anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND & AIMS: Dynapenia and obesity have been independently associated with cognitive decline in older adults, but their co-occurring effects has not been well-studied. The study objective is to examine the relationship between dynapenic-obesity and cognitive impairment in older adults 75 years and older with normal or high cognitive function at baseline over 12 years of follow-up. We hypothesize that those with dynapenic obesity will have greater odds of cognitive function impairment than those with dynapenia only, obesity only, or no dynapenia no obesity (reference group).
METHODS: A total of 761 participants with a mean age of 81.5 and Mini-Mental State Examination (MMSE) > 21 at baseline were divided into four groups: no dynapenia no obesity (n = 316), obesity only (n = 142), dynapenia only (n = 217), and dynapenic obesity (n = 86). Measures included socio-demographics, medical conditions, body mass index, depressive symptoms, handgrip strength, and limitations in activities of daily living. We performed a mixed models estimate for cognitive decline for these groups over a 12-year period. Handgrip strength (HGS) was measured with a handgrip dynamometer and cognitive function was assessed with MMSE.
RESULTS: Participants in the dynapenia-obesity group experienced a greater (β = - 1.29, Standard Error = 0.60, p-value = 0.0316) cognitive decline over time compared to those in the no dynapenia and no obesity group, after controlling for all covariates.
CONCLUSION: Older adults with dynapenic-obesity were at high risk of cognitive decline over time. These findings highlight the need for interventions that target both conditions in this population to help maintain cognitive health. Community-based strength training programs and educational initiatives on nutrition and diet can help older adults reduce their risk of age-related cognitive decline.
Empagliflozin (Jardiance) 10mg is an SGLT-2inhibitor. The drug will be taken qd for 4 weeks.
Cortical myoclonus is produced by abnormal neuronal discharges within the sensorimotor cortex, as demonstrated by electrophysiology. Our hypothesis is that the loss of cerebellar inhibitory control over the motor cortex, via cerebello-thalamo-cortical connections, could induce the increased sensorimotor cortical excitability that eventually causes cortical myoclonus. To explore this hypothesis, in the present study we applied anodal transcranial direct current stimulation over the cerebellum of patients affected by cortical myoclonus and healthy controls and assessed its effect on sensorimotor cortex excitability. We expected that anodal cerebellar transcranial direct current stimulation would increase the inhibitory cerebellar drive to the motor cortex and therefore reduce the sensorimotor cortex hyperexcitability observed in cortical myoclonus. Ten patients affected by cortical myoclonus of various aetiology and 10 aged-matched healthy control subjects were included in the study. All participants underwent somatosensory evoked potentials, long-latency reflexes and short-interval intracortical inhibition recording at baseline and immediately after 20 min session of cerebellar anodal transcranial direct current stimulation. In patients, myoclonus was recorded by the means of surface EMG before and after the cerebellar stimulation. Anodal cerebellar transcranial direct current stimulation did not change the above variables in healthy controls, while it significantly increased the amplitude of somatosensory evoked potential cortical components, long-latency reflexes and decreased short-interval intracortical inhibition in patients; alongside, a trend towards worsening of the myoclonus after the cerebellar stimulation was observed. Interestingly, when dividing patients in those with and without giant somatosensory evoked potentials, the increment of the somatosensory evoked potential cortical components was observed mainly in those with giant potentials. Our data showed that anodal cerebellar transcranial direct current stimulation facilitates-and does not inhibit-sensorimotor cortex excitability in cortical myoclonus syndromes. This paradoxical response might be due to an abnormal homeostatic plasticity within the sensorimotor cortex, driven by dysfunctional cerebello-thalamo-cortical input to the motor cortex. We suggest that the cerebellum is implicated in the pathophysiology of cortical myoclonus and that these results could open the way to new forms of treatment or treatment targets.
BACKGROUND: Estimates of proportions of people with migraine who report premonitory symptoms vary greatly among previous studies. Our aims were to establish the proportion of patients reporting premonitory symptoms and its dependency on the enquiry method. Additionally, we investigated the impact of premonitory symptoms on disease burden using Headache Impact Test (HIT-6), Migraine Disability Assessment (MIDAS) and World Health Organization Disability Assessment 2.0 (WHODAS 2.0), whilst investigating how various clinical factors influenced the likelihood of reporting premonitory symptoms.
