anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
A text analysis system is described. A natural language input unit ( 1 ) is arranged for enabling a user to input a free text ( 10 ) in a natural language. A natural language processing unit ( 2 ) is arranged for processing at least a portion of the free text ( 10 ) while it is being inputted, to obtain an explicit representation ( 11 ) of semantics represented by the free text. An explicit information input unit ( 3 ) is arranged for enabling the user to input explicit information ( 12 ) relating to the explicit representation ( 11 ) of semantics. The system comprises a visualization unit ( 4 ) for visualizing at least part of the explicit representation ( 11 ) to the user while the user is still inputting the free text ( 10 ). A user interface ( 5 ) is arranged for providing a user with simultaneous access to both the natural language input unit ( 1 ) and the explicit information input unit ( 3 )
1,244,564. Calcitonin. RESEARCH CORP. 19 June, 1969 [26 June, 1968], No. 31077/69. Heading A5B. Calcitonin is isolated and purified by a process comprising extracting mammalian thyroid glands with a butanol-acetic acid-water mixture, contacting the extract with silicic acid and recovering calcitonin from the extract. The calcitonin may be recovered from the extract by removing the butanol-acetic acid-water mixture by evaporation, dissolving the residue in aqueous acetic acid, adding trichloroacetic acid to precipitate calcitonin, and removing the calcitonin. Preferably defatted porcine thyroid glands are extracted with a mixture of nbutanol-acetic acid-water, 12:3:5 by volume, the extract is contacted with silicic acid, the extraction solvent is removed by evaporation, the residue after evaporation is dissolved in 20% aqueous acetic acid, the aqueous acetic acid solution is extracted with ether and calcitonin is precipitated from the aqueous acetic acid solution by the addition of trichloroacetic acid. The calcitonin precipitate may be dissolved in aqueous acetic acid, and the acetic acid solution extracted with ether and then lyophilized.
The present invention is an article of manufacture for use in alerting a person of exposure to an excessive amount of ultraviolet radiation. In one embodiment, the article of manufacture comprises a first strip comprising a backing member and first and second patches. Each of the first and second patches comprise an ultraviolet sensitive material releasably disposed upon the backing member. Each of the first and second patches comprise first and second outside edges and an inside edge. The first and second patches are nested and adjoined along said inside edges of the first and second patches, respectively. The ultraviolet sensitive material is adapted to change from a first color to a second color when exposed to an excessive amount of ultraviolet radiation. In operation, a person may remove the first and second patches from the backing member as desired and apply the patch to an area of exposed skin. The person is alerted of exposure to an excessive amount of ultraviolet radiation when the UV sensitive coating is changing from the first color to the second color.
The deubiquitylase OTU domain-containing ubiquitin aldehyde-binding protein 1 (OTUB1) has been implicated in the pathogenesis of various human diseases. However, the molecular mechanism by which OTUB1 participates in the pathogenesis of intracerebral hemorrhage (ICH) remains elusive. In the present study, we established an autologous whole blood fusion-induced ICH model in C57BL/6 J mice. We showed that the upregulation of OTUB1 contributes to the attenuation of Nuclear factor kappa B (NF-κB) and its downstream apoptotic signaling after ICH. OTUB1 directly associates with NF-κB precursors p105 and p100 after ICH, leading to attenuated polyubiquitylation of p105 and p100. Moreover, we revealed that NF-κB signaling was modestly activated both in ICH tissues and hemin-exposed HT-22 neuronal cells, accompanied with the activation of NF-κB downstream pro-apoptotic signaling. Notably, overexpression of OTUB1 strongly inhibited hemin-induced NF-κB activation, whereas interference of OTUB1 led to the opposite effect. Finally, we revealed that lentiviral transduction of OTUB1 markedly ameliorated hemin-induced apoptotic signaling and HT-22 neuronal death. Collectively, these findings suggest that the upregulation of OTUB1 serves as a neuroprotective mechanism in antagonizing neuroinflammation-induced NF-κB signaling and neuronal death, shed new light on manipulating intracellular deubiquitylating pathways as novel interventive approaches against ICH-induced secondary neuronal damage and death.
