anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Chronic hepatitis B virus (HBV) infection remains a significant global health challenge due to its link to severe conditions like HBV-related cirrhosis and hepatocellular carcinoma (HCC). Although current treatments effectively reduce viral levels, they have limited impact on certain HBV elements, namely hepatitis B surface antigen (HBsAg) and covalently closed circular DNA (cccDNA). This highlights the urgent need for innovative pharmaceutical and biological interventions that can disrupt HBsAg production originating from cccDNA. In this study, we identified a natural furanocoumarin compound, Imperatorin, which markedly inhibited the expression of HBsAg from cccDNA, by screening a library of natural compounds derived from Chinese herbal medicines using ELISA assay and qRT-PCR. The pharmacodynamics study of Imperatorin was explored on HBV infected HepG2-NTCP/PHHs and HBV-infected humanized mouse model. Proteome analysis was performed on HBV infected HepG2-NTCP cells following Imperatorin treatment. Molecular docking and bio-layer interferometry (BLI) were used for finding the target of Imperatorin. Our findings demonstrated Imperatorin remarkably reduced the level of HBsAg, HBV RNAs, HBV DNA and transcriptional activity of cccDNA both in vitro and in vivo. Additionally, Imperatorin effectively restrained the actions of HBV promoters responsible for cccDNA transcription. Mechanistic study revealed that Imperatorin directly binds to ERK and subsequently interfering with the activation of CAMP response element-binding protein (CREB), a crucial transcriptional factor for HBV and has been demonstrated to bind to the PreS2/S and X promoter regions of HBV. Importantly, the absence of ERK could nullify the antiviral impact triggered by Imperatorin. Collectively, the natural compound Imperatorin may be an effective candidate agent for inhibiting HBsAg production and cccDNA transcription by impeding the activities of HBV promoters through ERK-CREB axis.
The transmembrane metalloproteinase-disintegrin ADAM8 mediates cell adhesion and shedding of ligands, receptors, and extracellular matrix components. ADAM8 is abundantly expressed in breast tumors and derived metastases compared to normal tissue, especially in triple-negative breast cancers (TNBCs). High ADAM8 levels predicted poor patient outcome, and ADAM8 promoted an aggressive phenotype of TNBC cells in culture. Tumors derived from TNBC cells with ADAMS knockdown failed to grow beyond a palpable size and displayed poor vascularization. Circulating tumor cells and brain metastases were also significantly reduced. ADAMS stimulated angiogenesis through release of VEGF-A and cell migration through βΐ -integrin activation. Treatment with anti-ADAM8 antibody  in vivo  resulted in reduced primary tumor burden and reduced metastases. Furthermore, antibody treatment of established tumors profoundly decreased metastases in a resection model. ADAM8 represents a promising novel target for treatment of TNBCs, which currently lack targeted therapies and frequently progress with fatal dissemination.
1. Technical Result Improvement of medicinal properties of the compound. 2. Essence An amorphous torasemide modification is characterized with physical and chemical properties disclosed in the specification; use of said modification is possible as a raw material for the preparation of pharmaceutically acceptable salts of torasemide, as well as an active agent, as a diuretic and for treatment of other diseases, including thrombosis, angina pectoris, asthma, hypertension, nephroedema, pulmonary edema, cerebral edema caused by trauma, methods for their production and pharmaceutical compositions containing the same. 3. Field of Application Medicine.
The present disclosure provides a film for application to the living body, which contains a regenerated cellulose and is advantageous for reducing the time required for attachment of regenerated cellulose to living tissues. A film (10) for application to the living body according to the present disclosure contains a regenerated cellulose and an accelerator. The accelerator accelerates attachment of the regenerated cellulose to living tissues. This film (10) for application to the living body is self-supporting, and has a thickness of from 20 nm to 5,000 nm. The accelerator has an HLB value of 4-18. This film (10) for application to the living body is able to maintain the shape without having a supporting body.
Participants received GSK3884464 or placebo through oral administration in the treatment sequence: GSK3884464 1 mg/ GSK3884464 3 mg / Placebo C1 across 3 treatment periods. There was a minimum of 7 days washout period between dosing in each session.
