anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
150 patients at University of Washington affiliated hospitals who are found to be depressed by DSMIV criteria within the first four months following ischemic stroke will be invited to join the study, and randomly assigned to a problem-solving/pleasant events intervention provided by an advanced practice nurse, or to regular clinic follow-up. Both groups will receive standard antidepressant treatment and written materials from the American Stroke Association, and will be assessed for up to two years following the study. The primary outcome is reduction in depression at 12 months following stroke. Secondary outcomes are reductions in limitations in activity (Barthel Index), reduction in limitation in participation (Stroke Impact Scale) and overall stroke impact (Stroke Impact Scale) at 6, 12, and 24 months post- stroke. We hypothesize that all patients will improve their mood and functional ability related to their post-stroke standard treatment, but that those who receive the psychosocial intervention will have significantly greater improvement in mood, functional ability, social participation, and less overall stroke impact at all follow-up measurement. A supplemental aim is to expand aim 4 of the parent study, adding SERT genotype to our list of factors that might influence treatment outcome for PSD. Further, since we are screening both depressed and not depressed stroke survivors for this study, we will add a fifth aim: to compare ischemic stroke survivors who are and are not depressed within the first four months following stroke by their 5-HTTLPR genotypes (s/s, s/l, or l/l).
Fatal and/or serious hepatotoxicity occurred in 16% of patients treated with Zydelig in combination with rituximab or with unapproved combination therapies. Elevations in ALT or AST greater than 5 times the upper limit of normal have occurred [see Adverse Reactions (6.1)]. These findings were generally observed within the first 12 weeks of treatment and were reversible with dose interruption. After resumption of treatment at a lower dose, 26% of patients had recurrence of ALT and AST elevations. Discontinue Zydelig for recurrent hepatotoxicity.

Avoid concurrent use of Zydelig with other drugs that may cause liver toxicity.

Monitor ALT and AST in all patients every 2 weeks for the first 3 months of treatment, every 4 weeks for the next 3 months, then every 1 to 3 months thereafter. Monitor weekly for liver toxicity if the ALT or AST rises above 3 times the upper limit of normal until resolved. Withhold Zydelig if the ALT or AST is greater than 5 times the upper limit of normal, and continue to monitor AST, ALT and total bilirubin weekly until the abnormality is resolved [see Dosage and Administration (2.2)].
Chronic liver injury induces fibrosis that often proceeds to cirrhosis and hepatocellular carcinoma, indicating that prevention and/or resolution of fibrosis is a promising therapeutic target. Hepatic stellate cells (HSCs) are the major driver of fibrosis by expressing extracellular matrices (ECM). HSCs, in the normal liver, are quiescent and activated by liver injury to become myofibroblasts that proliferate and produce ECM. It has been shown that activated HSCs (aHSCs) become a "quiescent-like" state by removal of liver insults. Therefore, deactivation agents can be a therapeutic drug for advanced liver fibrosis. Using aHSCs prepared from human induced pluripotent stem cells, we found that aHSCs were reverted to a quiescent-like state by a combination of chemical compounds that either inhibit or activate a signaling pathway, Lanifibranor, SB431542, Dorsomorphin, retinoic acid, palmitic acid and Y27632, in vitro. Based on these results, we established a high throughput system to screen agents that induce deactivation and demonstrate that a single chemical compound can induce deactivation.
