anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Sepsis is a heterogeneous condition defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. For some, sepsis presents as a predominantly suppressive disorder, whilst others experience a pro-inflammatory condition which can culminate in a 'cytokine storm'. Frequently, patients experience signs of concurrent hyper-inflammation and immunosuppression, underpinning the difficulty in directing effective treatment. Although intensive care unit mortality rates have improved in recent years, one-third of discharged patients die within the following year. Half of post-sepsis deaths are due to exacerbation of pre-existing conditions, whilst half are due to complications arising from a deteriorated immune system. It has been suggested that the intense and dysregulated response to infection may induce irreversible metabolic reprogramming in immune cells. As a critical arm of immune protection in vertebrates, alterations to the adaptive immune system can have devastating repercussions. Indeed, a marked depletion of lymphocytes is observed in sepsis, correlating with increased rates of mortality. Such sepsis-induced lymphopenia has profound consequences on how T cells respond to infection but equally on the humoral immune response that is both elicited by B cells and supported by distinct CD4+ T follicular helper (TFH) cell subsets. The immunosuppressive state is further exacerbated by functional impairments to the remaining lymphocyte population, including the presence of cells expressing dysfunctional or exhausted phenotypes. This review will specifically focus on how sepsis destabilises the adaptive immune system, with a closer examination on how B cells and CD4+ TFH cells are affected by sepsis and the corresponding impact on humoral immunity.
The neurofeedback protocol will be the same during the 8 sessions constituting the protocol and taking place over a period of 4 weeks (2 neurofeedback sessions per week, the first and the last one in an MRI context). It will last 15 minutes per session, and during each session, the volunteer will have to increase the brain activity of his/her dlPFC using a visual gauge representing the "activity level" of his/her own dlPFC. No specific instructions will be given to the volunteer so that he/she can develop his/her own internal strategy to increase this "activity level".
The present invention relates to a natural hair dye. Specifically, the present invention relates to a method for preparing a natural hair dye containing, as an active ingredient, extract derived from various natural products, including henna containing black soybean seed coat extract. Specifically, in the present invention, a raw material extract is obtained by adding horseradish root, sorghum root, perila leaf, Ligularia fischeri (LEDEB.) TURCZ., and chamomile to black soybean seed coat powder extract. The raw material extract is aged under certain conditions, and an acidic mordant and other compositions are mixed with the aged raw material extract, thereby preparing a hair dye. A hair dye composition prepared according to the present invention has excellent dyeing properties, can be applied to people with sensitive scalp or damaged hair, and can have effects of alleviating damage to the scalp and hair and improving scalp health.
Neomycin and polymyxin B sulfates and hydrocortisone otic solution, USP is a sterile antibacterial and anti-inflammatory solution for otic use.

Each mL contains: Actives:neomycin sulfate equivalent to 3.5 mg neomycin base, polymyxin B sulfate equivalent to 10,000 polymyxin B units, and hydrocortisone 10 mg (1%); Inactives: propylene glycol, hydrochloric acid, potassium metabisulfite, cupric sulfate, glycerin, purified water. The pH range is 2.0 to 4.5.

Neomycin sulfate is the sulfate salt of neomycin B and C, which are produced by the growth of Streptomyces fradiae Waksman (Fam. Streptomycetaceae). It has a potency equivalent of not less than 600 micrograms of neomycin standard per mg, calculated on an anhydrous basis. The structural formulae are:

Polymyxin B sulfate is the sulfate salt of polymyxin B1 and B2, which are produced by the growth of Bacillus polymyxa, (Prazmowski) Migula (Fam. Bacillaceae). It has a potency of not less than 6,000 polymyxin B units per mg, calculated on an anhydrous basis. The structural formulae are:

Hydrocortisone, 11β, 17, 21 - trihydroxypregn-4-ene-3, 20-dione, is an anti-inflammatory hormone. Its structural formula is:
BACKGROUND: Neglected tropical diseases (NTDs) are a diverse group of debilitating diseases and conditions afflicting more than one billion people in impoverished communities. Control of these diseases is crucial to achieve Sustainable Development Goal 3 and the pledge to 'leave no one behind'. Relying on large-scale delivery of wide-spectrum drugs to individuals in at-risk communities irrespective of their health status, mass drug administration is a core strategy for tackling half of the NTDs targeted by the latest WHO roadmap (2021-2030). However, ethical challenges surround its implementation and long-term impact. This systematic review aims to give a comprehensive picture of the variety of ethical reasons for and against mass drug administration for NTD control and elimination, facilitating further debate in ethics and policy.
METHODS: PubMed and Web of Science Core Collection were searched for all relevant publications. Of the 486 retrieved records, 60 met the inclusion criteria for qualitative analysis. Ethical reasons discussing the topic at hand were extracted from full texts and synthesised through the Kuckartz method of qualitative content analysis.
RESULTS: Data extraction revealed 61 ethical reasons, of which 20 (32.7%) had positive, 13 (21.3%) had ambivalent and 28 (45.9%) had negative implications regarding mass drug administration for NTDs. The health benefits and cost-effectiveness of the measure were extensively highlighted. However, equity, autonomy and sustainability emerged as the domains with the most pressing ethical concerns. Many issues related to implementation are yet to be adequately addressed in policy documents.
CONCLUSIONS: This is the first systematic review of ethical reasons pertaining to mass drug administration for NTD control and elimination. Due to the diversity of included studies, no general recommendations can be made. Instead, context-specific strategies seem necessary. Alternative approaches tackling socioecological determinants of ill health are needed for long-term sustainability. Future research could benefit from contributions of non-Western philosophies and perspectives by local researchers.
One dose (1 packet or 1 level teaspoon) of colestipol hydrochloride granules contains 5 grams of colestipol hydrochloride. The recommended daily adult dose is one to six packets or level scoopfuls given once or in divided doses. Treatment should be started with one dose once or twice daily with an increment of one dose/day at one- or two-month intervals. Appropriate use of lipid profiles as per NCEP guidelines including LDL-cholesterol and triglycerides is advised so that optimal, but not excessive doses are used to obtain the desired therapeutic effect on LDL-cholesterol level. If the desired therapeutic effect is not obtained at one to six doses/day with good compliance and acceptable side effects, combined therapy or alternate treatment should be considered.

To avoid accidental inhalation or esophageal distress, colestipol hydrochloride granules should not be taken in its dry form. Colestipol hydrochloride granules should always be mixed with water or other fluids before ingesting. Patients should take other drugs at least one hour before or four hours after colestipol hydrochloride granules to minimize possible interference with their absorption. (See PRECAUTIONS, Drug Interactions.)
Therapeutic compsn. comprising a diamine oxidase obtd. from human placenta by virtually complete elimination of haemoglobin and its derivs., the diamine being a mixture of 4 molecular forms with a mol. wt. being a whole multiple of 1 to 4 x 125,000 plus-or-minus 5,000, the diamine oxidase catalysing the oxidation of histamine, putrescine and cadaverine but not phenethylamine and tyramine. Prepd. by fractionation of an acetone-dried placenta sample dissolved in 1% NaCl soln. with ethanol to remove haemoglobin and its derivs.
Benzene is a known leukemogen and may cause lymphoma as well, but its ability to , cause these conditions below 10 parts per million (ppm) in air are unclear. It is currently regulated in the United States at 1 ppm as an 8-hour time-weighted average and at a 5 ppm short-term exposure level for 15 minutes. There is a critical need to assess risks related to benzene exposure under 10 ppm because it is widely used industrially and a ubiquitous contaminant in the environment.

The National Cancer Institute (NCI) and the Chinese Academy of Preventive Medicine (CAPM), whose name was recently changed to the China Center for Disease Control (CDC) previously established a cohort of 75,000 workers exposed to benzene in 12 cities in China and 35,000 unexposed comparison workers, to investigate the relationship between benzene exposure and cancer risk, from 1972 to 1987. We followed up each worker using factory records and reported results suggesting that benzene exposure under 10 ppm may be associated with increased risk of acute non-lymphocytic cancer and could also be associated with increased risk of lymphoma and lung cancer. We have now laid the groundwork for a further epidemiologic investigation in China to evaluate health risks from lower levels of benzene exposure, particularly as present in the factories during the 1990s. The cohort was followed up through 1999, and through this effort we have identified 3260 subjects for study, including cases (HLD malignancies, n= 161; benzene poisoning, n= 1040; lung cancer, n= 560) and 1500 subjects in a cohort sub-sample to be used as the comparison group. In addition, we have identified a series of cases with benzene poisoning and controls from the same factories outside of the cohort (n = 600).