BACKGROUND: Post-translational modification pathway of protein ubiquitination is intricately associated with tumorigenesis. We previously reported elevated ubiquitin-conjugating enzyme 2T (UBE2T) as an independent risk factor in stage I lung adenocarcinoma and promoting cellular proliferation. However, its underlying mechanisms needed further investigation.
METHODS: Immunohistochemistry was used to assess the expression of UBE2T and retinoic acid receptor-related orphan receptor α (RORA) in stage I LUAD. Cell proliferation, migration, and invasion of LUAD cell lines were measured by Cell Counting Kit-8 assay (CCK-8), Colony-forming assay and Transwell assay, respectively. Western blot analysis was performed to determine the expression of epithelial-mesenchymal transition (EMT) markers. A xenograft model was established to evaluate the proliferative capacity of UBE2T and its interaction with RORA in promoting LUAD. Mechanistic insights into the promotion of early-stage LUAD by UBE2T were obtained through luciferase reporter assay, chromatin immunoprecipitation and co-immunoprecipitation.
RESULTS: UBE2T and RORA expression was significantly up- and down-regulated in early-stage LUAD patients which's proved to be associated with unfavorable outcomes, strengthened cell proliferation, migration, EMT and invasion through its interaction with RORA both in vivo and in vitro. The growth NSCLC xenografts was reduced by down-expression of UBE2T but was suppressed by RORA knockout. Mechanistically, UBE2T mediated the ubiquitination of the intermediate transcription factor PBX1, which played a transcriptional role in downstream regulation of RORA.
CONCLUSION: The oncogenic role of UBE2T and the UBE2T-PBX1-RORA axis in driving malignant progression in Stage I LUAD had been established. UBE2T might be a novel and promising therapeutic target for LUAD treatment.
PURPOSE:To provide a remedy for hepatic disease containing unsubstituted or alkyl-substituted 1,3-benzodioxol as an essential component, exhibiting by far strong remedying activity to hepatic disease compared with known compound having methylenedioxy group, and having high safety. CONSTITUTION:The objective remedy for hepatic disease contains the compound of formula I (R<1> and R<2> are H or 1-5C saturated alkyl) as an essential component. The compound of formula I has strong activity to cure hepatic disease compared with the compound having methylenedioxy group in the molecule and known as a remedy for hepatic disease, e.g. the compound of formula II, formula III, etc. Furthermore, it has no mutagenecity in contrast with safrole. Dose; preferably 1-10mg/kg daily for oral administration and 0.5-5mg/kg daily for parenteral administration.
Mothers without gestational diabetes will receive 18 months of educational intervention post-partum. They and their offspring will be evaluated at months 1,2,3,6,9,12,15,and 18.
Alpha-synuclein (αsyn) is an intrinsically disordered protein that aggregates in the brain in several neurodegenerative diseases collectively called synucleinopathies. Phosphorylation of αsyn at serine 129 (PSER129) was considered rare in the healthy human brain but is enriched in pathological αsyn aggregates and is used as a specific marker for disease inclusions. However, recent observations challenge this assumption by demonstrating that PSER129 results from neuronal activity and can be readily detected in the non-diseased mammalian brain. Here, we investigated experimental conditions under which two distinct PSER129 pools, namely endogenous-PSER129 and aggregated-PSER129, could be detected and differentiated in the mammalian brain. Results showed that in the wild-type (WT) mouse brain, perfusion fixation conditions greatly influenced the detection of endogenous-PSER129, with endogenous-PSER129 being nearly undetectable after delayed perfusion fixation (30-min and 1-h postmortem interval). Exposure to anesthetics (e.g., Ketamine or xylazine) before perfusion did not significantly influence endogenous-PSER129 detection or levels. In situ, non-specific phosphatase calf alkaline phosphatase (CIAP) selectively dephosphorylated endogenous-PSER129 while αsyn preformed fibril (PFF)-seeded aggregates and genuine disease aggregates (Lewy pathology and Papp-Lantos bodies in Parkinson's disease and multiple systems atrophy brain, respectively) were resistant to CIAP-mediated dephosphorylation. The phosphatase resistance of aggregates was abolished by sample denaturation, and CIAP-resistant PSER129 was closely associated with proteinase K (PK)-resistant αsyn (i.e., a marker of aggregation). CIAP pretreatment allowed for highly specific detection of seeded αsyn aggregates in a mouse model that accumulates non-aggregated-PSER129. We conclude that αsyn aggregates are impervious to phosphatases, and CIAP pretreatment increases detection specificity for aggregated-PSER129, particularly in well-preserved biological samples (e.g., perfusion fixed or flash-frozen mammalian tissues) where there is a high probability of interference from endogenous-PSER129. Our findings have important implications for the mechanism of PSER129-accumulation in the synucleinopathy brain and provide a simple experimental method to differentiate endogenous-from aggregated PSER129.
