anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Application of GPR31 inhibitor in preparation of medicines for treating cerebral ischemia-reperfusion injury and related diseases. Experimental research shows that the expression level of GPR31 protein is gradually increased along with the prolongation of tissue ischemia time, and a positive correlation exists between the expression level and the severity of tissue ischemia-reperfusion injury. Overexpression of GPR31 can increase activity of liver cells, cardiac muscle cells and kidney cells caused by H/R treatment. In addition, a decrease in GPR31 expression in hepatocytes may inhibit cellular lipid deposition caused by palmitate and oleate stimulation. Overexpression of GPR31 in cardiomyocytes aggravates cardiac hypertrophy due to angiotensin ii. Therefore, GPR31 inhibitors are useful for the preparation of medicaments for the treatment of diseases associated with ischemia reperfusion injury; myocardial hypertrophy and related diseases; metabolic disorders of the liver.
Subjects in the USA will choose to use the LF111 tablets or drospirenone (DRSP) 3.5 mg chewable tablets; 1/3 of subjects in the USA should receive DRSP 3.5 mg chewable tablets. Only LF111 will be available to subjects in Europe.
PCT No. PCT/AU95/00505 Sec. 371 Date Apr. 16, 1997 Sec. 102(e) Date Apr. 16, 1997 PCT Filed Aug. 16, 1995 PCT Pub. No. WO96/05218 PCT Pub. Date Feb. 22, 1996The present invention provides a method for introducing nucleic acids into cells. The method involves exposing the cells to a compound having formula (1), in which w is a nucleic acid, x is a peptide or amino acid, y is a linker having a chain length equivalent to 1 to 20 carbon atoms or is absent, R4 is H ir CH2O-R3; and R1, R2 and R3 are the same or different and are either hydrogen, methyl, ethyl, hydroxyl or an acyl group derived from a fatty acid having a carbon chain of 3 to 24 carbon atoms saturated or unsaturated, with the proviso that at least one of R1, R2 and R3 is an acyl group derived from a fatty acid, or to a compound having the formula (2): w . . . xyNHCH2CH2OR5, in which w is a nucleic acid, x is a peptide or amino acid, y is a linker having a chain length equivalent to 1 to 20 carbon atoms or absent, R5 is an acyl group derived from a fatty acid having a carbon chain of 3 to 24 carbon atoms saturated or unsaturated. The invention also relates to these compounds.
BACKGROUND: TC-325 powder has been successfully used in the management of malignancy-related upper gastrointestinal bleeding (UGIB) with favorable results. We conducted a meta-analysis of randomized controlled trials (RCTs) comparing TC-325 hemostatic powder with standard endoscopic treatments in the management of malignancy-related UGIB.
METHODS: Several databases were reviewed from inception to May 02, 2024 to identify RCTs comparing TC-325 and standard endoscopic treatments for the management of malignancy-related UGIB. Our outcomes of interest were immediate hemostasis, 30-day rebleeding, length of hospital stay, need for surgery, need for angiographic embolization, and all-cause mortality. We calculated pooled risk ratio (RR) with 95% confidence intervals (CI) for categorical variables and mean difference (MD) with 95% CI for continuous variables. We used a random effect model to analyze the data and heterogeneity was assessed by I2 statistic.
RESULTS: Four RCTs with 227 patients were included. We found that, the rate of immediate hemostasis was significantly higher in the TC-325 group compared to the standard therapy group, RR (95% CI): 1.48 (1.26, 1.74). There was no significant difference in 30-day rebleeding between the groups RR (95% CI): 0.52 (0.15, 1.76). We found no significant difference in other outcomes between groups such as the need for angiographic embolization, all-cause mortality, length of hospital stay, and need for surgery.
CONCLUSIONS: We found that, TC-325 hemostatic powder was superior to standard endoscopic treatments in achieving immediate hemostasis in patients with malignancy-related UGIB.