METHODS: In a cross-sectional study, premonitory symptoms were assessed among 632 patients with migraine. Unprompted enquiry was used first, followed by a list of 17 items (prompted). Additionally, we obtained clinical characteristics through a semi-structured interview.
RESULTS: Prompted enquiry resulted in a greater proportion reporting premonitory symptoms than unprompted (69.9% vs. 43.0%; p < 0.001) and with higher symptom counts (medians 2, interquartile range = 0-6 vs. 1, interquartile range = 0-1; p < 0.001). The number of symptoms correlated weakly with HIT-6 (ρ = 0.14; p < 0.001) and WHODAS scores (ρ = 0.09; p = 0.041). Reporting postdromal symptoms or triggers increased the probability of reporting premonitory symptoms, whereas monthly migraine days decreased it.
CONCLUSIONS: The use of a standardized and optimized method for assessing premonitory symptoms is necessary to estimate their prevalence and to understand whether and how they contribute to disease burden.
An in vitro model of a blood-brain barrier comprising a porous solid support upon which is disposed an essentially confluent monolayer of brain microvascular endothelial cells in contact with agents that elevate effective cyclic AMP concentrations in endothelial cells, with or without astrocyte-derived or endothelial cell-derived conditioned medium or the equivalent so that high electrical resistance tight junctions are formed between endothelial cells, and endothelial cells exhibit peripheral phalloidin staining and E-cadherin. Also disclosed is the use of agents that reduce effective cyclic AMP concentrations or interfere with the functioning of cyclic AMP or increase effective cyclic GMP concentrations to open up blood-brain barriers in vitro and in vivo, so that drugs normally excluded by such barriers may substantially penetrate such barriers. Also disclosed are uses of the model to screen for reagents with clinical utility in disorders involving brain endothelial cells. The prevention, treatment, and amelioration of a pathology characterized by brain inflammation are described herein. Uses of agents that inhibit binding of VLA-4 to brain endothelial receptor VCAM-1 are included. These agents may be antibodies, peptides, peptidomimetics, or related compounds.
Luminal cholecystokinin-releasing factor (LCRF) is a cholecystokinin (CCK) releasing protein isolated from rat intestinal secretion. Purified LCRF was characterized by molecular weight, partial amino acid sequence and CCK  releasing activity as shown in in vivo studies of anti-LCRF antibodies in blocking the CCK releasing effect of LCRF. Binding studies demonstrated localization in the duodenum, pancreas and in nerve fibers throughout the pancreas, sensory fibers and cell bodies of the nodose ganglia as well as in sympathetic nerve fibers in the adrenal medulla. LCRF appears to be a neuropeptide present in the enteric, parasympathetic and sympathetic nervous systems, but not in the brain. LCRF-IR is also present in enterocytes at the tips of small intestinal villi. Taken together, the studies indicate that LCRF  is a neuropeptide that may have several functions in the gastrointestinal systems and other systems. Immunoaffinity studies using antibodies raised to synthetic LCRF1-6 and small intestinal lumen infusion studies indicate LCRF  may be the CCK-releasing peptide present in intestinal secretion that mediates negative feedback regulation of pancreatic enzyme secretion and CCK release.  LCRF and functionally related species have potential for development for treatment of insulin secretion, gastric and gallbladder emptying and regimens requiring appetite control or suppression.
Venlafaxine hydrochloride extended-release capsules are indicated for the treatment of Generalized Anxiety Disorder (GAD) as defined in DSM-IV. Anxiety or tension associated with the stress of everyday life usually does not require treatment with an anxiolytic. 

The efficacy of venlafaxine hydrochloride extended-release capsules in the treatment of GAD was established in 8-week and 6-month placebo-controlled trials in adult outpatients diagnosed with GAD according to DSM-IV criteria (see Clinical Trials). 

Generalized Anxiety Disorder (DSM-IV) is characterized by excessive anxiety and worry (apprehensive expectation) that is persistent for at least 6 months and which the person finds difficult to control. It must be associated with at least 3 of the following 6 symptoms: restlessness or feeling keyed up or on edge, being easily fatigued, difficulty concentrating or mind going blank, irritability, muscle tension, sleep disturbance. 

