anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Due to their high-stress workloads, medical interns tend to have lower sleep and decreased physical activity. The goal of this study is to evaluate the efficacy of gamified competition (delivered through a smartphone) for improving the physical activity and sleep of medical interns. During the study, they are teamed up by programs and institutions and competes with other teams, which aim to motivate them to have more physical activity and sleep duration during their internship year.

The primary aim of this study is to investigate whether introducing competition mechanisms into mobile health (mHealth) interventions can improve a medical intern's activity-related behavioral outcomes: daily step counts and sleep duration. The first secondary aim is to assess the time-varying competition effect on their behavioral outcomes. The second secondary aim is to evaluate how social cooperation (competing within the same institution or program) moderates the effect of competition on behavioral outcomes. The first exploratory aim is to assess the competition effect on study engagement and the second exploratory aim is to evaluate the competition effect on mental outcome, mood score.
INTRODUCTION: Prior research has explored the relationship between inflammatory skin disorders and breast cancer (BC), yet the causality of this association remains uncertain.
METHODS: Utilizing a bidirectional two-sample Mendelian randomization (MR) approach, this study aimed to elucidate the causal dynamics between various inflammatory skin conditions-namely acne, atopic dermatitis, psoriasis vulgaris, urticaria, and rosacea-and BC. Genetic variants implicated in these disorders were sourced from comprehensive genome-wide association studies representative of European ancestry. In the forward MR, BC was posited as the exposure, while the reverse MR treated each inflammatory skin disease as the exposure. A suite of analytical methodologies, including random effects inverse variance weighted (IVW), weighted median (WME), and MR-Egger, were employed to probe the causative links between inflammatory skin diseases and BC. Sensitivity analyses, alongside evaluations for heterogeneity and pleiotropy, were conducted to substantiate the findings.
RESULTS: The MR analysis revealed an increased risk of acne associated with BC (IVW: OR = 1.063, 95% CI = 1.011-1.117, p = 0.016), while noting a decreased risk of atopic dermatitis (AD) in BC patients (IVW: OR = 0.941, 95% CI = 0.886-0.999, p = 0.047). No significant associations were observed between BC and psoriasis vulgaris, urticaria, or rosacea. Conversely, reverse MR analyses detected no effect of BC on the incidence of inflammatory skin diseases. The absence of pleiotropy and the consistency of these outcomes strengthen the study's conclusions.
CONCLUSION: Findings indicate an elevated incidence of acne and a reduced incidence of AD in individuals with BC within the European population.
PROBLEM TO BE SOLVED: To obtain a therapeutic agent having excellent antiallergic action with slight side effects, and useful as e.g. a medicament for preventing or treating diseases caused by various kinds of allergy by including a specific naphthoquinone derivative. SOLUTION: This allergic disease therapeutic agent contains a naphthoquinone derivative of formula I, II or III [2,2-"-methylenebis(3- hydroxy-1,4-naphthoquinone), 2,2'-ethylidenebis(3-hydroxy-1,4-naphthoquinone), 2-hydroxyethyl)-3-methoxy-1,4-naphthoquinone, respectively]. Each of these naphthoquinone derivatives can be extracted and isolated from lmpatience balsamina L.; it is obtained, for example, by cutting the whole grass, leaves, stems, rinds, or petals of the above plant with or without drying and subjecting them to extraction at normal or higher temperatures with a solvent (e.g. water, an organic solvent, a mixture thereof), or by synthesis. The daily dose of this agent is normally 0.1-500 or 0.01-100 mg/adult for external use or internal use, respectively.
OBJECTIVE: To explore the imaging and transcranial Doppler cerebral blood flow characteristics of cerebrovascular fenestration malformation and its relationship with the occurrence of ischemic cerebrovascular disease.
METHODS: A retrospective analysis was conducted on the imaging data of 194 patients with cerebrovascular fenestration malformation who visited the Heyuan People's Hospital from July 2021 to July 2023. The location and morphology of the fenestration malformation blood vessels as well as the presence of other cerebrovascular diseases were analyzed. Transcranial Doppler cerebral blood flow detection data of patients with cerebral infarction and those with basilar artery fenestration malformation were also analyzed.