A system for electronically recording and sharing medical data is provided, the system comprising an electronic source document, wherein the electronic source document comprises a database. In one particular embodiment, the medical data comprise clinical study data, and in another the medical data comprise patient specific data. In some embodiments, the system includes means for defining data parameters and storing the data parameters within the electronic source document, as well as a browser-based means for entering data into the electronic source document and storing the data therein. In a further embodiment, the system comprises means for one or more users of the system to view stored data. In a still further embodiment, means for one or more users to amend data stored in the electronic source document is provided, and in yet another embodiment the system comprises means for creating and maintaining an audit trail when one or more of the users amends data stored in the electronic source document. In other embodiments, the system further comprises an application specific navigation tool; in some embodiments, the application specific tool comprises a graphical user interface. Appropriate methods of using the system are also provided.
Fascin-1 (FSCN1) is recognized as an actin-binding protein, commonly exhibits up-regulation in breast cancer (BC) and is crucial for tumor invasion and metastasis. The existence of FSCN1 gene polymorphisms may raise the potential for developing BC, and there are still no studies focusing on the relationship between the FSCN1 rs2966447 variant and BC risk in Egyptian females. Thus, we investigated the serum fascin-1 levels in BC patients and the association between the FSCN1 rs2966447 variant with its serum levels and BC susceptibility. Genotyping was conducted in 153 treatment-naïve BC females with different stages and 144 apparent healthy females by TaqMan® allelic discrimination assay, whereas serum fascin-1 level quantification was employed by ELISA. The FSCN1 rs2966447 variant demonstrated a significant association with BC susceptibility under all utilized genetic models, cancer stages and estrogen receptor negativity. Also, BC females with AT and TT genotypes had higher serum fascin-1 levels and tumor size than those with the AA genotype. Moreover, serum fascin-1 levels were significantly elevated in the BC females, notably in those with advanced-stages. Furthermore, serum fascin-1 levels were markedly positively correlated with number of positive lymph nodes as well as tumor size. Collectively, these findings revealed that the FSCN1 rs2966447 variant may be regarded as a strong candidate for BC susceptibility. Also, this intronic variant is associated with increased serum fascin-1 levels and tumor size.
Previous studies reveal that psoriatic arthritis (PsA) and ankylosing spondylitis (AS) share susceptibility genes, such as HLA-B27, demonstrating a degree of genetic overlap between these diseases. Recent studies have identified a number of novel AS and PsA genetic susceptibility loci, but data on these loci in Chinese PsA patients are limited. To identify candidate genes that confer susceptibility to PsA in Chinese patients with PsA, psoriasis vulgaris (PsV), and healthy controls. Sixteen susceptibility loci, reported in a genome-wide association study of AS, and nine susceptibility loci, reported in candidate gene studies of PsA, were examined. Single-nucleotide polymorphisms (SNPs) were genotyped in 503 patients with PsA, 496 patients with PsV, and 979 healthy controls using the SNPscanTM multiplex SNP genotyping platform. PLINK software and logistic regression analysis were used to estimate the statistical significance of associations. PPP2R3C (rs8006884) was shown to significantly associate with PsA+PsV (p = 1.92×10-3, OR = 1.28) and was suggested to associate with PsV (p = 0.03, OR = 1.19). A suggestive association was also observed between IL-23R (rs12141575) and PsA as well as with axial PsA based on subtype analysis, KIF3A (rs2897442) and PsV, and ERN1 (rs196941) or IFIH1 (rs984971) and axial PsA. Our results suggest that PPP2R3C confers susceptibility to PsA and PsV, and that this gene may be related to the pathogenesis of psoriatic lesions and arthritis. Moreover, our results indicate a possible association between IL-23R, ERN1, or IFIH1 and subtypes of PsA, and between KIF3A and PsV.