A pressurized container contains a stable solubilized mixture of propellant, which is liquid under pressure, and an intermediate formulation, which comprises a pharmaceutical agent, water, first ingredient, second ingredient and at least one third ingredient.  The first ingredient is selected from the group consisting of glycerin and polyglycerin and mixtures thereof in an amount of from 1-50 wt./wt. % of the intermediate formulation. The second ingredient is selected from the group consisting of phenol, methyl phenol and mixtures thereof in an amount of from 1-20 wt./wt. % of the intermediate formulation. The third ingredient is selected from the group consisting of alkali metal C8 to C22 alkyl sulphate, polidocanol C6 to C40 alkyl ethers, trihydroxy sodium oxo-cholanyl glycines, polyoxethylene sorbitan ethers, alkyl-aryl polyether alcohols, hyaluronic acid and pharmaceutically suitable salts thereof, monoolein, triolein, lysine, polylysine, oleic acid, linoleic acid, linolenic acid, monooleates and laurates, glycolic acid, lactic acid, chenodeoxycholate, deoxycholate, chamomile extract, cucumber extract, borage oil and evening primrose oil and mixtures thereof, in an amount of from 1-50 wt./wt. % of the intermediate formulation. The total concentration of first, second and third ingredients is less than 90 wt./wt. % of the intermediate formulation. Also described is a process to making the stable aerosol pharmaceutical composition comprises solubilizing the propellant by a process comprising dissolving the proteinic agent in water and adjusting the pH to a level suitable for pharmaceutical use, mixing with the first ingredient, mixing with the second ingredient and subsequently mixing in the third ingredient. The intermediate formula is then charged to a pressurizable container and then the container is charged with a propellant. The pressurized container containing the stable solubilized mixture and intermediate formula is useful for administrating a proteinic agent bucally or into the lungs by spraying for the treatment of a medical condition.
Lipid matrix composition have a particular structure and associated physical properties. The present disclosure provides a drug delivery composition comprising a lipid matrix and a pharmaceutically acceptable carrier. The lipid matrix is, at least in part, in a lamellar phase. The lipid matrix comprises lysophosphoglyceride, monoglyceride and fatty acid. The molar ratio of lysophosphoglyceride:the sum of monoglyceride and fatty acid in the lipid matrix is between 1:3 and 1:12. The present disclosure also provides a nutritional supplement comprising the drug delivery composition.
PURPOSE:To obtain the titled extract for oral administration, containing a carcinostatic and immunity promoting component, keeping the taste, flavor, minor active components, etc. of the original fungus, by concentrating ethanol extract of Flammulina velutipes (an edible fungus) to a specific concentration, and adding a specific amount of ethanol to the concentrate. CONSTITUTION:For example, a mixture for a culture medium composed of the fruit body or mycelia of Flammulina velutipes and chaff, sawdust, rice bran, etc. is extracted with 30% ethanol. The obtained extract is concentrated to an extent to give a (raw material)/(product) ration of 1:1 when added with about 20% ethanol. Ethanol is added to the concentrate in an amount of about 20% to obtain the objective product.