Botulinum neurotoxins (BoNTs) are a family of neurotoxins produced by Clostridia and other bacteria that induce botulism. BoNTs are internalized into nerve terminals at the site of injection and cleave soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins to inhibit the vesicular release of neurotransmitters. BoNTs have been approved for multiple therapeutic applications, including the treatment of migraines. They have also shown efficacies for treating neuropathic pain, such as diabetic neuropathy, and postherpetic and trigeminal neuralgia. However, the mechanisms underlying BoNT-induced analgesia are not well understood. Peripherally administered BoNT is taken up by the nerve terminals and reduces the release of glutamate, calcitonin gene-related peptide, and substance P, which decreases neurogenic inflammation in the periphery. BoNT is retrogradely transported to sensory ganglia and central terminals in a microtubule-dependent manner. BoNTs decrease the expression of pronociceptive genes (ion channels or cytokines) from sensory ganglia and the release of neurotransmitters and neuropeptides from primary afferent central terminals, which likely leads to decreased central sensitization in the dorsal horn of the spinal cord or trigeminal nucleus. BoNT-induced analgesia is abolished after capsaicin-induced denervation of transient receptor potential vanilloid 1 (TRPV1)-expressing afferents or the knockout of substance P or the neurokinin-1 receptor. Although peripheral administration of BoNT leads to changes in the central nervous system (e.g., decreased phosphorylation of glutamate receptors in second-order neurons, reduced activation of microglia, contralateral localization, and cortical reorganization), whether such changes are secondary to changes in primary afferents or directly mediated by trans-synaptic, transcytotic, or the hematogenous transport of BoNT is controversial. To enhance their therapeutic potential, BoNTs engineered for specific targeting of nociceptive pathways have been developed to treat chronic pain. Further mechanistic studies on BoNT-induced analgesia can enhance the application of native or engineered BoNTs for neuropathic pain treatment with improved safety and efficacy.
Lactobacillus casei and application thereof relate to the field of microorganisms, in particular to lactobacillus casei and application thereof. The problem that the inhibition effect of the existing lactic acid bacteria on escherichia coli is not ideal is solved. The strain is Lactobacillus casei (Lactobacillus casei) R9, is preserved in China general microbiological culture Collection center of China Committee for culture Collection of microorganisms, has the preservation date of 10 months and 14 days in 2020, and has the preservation number of CGMCC No. 20888. The inhibition effect of the lactobacillus casei R9 on pathogenic escherichia coli can reach more than 70%, which shows that the lactobacillus casei R9 has better antagonistic action on the pathogenic escherichia coli and lays a good foundation for the development of microbial agents or additives for regulating the ecological balance of intestinal flora of livestock. The invention is used for inhibiting pathogenic escherichia coli.
The invention discloses an oral miracle drug, in particular to a concretion decomposing powdered medicine, belonging to a Chinese medicine preparation in curing renal calculus, capable of decomposing a solid renal calculus into liquid state and being discharged out of a human body with emiction successfully, indolence, and curing the diease completely in a short curative effect. The medicine is characterized in: the endothelium corneum gigeriae galli, Glauber's salt, climbing fern spore, rhizome dioscoreae hypoglaucae, turtleback and buffalo horn are mixed together and be made into powdereds or troches by being comminuted. The formula is bitter and cold, wherein the endothelium corneum gigeriae galli and climbing fern spore are capable of decomposing concretions and dredging emiction, the rhizome dioscoreae hypoglaucae, Glauber's salt and buffalo horn are capable of separating limpidity from turbidity, removing heat and damp, removing blood-heat and stopping bleeding, with all the medicine components working together, all kinds of concretion is capable of being decomposed into liquid state in immateriality and be drainaged successfully till all symptoms disappear. The turtleback in the formula is capable of nourishing Yin and Yang, invigorating the kidney, strengthening bones to prevent too much drainaging. Treating and nourishing are both used to work together in decomposing concretions, with an effect of benefiting for circulation and emiction. The beneficial effect is: indolence, fast curative effect and complete curing.
BACKGROUND: Knee osteoarthritis (KOA) is a very common musculoskeletal disorder, and patients with KOA often exhibit significant quadriceps femoris muscle atrophy. It is well established that curcumin (CUR) exerts protective effects on skeletal muscle. However, the efficacy of CUR in treating KOA-induced quadriceps femoris muscle atrophy and its underlying mechanisms remain uncertain. In this study, we employed network pharmacology to investigate the mechanism by which CUR promotes regenerative repair of the quadriceps femoris muscle in rats with KOA.
