anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Remifentanil, an ultra-short-acting µ-opioid receptor agonist, is commonly used for anesthetic management due to excellent adjustability. Remifentanil is known to cause sinus bradycardia, however, because it has a direct negative chronotropic effect on the cardiac conduction system and there is an indirect negative chronotropic effect via the parasympathetic nervous system.
CASE PRESENTATION: An 8-year-old Japanese boy was diagnosed with acute hydrocephalus due to a brain tumor in the fourth ventricle and underwent emergency surgery. Imaging examination showed brainstem compression. Endoscopic third ventriculostomy and ventriculoperitoneal shunt surgery were scheduled. Remifentanil was started during induction of general anesthesia, but electrocardiogram showed sinus bradycardia, then Wenckebach-type atrioventricular block, and then complete atrioventricular block. Remifentanil was immediately discontinued, and we administered atropine sulfate. Complete atrioventricular block was restored to sinus rhythm. When remifentanil was restarted, however, the electrocardiogram again showed sinus bradycardia, Wenckebach-type atrioventricular block, and then complete atrioventricular block. Remifentanil was again immediately discontinued, we administered adrenaline, and then complete atrioventricular block was restored to sinus rhythm. Fentanyl was used instead of remifentanil with continuous infusion of dopamine. There has since been no further occurrence of complete atrioventricular block.
CONCLUSIONS: This is the first known case of complete atrioventricular block in a pediatric patient with increased intracranial pressure seemingly caused by administration of remifentanil.
BACKGROUND: SAKI is a common and serious complication of sepsis, contributing significantly to high morbidity and mortality, especially in patients requiring RRT. Early identification of high-risk patients enables timely interventions and improvement in clinical outcomes. The objective of this study was to develop and validate a predictive model for in-hospital mortality in patients with SAKI receiving RRT.
METHODS: Patients with SAKI receiving RRT from the MIMIC-IV database were retrospectively enrolled and randomly assigned to either the training cohort or the testing cohort in a 7:3 ratio. LASSO regression and Boruta algorithm were utilized for feature selection. Subsequently, three machine learning models-CART, SVM and LR-were constructed, and their predictive efficacy was assessed using a comprehensive set of performance indicators. Feature importance analysis was performed to determine the contribution of each feature to a model's predictions. Finally, DCA was employed to evaluate the clinical utility of the prediction models. Additionally, a clinical nomogram was developed to facilitate the interpretation and visualization of the LR model.
RESULTS: A total of 1663 adults were ultimately enrolled and randomly allocated into the training cohort (n = 1164) or the testing cohort (n = 499). Twenty-eight variables were evaluated for feature selection, with eight ultimately retained in the final model: age, MAP, RR, lactate, Cr, PT-INR, TBIL and CVP. The LR model demonstrated commendable performance, exhibiting robust discrimination in both the training cohort (AUROC: 0.73 (95% CI 0.70-0.76); AUPRC: 0.75 (95% CI 0.72-0.79); accuracy: 0.66 (95% CI 0.63-0.68)) and the testing cohort (AUROC: 0.72 (95% CI 0.68-0.76); AUPRC: 0.73 (95% CI 0.67-0.79); accuracy: 0.65 (95% CI 0.61-0.69)). Furthermore, there was good concordance between predicted and observed values in both the training cohort (χ2 = 4.41, p = 0.82) and the testing cohort (χ2 = 4.16, p = 0.84). The results of the DCA revealed that the LR model provided a greater net benefit compared to other prediction models.
CONCLUSIONS: The LR model exhibited superior performance in predicting in-hospital mortality in patients with SAKI receiving RRT, suggesting its potential utility in identifying high-risk patients and guiding clinical decision-making.