RESULTS: A total of 194 patients with cerebral vascular fenestration malformation were found. Among the artery fenestration malformation, basilar artery fenestration was the most common, accounting for 46.08% (94/194). 61 patients (31.44%) had other vascular malformations, 97 patients (50%) had cerebral infarction, of which 30 were cerebral infarction in the fenestrated artery supply area. 28 patients with cerebral infarction in the fenestrated artery supply area received standardized antiplatelet, lipid-lowering and plaque-stabilizing medication treatment. During the follow-up period, these patients did not experience any symptoms of cerebral infarction or transient ischemic attack again. There were no differences in peak systolic flow velocity and end diastolic flow velocity, pulsatility index and resistance index between the ischemic stroke group and the no ischemic stroke group in patients with basal artery fenestration malformation (P > 0.05).
CONCLUSION: Cerebrovascular fenestration malformation is most common in the basilar artery. Cerebrovascular fenestration malformation may also be associated with other cerebrovascular malformations. Standardized antiplatelet and statin lipid-lowering and plaque-stabilizing drugs are suitable for patients with cerebral infarction complicated with fenestration malformation. The relationship between cerebral blood flow changes in basilar artery fenestration malformation and the occurrence of ischemic stroke may not be significant.
Advanced urothelial carcinoma (UC) has a poor long-term prognosis. The disease has not seen improved outcomes despite research efforts in over two decades. Novel therapeutic options are needed. Regorafenib is a novel oral multikinase inhibitor but is more potent than a similar multikinase inhibitor drug that treats advanced renal cell carcinoma and hepatocellular carcinoma. Regorafenib has been shown to have a broader capacity to inhibit blood supply to tumor sources.

This trial evaluates a proof-of-concept using Regorafenib in patients with metastatic progressive urothelial carcinoma following chemotherapy but still have a high level of activity performance in their daily living. The initial dose of Regorafenib will be 120 mg daily and then be escalated to 160 mg daily before gradually tapering.
BACKGROUND: Ischemia-reperfusion injury (IRI) is a significant clinical concern in liver transplantation, with a key influence on short-term and long-term allograft and patient survival. Myeloid cells trigger and sustain tissue inflammation and damage associated with IRI, but the mechanisms regulating these activities are unknown. To address this, we investigated the molecular characteristics of intragraft myeloid cells present in biopsy-proven IRI- and IRI+ liver transplants.
METHODS: RNA-sequencing was performed on 80 pre-reperfusion and post-reperfusion biopsies from 40 human recipients of liver transplantation (23 IRI+, 17 IRI-). We used transcriptional profiling and computational approaches to identify specific gene coexpression network modules correlated with functional subsets of MPO+, lysozyme+, and CD68+ myeloid cells quantified by immunohistochemistry on sequential sections from the same patient biopsies.
RESULTS: A global molecular map showed gene signatures related to myeloid activation in all patients regardless of IRI status; however, myeloid cell subsets differed dramatically in their spatial morphology and associated gene signatures. IRI- recipients were found to have a natural corticosteroid production and response profile from pre-reperfusion to post-reperfusion, particularly among monocytes/macrophages. The pre-reperfusion signature of IRI+ recipients included acute inflammatory responses in neutrophils and increased translation of adaptive immune-related genes in monocytes/macrophages coupled with decreased glucocorticoid responses. Subsequent lymphocyte activation at post-reperfusion identified transcriptional programs associated with the transition to adaptive immunity found only among IRI+ recipients.
CONCLUSIONS: Myeloid subset-specific genes and related signaling pathways provide targets for the development of therapeutic strategies aimed at limiting IRI in the clinical setting of liver transplantation.
No-treatment was administered during control period. After 3 months, participants were eligible to receive treatment with JUVÉDERM® VOLBELLA® XC with lidocaine if applicable followed by an optional touch-up retreatment one month following initial treatment.