Although the effectiveness of venlafaxine hydrochloride extended-release capsules have been demonstrated in 6-month clinical trials in patients with GAD, the physician who elects to use venlafaxine hydrochloride extended-release capsules for extended periods should periodically re-evaluate the long-term usefulness of the drug for the individual patient (see DOSAGE AND ADMINISTRATION).
Patients with orbital injuries are entered into the trial. Age: 20 - 70. After obtaining appropriate consent, they are entered into either a control arm where reconstruction of the orbit is done with a titanium mesh (established practice) or the experimental arm where reconstruction is by a bioresorbable implant made of polycaprolactone. Patients are followuped at 1 week, 1 month, 3 months, 6 months \& 12 months. CT scan of the orbits are performed preop, 6 months \& 12 months. End point is the 12 month follow-up appointment. Visual acuity, range of motion, enophthalmos \& diplopia are assessed in follow-up.
Losartan potassium tablet is a prescription medicine called an angiotensin receptor blocker (ARB). It is used: 

  * alone or with other blood pressure medicines to lower high blood pressure (hypertension). 
  * to lower the chance of stroke in patients with high blood pressure and a heart problem called left ventricular hypertrophy. Losartan potassium tablets may not help Black patients with this problem.
  * to slow the worsening of diabetic kidney disease (nephropathy) in patients with type 2 diabetes who have or had high blood pressure. 



Losartan potassium tablets have not been studied in children less than 6 years old or in children with certain kidney problems. 

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High Blood Pressure (hypertension). Blood pressure is the force in your blood vessels when your heart beats and when your heart rests. You have high blood pressure when the force is too much. Losartan potassium tablets can help your blood vessels relax so your blood pressure is lower. 

Left Ventricular Hypertrophy (LVH) is an enlargement of the walls of the left chamber of the heart (the heart’s main pumping chamber). LVH can happen from several things. High blood pressure is the most common cause of LVH. 

Type 2 Diabetes with Nephropathy. Type 2 diabetes is a type of diabetes that happens mainly in adults. If you have diabetic nephropathy it means that your kidneys do not work properly because of damage from the diabetes.
BACKGROUND: Despite the health effects of basal metabolic rate (BMR), the causal effect of BMR on cardiovascular diseases (CVDs) remains undetermined. To elucidate the causal nature, Mendelian randomization (MR) analyses were performed.
METHODS AND RESULTS: Summary genome-wide association statistics regarding BMR and 5 CVDs were obtained from European databases. A 2-sample bidirectional MR was performed to assess the causal association between BMR and CVDs. The causal effects were estimated using inverse variance weighting. Simultaneously, multiple sensitivity analyses were performed to validate the robustness and reliability of the results. Our results indicated that genetically predicted BMR was significantly positively associated with the risk of heart failure (odds ratio, 1.53 [95% CI, 1.39-1.67]; P<0.001), atrial fibrillation and flutter (odds ratio, 2.12 [95% CI, 1.87-2.40]; P<0.001), and aortic aneurysm (odds ratio, 1.64 [95% CI, 1.41-1.92]; P<0.001). Genetically predicted BMR may not be causally associated with coronary artery disease and ischemic stroke risk. Furthermore, a significant causal effect of CVDs on BMR was not found in the reverse MR analysis. Multivariable MR was applied to further assess the direct effect of BMR on CVDs. Multivariable MR indicated that a high level of BMR still increased the risk of heart failure and atrial fibrillation and flutter after adjustment independent of possible confounders. However, the P value of aortic aneurysm was not significant.
CONCLUSIONS: The present study provides robust evidence that genetically predicted BMR is independently causally associated with heart failure and atrial fibrillation and flutter but not vice versa. These findings have implications for the prevention and treatment of CVDs in clinical practice.
Cisplatin 50mg/m2 or carboplatin AUC 5 + paclitaxel 175mg/m2+ bevacizumab 15mg/kg i.v D1 Q3W. Patients who achieve a complete response after ≥6 treatment cycles may be allowed to continue only on biologic therapy, namely bevacizumab, upon investigator discussion.