Plant extracts are actively being used worldwide due to the presence of biologically active constituents helping in the preservation of food, and to aid against various diseases owing to their antimicrobial and antioxidant potential. The present research work was carried out to investigate the phytochemical constituents, antimicrobial activity, and antioxidant activity of different extracted samples of Euphorbia parviflora. Anti-microbial studies were carried out by Agar well diffusion while the DPPH method was employed for investigating anti-oxidant activity. Three samples from methanol, chloroform, and ethyl acetate extract were tested against five different bacterial strains comprising two species from Gram-negative bacteria i.e., Staphylococcus aureus and Bacillus subtilis and three species from Gram-positive bacteria i.e. Escherichia coli, Pseudomonas aeruginosa and Klebsiella pneumonia along two fungal strains i.e. Candida albicans and Aspergillus niger. The results of the qualitative phytochemical analysis showed that methanolic, chloroformic, and ethylacetate extract of Euphorbia parviflora consist of alkaloids, reducing sugars, flavonoids, terpenoids, tannins, and saponins. The total phenol and flavonoid content of E. parviflora showed that the methanolic extract of E. parviflora had a significantly higher total phenolic content (53.73 ± 0.30 mg of GAE/g) and flavonoid content (44.62 ± 0.38 mg of than other extracts. The content of total phenolic and flavonoids was more in methanolic extract as compared to other extracts of E. prolifera. The HPLC analysis showed that in the chloroform extract of E. parviflora Cinnamic acid (4.32 ± 2.89 mg/g) was dominant, in methanol extract quercetin (3.42 ± 2.89 mg/g) was dominant and in ethyl acetate extract of E. parviflora catechin (4.44 ± 2.89 mg/g) was found dominant. The antimicrobial activity revealed that amongst all the extracts the highest antibacterial activity was shown by methanolic extract against B. subtilis and Staphylococcus aureus as compared to the other extracts. The antioxidant activity revealed that methanolic extract of E. parviflora demonstrated higher antioxidant activity (82.42 ± 0.02) followed by chloroform extract (76.48 ± 0.08) at 150 µg/mL. The aim of this study was primarily to evaluate the potential of this plant as a reliable source of antimicrobials and antioxidants that may be used for the treatment of various infectious diseases in the future. The study provides evidence that this plant can act as a reliable source of antimicrobial and antioxidant agents and might be used against several infectious diseases.
The susceptible-infected-recovered (SIR) model and its variants form the foundation of our understanding of the spread of diseases. Here, each agent can be in one of three states (susceptible, infected, or recovered), and transitions between these states follow a stochastic process. The probability of an agent becoming infected depends on the number of its infected neighbors, hence all agents are correlated. The simplest mean-field theory of the same stochastic process, however, assumes that the agents are statistically independent. This leads to a self-feedback effect in the approximation: when an agent infects its neighbors, this infection may subsequently travel back to the original agent at a later time, leading to a self-infection of the agent which is not present in the underlying stochastic process. We here compute the first-order correction to the mean-field assumption from a systematic expansion, called dynamical TAP theory. This correction, which takes fluctuations up to second order in the interaction strength into account, cancels the self-feedback effect, leading to smaller infection rates. The correction significantly improves predictions compared to mean-field theory. In particular, it captures how sparsity dampens the spread of the disease: this indicates that reducing the number of contacts is more effective than predicted by mean-field models. We further apply the expansion to variants of the SIR model, such as the SIRS model, in which the immunity of an individual to the disease wanes over time. We find that up to the second order, the correction terms in the SIR and SIRS model are equivalent, meaning that fluctuations partially cancel the self-feedback effect even when self-feedback is in principle allowed.
The Neurotrac® Simplex device will be used for EMG-Biofeedback treatment. As in the muscle strength assessment procedure, the EMG reference electrode will be placed on the patient's forearm, and 2 adhesive electrodes in the EMG channel will be placed on the patient's perineal muscles. The patient will be asked to contract and relax the pelvic floor muscles at certain intervals in accordance with the visual and auditory stimuli made on the device screen or computer screen. The pelvic floor muscle contraction and rest period will last 5 seconds each. The program will continue for 2 days a week, 25 minutes per session and 8 weeks and will be performed in a clinical environment. During the treatment, the treatment will be visualized for the patient with different imagery. At the end of the games played, the patients' scores (%), the lowest and highest EMG values will be recorded in mV. The treatment will be applied to the patients in two sessions per week.