METHODS: The potential targets of CUR were obtained from Swiss Target Prediction. The targets of skeletal muscle regeneration were identified from GeneCard and OMIM. A Venn diagram was generated to visualize the intersection of CUR targets and skeletal muscle regeneration targets, and the core targets were identified using STRING. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were conducted using DAVID. Finally, the network pharmacology results were further validated by establishing a KOA rat model using the Hulth method.
RESULTS: Network pharmacology analysis and molecular docking results revealed that CUR affects skeletal muscle regeneration through multiple targets and pathways. In vivo experimental results were validated by demonstrating that KOA causes atrophy and induces apoptosis in the quadriceps femoris muscle. Furthermore, CUR was shown to inhibit apoptosis in the quadriceps femoris muscle by regulating STAT3 and FOS, as well as the PI3K/AKT signaling pathway.
CONCLUSIONS: Our study revealed the apoptosis-inhibiting effects of CUR and its underlying mechanisms. Consequently, CUR has the potential to improve quadriceps femoris muscle atrophy caused by KOA.
Patients should be placed on an appropriate lipid-lowering diet before receiving fenofibrate capsules (micronized) and should continue this diet during treatment with fenofibrate capsules (micronized). Fenofibrate capsules (micronized) should be given with meals, thereby optimizing the bioavailability of the medication.

For the treatment of adult patients with primary hypercholesterolemia or mixed hyperlipidemia, the initial dose of fenofibrate capsules (micronized) is 200 mg per day.

For adult patients with hypertriglyceridemia, the initial dose is 67 to 200 mg per day.Dosage should be individualized according to patient response and should be adjusted if necessary following repeat lipid determinations at 4 to 8 week intervals. The maximum dose is 200 mg per day.

Treatment with fenofibrate capsules (micronized) should be initiated at a dose of 67 mg/day in patients having impaired renal function, and increased only after evaluation of the effects on renal function and lipid levels at this dose. In the elderly, the initial dose should likewise be limited to 67 mg/day.

Lipid levels should be monitored periodically and consideration should be given to reducing the dosage of fenofibrate capsules (micronized) if lipid levels fall significantly below the targeted range.
PURPOSE:To obtain a high-precision multigate image (MGI) where the variance of R-R waves is eliminated, by providing an RAM where two-heartbeat components of data of generated gamma rays obtained through an A/D converter can be stored and adding MGIs viewed form the rise order and the reverse rise order with respect to several hundreds heartbeats. CONSTITUTION:When detecting the first R wave through an electrocardiogram tuning circuit 2, a CPU10 generates an address and sends it to an address generating circuit 8. The circuit 8 stores an R wave rise code in the address of an RAM4. Meanwhile, the CPU10 stores this R wave rise code in an RAM5. When the next R wave rise code is attained, the CPU10 stores this rise code in an address of the RAM4 and stores the address in an RAM6. Data stored in RAMs 4, 5, and 6 are converted by a listframe converting circuit 7, and data in the rise order and the reverse rise order which are the output of the converter 7 are stored in an RAM9. This processing is performed for several hundreds heartteats, and individual MGI are added to attain an average MGI for all heartbeats.
The invention is accomplished by preventing and/or reversing inner ear damage due to noise or toxins. In part, this is accomplished by upregulating antioxidant enzyme activity by applying agents such as R-N6-Phenylisopropyl adenosine (R-PIA) to the round window membrane of the inner ear or systemically, and/or by also applying agents such as 1-2-oxothiazolidine-4-carboxylic acid (Procysteine) to the round window membrane. Also, the invention is accomplished by giving the compounds systemically. Selective auditory hair cell protection in the face of gentamicin exposure by concomitant delivery of an NMDA antagonist or glial dervied neurtrophic factor (GDNF) with the gentamicin. These and additional agents are also accomplished by curtailing activated programmed cell death pathways and/or inducing/enhancing cell repair mechanisms in the inner ear. The agent(s) may be applied before, during or after the noise trauma or toxin exposure.