PURPOSE: A composition containing Rhizoma Polygoni Cuspidati extract for reducing blood glucose is provided to use in food or pharmaceutical composition for preventing and treating diabetes. CONSTITUTION: A composition for reducing blood glucose contains crude extract of Rhizoma Polygoni Cuspidati isolated using ethanol or spirit or extract isolated using ethylacetate or butanol from the crude extract. The composition is a food or pharmaceutical composition. The food is manufactured in the form of tablet, granule, powder, capsule and liquid. The pharmaceutical composition is manufactured in the form of tablet, pill, powder, granule, capsule, suspension, emulsion, syrup, aerosol or injection. A composition for preventing or treating diabetes contains the extract of Rhizoma Polygoni Cuspidati as an active ingredient.
1. Technical Result Improvement of anti thrombotic properties. 2. Essence Compounds of the formula (I), (wherein A, B, C, W¹ and G have the values defined in the specification) or pharmaceutically acceptable salt thereof, method for its production, a pharmaceutical composition comprising the same and use thereof. 3. Field of Application Medicine.
Neonatal hypoxic-ischemic encephalopathy, an important cause of death as well as long-term disability in survivors, is caused by oxygen and glucose deprivation, and limited blood flow. Following hypoxic-ischemic injury in the neonatal brain, three main biochemical damages (excitotoxicity, oxidative stress, and exacerbated inflammation) are triggered. Mitochondria are involved in all three cascades. Mitochondria are the nexus of metabolic pathways to offer most of the energy that our body needs. Hypoxic-ischemic injury affects the characteristics of mitochondria, including dynamics, permeability, and ATP production, which also feed back into the process of neonatal hypoxic-ischemic encephalopathy. Mitochondria can be a cellular hub in inflammation, which is another main response of the injured neonatal brain. Some treatments for neonatal hypoxic-ischemic encephalopathy affect the function of mitochondria or target mitochondria, including therapeutic hypothermia and erythropoietin. This review presents the main roles of mitochondria in neonatal hypoxic-ischemic encephalopathy and discusses some potential treatments directed at mitochondria, which may foster the development of new therapeutic strategies for this encephalopathy.
BACKGROUND: Locomotive syndrome is a major challenge for older adults, and anthropometric indices can greatly affect the musculoskeletal system. This study aimed to compare the anthropometric indices between older adults with and without locomotive syndrome.
METHODS: This descriptive-analytical study was performed on 211 older adults using random cluster sampling from a population of over-60 individuals covered by comprehensive health service centers in Sari in Autumn, 2021. Participants were divided into two groups: with and without locomotive syndrome. Locomotive syndrome was assessed via the 25-item Geriatric Locomotive Function Scale questionnaire, and the level of anthropometric indices was determined through the Bioelectrical Impedance Analysis device. Data were analyzed by independent t-test, Mann-Whitney U, Chi-Square, and Binary logistic regression in SPSS, Version 23 (P < 0.05).
RESULTS: The average age of older adult participants was 78.4 ± 6.6 years. In older adults with locomotive syndrome, the average percentage of fat-free mass (P < 0.001) was significantly lower while the average percentage of fat mass and fat mass index (P < 0.001) was significantly higher. Older adults with locomotive syndrome were shorter in height (P < 0.001) and had a higher body mass index (P < 0.05). Fat-free mass percentage (OR = 0.59) and body mass index (OR = 1.4) predicted the incidence of locomotive syndrome in the subjects. Significant differences such as chronic diseases, chronic pain, falls, age, and gender were observed between the two groups (P < 0.05).
CONCLUSION: Anthropometric indices can play an important role in the occurrence of locomotive syndrome in older adults. Evaluation of anthropometric indices and management of body composition can help prevent locomotive syndrome and improve the quality of life of older adults.