The targeted delivery of therapeutic agents to specific cells remains a challenge in drug delivery. Provided herein are nanoparticle-targeting agent conjugates that can be used for the targeted delivery of therapeutic agents to certain cells and target tissues. The conjugates comprise nanoparticles (e.g., metal nanoparticles such as gold nanoparticles) with organic outer shells capable of adsorbing large numbers of therapeutic agents (e.g., small molecule drugs). The nanoparticles are covalently linked to targeting agents (e.g., proteins such as antibodies). The present invention also provides formulations comprising the nanoparticle-targeting agent conjugates, and kits comprising the same. In another aspect, the present invention provides methods of using the conjugates for the delivery of therapeutic agents to cells, and the treatment and/or prevention of diseases (e.g., autoimmune diseases, infectious diseases, proliferative diseases such as cancer). In another aspect, the present invention provides methods of preparing the nanoparticle-targeting agent conjugates described herein.
Generic name:Felbinac Trometamol Injection; Placebo:normal saline Dosage form:Injection Dosage:188.5mg Volume:8ml Frequency:Multi-dose Duration:1 day. A total of 40 subjects,40 received the test drug .
Disease detection from medical images is provided. In various embodiments, a medical image of a patient is read. The medical image is provided to a trained anatomy segmentation network. A feature map is received from the trained anatomy segmentation network. The feature map indicates the location of at least one feature within the medical image. The feature map is provided to a trained classification network. The trained classification network was pre-trained on a plurality of feature map outputs of the segmentation network. A disease detection is received from the trained classification network. The disease detection indicating the presence or absence of a predetermined disease.
Intracerebral hemorrhage (ICH) is a severe stroke subtype with limited therapeutic options. Programmed cell death (PCD) is crucial for immunological balance, and includes necroptosis, pyroptosis, apoptosis, ferroptosis, and necrosis. However, the distinctions between these programmed cell death modalities after ICH remain to be further investigated. We used single-cell transcriptome (single-cell RNA sequencing) and spatial transcriptome (spatial RNA sequencing) techniques to investigate PCD-related gene expression trends in the rat brain following hemorrhagic stroke. Ferroptosis was the main PCD process after ICH, and primarily affected mature oligodendrocytes. Its onset occurred as early as 1 hour post-ICH, peaking at 24 hours post-ICH. Additionally, ferroptosis-related genes were distributed in the hippocampus and choroid plexus. We also elucidated a specific interaction between lipocalin-2 (LCN2)-positive microglia and oligodendrocytes that was mediated by the colony stimulating factor 1 (CSF1)/CSF1 receptor pathway, leading to ferroptosis induction in oligodendrocytes and subsequent neurological deficits. In conclusion, our study highlights ferroptosis as the primary PCD mechanism, emerging as early as 1 hour post-ICH. Early therapeutic intervention via the suppression of microglial LCN2 expression may alleviate ferroptosis-induced damage in oligodendrocytes and associated neurological deficits, thus offering a promising neuroprotective strategy following ICH.
Persons with multiple sclerosis (MS) MS commonly experience muscle weakness and fatigue which may contribute to the commonly reported symptomatic fatigue. Photobiomodulation therapy (PBMT) induced with light in the visible red to near infrared (VIS/NIR) region of the spectrum (600-1000 nm) can stimulate cytochrome c oxidase and improve mitochondrial function. PBMT is an emerging therapeutic modality for soft tissue injury, chronic inflammation, neurodegeneration , and retinal diseases. PBMT has also been used to enhance muscle endurance, strength and recovery in healthy adults. We propose that in persons with MS, PBMT will 1) enhance regional muscle endurance after acute treatment and 2) enhance functional endurance after extended treatment. We will also test to determine if improvements are due to central or peripheral neuromuscular or cardiovascular mechanisms. Final, we will explore if regional PBMT can result in systemic anti-inflammatory effects.