The education program developed within the scope of the research consists of five modules. In order to use the question and answer method in education, to make the education interactive and to receive feedback, 4 separate training groups of 7 people will be formed. The training will take place on the online platform, not face to face. Midwives will be contacted by phone and / or e-mail and the researcher will give a brief information about the research after introducing himself. A social media group will be created for each training group in order to communicate, announce trainings and inform changes.
Systemic lupus erythematosus (SLE) is a serious autoimmune disease that can lead to extensive damage in multiple organs and systems, ultimately resulting in disability and even death. Children with SLE are particularly at risk of organ damage, especially to the kidneys, and tend to have a more severe and protracted course of the disease compared to adults. Since 2019, CAR T-cell therapy has been successfully applied to autoimmune diseases. Clinical studies have demonstrated that targeted auto-CD19 CAR T-cells hold significant therapeutic potential for SLE. These cells effectively slow down the pathological progression of SLE and can also effectively treat severe cases. However, there are many limitations to the wide application of autologous CAR T-cells, autologous CAR T-cells are "personalized" products, which take a long time to produce, and their quality is affected by the patient's own physique, which is not conducive to scale and standardization. Besides, due to the personalized and complex preparation process of autologous CAR-T cell products, the costs are quite high which limits the promotion of use in the population. Compared with autologous CAR-T cell product, universal CAR-T cell products derived from healthy donors, it is not affected by the quantity and quality of the patient's T cells, leading to a high success rate in preparation. A single batch can meet the needs of hundreds of people, offering absolute advantages in time and cost. Compared to traditional autologous CAR-T cells, allogeneic universal CAR T-cells can greatly expand the accessibility of the product to patients, benefiting more patients. The purpose of this study is to assess the safety and efficacy of the CD19 universal CAR-T cells in the treatment of refractory SLE.
This study comprised a randomized crossover trial of adult United States Army combat medic volunteers participating in a cadaver laboratory as part of their training. The study took place in Bulverde, TX. Participants were randomized to perform cadaver ventilation first using either the novel Nu-MaskR intraoral device or conventional bag valve mask. A one handed seal technique was used to simulate single operator ventilation. Participants were responsible for mask placement while a ventilator delivered 10 breaths each with a standardized tidal volume of 750 ml. After a 5-minute washout period, they performed ventilation using the alternative device. The primary outcome measure was air leak as calculated by subtracting tidal volume received from tidal volume delivered as measured by the ventilator.
Parkinson's Disease (PD) is a chronic condition, with extensive research on initial medication selection for treatment, but limited guidance on long-term medication management. This study aims to identify optimal medication adjustment strategies based on patient clusters, focusing on either maximizing time spent in favorable health states or minimizing time spent in unfavorable ones while avoiding adverse effects. To guide treatment, we developed decision models using prescription dosages converted into standardized units for various medications. Using data from the Parkinson's Progression Markers Initiative, we employed a multivariate time-series clustering approach to capture symptom progression dynamics. This analysis identified four distinct clusters: two representing desirable and undesirable states, and two highlighting motor-focused and non-motor-focused failures across multiple domains. We developed two separate Markov Decision Process (MDP) models to address these dual objectives, which were then integrated into a comprehensive framework that suggests optimal actions and cautions against risky ones for each patient state. This model provides valuable insights for clinical decision-making by offering flexible guidance on adjusting medication intensity rather than prescribing specific medication types, enhancing its applicability in clinical practice.
Parkinson's disease (PD) is a chronic, age-related, progressive multisystem disease associated with neuroinflammation and immune dysfunction. This review discusses the methodological approaches used to study the changes in central and peripheral immunity in PD, the advantages and limitations of the techniques, and their applicability to humans. Although a single animal model cannot replicate all pathological features of the human disease, neuroinflammation is present in most animal models of PD and plays a critical role in understanding the involvement of the immune system (IS) in the pathogenesis of PD. The IS and its interactions with different cell types in the central nervous system (CNS) play an important role in the pathogenesis of PD. Even though culture models do not fully reflect the complexity of disease progression, they are limited in their ability to mimic long-term effects and need validation through in vivo studies. They are an indispensable tool for understanding the interplay between the IS and the pathogenesis of this disease. Understanding the immune-mediated mechanisms may lead to potential therapeutic targets for the treatment of PD. We believe that the development of methodological guidelines for experiments with animal models and PD patients is crucial to ensure the validity and consistency of the results.