We propose to contact next-of-kin of deceased subjects (essentially all cancer cases and some members of the sub-cohort are deceased), for questionnaire-based evaluation of benzene and other exposures, and to contact living subjects (primarily the benzene poisoning cases and the sub-cohort sample) for collection of questionnaires and biologic samples. The questionnaires (formatted for direct interview of living subjects or for next-of-kin) will collect information on potential confounders needed in the analysis of benzene's effects and information on work experience outside of the study cohort factories. The biologic sample collection (13 ml blood and buccal cell rinse) will provide material primarily for study of genetic polymorphisms potentially associated with benzene metabolism and disease status. The polymorphisms being studied are relatively common in the Chinese population and may be associated with a relatively modest increase in risk (1.5 to 2-fold). Written informed consent will be obtained from all next-of-kin and all live study subjects. We will attempt to enroll 3,860 study subjects or next-of-kin. The study will be carried out with Drs. Gui-Lan Li and Song-Nian Yin and colleagues from the China CDC, Beijing, China.
FIELD: biotechnology, immunology, virology. SUBSTANCE: composition has polypeptides from different isolates of hepatitis C virus and containing at least one epitope in variable domain of envelope polypeptide HCV E2/NS1 exhibiting an amino acid sequence 384-414 and/or one epitope in variable domain E1 exhibiting an amino acid sequence 215-255. Immunogenic composition is used for preparing antibodies against hepatitis C virus, detection of antibodies in sample, preparing immunogenic polypeptide compositions showing and cross-reactions with many isolates of hepatitis C virus. Invention ensures to make new diagnostics and vaccines. EFFECT: improved method of preparing, enhanced effectiveness of composition, improved method of producing and detection of antibodies. 18 dwg, 6 tbl, 7 ex
The utility model provides a POCT sharing cabinet, which comprises a cabinet main body, a main control circuit board, a supply control circuit, a charging seat and POCT equipment for sharing. Also included is a device compartment housing a POCT device, wherein there is a first transfer assembly, a first transfer window, and a charging assembly. When the POCT equipment is sent out or returned, the first transmission assembly moves towards or back to the first transmission window, the first transmission window is matched with the movement of the first transmission assembly to be opened and closed, and the first transmission assembly sends out or returns the POCT equipment through the first transmission window. The charging component charges the POCT device. The POCT device also comprises consumable matched with POCT equipment, the consumable is contained in a consumable chamber, and the consumable chamber comprises a second transmission assembly and a second transmission window, and the consumable is sent out through the second transmission window. The POCT detection method and the POCT detection system achieve the purpose of carrying out required POCT detection anytime and anywhere by sharing POCT equipment and consumable materials.
Mitochondrial dysfunction has been implicated in various types of cardiovascular disease including hypertension. Mitochondrial fission fusion balance is critical to mitochondrial quality control, whereas enhanced fission has been reported in several models of cardiovascular disease. However, limited information is available regarding the contribution of mitochondrial fission in hypertension. Here, we have tested the hypothesis that inhibition of mitochondrial fission attenuates the development of hypertension and associated vascular remodeling. In C57BL6 mice infused with angiotensin II for 2 weeks, co-treatment of mitochondrial fission inhibitor, mdivi1, significantly inhibited angiotensin II-induced development of hypertension assessed by radiotelemetry. Histological assessment of hearts and aortas showed that mdivi1 inhibited vessel fibrosis and hypertrophy induced by angiotensin II. This was associated with attenuation of angiotensin II-induced decline in mitochondrial aspect ratio seen in both the endothelial and medial layers of aortas. Mdivi1 also mitigated angiotensin II-induced cardiac hypertrophy assessed by heart weight-to-body weight ratio as well as by echocardiography. In ex vivo experiments, mdivi1 inhibited vasoconstriction and abolished the enhanced vascular reactivity by angiotensin II in small mesenteric arteries. Proteomic analysis on endothelial cell culture media with angiotensin II and/or mdivi1 treatment revealed that mdivi1 inhibited endothelial cell hypersecretory phenotype induced by angiotensin II. In addition, mdivi1 attenuated angiotensin II-induced protein induction of periostin, a myofibroblast marker in cultured vascular fibroblasts. In conclusion, these data suggest that mdivi1 prevented angiotensin II-induced hypertension and cardiovascular remodeling via multicellular mechanisms in the vasculature.
BACKGROUND: Liver hepatocellular carcinoma (LIHC) is a prevalent form of primary liver cancer. Research has demonstrated the contribution of tumor stem cells in facilitating tumor recurrence, metastasis, and treatment resistance. Despite this, there remains a lack of established cancer stem cells (CSCs)-associated genes signatures for effectively predicting the prognosis and guiding the treatment strategies for patients diagnosed with LIHC.