Exposures to endocrine disrupting chemicals (EDCs) have been linked to chronic diseases and conditions including breast cancer, metabolic syndrome, diabetes, and infertility. Timing of exposure, especially during pregnancy, may have a lifelong impact on the fetus, including neurodevelopmental problems and asthma. However, there have been no tools to allow those in the preconception, conception, and pregnancy stages to assess EDC exposures to ensure a healthy pregnancy and normal child development. Million Marker (MM) was born to fill this need. MM is a precision health company, built by a team of multidisciplinary scientists who are trained in environmental epidemiology, toxicology, analytical chemistry, biostatistics, data engineering, and business. MM's missions are to crowdsource and scale the biomonitoring of environmental chemicals and provide actionable results to consumers in a timely manner in order to empower individuals to proactively assess, track, and reduce their harmful environmental exposures. Starting with a few biomarkers of common EDCs, MM's ultimate vision is to discover all possible ("a million") biomarkers of harmful exposures to inform and improve individual health outcomes and advance precision medicine. Less than a year after it was founded, Million Marker developed and sold the first product-a mail-in urine test for BPA and phthalates-and successfully helped users reduce exposures through personalized intervention plans. Customers are able to order a test kit online, receive the test kit via mail, take a comprehensive exposure survey (via the Million Marker app), send back samples via mail, view personalized reports with tailored product recommendations through a secure online portal, make lifestyle changes to reduce exposures, and retest to monitor progress. MM's initial target audience are individuals of reproductive age, due to the vulnerability pregnancy and preconception to EDC exposures. However, it is unclear to what extent the MM platform educates, motivates, and ultimately reduces EDC exposure in individuals in this age range. Therefore, the aims of the current proposal are to 1) test and validate a this first-of-its-kind mobile EDC reduction program in a prospective longitudinal cohort intervention trial; 2) assess changes in participants' environmental health literacy, attitudes, knowledge, and behaviors after using MM's products and services; and 3) evaluate the MM app and platform usability to improve the user experience. Validating this population with MM's program is a step towards these types of future studies. At the conclusion of the project, MM will be well-positioned to begin Phase II and will scale the EDCs testing and personalized intervention plan to fertility clinics and the general public.
With growing emphasis on the development and maintenance of healthy lifestyles, the family role has increasing importance. A family-based health promotion strategy can be instrumental in helping disseminate and reinforce knowledge and behaviours on family well-being and better equip families to protect themselves and promote family well-being beyond the COVID-19 pandemic. Additionally, the pandemic led to increased sedentary behavior and unhealthy eating. New, innovative health promotion strategies and approaches to increase physical activity and healthy diet and enhance well-being are needed.

This study aims to investigate and use a game-based approach to enhance knowledge and behaviours on healthy living and family well-being. We will conduct quantitative and qualitative evaluation. The findings would provide evidence of the feasibility and effectiveness of such an approach in a family-based context. It would also guide the direction for future health education and awareness trials and related projects and campaigns for health promotion efforts and to help improve family well-being in the Hong Kong community and elsewhere.