1. A Symptom Experience Assessment Questionnaire for COVID-19 patients after recovery; a self-designed symptom assessment tool. The questionnaire takes the Symptom Experience Model (Armstrong et al., 2003) as the theoretical framework, and combines it with a systematic review of COVID-19 symptoms of patients in recovery to form the entry pool. The questionnaire included twenty-four symptoms, and each symptom included three dimensions: frequency, severity, and distress. Each dimension was scored using Likert scales. Taking frequency as an example, zero represents "never happened" and 4 represents "always existed". Cronbach's α coefficient: 0.953, split half reliability: 0.949; KMO: 0.842; (Bartlett's Test of Sphericity) Sig is 0.
2. A questionnaire on risk factors of symptom experience of COVID-19 patients after recovery: a self-designed survey tool.The questionnaire is based on the Symptom Experience Model. In this model, sociodemographic characteristics, disease-related characteristics, and personal characteristics are taken to be the leading factors of symptom experience, and three factors jointly mediate the occurrence and development of symptom experience. Based on this, combined with the results of the literature analysis and the clinical experience in our team, the investigators developed a questionnaire on the factors that influence the experience of symptoms in COVID-19 patients after recovery This included three parts, (a) sociodemographic characteristics (age, marital status, educational background) (b) disease-related characteristics (length of hospitalization, days following discharge, retesting positive for COVID-19, chronic disease) (c) individual factors (the main ways of acquiring knowledge of COVID-19, authenticity of optimism, the degree to which work is affected by symptoms, satisfaction with daily life). Each item was scored by the Likert 5-level scoring method, with zero representing "never" and 4 representing "always".
OBJECTIVE: This study investigates the relationship between hypertension, dysregulation of the autonomic nervous system, heart rate variability (HRV), and chronic inflammation.
METHODS: We analysed a cohort of 50 hypertensive patients treated at the affiliated Hospital of Jianghan University. The average systolic and diastolic blood pressures (BPs) in this group were 155.26 and 95.32 mmHg, respectively. A control group of 50 healthy volunteers, undergoing routine physical examinations at the same hospital, was also analysed.
RESULTS: The average systolic BP of the control group was 115.64 ± 10.27 mmHg, and the average diastolic BP was 75.33 ± 8.25 mmHg. In contrast, the experimental group exhibited an average systolic BP of 155.26 ± 20.13 mmHg and an average diastolic BP of 95.32 ± 12.16 mmHg. Both systolic and diastolic BPs were significantly higher in the hypertensive group (p < 0.05). The experimental group also demonstrated reduced HRV and skin conductance response, alongside increased BP variability (BPV), urinary epinephrine levels and prolonged pupillary light reaction time compared to controls (p < 0.05). Notably, Standard Deviation of Normal to Normal Intervals (SDNN) and Root Mean Square of Successive Differences (RMSSD) values were significantly lower in the experimental group (p < 0.05). Furthermore, levels of inflammatory markers such as CRP, TNF-α, IL-6 and IL-1β were markedly elevated in hypertensive patients (p < 0.05). Negative correlations were observed between systolic and diastolic BP with HRV metrics, while positive correlations were found between BP and BPV as well as urinary adrenaline levels.
CONCLUSIONS: The findings indicate that hypertension is closely associated with autonomic nervous system dysfunction, reduced HRV and increased chronic inflammation. A comprehensive approach to hypertension management should integrate these interrelated physiological and pathological mechanisms, with potential therapeutic interventions targeting autonomic function and inflammatory states.
In this particular arm of the study, participants also undergo an initial electroencephalography (EEG) procedure. Subsequently, intermittent theta burst stimulation (iTBS) is administered using the standard theta burst stimulation frequency of 5Hz. The participants receive this treatment once daily, five times a week, over a total duration of three weeks.