PURPOSE: To explore the effect of calcium peroxide nanoparticles (CaO2 NPs) combined with programmed cell death protein 1 (PD-1) inhibitors in the treatment of liver cancer and its related mechanism.
METHODS: Hepa1-6 cells were cultured to construct the Hepa1-6 mouse liver cancer model. In vivo mechanism study, a unilateral tumor model was established. Eighteen tumor-bearing mice were randomly divided into the control group (intra-tumoral injection of PBS solution) and the experimental group (intra-tumoral injection of CaO2 NPs). A hypoxic probe, pH probe, and micro-CT were used to evaluate the effect of CaO2 NPs on improving hypoxia, neutralizing acidity, and inducing calcium overload within the tumor. To study the effect of CaO2 NPs combined with PD-1 inhibitors on proximal and distal tumors, the bilateral tumor model was established. Forty tumor-bearing mice were randomly divided into the control group (intra-tumoral/intra-peritoneal injection of PBS solution), CaO2 NPs group (intra-tumoral injection of CaO2 NPs), PD-1 group (intra-peritoneal injection of PD-1 inhibitor), and the combination group (intra-tumoral injection of CaO2 NPs and intra-peritoneal injection of PD-1 inhibitors). The administered side was recorded as the proximal tumor. Tumor volume and body weight were measured every 2 days after treatment. On day 8, serum and tumor samples were collected. The immune factors in serum (Interferon-γ (IFN-γ), Tumour necrosis factor-α (TNF-α), Interleukin-2 (IL-2), and Interleukin-10 (IL-10)) and tumor tissue (IFN-γ and TNF-α) were detected by ELISA. H&E staining was used to detect tumor necrosis. Immunohistochemical staining was used to detect the amount of CD4+ and CD8+ T cells within the tumor. By analyzing the tumor volume, pathological indexes, and immune-related indexes, the effects of CaO2 NPs combined with PD-1 inhibitors on proximal and distal tumors were evaluated, and they mediated immunomodulatory effects (including local and systemic immunity), and their effects on tumor burden were studied. In addition, a unilateral tumor model was established to study the effect of CaO2 NPs combined with PD-1 inhibitors on survival time.
RESULTS: The results of in vivo mechanism study showed that CaO2 NPs can improve hypoxia, neutralize acidity, and induce calcium overload within tumors. The results of the study on the effect of CaO2 NPs combined with PD-1 inhibitor on proximal and distal tumors showed that, compared with the other three groups, the bilateral tumor burden of the combination group was significantly reduced, the intra-tumoral infiltration of CD8+ and CD4+ T cells were significantly increased, the secretion of anti-tumor immune factors in tumor and serum was increased, and the secretion of pro-tumor immune factors was decreased. Mice in the combination group showed the longest survival compared with the other groups.
CONCLUSION: CaO2 NPs can improve hypoxia, neutralize acidity, and induce calcium overload within tumors, so as to reduce tumor burden and realize an immunosuppressive tumor transformation to a hot tumor, and play a synergistic role with PD-1 inhibitors in anti-liver cancer.
BACKGROUND: Juvenile idiopathic arthritis (JIA) is the most common chronic rheumatic condition of childhood. Temporomandibular joint (TMJ) is among the most commonly affected joints in JIA patients. When JIA involves the TMJ, it may affect condylar growth in the joint; therefore, JIA patients are at risk of unfavourable long-term outcomes from associated joint damage. If undetected, TMJ involvement can lead to various functional disabilities such as reduced mandibular mobility and disorders of the mastication muscles. Limitations in sagittal and vertical mandibular growth can result in micrognathia and anterior open bite with aesthetic and functional restrictions.
OBJECTIVE: Genetic factors may play a role in determining which individuals are more prone to develop TMJ disorders or in predicting the severity of the disease process. Therefore, we applied a GWAS approach to identify loci associated with TMJ involvement in a sample of Estonian patients with JIA. Our aim was to address the potential role of genetic susceptibility factors in TMJ-JIA, a condition not previously studied in this context.
