anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
OBJECTIVE: To investigate the relationship between the anatomical position of the anterior arm of the mesh, measured by ultrasound through the bladder neck-mesh distance technique and the surgical outcomes after laparoscopic sacrocolpopexy (SCP) for apical prolapse.
STUDY DESIGN: It was a retrospective analysis of prospectively collected data in a tertiary care hospital. Between January 2019 and September 2019, 63 women who underwent laparoscopic SCP due to apical prolapse were included. Bladder neck-mesh distance was measured immediately after surgery. The pelvic floor was evaluated using the Pelvic Organ Prolapse Quantification (POP-Q) System before, 1 month, and 2.7 years (mid-term) after the surgery. Post-operative stress urinary incontinence (SUI) and Patient Global Impression of Improvement (PGI-I) scores were also assessed. The correlation between bladder neck-mesh distance and the post-operative outcomes was investigated using the Spearman rank correlation coefficient.
RESULTS: At mid-term follow-up visit, bladder neck-mesh distance was inversely correlated with the correction of apical prolapse and post-operative SUI. No correlation was detected with the anterior compartment prolapse correction. PGI-I scores were high in all patients at mid-term follow-up, irrespective of bladder neck-mesh distance values.
CONCLUSION: The shorter the bladder neck-mesh distance, the better the outcome for apical compartment repair. Bladder neck-mesh distance had no correlation with the anterior anatomical correction. Shorter bladder neck-mesh distance values were positively correlated to better PGI-I scores and a higher risk of SUI.
Porcine reproductive and respiratory syndrome (PRRS), which has also been termed mystery swine disease, swine infertility and respiratory syndrome (SIRS), and porcine epidemic abortion and respiratory syndrome (PEARS), induces severe disease in pigs and causes considerable economic loss to farmers. The pathology of PRRS is characterized by severe reproductive failure in sows, mild to severe respiratory distress, increased mortality in weaning pigs, conjunctivitis, and lymphnode enlargement. The pathogen responsible for PRRS is an enveloped RNA virus belonging to the Arterivirus group within the Togaviridae family. The PRRS viruses are single stranded RNA viruses having a viral genome of positive polarity and a size of approximately 15 kb. The positive-strand RNA genome possesses at least three major structural proteins designated N, M, and E. The PRRS viruses exist as a quasispecies and display considerable genotypic and phenotypic heterogeneity. The present invention is directed toward the isolation, characterization, and utilization of a novel PRRS viral isolate designated JK-100.
The treatment period was set at 20 weeks, in order to realize adequate treatment efficacy of imiquimod, while minimizing the risk of progression of cervical dysplasia to invasive disease in the conservative treatment group. Based on the available literature on the natural history of CIN and several studies on cervical dysplasia that included a conservative treatment group, the risk of disease progression within the treatment period of 20 weeks is estimated to be marginal. Approximately 30% of high-grade CIN progresses to cervical cancer. \[Peto, 2004; McCredie, 2008\]. This is believed to be a slow process, which can take many years. The annual risk of progression of CIN 3 to invasive cervical cancer is estimated to be less than 1%.\[Canfell, 2004\]. Ten studies were identified in which a total of 637 patients with high grade CIN were included either as a control group, receiving conservative treatment during 6 weeks to 15 months, or followed during the period between diagnosis and LLETZ.\[Grimm, 2012, Follen, 2001; Meyskens, 1994; Keefe, 2001; Alvarez, 2003; Garcia, 2004; Van Pachterbeke, 2009; Kaufmann, 2007; Trimble 2005; Munk, 2012\] Three cases of invasive disease were identified: all occured in the same study after 16 weeks of conservative treatment. Other studies showed no progression to invasive disease. One case of progression was reported with undefined disease grade and follow-up term. The possibility of invasive disease already present at the initial colposcopy (biopsy error) cannot be excluded. Based on these results, the investigators selected a treatment period of 20 weeks, with a control colposcopy with diagnostic biopsies after ten weeks.

