anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Optimal risk stratification of patients with cancer and pulmonary embolism (PE) remains unclear. We constructed a clinical prediction rule (CPR) named 'MAUPE-C' to identify patients with low 30 days mortality. The study retrospectively developed and internally validated a CPR for 30 days mortality in a cohort of patients with cancer and PE (both suspected and unsuspected). Candidate variables were chosen based on the EPIPHANY study, which categorized patients into 3 groups based on symptoms, signs, suspicion and patient setting at PE diagnosis. The performance of 'MAUPE-C' was compared to RIETE and sPESI scores. Univariate analysis confirmed that the presence of symptoms, signs, suspicion and inpatient diagnosis were associated with 30 days mortality. Multivariable logistic regression analysis led to the exclusion of symptoms as predictive variable. 'MAUPE-C' was developed by assigning weights to risk factors related to the β coefficient, yielding a score range of 0 to 4.5. After receiver operating characteristic (ROC) curve analysis, a cutoff point was established at ≤ 1. Prognostic accuracy was good with an area under the curve (AUC) of 0.77 (95% CI 0.71-0.82), outperforming RIETE and sPESI scores in this cohort (AUC of 0.64 [95% CI 0.57-0.71] and 0.57 [95% CI 0.49-0.65], respectively). Forty-five per cent of patients were classified as low risk and experienced a 2.79% 30 days mortality. MAUPE-C has good prognostic accuracy in identifying patients at low risk of 30 days mortality. This CPR could help physicians select patients for early discharge.
EN3835 0.84 mg (Collagenase Clostridium Histolyticum). Each subject can receive up to three treatment sessions. Each treatment session will be separated by approximately 21 days.
A calorie monitoring device is provided for providing a visual output which compares the number of calories burned by an individual versus the calorie intake for the individual. The device has a keyboard which functions as a first input to input the calorie intake of the individual. The calorie intake input is applied to a first calculator through an interface and the calculator adds the calorie intake input to the total calorie intake in storage and displays the new total calorie intake. The keyboard also functions as a second input to receive a value indicative of the calories burned per unit of time for the individual under normal conditions. This value is applied to a second calculator through the interface circuit. The second calculator calculates and displays the total number of calories burned during a total time period which extends over a plurality of the predetermined time periods. Thus, the second calculator provides an output which is a real time display of the total calories burned by the individual. 
     The device also includes an exercise mode circuit which controls the second calculator to add, to the total calories burned, additional calories when the individual exercises. The exercise mode circuit can be adjusted to add calories burned which are indicative of the level of exercise being performed.
Participants in this arm will receive a physical activity program delivered by DVD that focuses on exercises targeting flexibility, toning and balance. These exercises will be progressive in nature throughout the six months and will also focus on modifications for all ability levels. Participants will be provided with three DVDs including: an Introduction to physical activity, Sessions 1-3, and Sessions 4-6, which they will be asked to watch and participate in over the course of six months.
Kidney transplantation is the preferred treatment for end-stage renal disease (ESRD) given improved quality of life, longer survival and lower costs compared with chronic dialysis. Despite these long-term benefits, the first year post-transplant is a critical period that influences health care costs for transplantation and long-term patient and allograft survival. The two most common complications in the first year are delayed graft function (DGF), which affects nearly 25% of deceased-donor transplants, and acute allograft rejection, which affects nearly 10% of all transplants (deceased and living donor). DGF is most commonly caused by severe ischemia-reperfusion injury at transplantation and is a known risk factor for acute rejection and premature failure. Driven by an ever-growing transplant waiting list and limited organs, efforts to utilize higher-risk kidneys for increasingly higher-risk recipients may further increase these complication rates. While treatments exist for DGF and acute rejection, the current diagnostic paradigm is to obtain a duplex ultrasound (DUS) of the allograft, based on serial changes in serum creatinine, and then proceed to biopsy if there is clinical concern for rejection. Biopsy is the gold standard to differentiate between causes of allograft dysfunction, but the procedure is invasive and typically takes 24 hours or longer for an interpretation. Thus, early detection of these complications using non-invasive diagnostic methods (a major transplant research goal) could reduce our reliance on biopsies and help improve long-term patient and allograft survival.