Embodiments described herein relate generally to apparatus, methods and systems for low energy processing of consumer personal hygiene products (PHPs) and formulations of the same. In some embodiments, a method of manufacturing a consumer PHP comprises combining a first material and second material at room temperature to form a first mixture, mixing the first mixture at room temperature, adding a third material at room temperature to form a second mixture; mixing the second mixture at room temperature, adding a fourth material at room temperature to form a third mixture; and mixing the third mixture at room temperature. In some embodiments, the third material and the fourth material can be mixed to form the second mixture and the first mixture and second mixture can be combined to form the third mixture. In some embodiments, the mixing can be accomplished using a propeller mixer. In some embodiments, the propeller mixer can be rotated at a speed of greater than about 200 rpm during at least one of the mixing steps. In some embodiments, the pH of the third mixture can be adjusted to between about 4.5 and about 6.5 using an acidifier. In some embodiments, the viscosity of the third mixture can be adjusted to between about 100 cP and about 25,000 cP using a thickener.
BACKGROUND: Frailty increases the risk of needing nursing care and significantly affects the life and functional prognosis of older individuals. Early detection and tailored interventions are crucial for maintaining and enhancing their life functions. Recognizing distinct clinical phenotypes is essential for devising appropriate interventions. This study aimed to explore diverse frailty phenotypes, focusing on poor nutrition in older Japanese individuals through observational research.
METHODS: Twenty-one nursing home residents underwent a comprehensive survey covering physical, blood, dietary, cardiac, cognitive, nutritional, nursing care, frailty, agitated behavior, and gut microbiome assessments (high-throughput 16S rRNA gene sequencing). Using clustering analysis with 239 survey items (excluding gut microbiome), participants were classified into subgroups based on clinical phenotypes, and group characteristics were compared through analysis.
RESULTS: Individuals with moderate or severe frailty and suspected dementia formed subgroups with distinct clinical phenotypes based on nutritional, defecation, and nursing care statuses. The gut microbiome significantly varied among these groups (p = 0.007), indicating its correlation with changes in clinical phenotype. Nutritional status differences suggested poor nutrition as a differentiating factor in the core clinical phenotype.
CONCLUSIONS: This study proposes that the gut microbiome differs based on the clinical phenotype of Japanese older individuals with frailty, and targeted interventions addressing the gut microbiome may contribute to preventing frailty in this population.
In a randomized, double-blind, clinical trial in patients undergoing hip fracture surgery, fondaparinux sodium 2.5 mg SC once daily was compared to enoxaparin sodium 40 mg SC once daily, which is not approved for use in patients undergoing hip fracture surgery. A total of 1,711 patients were randomized and 1,673 were treated. Patients ranged in age from 17 to 101 years (mean age 77 years) with 25% men and 75% women. Patients were 99% Caucasian, 1% other races. Patients with multiple traumas affecting more than one organ system, serum creatinine level more than 2 mg/dL (180 micromol/L), or platelet count less than 100,000/mm3 were excluded from the trial. Fondaparinux sodium was initiated after surgery in 88% of patients (mean 6 hours) and enoxaparin sodium was initiated after surgery in 74% of patients (mean 18 hours). For both drugs, treatment was continued for 7 ± 2 days. The primary efficacy endpoint, venous thromboembolism (VTE), was a composite of documented deep vein thrombosis (DVT) and/or documented symptomatic pulmonary embolism (PE) reported up to Day 11. The efficacy data are provided in Table 7 and demonstrate that under the conditions of the trial fondaparinux sodium was associated with a VTE rate of 8.3% compared with a VTE rate of 19.1% for enoxaparin sodium for a relative risk reduction of 56% (95% CI: 39%, 70%; P <0.001). Major bleeding episodes occurred in 2.2% of patients receiving fondaparinux sodium and 2.3% of enoxaparin sodium patients [see Adverse Reactions (6.1)].

Table 7. Efficacy of Fondaparinux Sodium in the Peri-operative Prophylaxis of Thromboembolic Events Following Hip Fracture Surgery 

a N = all evaluable hip fracture surgery patients. Evaluable patients were those who were treated and underwent the appropriate surgery (i.e., hip fracture surgery of the upper third of the femur), with an adequate efficacy assessment up to Day 11. 

b P value versus enoxaparin sodium <0.001.

c P value versus enoxaparin sodium: NS.