The current study protocol includes a substantial amendment to the original study protocol, which consisted of three study arms: imiquimod treatment arm, LLETZ treatment arm and an observational arm. The purpose of the observational arm was to assess spontaneous regression of high-grade CIN and to develop a prognostic biomarker panel to predict spontaneous regression of high-grade CIN. Patients in the observational arm underwent no treatment for a period of maximum 20 weeks. Histological assessment of disease development was performed after 10 and 20 weeks by colposcopy with diagnostic biopsies. Inclusion of patients into the study was hampered by the observational arm: patients declined the study because they wished to be treated, rather than undergo observational management. The observational arm was removed from the study.
Disclosed are a human sDR5-Fc recombinant fusion protein and the use of same in the preparation of a drug for treating reproductive system inflammation. In particular, a fusion protein of the soluble fragment of the human DR5 and the Fc fragment of the human IgG1 is constructed, wherein the amino acid sequence of the soluble fragment of the human DR5 is as shown in SEQ ID No. 1, SEQ ID No. 2, SEQ ID No. 3 or SEQ ID No. 4, and the amino acid sequence of the Fc fragment of the human IgG1 is as shown in SEQ ID No. 5, or a recombinant fusion protein having at least 95% homology to SEQ ID No. 1, SEQ ID No. 2, SEQ ID No. 3, SEQ ID No. 4 or SEQ ID No. 5 and having the same function is constructed. Also provided is the use of the human sDR5-Fc recombinant fusion protein in the preparation of a drug for treating or preventing inflammation. The inflammation is selected from seminal vesiculitis, prostatitis and urethritis. The recombinant fusion protein has good stability and high biological activity, and can be efficiently and safely used in the treatment of reproductive system inflammation.
Patients undergo blood sample collection and bone marrow biopsies at baseline and during and after induction therapy for immunophenotyping for ALL confirmation and classification, DNA ploidy, genomic variation, and cytogenetic (BCR-ABL, trisomies 4+10, and molecular testing for translocations) analysis by flow cytometry and FISH. Immunophenotype results obtained on this study are used to determine patient's assignment to specific clinical-trial treatments. Some samples (leukemic and germline) may be banked for current and/or future analyses.
During the baseline phase, participants were instructed to sit quietly and relax. For the neutral control, they viewed an informative video demonstrating the process of plastic injection molding. As for the sadness induction, they were presented with sad film clips from either Hachi: A Dog\'s Tale or My Brother and Sister. The order of the sad videos was randomized across participants. The intervention stages involved listening to either the cheerful Cuckoo Waltz music or a clip of birdsongs from laughing thrushes. The order of the interventions was randomized as well. The calculation task was employed as a distracter, enabling participants to return to a neutral state. Except for the computational task, the remaining six phases each had a duration of 6 minutes.
Bleeding has been reported in patients treated with Pentoxifylline Extended-Release Tablets with or without concomitant NSAIDS, anticoagulants, or platelet aggregation inhibitors. Increased prothrombin time has been reports in patients concomitantly treated with pentoxifylline and vitamin K antagonists. Monitoring of anticoagulant activity in these patients is recommended when pentoxifylline is introduced or the dose is changed.

Concomitant administration of pentoxifylline- and theophylline-containing drugs leads to increased theophylline levels and theophylline toxicity in some individuals. Monitor theophylline levels when starting Pentoxifylline Extended-Release Tablets or changing dose.

Concomitant administration of strong CYP1A2 inhibitors (including e.g. ciprofloxacin or fluvoxamine) may increase the exposure to pentoxifylline (see ADVERSE REACTIONS). Pentoxifylline has been used concurrently with antihypertensive drugs, beta blockers, digitalis, diuretics, and antiarrhythmics, without observed problems. Small decreases in blood pressure have been observed in some patients treated with pentoxifylline; periodic systemic blood pressure monitoring is recommended for patients receiving concomitant antihypertensive therapy. If indicated, dosage of the antihypertensive agents should be reduced. 

Postmarketing cases of increased anticoagulant activity have been reported in patients concomitantly treated with pentoxifylline and vitamin K antagonists. Monitoring of anticoagulant activity in these patients is recommended when pentoxifylline is introduced or the dose is changed.

Concomitant administration with cimetidine is reported to increase the average steady state plasma concentration of pentoxifylline (~ 25%) and Metabolite I (~ 30%).   