The efficacy of Cymbalta as a treatment for depression was established in 4 randomized, double-blind, placebo-controlled, fixed-dose studies in adult outpatients (18 to 83 years) meeting DSM-IV criteria for major depression. In 2 studies, patients were randomized to Cymbalta 60 mg once daily (N=123 and N=128, respectively) or placebo (N=122 and N=139, respectively) for 9 weeks; in the third study, patients were randomized to Cymbalta 20 or 40 mg twice daily (N=86 and N=91, respectively) or placebo (N=89) for 8 weeks; in the fourth study, patients were randomized to Cymbalta 40 or 60 mg twice daily (N=95 and N=93, respectively) or placebo (N=93) for 8 weeks. There is no evidence that doses greater than 60 mg/day confer additional benefits. 

In all 4 studies, Cymbalta demonstrated superiority over placebo as measured by improvement in the 17-item Hamilton Depression Rating Scale (HAMD-17) total score. 

In all of these clinical studies, analyses of the relationship between treatment outcome and age, gender, and race did not suggest any differential responsiveness on the basis of these patient characteristics. 

In another study, 533 patients meeting DSM-IV criteria for MDD received Cymbalta 60 mg once daily during an initial 12-week open-label treatment phase. Two hundred and seventy-eight patients who responded to open label treatment (defined as meeting the following criteria at weeks 10 and 12: a HAMD-17 total score ≤9, Clinical Global Impressions of Severity (CGI-S) ≤2, and not meeting the DSM-IV criteria for MDD) were randomly assigned to continuation of Cymbalta at the same dose (N=136) or to placebo (N=142) for 6 months. Patients on Cymbalta experienced a statistically significantly longer time to relapse of depression than did patients on placebo. Relapse was defined as an increase in the CGI-S score of ≥2 points compared with that obtained at week 12, as well as meeting the DSM-IV criteria for MDD at 2 consecutive visits at least 2 weeks apart, where the 2-week temporal criterion had to be satisfied at only the second visit. The effectiveness of Cymbalta in hospitalized patients with major depressive disorder has not been studied.
Arm 1 (Phase I dose level 1) Participants receive spartalizumab 300 mg IV over 30 minutes on day 1 and siltuximab 6 mg/Kg IV over 1 hour on day 1. Cycles repeat every 3 weeks in the absence of disease progression or unacceptable toxicity.
In pediatric cancer, structural variants (SVs) and copy-number alterations contribute to cancer initiation as well as progression, thereby aiding diagnosis and treatment stratification. Although suggested to be of importance, the prevalence and biological relevance of complex genomic rearrangements (CGRs) across pediatric solid tumors is largely unexplored. In a cohort of 120 primary tumors, we systematically characterized patterns of extrachromosomal DNA, chromoplexy, and chromothripsis across five pediatric solid cancer types. CGRs were identified in 56 tumors (47%), and in 42 of these tumors, CGRs affect cancer driver genes or result in unfavorable chromosomal alterations. This demonstrates that CGRs are prevalent and pathogenic in pediatric solid tumors and suggests that selection likely contributes to the structural variation landscape. Moreover, carrying CGRs is associated with more adverse clinical events. Our study highlights the potential for CGRs to be incorporated in risk stratification or exploited for targeted treatments.
Metabolic-associated steatotic liver disease (MASLD) is closely associated with obesity. MASLD affects over 1 billion adults globally but there are few treatment options available. Glucagon is a key metabolic regulator, and its actions include the reduction of liver fat through direct and indirect means. Chronic glucagon signalling deficiency is associated with hyperaminoacidaemia, hyperglucagonaemia and increased circulating levels of glucagon-like peptide 1 (GLP-1) and fibroblast growth factor 21 (FGF-21). Reduction in glucagon activity decreases hepatic amino acid and triglyceride catabolism; metabolic effects include improved glucose tolerance, increased plasma cholesterol and increased liver fat. Conversely, glucagon infusion in healthy volunteers leads to increased hepatic glucose output, decreased levels of plasma amino acids and increased urea production, decreased plasma cholesterol and increased energy expenditure. Patients with MASLD share many hormonal and metabolic characteristics with models of glucagon signalling deficiency, suggesting that they could be resistant to glucagon. Although there are few studies of the effects of glucagon infusion in patients with obesity and/or MASLD, there is some evidence that the expected effect of glucagon on amino acid catabolism may be attenuated. Taken together, this evidence supports the notion that glucagon resistance exists in patients with MASLD and may contribute to the pathogenesis of MASLD. Further studies are warranted to investigate the direct effects of glucagon on metabolism in patients with MASLD.