PURPOSE: Bromodomain-containing protein 7 (BRD7) is downregulated and functions as a tumor suppressor in many types of cancers including breast cancer, and the dysregulation of BRD7 expression is closely related to the development and progression of breast cancer. Whereas little attention has been focused on the regulation of BRD7 protein levels in breast cancer, which needs to be further elucidated.
METHODS: The protein stability of BRD7 in breast cancer cells and BRD7 protein level in breast cancer tissues was examined by Western Blotting. The potential E3 ubiquitin ligase proteins that interact with the BRD7 was screened by coimmunoprecipitation combined with mass spectrometry analysis in MDA-MB-231 cells. We proved the interaction between BRD7 and tripartite motif containing 28 (TRIM28) through Co-Immunoprecipitation (Co-IP) and immunofluorescence assays. Co-IP and ubiquitination assay were used to explore the specific binding domain between BRD7 and TRIM28 and the ubiquitination site of BRD7. The effects of TRIM28 on the BRD7 protein stability and ubiquitination level was investigated by qPCR, Western Blot and Co-IP assay. CCK-8 and clone formation assays were carried out to assess the effect of TRIM28 on proliferation ability of breast cancer ells. Transwell assay and wound healing assay were used to investigate the effect of TRIM28 on breast cancer cell invasion and migration. Flow cytometry was used to detect the effect of TRIM28 on cell cycle and apoptosis of breast cancer cells. In addition, we confirmed effect of TRIM28 on tumor growth and metastasis by xenograft and metastatic mouse models. We designed some recovery assays to explore the role of recovery BRD7 in TRIM28-mediated promotion of malignant progression of breast cancer in vivo and in vitro. Finally, the clinical significance of TRIM28 and BRD7 was proved by immunohistochemistry.
RESULTS: In this study, we demonstrated that BRD7 was an unstable protein and might be regulated by ubiquitination in breast cancer; furthermore, we found that the Coiled-Coil region of TRIM28 could directly bind to N-terminal of BRD7, and TRIM28 mediates BRD7 ubiquitination and degradation dependent on K21 by acting as a potential E3 ubiquitin ligase. Moreover, TRIM28 promoted cell proliferation, migration, invasion, xenograft tumor growth and metastasis, thus playing an oncogenic role in breast cancer. Furthermore, the restoration of BRD7 expression in breast cancer significantly reversed the promotional effects of TRIM28 on malignant progression both in vitro and in vivo. In addition, TRIM28 was highly expressed in the biopsy tissues of breast cancer, and its expression was negatively correlated with BRD7 expression and positively correlated with TNM stage and poor prognosis of BC patients.
CONCLUSIONS: Our findings provide a novel mechanism by which TRIM28 significantly facilitates BRD7 ubiquitination and degradation, thus promoting breast cancer malignant progression. Targeting the TRIM28/BRD7 axis might be a novel potential strategy for the clinical diagnosis and treatment of breast cancer.
FIELD: medicine. ^ SUBSTANCE: invention relates to medicine, namely to cardiology, and can be used for optimisation of cardiovascular system (CVS) functional reactivity. Method is realised in the following way: evaluation of state of CVS functional reactivity is carried out under psychoemotional load, for which purpose systolic, diastolic, mean dynamic (APm.dyn.) pressure, heart rate (HR) are registered. On the basis of these data index of functional reactivity (IFR) before and after load is determined by formula: IFR=(APm.dyn.xHR)/100 (conv.units). If IFR value increase is more than 20 conv.units, administered is combination of daily swimming in swimming pool for not less than 15 minutes per day, lisinopril 10 mg in the morning 1 time and amlodipine 5 mg in the morning 1 time for not less than 3 months. ^ EFFECT: method allows to normalise CVS functional reactivity due to potentiation of their medicinal action in patients of elderly and senile age with arterial hypertension during three months of treatment. ^ 2 ex
The invention provides a SHINC-2 polynucleotide, which can be a nucleic acid encoding all or a portion of a SHINC-2 protein, or a complementary polynucleotide or antisense polynucleotide. The invention provides a SHINC-2 polypeptide, which can be a full-length SHINC-2 protein or a fragment thereof or an analog or homolog thereof. Desirably, the SHINC-2 polypeptide modulates apoptosis. The invention provides an antibody that specifically binds a SHINC-2 polypeptide. The invention provides diagnostic methods. For example, the invention affords a method for identifying compounds that modulate apoptosis. The invention provides a method for detecting or evaluating the prognosis of a cancer. The invention provides diagnostic compositions for detection of cancer. The invention provides a method of modulating apoptosis or treating or preventing a cancer, tumor growth and/or metastasis by administration of an agent that modulates the expression and/or activity of SHINC-2. The invention provides formulations of SHINC-2 polynucleotides or proteins. Preferably, such compositions will comprise liposomal formulations.