Carcinogenesis, Mutagenesis, and Impairment of Fertility

Long-term studies of the carcinogenic potential of pentoxifylline were conducted in mice and rats by dietary administration of the drug at doses up to 450 mg/kg (approximately 19 times the maximum recommended human daily dose (MRHD) in both species when based on body weight; 1.5 times the MRHD in the mouse and 3.3 times the MRHD in the rat when based on body surface area). In mice, the drug was administered for 18 months, whereas in rats, the drug was administered for 18 months followed by an additional 6 months without drug exposure. In the rat study, there was a statistically significant increase in benign mammary fibroadenomas in females of the 450 mg/kg group. The relevance of this finding to human use is uncertain. Pentoxifylline was devoid of mutagenic activity in various strains of Salmonella (Ames test) and in cultured mammalian cells (unscheduled DNA synthesis test) when tested in the presence and absence of metabolic activation. It was also negative in the in vivo mouse micronucleus test.
* Mix each VISTOGARD dose with 3 to 4 ounces of soft foods such as applesauce, pudding or yogurt and ingest within 30 minutes. Do not chew the VISTOGARD granules. Drink at least 4 ounces of water. 
  * If a patient vomits within 2 hours of taking a dose of VISTOGARD, initiate another complete dose as soon as possible after the vomiting episode. Administer the next dose at the regularly scheduled time. 
  * If a patient misses a dose at the scheduled time, administer that dose of VISTOGARD as soon as possible. Administer the next dose at the regularly scheduled time. 
  * Administer VISTOGARD via a nasogastric tube (NG tube) or gastrostomy tube (G-Tube) when necessary (eg, severe mucositis or coma). Follow the instructions below for each dose administration: 
    1. Prepare approximately 4 fluid ounces (about 100 mL) of a food starch-based thickening product in water and stir briskly until the thickener has dissolved. 
    2. Crush the contents of one full 10 gram packet of VISTOGARD granules to a fine powder. 
    3. Add the crushed VISTOGARD granules to 4 ounces (about 100 mL) of the reconstituted food starch-based thickening product. For pediatric patients receiving less than 10 grams, prepare the mixture at a ratio of no greater than 1 gram per 10 mL of reconstituted food starch-based thickening product and mix thoroughly. 
    4. After administration of the mixture using the NG tube or G-Tube, flush the tube with water.
Full Intervention participants will meet twice per week for one hour each time, for approximately 6 months. Participants will learn and practice good nutrition and physical activity for improved individual, family and community health.
Procedure for obtaining styrene resins of ionic, anionic and atoxic exchange. Polymerize at low speed a mixture of monomers, containing 1.5 to 2.5 per 100 of divinil compound, in the presence of a polymerization catalyst constituted by an organic peroxide at a concentration of 0.3 to 3 per 100, at a polymerization temperature of 50 to 80gc. The compound of divinil that is polymerized is divinylbenzene. The resins that are obtained have an apparent density in water of 0.18 to 0.20 gr. Of dry material/cc, and a capacity of absorption of water of 69 to 73 per 100 in weight of the polymer, with a reticulation ratio of 1.5-2.5 per 100 and a power of exchange of 2.8 to 4, 0 meq/gr. Cholesterol rebuilding activity. M (Machine-translation by Google Translate, not legally binding)
Group B included Graston Technique to Upper Trapezius and Levator Scapulae.This instrumented-assisted soft tissue massage applied with deeper pressure to the area of concern.The protocol consist of Longitudinal stroking parallel to muscle fiber for 1min , spin over trigger points for 1 min using knob of instrument and fanning for 2 min Hot pack placed over the painful area in cervical region before the treatment ( 20 minutes).Strengthening exercises for deep neck flexors, rhomboids, lower trapezius and serratus anterior due to weak muscles (2 sets of 10 repetitions once a day) Stretching exercises for pectoralis muscles (20-second hold, 5 repetitions). This exercise protocol was for 4 weeks and 3 sessions per week. Measurements taken at baseline level and at the END of treatment , i.e. ROM, pain intensity by NPRS and PPT , functional disability.
This study design is a prospective randomized control trial to compare outcomes between the utilization of coronary computed tomography angiography (CCTA) vs conservative treatment in type 2 NSTEMI. The targeted population is expectedly heterogeneous and inpatient setting who are admitted and diagnosed with type 2 NSTEMI. Patients are randomized into 2 groups. Group 1 undergoes coronary 64-detector row computed tomography angiography (CCTA) and Group 2 receives conservative management and treatment for underlying conditions. The investigators will evaluate cross-sectional and time-varying clinical, laboratory, and imaging characteristics in association with clinical events. The exclusion criteria are an absence of information for follow-up of clinical events, and patients who have absolute and relative contraindications for CCTA. Absolute contraindications are a patient history of severe or anaphylactic reaction to iodinated contrast, inability to cooperate with scan protocols, hemodynamic instability, decompensated heart failure, acute myocardial infarction, and renal impairment with GFR \< 30. Relative contraindications include pregnancy, inability to tolerate heart rate-slowing medications or nitroglycerin, recent phosphodiesterase inhibitor use, severe aortic stenosis, bronchospastic disease, and patient's weight and height.
BACKGROUND: The minimal clinically important difference (MCID) is the smallest change in outcome that physicians or patients would consider meaningful and is relevant when evaluating disease progression or the efficacy of interventions. Studies of patients with late-onset Pompe disease (LOPD) have used the 6-min walk distance (6MWD) as an endpoint to assess motor function. However, an MCID for 6MWD (% predicted and meters) has yet to be established in LOPD. The objective of the study was to derive 6MWD MCID (% predicted and meters) with different analysis methods and for subgroups of different disease severity for LOPD.
METHODS: Data from the PROPEL trial were used to calculate 6MWD MCID in the overall PROPEL population and subgroups of baseline severity as assessed by walking distance and body mass index (BMI), using anchor- and distribution-based approaches.
RESULTS: The 6MWD MCIDs varied widely, depending on the method and subgroup, ranging from 2.27%-8.11% predicted for the overall LOPD population (23.7 m-57.2 m). For patients with baseline 6MWD < 150 m, MCIDs ranged from -0.74%-3.37% (-2.1 m-11.3 m). MCIDs increased with distance walked at baseline until a plateau was reached. For BMI subgroups, the MCIDs were generally lowest in obese patients.
CONCLUSION: Our analysis shows that MCID depends on the chosen method and disease severity. The findings suggest that applying a single MCID to all patients can be misleading; consequently, a range of possible MCIDs should be considered. This may also be highly relevant for other neuromuscular diseases. This study provides a range of 6MWD MCIDs for LOPD, with lower MCIDs for more severe patients.
Sensorcaine ® (bupivacaine HCl) injections are sterile isotonic solutions that contain a local anesthetic agent with and without epinephrine (as bitartrate) 1:200,000 and are administered parenterally by injection. See INDICATIONS AND USAGE for specific uses. Solutions of bupivacaine HCl may be autoclaved if they do not contain epinephrine. 