METHODS: The case group consisted of 55 JIA patients with TMJ involvement and 208 patients without TMJ involvement comprised the control group. The entire cohort was genotyped using the Illumina HumanOmniExpress BeadChip arrays. Imputation was performed using a nationwide reference panel obtained of 2240 individuals whose data were obtained from the Estonian Biobank.
RESULTS: We identified six loci as being associated with the risk of TMJ-JIA in Estonian JIA patients. The strongest associations were identified at CD6 rs3019551 (P = 3.80 × 10-6), SLC26A8/MAPK14 rs9470191 (P = 6.15 × 10-6), NLRP3 rs2056795 (P = 8.91 × 10-6) and MAP2K4 rs7225328 (P = 1.64 × 10-5).
CONCLUSION: This study provides first insights into the risk-associated loci between JIA and its manifestation in the TMJ. The reported loci are involved in molecular pathways of immunological relevance and likely represent genomic regions that render the TMJ susceptible to involvement by JIA in Estonian patients.
The present invention discloses an inhibitor of SFTSV which is a monoclonal antibody against SFTSV wherein the variable domain of the heavy chain comprises the sequence of CDR-H1 given in SEQ ID NO. 1, the sequence of CDR-H2 given in SEQ ID NO. 2 and the sequence of CDR-H3 given in SEQ ID NO. 3 and the variable domain of the light chain comprises the sequence of CDR-L1 given in SEQ ID NO. 4, the sequence of CDR-L2 given in SEQ ID NO. 5 and the sequence of CDR-L3 given in SEQ ID NO. 6. The invention also extends to therapeutic uses of the inhibitors, compositions and methods for detecting SFTSV.
Volunteers without history, signs or symptoms of acute traumatic injuries. Volunteers consent to have 7ml peripheral blood to be drawn.
This study aims to improve the 24 weeks response rate. The sample size is calculated based on Simon's two-stage design. The first stage of the study enrolled a cohort of 15 patients. If after 24 weeks at least 9 patients achieved a response, then enrollment was expanded to a total of 43 patients. The null hypothesis was unaccepted if more than 26 of 43 patients achieved the response. Accounting for a 20% dropout rate, the estimated final sample size was 54 patients.
PROBLEM TO BE SOLVED: To obtain a new human neuropsin exhibited by a specific amino acid sequence, specifically expressed in the cerebral hippocampus and useful for the elucidation of the mechanism of human brain and development of therapeutic medicines for brain disorders. SOLUTION: This new human neuropsin is shown by an amino acid sequence of formula I. The DNA sequence encoding this human neuropsin is expressed by a base sequence of formula I. The gene for this human neuropsin consists of 6 exons and 5 introns. The 6 exons are shown by base Nos.1-26, Nos.27-104, Nos.l05-264, Nos.26-27, Nos.528-661 and Nos.662-868 of the base sequence of formula I, respectively. The promoter region is shown by a base sequence of formula II. The primer of this human neuropsin is shown by the base sequence such as GTGACCCCGC-CCCTGGATT.
PURPOSE:To provide a modified ultramarine excellent in stability, resistance to acids, and heat and mechanical shearing force, by bringing a specific treated ultramarine into contact with the vapor of a silicon compd. to support a film of a silicon polymer on the whole surface of the treated ultramarine. CONSTITUTION:An ultramarine powder (a) having a particle size of 0.1-20mu is dispersed in an aq. medium 0.1-20wt.% [in terms of Zn based on the amount of the components (a)] zinc compd. is added thereto. The mixture is filtered, dried, optionally, fired at 110-250 deg.C and crushed to obtain a treated ultramarine (A) wherein sulfur on the surface of the component (a) is blocked by the component (b). The component A is brought into contact with the vapor of at least one silicon compd. (B) of the formula [wherein R<1>, R<2>, R<3>, R<4>, R<5> and R<6> are each H or a 1-10C hydrocarbon group substd. by at least one halogen atom and at least one of R<1>, R<2> and R<3> is always a group other than H; a and b are each o or 0 or at least one; C is 0 or 2 and a+b is at least 3 when C is O] to polymerize the component B on the whole surface of the component A, thus obtaining a modified ultramarine wherein a film of a silicon polymer is supported on the whole surface thereof.