Background. Sleep is an activation procedure and is considered the most potent and best-documented modulator of seizures and interictal epileptiform discharges (IEDs) on electroencephalogram (EEG). The precise role of sleep deprivation in the diagnostic process of epilepsy has not been fully clarified after more than 50 years of use. Sleep deprivation is a procedure that is accompanied by discomfort for patients and their families. Therefore, an accurate indication according to each patient-specific characteristic is needed. This study aims to assess the effectiveness of sleep deprivation EEG in the diagnostic process of patients with suspected epilepsy in our center. Methods. We included patients with a first unprovoked seizure and patients with paroxysmal events suspecting seizures who underwent a sleep deprivation EEG (sdEEG) or routine EEG (rEEG). All patients were subsequently classified with confirmed epilepsy or not. Results. We included 460 patients. The group with sdEEG consisted of 115 patients, while the group with rEEG comprised 345 patients. In the sdEEG group, 19 patients (17%) were confirmed with epilepsy, of which 17 presented interictal epileptiform discharges (IEDs). For the rEEG group, 66 patients (19%) were confirmed with epilepsy, of which 63 presented IEDs. The difference was not statistically significant. Conclusion. Our study failed to find a difference in the yield of sleep deprivation versus routine EEG in patients with epilepsy, but there are many significant confounders/sample biases that limit the generalizability of the findings, particularly to the majority of adult practices.
In mammals, the maintenance of energy homeostasis relies on complex mechanisms requiring tight synchronization between peripheral organs and the brain. Thyroid hormones (THs), through their pleiotropic actions, play a central role in these regulations. Hypothyroidism, which is characterized by low circulating TH levels, slows down the metabolism, which leads to a reduction in energy expenditure as well as in lipid and glucose metabolism. The objective of this study was to evaluate whether the metabolic deregulations induced by hypothyroidism could be avoided through regulatory mechanisms involved in metabolic flexibility. To this end, the response to induced hypothyroidism was compared in males from two mouse strains, the wild-derived WSB/EiJ mouse strain characterized by a diet-induced obesity (DIO) resistance due to its high metabolic flexibility phenotype and C57BL/6J mice, which are prone to DIO. The results show that propylthiouracil (PTU)-induced hypothyroidism led to metabolic deregulations, particularly a reduction in hepatic lipid synthesis in both strains. Furthermore, in contrast to the C57BL/6J mice, the WSB/EiJ mice were resistant to the metabolic dysregulations induced by hypothyroidism, mainly through enhanced lipid metabolism in their adipose tissue. Indeed, WSB/EiJ mice compensated for the decrease in hepatic lipid synthesis by mobilizing lipid reserves from white adipose tissue. Gene expression analysis revealed that hypothyroidism stimulated the hypothalamic orexigenic circuit in both strains, but there was unchanged melanocortin 4 receptor (Mc4r) and leptin receptor (LepR) expression in the hypothyroid WSB/EiJ mice strain, which reflects their adaptability to maintain their body weight, in contrast to C57BL/6J mice. Thus, this study showed that WSB/EiJ male mice displayed a resistance to the metabolic dysregulations induced by hypothyroidism through compensatory mechanisms. This highlights the importance of metabolic flexibility in the ability to adapt to disturbed circulating TH levels.
BACKGROUND AND AIM: Early identification of liver fibrosis is essential for the prognosis of metabolic-associated fatty liver disease (MAFLD), particularly in type 2 diabetes mellitus (T2DM) patients. Here, we explored the association of chitinase-3-like protein 1 (CHI3L1) and liver fibrosis in T2DM-MAFLD patients.
METHODS: Liver fibrosis was staged in T2DM-MAFLD patients, and a liver stiffness measurement (LSM) of ≥ 8 kPa was used to differentiate between non-significant (NSLF) and significant liver fibrosis (SLF) subgroups. The two subgroups were compared for serum CHI3L1 and other parameters. Linear correlation, logistic regression, and restricted cubic spline (RCS) analyses were performed to evaluate the association between CHI3L1 and liver fibrosis. Receiver operating characteristic (ROC) curve analysis was performed to assess the diagnostic accuracy of CHI3L1.
