMONDYS 45. Consider also measuring glomerular filtration rate using an exogenous filtration marker before starting AMONDYS 45. During treatment, monitor urine dipstick every month, and serum cystatin C and urine protein-to-creatinine ratio (UPCR) every three months. Only urine expected to be free of excreted AMONDYS 45 should be used for monitoring of urine protein. Urine obtained on the day of AMONDYS 45 infusion prior to the infusion, or urine obtained at least 48 hours after the most recent infusion, may be used. Alternatively, use a laboratory test that does not use the reagent pyrogallol red, as this reagent has the potential to cross react with any AMONDYS 45 that is excreted in the urine and thus lead to a false positive result for urine protein. 

If a persistent increase in serum cystatin C or proteinuria is detected, refer to a pediatric nephrologist for further evaluation.
Acute haemorrhagic diarrhoea is a common complaint in dogs. In addition to causes like intestinal parasites, dietary indiscretion, intestinal foreign bodies, canine parvovirus infection, or hypoadrenocorticism, acute haemorrhagic diarrhoea syndrome (AHDS) is an important and sometimes life-threatening differential diagnosis. There is some evidence supporting the link between Clostridium perfringens toxins and AHDS. These toxins may be partially responsible for the epithelial cell injury, but the pathogenesis of AHDS is still not fully understood. Recent studies have suggested that severe damage to the intestinal mucosa and associated barrier dysfunction can trigger chronic gastrointestinal illnesses. Besides bloodwork and classical markers for AHDS such as protein loss and intestinal bacterial dysbiosis, we focused mainly on the plasma-proteome to identify systemic pathological alterations during this disease and searched for potential biomarkers to improve the diagnosis. To accomplish the goals, we used liquid chromatography-mass spectrometry. We compared the proteomic profiles of 20 dogs with AHDS to 20 age-, breed-, and sex-matched control dogs. All dogs were examined, and several blood work parameters were determined and compared, including plasma biochemistry and cell counts. We identified and quantified (relative quantification) 207 plasmatic proteins, from which dozens showed significantly altered levels in AHDS. Serpina3, Lipopolysaccharide-binding protein, several Ig-like domain-containing proteins, Glyceraldehyde-3-phosphate dehydrogenase and Serum amyloid A were more abundant in plasma from AHDS affected dogs. In contrast, other proteins such as Paraoxonase, Selenoprotein, Amine oxidases, and Apolipoprotein C-IV were significantly less abundant. Many of the identified and quantified proteins are known to be associated with inflammation. Other proteins like Serpina3 and RPLP1 have a relevant role in oncogenesis. Some proteins and their roles have not yet been described in dogs with diarrhoea. Our study opens new avenues that could contribute to the understanding of the aetiology and pathophysiology of AHDS.
One randomized, open-label, active-controlled study was conducted to evaluate the efficacy of IMPAVIDO in the treatment of visceral leishmaniasis in Bihar, India, an area where L. donovani is known epidemiologically to be the prevalent infecting species. Patients 12 years of age and older with clinical signs and symptoms compatible with visceral leishmaniasis (fever, splenomegaly, and cytopenia) confirmed by the presence of Leishmania amastigotes in aspirates of spleen or bone marrow were randomized to receive oral IMPAVIDO or intravenous amphotericin B deoxycholate in a 3:1 ratio. Patients weighing greater than or equal to 25 kg received an IMPAVIDO 50 mg capsule with meals twice a day. Patients weighing less than 25 kg received an IMPAVIDO 50 mg capsule with meals once a day in the morning. Weight ranged between 15 and 67 kg (mean weight 38.6 kg) and BMI ranged between 8.2 and 24 (mean 16.1). No patient weighed more than 70kg. Amphotericin B was administered intravenously over 6 continuous hours at 1 mg/kg every other day for 15 doses. Patients were hospitalized for the duration of therapy.

Exclusion criteria included platelet count <50 × 109/L, white cell count <1 × 109/L, hemoglobin <6 g/100 mL, AST or ALT ≥3 times upper limit of the normal range, bilirubin ≥2 times upper limit of the normal range, serum creatinine or BUN >1.5 times upper limit of the normal range, prothrombin time >5 seconds above control, and any non-compensated or uncontrolled condition including human immunodeficiency virus (HIV) infection. Women of reproductive potential were required to use effective contraception for the duration of therapy and for 2 months post therapy.

Final cure was defined as initial cure at end of therapy plus absence of signs and symptoms of visceral leishmaniasis at 6 months follow up. Initial cure at the end of therapy was evaluated by repeat spleen or bone marrow aspiration. Patients with initial parasitologic cure were followed for 6 months; patients without absence of clinical signs and symptoms of visceral leishmaniasis were to be evaluated with repeat spleen or bone marrow aspiration to determine final cure. 

Two hundred and ninety nine (299) patients received IMPAVIDO and 99 patients received amphotericin B. Approximately, 70% of patients in each arm had previously failed treatment with pentavalent antimony. Initial cure was achieved in 98% of patients in each treatment arm. At 6 months after therapy, 88 (29.5%) IMPAVIDO recipients and 12 (12.1%) amphotericin B recipients continued to have signs and symptoms suggestive of visceral leishmaniasis. These signs or symptoms were attributed to alternative diagnosis in 73 patients. The remaining 27 patients, all in the IMPAVIDO arm, underwent evaluation with splenic or bone marrow aspiration, and 9 (3.0%) were positive for Leishmania amastigotes, indicating relapse. The final cure rates for IMPAVIDO and amphotericin B were 94% and 97%, respectively.