Huanglian Jiedu decoction (HLJD) has been used to treat ischemic stroke in clinic. However, the detailed protective mechanisms of HLJD on ischemic stroke have yet to be elucidated. The aim of this study is to elucidate the underlying pharmacological mechanisms of HLJD based on the inhibition of neuroinflammation and the amelioration of nerve cell damage. A middle cerebral artery occlusion reperfusion (MCAO/R) model was established in rats and received HLJD treatment. Effects of HLJD on neurological function was assessed based on Bederson's score, postural reflex test and asymmetry score. 2, 3, 5-Triphenyltetrazolium chloride (TTC) staining, Hematein and eosin (HE) and Nissl staining were used to observe the pathological changes in brain. Then, transcriptomics was used to screen the differential genes in brain tissue in MCAO/R model rats following HLJD intervention. Subsequently, the effects of HLJD on neutrophil extracellular trap (NET) formation-related neuroinflammation, gamma-aminobutyric acid (GABA)ergic synapse activation, nerve cell damage and proliferation were validated using immunofluorescence, western blot and enzyme-linked immunosorbent assay (ELISA). Our results showed that HLJD intervention reduced the Bederson's score, postural reflex test score and asymmetry score in MCAO/R model rats. Pathological staining indicated that HLJD treatment decreased the cerebral infarction area, mitigated neuronal damage and increased the numbers of Nissl bodies. Transcriptomics suggested that HLJD affected 435 genes in MCAO/R rats. Among them, several genes involving in NET formation and GABAergic synapses pathways were dysregulated. Subsequent experimental validation showed that HLJD reduced the MPO+CitH3+ positive expression area, reduced the protein expression of PAD4, p-P38/P38, p-ERK/ERK and decreased the levels of IL-1β, IL-6 and TNF-α, reversed the increase of Iba1+TLR4+, Iba1+p65+ and Iba1+NLRP3+ positive expression area in brain. Moreover, HLJD increased GABA levels, elevated the protein expression of GABRG1 and GAT3, decreased the TUNEL positive expression area and increased the Ki67 positive expression area in brain. HLJD intervention exerts a multifaceted positive impact on ischemia-induced cerebral injury in MCAO/R rats. This intervention effectively inhibits neuroinflammation by mitigating NET formation, and concurrently improves nerve cell damage and fosters nerve cell proliferation through activating GABAergic synapses.
In the course of chronic liver disease a systemic inflammatory reaction promotes mediators leading to a loss of appetite, as well as to metabolic and hormonal changes. Consequences hereof are a decreased food uptake, a deteriorated nutrient utilization and a loss of muscles, with or without fat loss leading to cachexia. Especially muscle loss has a relevant influence on morbidity and mortality of chronic liver patients. The loss of muscle is probably due to a deteriorated protein synthesis with concurrent anabolic resistance. These pathologic processes increase the protein requirements of chronic liver patients dramatically.

The purpose of this study is to establish an innovative combined therapy involving optimized nutritional therapy and highly effective muscle training by personalized whole-body electromyostimulation (WB-EMS) exercise to improve the quality of life (QLQ) of patients with serious chronic disease. An improvement of QLQ results from an increase in muscle mass and strength, thereby increasing physical activity, physical capability as well as tolerance to and applicability of therapy. In the course of a 3-months intervention study the efficacy of a combined German-guidelines-recommended protein-rich nutritional therapy with an innovative exercise therapy will be documented for patients with chronic liver disease. An effective stopping of the progress of muscle wasting or even increase of muscle mass, strength and function in the patients of the trial would benefit each patient and his family individually, since it could mean a considerable improvement in his QLQ and tolerability of therapeutical treatment.
NEW MATERIAL:An isoquinoline derivative expressed by formula I [R1 is lower alkyl or lower alkoxyalkyl; R2 and R3 are H, lower alkyl, lower alkoxy, cyclohexyl, substituted cyclohexyl, phenyl, substituted phenyl, benzyl, substituted benzyl, pyridyl or oxo (=0)] and a salt thereof. EXAMPLE:4-Cyano-2,3,5,6,7,8-hexahydro-7-methoxy-1-methyl-3-oxoisoquino line. USE:A cardiotonic agent, exhibiting high cardiotonic activity, and having low toxicity. PREPARATION:A compound expressed by formula III is condensed with any of compounds expressed by formulas V-VII (X is halogen; R4 is methyl or ethyl) in the presence of sodium hydride, etc. in an organic solvent to give a compound expressed by formula IV, which is then condensed with cyanoacetamide in the presence of piperidine, etc. to afford the aimed compound expressed by formula I.
PROBLEM TO BE SOLVED: To sufficiently improve the freshness of aftertaste of a composition for oral cavity. SOLUTION: This composition contains a functional substance capable of masking foreign tastes originated from compounding components and intensifying fresh feeling as an improving agent for aftertaste. The functional substance is selected from group consisting of substances having bitterness, sourness and astringency. A substance having bitterness (sourness or astringency) is a natural product having bitterness (sourness or astringency), an extract of a natural product having bitterness (sourness or astringency) and/or a compound having bitterness (sourness or astringency). A preferable mode of composition has a water content of 5 wt.% or less, and contains a heat generating body. In this case, the heat generating body is anhydrous zeolite, anhydrous magnesium sulfate, dextrin, sodium metaphosphate and/or calcium chloride.