RESULTS: Among T2DM-MAFLD, SLF patients had higher CHI3L1 compared to NSLF patients. CHI3L1 was found to be positively correlated with LSM. Multivariate logistic regression analysis suggested that CHI3L1 may be a potential independent risk factor for SLF. Further stratified analysis indicated that the odds ratios of SLF in the high CHI3L1 group were higher than in the low CHI3L1 group in the subgroups. RCS analysis suggested an increasing trend in the incidence of significant fibrosis with the rising level of CHI3L1. The area under the ROC curve for detecting significant fibrosis was 0.749 (95% CI: 0.668-0.829).
CONCLUSIONS: Serum CHI3L1 demonstrates an association with significant liver fibrosis. High serum levels of CHI3L1 may indicate the existence of significant liver fibrosis in T2DM-MAFLD patients.
Intervention group goes through a web-based neuropsychological intervention program. The program includes eight structured sessions regarding general neuropsychological symptoms after ABI - problems with fatigue, attention, executive functions and memory. A new session opens after the previous one is completed, and after a minimum of 3 days between the sessions. The intervention takes approximately 2 months depending on the progression pace of a patient. The eight sessions consist of psychoeducation, self-assessments, cognitive strategy training and feedback (automatic or given by a monitoring neuropsychologist). A neuropsychologist from HUS monitors patients' progression and provides personal feedback when needed. Participants can also be in contact with a monitoring neuropsychologist via message feature of the program.
Parkinson's disease (PD) is a neurodegenerative disorder that causes a variety of motor and non-motor symptoms. Typically, patients with PD suffer from disabilities and secondary complications even when the disease is optimally treated, and many patients still have sedentary lifestyles, which in turn result in higher rates of mortality and comorbidity. Physical activity is an essential element in maintaining daily functional capabilities and quality of life. However, patients with PD have motor and non-motor deficits that can prevent or limit physical exercise, such as running or resistance exercise. Ischemic conditioning (IC) is a promising therapy that can mimic the physiological effects of physical exercise. IC consists of using a cuff to measure blood pressure, calibrated between 180 and 200 mmHg on the upper or lower limb. Thus, at alternating intervals of 5 minutes, ischemia or reperfusion occurs, depending on whether the cuff is inflated or deflated. IC induces changes in spinal cord excitability for the last reflex reactions of recruited motoneurons with improved balance control in healthy young people and improved learning in the elderly. Recently, IC has been shown to improve cognitive performance in neurological patients with stroke, subcortical ischemia, and vascular dementia. However, there are no studies that have evaluated the effect of IC on motor and cognitive performance in patients with PD. The objective of the present study is to evaluate the chronic effect of IC on the motor and cognitive performance of patients with PD. Furthermore, the investigators intend to evaluate other secondary outcomes such as mobility, quality of life, and immunological responses.
ETHNOPHARMACOLOGICAL RELEVANCE: Cerebral ischemia-reperfusion injury (CIRI) is a complex pathophysiological process involving multiple factors, and becomes the footstone of rehabilitation after ischemic stroke. Sanpian decoction (SPD) has exhibited protective effects against CIRI, migraine, and other cerebral vascular diseases. However, the underlying mechanisms have not been completely elucidated.
AIM OF THE STUDY: This study sought to explore the potential mechanisms underlying the effect of SPD against CIRI.
MATERIALS AND METHODS: High-performance liquid chromatography (HPLC) and ultra-high-performance liquid chromatography (UPLC) were carried out to determine the chemical constituents of SPD. A network pharmacology approach combined with experimental verification was conducted to elucidate SPD's multi-component, multi-target, and multi-pathway mechanisms in CIRI occurrence. The pharmacodynamics of the decoction was evaluated by establishing the rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). In vivo and in vitro experiments were carried out, and the therapeutic effects of SPD were performed using 2,3,5-triphenyltetrazolium chloride (TTC) staining, hematoxylin-eosin (HE) staining, and Nissl staining. We used terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and flow cytometry to evaluate cortex apoptosis. The quantification of mRNA and corresponding proteins were performed using real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot respectively.
RESULTS: Our research showed that pretreatment with SPD improved neurological function and inhibited CIRI. Network pharmacology revealed that the hypoxia-inducible factor-1 (HIF-1) signaling pathway and mitogen-activated protein kinase (MAPK) signaling pathway-mediated apoptosis may be associated with CIRI. In vivo and in vitro experiments, we confirmed that SPD increased cerebral blood flow, improved neural function, and reduced neural apoptosis via up-regulating the expression of sirtuin 1 (SIRT1) and down-regulating phospho-extracellular regulated protein kinases (p-ERK)/ERK and HIF-1α levels in CIRI rats.