Sensorcaine injections contain bupivacaine HCl which is chemically designated as 2- piperidinecarboxamide, 1-butyl- N-(2,6-dimethylphenyl)-, monohydrochloride, monohydrate and has the following structure: 

Epinephrine is (-)-3,4-Dihydroxy-α [(methylamino)methyl] benzyl alcohol. It has the following structural formula: 

The pK a of bupivacaine (8.1) is similar to that of lidocaine (7.86). However, bupivacaine possesses a greater degree of lipid solubility and is protein bound to a greater extent than lidocaine. 

Bupivacaine is related chemically and pharmacologically to the aminoacyl local anesthetics. It is a homologue of mepivacaine and is chemically related to lidocaine. All three of these anesthetics contain an amide linkage between the aromatic nucleus and the amino, or piperidine group. They differ in this respect from the procaine-type local anesthetics, which have an ester linkage.
A method and system for producing petroleum jelly from hydrocarbons. The method converts the hydrocarbon source into a synthesis gas. The synthesis gas is converted into at least a light-hydrocarbons stream and a heavy-hydrocarbons stream, which both include a plurality of paraffins and a plurality of olefins. The plurality of paraffins is reacted with the plurality of olefins in the presence of a dialkyl peroxide initiator to form the petroleum jelly. A synthesis gas production system is adapted to produce a synthesis gas from at least a natural gas source. A hydrocarbon conversion system is adapted to produce heavier hydrocarbons from at least the synthesis gas, the heavier hydrocarbons containing at least a plurality of paraffins and a plurality of olefins. A petroleum-jelly production system is adapted to convert the produced heavier hydrocarbons into petrolatum.
Naproxen is rapidly and completely absorbed from the gastrointestinal tract with an in vivo bioavailability of 95%. The elimination half-life of naproxen ranges from 12 to 17 hours. Steady-state levels of naproxen are reached in 4 to 5 days, and the degree of naproxen accumulation is consistent with this half-life.