Researchers in the United States have safely performed contrast-enhanced ultrasounds of the kidney in healthy participants, and radiologists have used ultrasound contrast agents off-label to better visualize organs other than the heart when clinically indicated. In terms of kidney transplants, European data suggest CEUS of the allograft on post-operative day (POD) 7 is superior to DUS for predicting 12-month allograft function, but there are no published studies using CEUS on POD 1 to diagnose DGF or acute rejection.

The pathophysiology of both DGF and acute rejection involve interactions between the microvasculature, parenchymal cells and inflammatory cells, though with differences in timing and within different zones of the kidney itself. A very important feature of CEUS is its capacity to measure microvascular perfusion, whereas DUS can only estimate flow within larger vessels. This potential innovation for assessing the renal macro- and microvasculature may allow for earlier non-invasive detection of DGF and acute rejection. With additional research, it may ultimately be shown that non-invasive CEUS will revolutionize early DGF and acute rejection diagnosis to enable improvement in long-term patient and allograft survival.
Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogs, including VIREAD, a component of TRUVADA, in combination with other antiretrovirals [See Warnings and Precautions (5.1)].

TRUVADA is not approved for the treatment of chronic hepatitis B virus (HBV) infection and the safety and efficacy of TRUVADA have not been established in patients coinfected with HBV and HIV-1. Severe acute exacerbations of hepatitis B have been reported in patients who are coinfected with HBV and HIV-1 and have discontinued TRUVADA. Therefore, hepatic function should be monitored closely with both clinical and laboratory follow-up for at least several months in patients who are infected with HBV and discontinue TRUVADA. If appropriate, initiation of anti-hepatitis B therapy may be warranted [See Warnings and Precautions (5.2)].

TRUVADA used for a PrEP indication must only be prescribed to individuals confirmed to be HIV-negative immediately prior to initiating and periodically (at least every 3 months) during use. Drug-resistant HIV-1 variants have been identified with use of TRUVADA for a PrEP indication following undetected acute HIV-1 infection. Do not initiate TRUVADA for a PrEP indication if signs or symptoms of acute HIV-1 infection are present unless negative infection status is confirmed [See Warnings and Precautions (5.9)].
During clinical studies in Dupuytren’s contracture and Peyronie’s disease, patients were tested at multiple time points for antibodies to the protein components of XIAFLEX (AUX-I and AUX-II).

In the Dupuytren’s contracture clinical studies (Studies 1 and 2), at 30 days post the first injection of XIAFLEX 0.58 mg, 92% of patients had antibodies against AUX-I detected and 86% of patients had antibodies against AUX-II detected. After the fourth injection of XIAFLEX, every XIAFLEX-treated patient developed high titers of antibodies to both AUX-I and AUX-II. After 5 years more than 90% of patients remained seropositive for anti-AUX-I and anti-AUX-II antibody (Study 4). Neutralizing antibodies were assayed for all patients (204) in Study 1. Neutralizing antibodies to AUX-I or AUX-II, were detected in 10% and 21%, respectively, of patients treated with XIAFLEX. Among patients in Study 3 who reported no prior exposure to XIAFLEX, 97% of patients had antibodies against AUX-I and AUX-II after two concurrent doses of XIAFLEX 0.58 mg (total dose of 1.16 mg) in the same hand. In Study 5, treatment of recurrent contractures with XIAFLEX resulted in similar immunogenicity results as seen in Studies 1 and 2.

In the Peyronie’s disease clinical studies, at 6 weeks after the first treatment cycle of XIAFLEX 0.58 mg, approximately 75% of patients had antibodies against AUX-I and approximately 55% of patients had antibodies against AUX-II. Six weeks after the eighth injection (fourth treatment cycle) of XIAFLEX, >99% of XIAFLEX-treated patients developed high titers of antibodies to both AUX-I and AUX-II. Neutralizing antibodies were assayed for a subset of 70 samples selected to be representative of high and low titer binding antibody responses at Week 12 of treatment. For each subject in whom a Week 12 sample was selected, the corresponding Week 6, 18, 24, and 52 samples were assayed if they were also binding antibody positive. Neutralizing antibodies to AUX-I or AUX-II, were detected in 60% and 51.8%, respectively, of patients tested. 