During completion of the star shaped manual dexterity test, the test subject is asked to identify cards from a regular deck of playing card by naming the suit and rank of the card. They will be asked to identify one random card during each of the 10 rounds in the completion of the test. Completion time and number of errors are recorded.
Exacerbation of pain by chronic stress and comorbidity of pain with stress-related disorders such as depression and post-traumatic stress disorder, represent significant clinical challenges. Previously we have documented that chronic forced swim (FS) stress exacerbates neuropathic pain in spared nerve injury (SNI) rats, associated with an up-regulation of GluN2B-containing N-methyl-D-aspartate receptors (GluN2B-NMDARs) in the central nucleus of the amygdala (CeA). However, the molecular mechanisms underlying chronic FS stress (CFSS)-mediated exacerbation of pain sensitivity in SNI rats still remain unclear. In this study, we demonstrated that exposure of CFSS to rats activated the corticotropin-releasing factor (CRF)/CRF receptor type 1 (CRFR1) signaling in the CeA, which was shown to be necessary for CFSS-induced depressive-like symptoms in stressed rats, and as well, for CFSS-induced exacerbation of pain hypersensitivity in SNI rats exposed to chronic FS stress. Furthermore, we discovered that activation of CRF/CRFR1 signaling in the CeA upregulated the phosphorylation of GluN2B-NMDARs at tyrosine 1472 (pGluN2BY1472) in the synaptosomal fraction of CeA, which is highly correlated to the enhancement of synaptic GluN2B-NMDARs expression that has been observed in the CeA in CFSS-treated SNI rats. In addition, we revealed that activation of CRF/CRFR1 signaling in the CeA facilitated the CFSS-induced reinforcement of long-term potentiation as well as the enhancement of NMDAR-mediated excitatory postsynaptic currents in the basolateral amygdala (BLA)-CeA pathway in SNI rats. These findings suggest that activation of CRF/CRFR1 signaling in the CeA contributes to chronic stress-induced exacerbation of neuropathic pain by enhancing GluN2B-NMDAR-mediated synaptic plasticity in rats subjected to nerve injury. PERSPECTIVE: Our present study provides a novel mechanism for elucidating stress-induced hyperalgesia and highlights that the CRF/CRFR1 signaling and the GluN2B-NMDAR-mediated synaptic plasticity in the CeA may be important as potential therapeutic targets for chronic stress-induced pain exacerbation in human neuropathic pain. DATA AVAILABILITY: The data that support the findings of this study are available from the corresponding author upon reasonable request.
Along with standard manual physical therapy, patients will have a stretching device (Dynasplint) used in rehabilitation to regain ROM in stiff joints. Patients will use this device 20-30 minutes 2 times per day at home.
Cosmetic, non-therapeutic use of (a) at least one extract of Fucus vesiculosusand/or (b) carnitine and/or at least one carnitine derivative for increasing the expression or activity of at least one gene or protein from the group of the mitochondrial enzyme complexes and associated transcription factors in skin and/or skin appendages, is claimed. An independent claim is also included for a cosmetic agent comprising (in wt.%): (a) at least one extract of Fucus vesiculosus(0.00001-10) and (b) carnitine and/or at least carnitine derivative (0.000001-15). ACTIVITY : Dermatological. MECHANISM OF ACTION : Mitochondrially encoded cytochrome-c oxidase subunit-I activator; Mitochondrial transcription factor-A activator; Transcriptional co-activator peroxisome proliferator-activated receptor gamma co-activator 1-alpha activator. The ability of the extract for increasing expression of mitochondrially encoded cytochrome-c oxidase subunit-I was tested in hair follicle cultures from dermal papilla cells. The results showed that the expression was increased by 1.8 folds, compared to the control (0.55 fold).