Background: According to the National Pressure Ulcer Association Panel (NPUAP) data, the incidence of pressure wounds (PW) in acute care units varies between 0.4-38%, in long-term care units 2.2-23.9%. While it is stated that more than 700,000 patients develop PW each year in the UK and 180,000 of them start in the hospital, PW is a significant health burden affecting more than 2.5 million adults per year in the United States (USA) and will affect the growing elderly population in the future. According to the National Health Service (NHS), it is claimed that the daily cost of treatment applied in the treatment of PW is more than 3.8 million. European Pressure Ulcer Association Panel (EPUAP) according to, PW is defined as localized skin/subcutaneous tissue damage, usually occurring on bone prominences, caused by additional factors together with pressure or shearing. It is said that hand massage is effective in preventing the development of PW; when the literature results are examined, it has been determined that there are insufficient studies at the level of evidence to measure the effectiveness of massage applications or hand massage. Therefore, our study, it was aimed to evaluate the effect of classical hand massage on the prevention of PW.

Method: A total of 60 patients over the age of 18 who were hospitalized in the intensive care unit of the hospital with undeveloped PW and who had not undergone surgery were randomly assigned to the experimental and control groups. The patients included in the experimental group were massaged twice a day, in the morning and evening, together with nursing care, for 15-20 minutes. Admitted to the control group. only nursing care was applied to the basta. Due to the lack of a clear time for PW development in the literature, patients; In the hospital where the research was conducted, patients were followed up for 12 days, since the average duration of opening RF was 12 days in 2019-2020. Patients who were opened BY were followed up until the day they were opened.
Post isometric relaxation technique is performed after positioning the patient and was asked to apply 30% force against therapist force and hold that contraction for 7- 10seconds and after that relax for 5seconds and when patient exhale. Therapists take muscle to new restriction barrier; hold this position for 10-60 seconds . Technique is performed 3-5 reps along with conventional treatment for 3 consecutive weeks.
A measurement system includes a light source having semiconductor sources, a multiplexer, and one or more fused silica fibers configured to form an output optical beam having one or more optical wavelengths modulated at a modulation frequency. A light beam set-up includes a monochromator forming a filtered optical beam. A measurement apparatus delivers the filtered optical beam to a sample. A receiver receives a spectroscopy output beam generated from the sample by the filtered optical beam. The receiver is configured to use a lock-in technique that detects the modulation frequency, and to generate first and second signals responsive to light received while the light source is off and on, respectively. The measurement system improves a signal-to-noise ratio of the spectroscopy output beam by differencing the first and second signals. The receiver processes the spectroscopy output beam using chemometrics or multivariate analysis to permit identification of materials within the sample.
Participants will sit continuously for 3 hours. They will interrupt solitary sitting activities (while remaining seated) by talking to a researcher for 3 min on pre-selected topics of general interest.
Participants will be submitted to a linear pressure resistance (PowerBreathe) with an inspiratory load of 30% of maximal inspiratory pressure (adjusted weekly), seven days a week, session duration of 30 minutes for 12 weeks. During training, participants will be instructed to maintain diaphragmatic breathing with a breathing rate of 15-20 cycles/min. Inspiratory load will be set at 30% of maximum static inspiratory pressure, and weekly training loads will be adjusted to maintain 30% of MIP. Each week, six training sessions will be held at home and a training session will be supervised in the research center.
A classic "3+3" design will be used to explore the maximum tolerated dose (MTD) and to determine the recommended phase II dose (RP2D). Three to four patients will be enrolled to ensure at least 3 evaluable patients for DLT (Dose Limiting Toxicity). ABM-168 monotherapy will be conducted in seven provisional dose levels starting at 0.5mg oral administration per day and up to and including 12mg oral administration. Each treatment cycle is 28-days. DLT will be evaluated in the first 28-day cycle. Patients will receive daily doses of ABM-168 until disease progression; intolerable toxicity; withdrawal consent; or other clinical observation is met.
The invention relates to a polypeptide capable of binding to human CD19, which comprises 3 complementarity determining regions CDR1-3, wherein the sequence of CDR1 is or comprises one of the sequences shown in SEQ ID NO. 1-15, the sequence of CDR2 is or comprises one of the sequences shown in SEQ ID NO. 16-30, and the sequence of CDR3 is or comprises one of the sequences shown in SEQ ID NO. 31-48. The invention carries out nano antibody drug development and diagnostic kit development aiming at B cell malignant tumor, and selects the nano antibody VHH specifically combined with CD19 by preparing CD19 protein, immune alpaca, platform technology for displaying nano monoclonal antibody by using phage library, etc., identifies the CDR sequence thereof, and constructs humanized antibody C19 NB; and simultaneously, identifying the binding of the humanized antibody and the cell surface CD19 protein by using a flow cytometry detection method. The invention provides a potential nano-antibody new drug for the clinical treatment of cancers expressed by the CD19 antibody, such as B cell malignant tumor.