In patients treated for these two indications, there was no apparent correlation of antibody frequency, antibody titers, or neutralizing status to clinical response or adverse reactions.

Since the protein components in XIAFLEX (AUX-I and AUX-II) have some sequence homology with human matrix metalloproteinases (MMPs), anti-product antibodies could theoretically interfere with human MMPs. In vitro studies showed no evidence of cross-reactivity between anti-drug-antibody positive patient sera and a series of relevant MMPs. In addition, no clinical safety concerns related to the inhibition of endogenous MMPs have been observed. 

Immunogenicity assay results are highly dependent on the sensitivity and specificity of the assay used in detection and may be influenced by several factors, including sample handling, timing of sample collection, concomitant medications, and underlying disease. For these reasons, comparison of incidence of antibodies to collagenase clostridium histolyticum with the incidence of antibodies to other products may be misleading.
PURPOSE:To obtain a dental material having low odor, low irritation and low water-absorption of polymer and giving a proper glutinous period when mixed with a powdery polymer by compounding a specific methacrylic acid ester compound. CONSTITUTION:The dental material is produced by compounding a methacrylic acid ester compound of formula I (m is 0 or integer of >=1; n is integer of >=1; m+n is integer of >=2; R is H or methyl) (e.g. the compound of formula II or formula III). The compound of formula 1 is preferably further compounded with a polyfunctional methacrylate copolymerizable with the compound of formula I (e.g. ethylene glycol dimethacrylate or 1,6-hexanediol dimethacrylate). The material does not cause discomfortable feeling such as malodor and irritation of mucous membrane, etc. It has excellent durability of the dimension, strength, color, etc., in the palate as a cured material and is usable for a long period.
Immune cells and interleukins play a crucial role in female-specific pain signaling. Interleukin 16 (IL-16) is a cytokine primarily associated with CD4+ T cell function. While previous studies have demonstrated the important role of spinal CD4+ T cells in neuropathic pain, the specific contribution of IL-16 to neuropathic pain remains unclear. In this study, by using a spinal nerve ligation (SNL)-induced neuropathic pain mice model, we found that SNL induced an increase in IL-16 mRNA levels, which persisted for a longer duration in female mice compared to male mice. Immunofluorescence analysis further confirmed enhanced IL-16- and CD4-positive signals in the spinal dorsal horn following SNL surgery in female mice. Knockdown of spinal IL-16 by siRNA or inhibition of CD4 by FGF22-IN-1, a CD4 inhibitor, attenuated established mechanical and thermal pain hypersensitivity induced by SNL. Furthermore, female mice injected with IL-16 intrathecally exhibited significant spontaneous pain, mechanical and thermal hyperalgesia, all of which could be alleviated by FGF22-IN-1 or a CD3 antibody. Additionally, IL-16 induced astrocyte activation but not microglial activation in the spinal dorsal horn of female mice. Meanwhile, astrocyte activation could be suppressed by the CD3 antibody. These results provide compelling evidence that IL-16 promotes astrocyte activation via CD4 on CD3+ T cells, which is critical for maintaining neuropathic pain in female mice.
All participants who complete Part 1, and who meet eligibility criteria for Part 2, as well as direct entry participants, will enter Part 2 of the study. Participants who achieve a stable response during the open-label phase will receive treatment with seltorexant orally once daily during DB Maintenance Phase in Part 2 of the study. Participants will continue to take their single baseline SSRI/SNRI antidepressant throughout the study.
Patients receive CXCR4 antagonist BL-8040 SC on days 1-5 and 8-12 of cycle 1 and days 1, 4, 8, and 11 of subsequent cycles. Beginning cycle 2, patients also receive pembrolizumab IV over about 30 minutes on day 1. Cycles repeat every 21 days for up to 1 year in the absence of disease progression or unacceptable toxicity.
This is a prospective, phase II single center one arm, open label clinical trial testing the efficacy and feasibility of a combination salvage therapy with Venetoclax and intensified Decitabine in relapsed or refractory AML and MDS IB2. Enrolled will be twenty-seven patients with newly diagnosed AML and primary induction failure to conventional anthracycline-based induction chemotherapy, as well as patients with a relapse of AML oder MDS IB2 after chemotherapy. Patients will receive a combination therapy of ten days of Decitabine and twenty-eigt days of Venetoclax. If hematologic remission is not achieved after one cycle of treatment, patients receive a second cycle. After treatment, a follow-up period of 100 days will ensue. The main aim of the trial is the assessment of hematologic remission after combining Venetoclax with a time-dense immediate application of the hypomethylating agent Decitabine after failure of a chemotherapy approach, thus additionally altering backbone treatment modalities from chemotherapy to epigenetic and anti-BCL2 (B-cell lymphoma 2) treatment. A first assessment of safety and feasibility will take place after the treatment of three patients and a second assessment for safety, feasibility and efficacy/futility after nine patients.
Increased exposure to PAA, the major metabolite of RAVICTI, may be associated with neurotoxicity in patients with UCDs. In a study of adult cancer patients, subjects received sodium phenylacetate administered as a 1-hour infusion twice daily at two dose levels of 125 and 150 mg/kg for a 2-week period. Of 18 subjects enrolled, 7 had a history of primary central nervous system tumor. Signs and symptoms of potential PAA neurotoxicity, which were reversible, were reported at plasma PAA concentrations above 500 micrograms/mL and included somnolence, fatigue, lightheadedness, headache, dysgeusia, hypoacusis, disorientation, impaired memory, and exacerbation of preexisting neuropathy. PAA concentrations were not measured when symptoms resolved. 