The efficacy of VISTOGARD was assessed in 135 patients who were treated in two open-label trials, Study 1 (n=60) and Study 2 (n=75). The patients in both studies had either received an overdose of fluorouracil or capecitabine, or presented with severe or life-threatening toxicities within 96 hours following the end of fluorouracil or capecitabine administration. Overdose was defined as administration of fluorouracil at a dose, or infusion rate, greater than the intended dose or maximum tolerated dose for the patient's intended regimen of fluorouracil. VISTOGARD was administered at 10 grams orally every 6 hours for 20 doses or at a body surface area adjusted dosage of 6.2 grams/m2/dose for 20 doses for four patients between 1 and 7 years of age. The major efficacy outcome was survival at 30 days or until the resumption of chemotherapy if prior to 30 days. 

In Study 1 and Study 2 combined, the median age of the patients was 59 years (range: 1 to 83), 56% were male, 72% were white, 9% were Black/African American, 6% were Hispanic, 4% were Asian, and 95% had a cancer diagnosis. Of the 135 patients, 117 were treated with VISTOGARD following an overdose of fluorouracil (n=112) or capecitabine (n=5), and 18 were treated after exhibiting severe or life-threatening fluorouracil toxicities within 96 hours following the end of fluorouracil administration. The severe or life-threatening toxicities involved the central nervous system (such as encephalopathy, acute mental status change), cardiovascular system, gastrointestinal system (such as mucositis), and bone marrow. A total of six pediatric patients were administered VISTOGARD. Four patients initiated VISTOGARD more than 96 hours following the end of fluorouracil or capecitabine administration. Of the 112 patients overdosed with fluorouracil, 105 (94%) were overdosed by infusion rate only (range 1.3 to 720 times the planned infusion rate), four (4%) were overdosed by dose only, and three (3%) were overdosed by both dose and rate.

The survival results are shown in Table 4. Of the 135 patients who were treated with VISTOGARD in Studies 1 and 2 there were five deaths due to fluorouracil or capecitabine toxicity (4%). Of the five patients who died, two were treated after 96 hours following the end of fluorouracil administration. In the patients treated with VISTOGARD for an overdose of fluorouracil or capecitabine in Studies 1 and 2 combined (n=117), survival at 30 days was 97% (n=114). In the patients receiving VISTOGARD for early-onset severe or life-threatening toxicity in Studies 1 and 2 combined (n=18), the survival at 30 days was 89% (n=16). In these studies 33% of patients (n=45) resumed chemotherapy in less than 30 days. Based on retrospective historical case reports of 25 patients who were overdosed with fluorouracil and received supportive care only, all were overdosed by rate with a range 1.9 to 64 times the planned infusion rate, and 84% died.
The invention provides a recombinant Newcastle disease virus LaSota vaccine strain rLa-WNV-PrM/E for expressing a West Nile virus (WNV) PrM/E protein. The collection number of the vaccine strain is CGMCC No. 10199; the body fluid generated by the recombinant virus and the cellular immune response are systematically evaluated in a mouse mold. Results indicate that the vaccine strain is capable of correctly expressing the PrM/E protein. A C57BL/6 mouse is immunized twice by use of the recombined virus, and then an ELISA result indicates that the immunized mouse is capable of generating high-level PrM/E protein-specific IgG; a neutralization test result indicates that the immunized mouse is capable of generating high-level WNV neutralization antibodies; the flow cytometry indicates that the immunized mouse is capable of generating WNVE protein epitope-specific CD4+ and CD8+T cell immune response. The vaccine strain is a safe, efficient West Nile virus prevention and control candidate vaccine having perspectiveness and reservation property, and has great strategic importance for China to cope with the potential threats of the virus.