Experimental: emotion-oriented Cognitive Behavior Therapy focused on delusions for patients with schizophrenia-spectrum disorders and delusions. The therapeutical intervention follows a treatment-manual consisting of two modules. Patients work on two modules every week for 25 weeks in a row. Module I comprises psychoeducation on emotions, training radical acceptance of emotions and mindfulness, cognitive and behavioral strategies in order to change negative emotions and in order to foster positive emotions and suggestions for life-style changes (positive activities, sports, stress reduction). In the second module, the focus is on self-acceptance. Patients receive psychoeducation on self-acceptance and learn strategies in order to reduce negative self-schema and foster positive self-schema.
[Problem] To provide a pyridine N-oxide compound: that is superior in terms of pest control activities, particularly insecticidal activity and/or acaricidal activity among such activities; that is superior in terms of safety; and that can be industrially synthesized in an advantageous manner. [Solution] The present invention provides a pyridine N-oxide compound that is a compound represented by formula (II), a stereoisomer, a tautomer, a hydrated object, or a salt thereof. In formula (II), R1 is an alkylsulfonyl group that has a substitution or does not have a substitution and that has 1-6 carbon atoms. R2 is a hydrogen atom, an alkyl group that has a substitution or does not have a substitution and that has 1-6 carbon atoms, or the like. A1 is an oxygen atom, a sulfur atom, or the like. Each of A2 and A3 independently indicates a carbon atom or a nitrogen atom. X is an alkyl group that has a substitution or does not have a substitution and that has 1-6 carbon atoms, an alkoxy group that has a substitution or does not have a substitution and that has 1-6 carbon atoms, or the like. n is an integer of 0-2.
Fibromyalgia syndrome occurs in around 2% of the population (predominantly women), and is characterized by its poor response to conventional therapies. Therapeutic approaches modulating inhibitory pathways, including pharmacologic options as pregabalin, and non pharmacological ones as transcranial direct current stimulation (tDCS) have been proven to be of limited utility independently. Aiming to evaluate a better understanding of the pathophysiogenic mechanisms and the effect of these treatments on neuroplasticity, this study was designed evaluating neurophysiologic, neurochemical and clinical parameters. Neurophysiologic parameters and functions to be assessed will include pain threshold, motor evoked potential, silent period, intracortical facilitation and inhibition assessed by Transcranial Magnetic Stimulation (TMS) and optic functional neuroimaging. Neurochemical measurements considered will be neurotrophins (BDNF) and inflammatory mediators (TNF, IL1, IL6, IL10 and cortisol). Clinical characteristics will be assessed using validated scales capable to detect functional capacity, quality of life (WHOCOHL), catastrophism, sleep disruptions (Pittsburgh) and depressive symptoms (Beck Depression Inventory). Considering the above described hypothesis, the present randomized clinical trial with blinded patients and evaluators is proposed. It pretends to analyze short-, mid- and long-term neurobiological mechanisms triggered by the selected interventions.
Participants will receive VRd regimen for 6 cycles before randomization. Following randomization, participants in Arm B will undergo apheresis and receive two more cycles of VRd as bridging therapy. In VRd treatment, participants will receive bortezomib 1.3 mg/m\^2 SC on Days 1, 4, 8 and 11 of each cycle for Cycles 1 to 8; oral lenalidomide 25 mg on days 1 to 14 of each cycle for Cycles 1 to 8 and oral dexamethasone 20 mg on days 1, 2, 4, 5, 8, 9, 11 and 12 of each cycle for Cycles 1 to 8. Each cycle will consist of 21 days. After 8 cycles of VRd, participants will receive a conditioning regimen (cyclophosphamide 300 mg/m\^2 intravenous \[IV\] and fludarabine 30 mg/m\^2 IV daily for 3 days) and Cilta-cel infusion 0.75\*10\^6 chimeric antigen receptor (CAR)-positive viable T cells/kilogram (kg).