In healthy subjects, after administration of 4 mL and 6 mL RAVICTI 3 times daily (13.2 g/day and 19.8 g/day, respectively) for 3 days, a dose-dependent increase in non-serious nervous system adverse reactions were observed. In subjects who had nervous system adverse reactions, plasma PAA concentrations, which were measured on Day 3 per protocol and not always at onset of symptoms, ranged from 8 to 56 micrograms/mL with 4 mL RAVICTI 3 times daily and from 31 to 242 micrograms/mL with 6 mL RAVICTI 3 times daily. 

In clinical trials in patients with UCDs who had been on sodium phenylbutyrate prior to administration of RAVICTI, adverse reactions of headache, fatigue, symptoms of peripheral neuropathy, seizures, tremor and/or dizziness were reported. No correlation between plasma PAA concentration and neurologic symptoms was identified but plasma PAA concentrations were generally not consistently measured at the time of neurologic symptom occurrence [see Clinical Pharmacology (12.3)]. 

If symptoms of vomiting, nausea, headache, somnolence or confusion are present in the absence of high ammonia or other intercurrent illness which explains these symptoms, consider the potential for PAA neurotoxicity which may need reduction in the RAVICTI dosage [see Dosage and Administration (2.4)].
Montelukast sodium 4 mg oral granules can be administered either directly in the mouth, dissolved in 1 teaspoonful (5 mL) of cold or room temperature baby formula or breast milk, or mixed with a spoonful of cold or room temperature soft foods; based on stability studies, only applesauce, carrots, rice, or ice cream should be used. The packet should not be opened until ready to use. After opening the packet, the full dose (with or without mixing with baby formula, breast milk, or food) must be administered within 15 minutes. If mixed with baby formula, breast milk, or food, montelukast sodium oral granules must not be stored for future use. Discard any unused portion. Montelukast sodium oral granules are not intended to be dissolved in any liquid other than baby formula or breast milk for administration. However, liquids may be taken subsequent to administration. Montelukast sodium oral granules can be administered without regard to the time of meals.
AIM: Rotator cuff tears (RCTs) are a major cause of shoulder pain and disability, affecting millions worldwide. Understanding the risk factors and developing reliable predictive measures for RCTs is essential for early diagnosis, targeted prevention, and effective treatment of this patient population. This study seeks to enhance our understanding by analyzing the acromiohumeral distance (AHD) and Constant-Murley Score (CMS) in patients with and without RCTs, thereby aiding the development of a predictive model aimed at improving clinical outcomes and prevention strategies in rotator cuff pathology.
METHODS: This retrospective analysis involved 201 patients with shoulder pain, categorized into RCT (n = 72) and no RCTs (N-RCTs, n = 129) groups based on Magnetic Resonance Imaging (MRI) findings. We compared demographics, AHD, CMS, and rotator cuff status between groups and utilized logistic regression for identifying RCT predictors, leading to the development of a multifactorial predictive model.
RESULTS: The mean AHD was 6.60 ± 1.12 mm. The RCT group showed a marginally higher AHD than the N-RCT group (p = 0.669). CMS scores were significantly lower in the RCT group (p < 0.001). Dominant side involvement (Odds Ratio (OR) 2.244), type III acromion (OR 6.106), and lower CMS (OR 0.938) significantly correlated with RCTs. The predictive model demonstrated an area under the curve (AUC) of 0.701 for RCT diagnosis.