###  Absorption 

After administration of naproxen tablets, peak plasma levels are attained in 2 to 4 hours.

###  Distribution 

Naproxen has a volume of distribution of 0.16 L/kg. At therapeutic levels naproxen is greater than 99% albumin-bound. At doses of naproxen greater than 500 mg/day there is less than proportional increase in plasma levels due to an increase in clearance caused by saturation of plasma protein binding at higher doses (average trough Css 36.5, 49.2 and 56.4 mg/L with 500, 1000 and 1500 mg daily doses of naproxen, respectively). The naproxen anion has been found in the milk of lactating women at a concentration equivalent to approximately 1% of maximum naproxen concentration in plasma (see PRECAUTIONS: Nursing Mothers). 

###  Metabolism 

Naproxen is extensively metabolized in the liver to 6-0-desmethyl naproxen, and both parent and metabolites do not induce metabolizing enzymes. Both naproxen and 6-0-desmethyl naproxen are further metabolized to their respective acylglucuronide conjugated metabolites.

###  Excretion 

The clearance of naproxen is 0.13 mL/min/kg. Approximately 95% of the naproxen from any dose is excreted in the urine, primarily as naproxen (<1%), 6-0-desmethyl naproxen (<1%) or their conjugates (66% to 92%). The plasma half-life of the naproxen anion in humans ranges from 12 to 17 hours. The corresponding half-lives of both naproxen’s metabolites and conjugates are shorter than 12 hours, and their rates of excretion have been found to coincide closely with the rate of naproxen disappearance from the plasma. Small amounts, 3% or less of the administered dose, are excreted in the feces. In patients with renal failure metabolites may accumulate (see WARNINGS: Renal Effects).
Intercostobrachial nerve preserving axillary lymph node dissection will be carried out. Post-operatively, the patients will be monitored in the post anesthesia care unit (PACU). Acute Post-Operative pain will be controlled using a standardized pain management regimen in accordance with World Health Organization (WHO) analgesia ladder. The patients will be discharged from PACU and admitted to surgical ward once numerical rating score (NRI) is below 4.
Frostbite, a debilitating condition, significantly affects the well-being of military veterans and high-altitude residents, causing severe clinical complications such as chronic pain that markedly impacts overall quality of life. There has been a notable increase in the development of pre-clinical models for studying frostbite injury, but their suitability for pain evaluation remains limited. The major hurdle in the development of novel therapeutics for the treatment of frostbite-induced chronic pain is the unavailability of well-established preclinical models. In this study, we employed deep-frozen magnets to induce frostbite injury and conducted validation for chronic pain through assessments of face, predictive, and mechanistic validity. Behavioral assays demonstrated that frostbite injury exhibited significant mechanical, thermal & cold hypersensitivity in rats. Further, molecular analysis indicated that frostbite injury triggered the activation of TRP channels (TRPA1, TRPV1 and TRPM8), microgliosis, and neuroinflammation in the dorsal root ganglion (DRG) and spinal cord of rats. Notably, NR2B protein expressions were significantly upregulated in the DRG of injured rats, while no changes were observed in spinal NR2B expressions. Furthermore, the administration of ibuprofen (25, 50, and 100 mg/kg, i.p.) resulted in a significant improvement in behavioral, biochemical, and molecular alterations in frostbite-injured rats. Overall, results suggested that established frostbite model effectively recapitulates face, pharmacological, and mechanistic validity, highlighting its potential for screening future treatment modalities and exploring the intricate mechanisms associated with frostbite-induced chronic pain.