The present disclosure provides a system. In an embodiment, a system for medication management is provided and includes a mobile device. The mobile device includes a dose software application (dose-app) configured to notify a user to take a medication from a medication container. The system also includes a motion detection component attached to the medication container. The motion detection component includes a motion detection device configured to detect container motion data and wirelessly transmit the motion data to the mobile device. The mobile device includes a wireless receiver configured to receive the motion data from the motion detection device and send the motion data to the dose-app. The dose-app is configured to determine whether the received motion data constitutes a valid medication dosage.
The present invention relates to secondary functional moieties comprising a transition metal-based linker and a primary functional moiety bound thereto. The secondary functional moieties according to the present invention comprise a transition metal complex, such as a cis-platinum(ll) complex, which complex has a primary functional moiety (e.g. an unmodified or modified cytotoxic drug) as a first ligand and iodide, bromide or chloride as a second ligand. It has been found that secondary functional moieties comprising an iodide or bromide group as a leaving ligand, in particular an iodide group as a leaving ligand, show an even improved binding efficiency to cell binding moieties (e.g. antibodies). Furthermore, the secondary functional moieties containing iodide or bromide as a leaving ligand are hydrolytically considerably more stable compared with secondary functional moieties containing chloride as a leaving ligand. The invention also relates to cell targeting conjugates comprising a linker of the invention. The present invention further relates to a medicament comprising said cell targeting conjugate and to the use of the cell targeting conjugates in the diagnosis and treatment of cancer.
Nucleic acid condensing agents with reduced immunogenicity are generated either by conjugation of polycations or by selection of basic amino acid regions from proteins. Conjugation involves a chemical linkage between a polyalkylene glycol, such as polyethylene glycol, or a polysaccharide, such as dextran, and a polycation. Additionally, gene delivery vehicles, such as viral vectors, may be conjugated with polyalkylene glycol or polysaccharide, to reduce their immunogenicity. Basic amino acid regions of proteins are identified by isoelectric point, and amino acid composition. These condensing agents are complexed with nucleic acids and used to deliver genes to cells. Immunogenicity is assessed by whether neutralizing antibody is induced and by whether a serum component  inactivates the complexes.
Patients receive fludarabine IV over 1 hour on days -5 to -2, melphalan IV over 30 minutes on days -5 and -4, and undergo TBI on day -1 and stem cell transplantation IV over 2-6 hours on day 0. Depending on when the trial was joined, patients receive cyclophosphamide IV over 3 hours or bendamustine IV over 30-60 minutes or cyclophosphamide IV over 3 hours and bendamustine IV over 30-60 minutes on day 3. Patients also receive bendamustine IV over 30-60 minutes on day 4. Beginning day 5, patients receive tacrolimus IV followed by PO QD or BID for 6 months and mycophenolate mofetil PO TID until day 100. Beginning day 7, patients receive filgrastim-sndz SC QD until blood cell levels return to normal.
PURPOSE: A functional health food composition containing chrysophanol, physcion, or emodin, which suppresses metastasis is provided to improve an anticancer function. CONSTITUTION: A chrysophanol compound of chemical formula 1 suppresses metastasis. A physcion compound of chemical formula 2 suppresses metastasis. An emodin compound of chemical formula 3 suppresses metastasis. The compounds are derived from Microsporum sp. A functional health food composition for anticancer therapy aid contains the compounds as active ingredients.