CONCLUSIONS: Reduced CMS, dominance of the affected side, and type III acromion emerged as key risk factors for RCTs. Our predictive model, incorporating these factors, holds promise for RCT diagnosis, with future studies needed for further validation.
Process for enzymatic isolation of aminoacid and peptide solns. of animal origin, by removal of the fatty constituents of an aqueous soln. of animal origin by extn. or centrifugation and then adjustment of the temp. and pH to an appropriate value and elimination of the formed-sediment by filtration or centrifugation. Treatment of nerve cell disorders by intramuscular injection of the peptide-aminoacid soln. e.g. tests show the solns. reverse the effects of neuro-toxic agents, such as nitrofurantoine or acrylamide and their regeneration capacity is greater than that of coenzyme B12. Tests show the solns. have no specific antiinflammatory or analgesic activity. The solns. may be used as solvents for other therapeutic substances having metabolic activity on neurones, such as vitamins B1, B6 or B12 etc.
Exercise has long been acknowledged for its powerful disease-preventing, health-promoting effects. However, the cellular and molecular mechanisms responsible for the beneficial effects of exercise are not fully understood. Inflammation is a component of the stress response to exercise. Recent work has revealed that such inflammation is not merely a symptom of exertion; rather, it is a key regulator of exercise adaptations, particularly in skeletal muscle. The purpose of this piece is to provide a conceptual framework that we hope will integrate exercise immunology with exercise physiology, muscle biology, and cellular immunology. We start with an overview of early studies in the field of exercise immunology, followed by an exploration of the importance of stromal cells and immunocytes in the maintenance of muscle homeostasis based on studies of experimental muscle injury. Subsequently, we discuss recent advances in our understanding of the functions and physiological relevance of the immune system in exercised muscle. Finally, we highlight a potential immunological basis for the benefits of exercise in musculoskeletal diseases and aging.
Rates of obesity are increasing world-wide with an estimated 1billion people projected to be obese by 2030 if current trends remain unchanged. Obesity currently considered one of the most significant associated factors of non-communicable diseases poses the greatest threat to health. Diabetes mellitus is an important metabolic disorder closely associated with obesity. It is therefore expected that with the increasing rates of obesity, the rates of diabetes in pregnancy will also be rising. This disorder may pre-date pregnancy (diagnosed or undiagnosed and diagnosed for the first time in pregnancy) or may be of onset in pregnancy. Irrespective of the timing of onset, diabetes in pregnancy is associated with both fetal and maternal complications. Outcomes are much better if control is maximised. Early diagnosis, multidisciplinary care and tailored management with optimum glycaemic control is associated with a significant reduction in not only pregnancy complications but long-term consequences on both the mother and offspring. This review brings together the current understanding of the pathogenesis of the endocrine derangements that are associated with diabetes in pregnancy how screening should be offered and management including pre-pregnancy care and the role of newer agents in management.