CONCLUSION: Taken together, the present study systematically revealed the potential targets and signaling pathways of SPD in the treatment of CIRI using in silico prediction and verified the therapeutic effects of SPD against CIRI via ameliorating apoptosis by regulating SIRT1/ERK/HIF-1α.
FIELD: microbiology. SUBSTANCE: suspension of microbial cells with added glass beads (diameter is 1-1.5 mm) is centrifuged at 600g for 45 min, precipitate is suspended in tris-HCl buffer, pH 7.2 (buffer A) containing 2% Triton X-100 and extracted with at 4 C for 2 h with vigorous stirring. Precipitate is separated by centrifugation at 20000g for 15 min, washed with buffer A, suspended in 200 ml buffer, and 1M MgClsolution and DNAase are added and incubated for 12 h. Precipitate is separated by centrifugation at 20000g for 30 min, washed with buffer A, suspended in buffer A containing 2% sodium dodecylsulfate, and extracted at 60 C for 15 min. Complex of peptidiglycan-protein is separated by centrifugation at 45000g for 1 h. Precipitate is washed, suspended in 100 ml buffer A containing 0.5% sodium dodecylsulfate and 0.5M NaCl, precipitate i separated by centrifugation at 100000g for 30 min, suspended in 50 ml buffer A, precipitate is separated by centrifugation at 150000g for 1 h. Protein is separated from supernatant with 9.5 volumes of cold acetone, kept at 2-10 C for 12 h. Precipitate is separated, suspended in distilled water and lyophilized. Product yield is 3.5% , low-molecular proteins are absent. Product is used for diagnosis of pseudotuberculosis infection and protection of organism against of its. EFFECT: increased purification of protein porine from pseudotuberculosis microbe, simplified method.
Effects of zonisamide on the pharmacokinetics of other antiepilepsy drugs (AEDs): Zonisamide had no appreciable effect on the steady state plasma concentrations of phenytoin, carbamazepine, or valproate during clinical trials. Zonisamide did not inhibit mixed-function liver oxidase enzymes (cytochrome P450), as measured in human liver microsomal preparations, in vitro. Zonisamide is not expected to interfere with the metabolism of other drugs that are metabolized by cytochrome P450 isozymes.

Effects of other drugs on zonisamide pharmacokinetics: Drugs that induce liver enzymes increase the metabolism and clearance of zonisamide and decrease its half-life. The half-life of zonisamide following a 400 mg dose in patients concurrently on enzyme-inducing AEDs such as phenytoin, carbamazepine, or phenobarbital was between 27 to 38 hours; the half-life of zonisamide in patients concurrently on the non-enzyme inducing AED, valproate, was 46 hours. Concurrent medication with drugs that either induce or inhibit CYP3A4 would be expected to alter serum concentrations of zonisamide.

Interaction with cimetidine: Zonisamide single dose pharmacokinetic parameters were not affected by cimetidine (300 mg four times a day for 12 days).

Drug Interactions with CNS Depressants: Concomitant administration of zonisamide and alcohol or other CNS depressant drugs has not been evaluated in clinical studies. Because of the potential of zonisamide to cause CNS depression, as well as other cognitive and/or neuropsychiatric adverse events, zonisamide should be used with caution if used in combination with alcohol or other CNS depressants.

Other Carbonic Anhydrase Inhibitors: Concomitant use of zonisamide, a carbonic anhydrase inhibitor, with any other carbonic anhydrase inhibitor (e.g., topiramate, acetazolamide or dichlorphenamide), may increase the severity of metabolic acidosis and may also increase the risk of kidney stone formation. Therefore, if zonisamide is given concomitantly with another carbonic anhydrase inhibitor, the patient should be monitored for the appearance or worsening of metabolic acidosis (see CLINICAL PHARMACOLOGY, Interactions of Zonisamide with Other Carbonic Anhydrase Inhibitors subsection).