METHODS: The single-cell RNA sequencing (scRNA-seq) and bulk RNA transcriptome data were obtained based on public datasets and computerized firstly using CytoTRACE package and One Class Linear Regression (OCLR) algorithm to evaluate stemness level, respectively. Then, we explored the association of stemness indicators (CytoTRACE score and stemness index, mRNAsi) with survival outcomes and clinical characteristics by combining clinical information and survival analyses. Subsequently, weighted co-expression network analysis (WGCNA) and Cox were applied to assess mRNAsi-related genes in bulk LIHC data and construct a prognostic model for LIHC patients. Single-sample gene-set enrichment analysis (ssGSEA), Cell-type Identification By Estimating Relative Subsets Of RNA Transcripts (CIBERSORT) and Tumor Immune Estimation Resource (TIMER) analysis were employed for immune infiltration assessment. Finally, the potential immunotherapeutic response was predicted by the Tumor Immune Dysfunction and Exclusion (TIDE), and the tumor mutation burden (TMB). Additionally, pRRophetic package was applied to evaluate the sensitivity of high and low-risk groups to common chemotherapeutic drugs.
RESULTS: A total of four genes (including STIP1, H2AFZ, BRIX1, and TUBB) associated with stemness score (CytoTRACE score and mRNAsi) were identified and constructed a risk model that could predict prognosis in LIHC patients. It was observed that high stemness cells occurred predominantly in the late stages of LIHC and that poor overall survival in LIHC patients was also associated with high mRNAsi scores. In addition, pathway analysis confirmed the biological uniqueness of the two risk groups. Personalized treatment predictions suggest that patients with a low risk benefited more from immunotherapy, while those with a high risk group may be conducive to chemotherapeutic drugs.
CONCLUSION: The current study developed a novel prognostic risk signature with genes related to CSCs, which provides novel ideas for the diagnosis, prognosis and treatment of LIHC.
Stable HIV-1 infected subjects will be followed-up using an mHealth platform. The platform will provide users with web based and mobile device applications which interface securely with relevant medical data and facilitate remote access to healthcare providers. The minimum length of follow-up will be 12 months and the maximum 35 months.
A transdermal drug delivery patch 10 for the pre-treatment and treatment of poisoning by highly toxic organophosphates comprises a backing layer 12, a drug containing adhesive layer 11 and a release liner 13. The drug containing adhesive layer 11 comprises a neutral polyacrylate without functionality, preferably a co-polymer of 2-ethylhexyl acrylate and vinyl acetate, having a uniform dispersion of a parasympathomimetic, preferably physostigmine and a parasympatholytic, preferably scopolamine. The drug containing adhesive layer may further comprise a permeation enhancer, preferably oleic acid. The patch 10 may include an overtape 14 comprising a backing foil 15 provided with an additional adhesive layer 16 which circumferentially bounds the drug containing adhesive layer 11. The additional adhesive layer 16 preferably comprises an acidic polyacrylate. A method for the manufacture of the device 10 and a kit of parts including the transdermal drug patch 10 and a compression bandage are also provided.
This is a prospective, non-interventional, longitudinal study of the natural history and function of patients with MTM. The study duration is 36 months. The enrollment period will be 12 months and each patient will be assessed over 24 months. Data will be analyzed at baseline and annually thereafter and reports will be prepared based on these analyses. A final report will summarize findings after all patients have completed 24 months of follow-up. Assessments performed in this study will be based on the age and ambulatory status of the patient. The assessments will also be adjusted to account for the variability in both phenotypes and age of the patients who may participate in this study. Patients will be evaluated at Baseline, Month 6, Month 12 and Month 24. It is anticipated that approximately 60 patients from the United States, Canada and Europe will be included in this study.
Character strengths-based intervention, 3 sessions every week for three weeks. 30 minutes each session.
When adding other blood-glucose-lowering agents to Glipizide XL for combination therapy, the agent should be initiated at the lowest recommended dose, and patients should be observed carefully for hypoglycemia. Refer to the product information supplied with the oral agent for additional information.

When adding Glipizide XL to other blood-glucose-lowering agents, Glipizide XL can be initiated at 5 mg. Those patients who may be more sensitive to hypoglycemic drugs may be started at a lower dose. Titration should be based on clinical judgment.

When colesevelam is coadministered with glipizide ER, maximum plasma concentration and total exposure to glipizide is reduced. Therefore, Glipizide XL should be administered at least 4 hours prior to colesevelam.
Systems, methods and computer-readable storage media for securely authenticating client computing devices and receiving medical information at a medical information system are described. Patients and client computing devices associated with the patients may be enrolled with the medical information system. A client computing device may capture medical information, such as an image of a portion of the body of medical significance (for example, a wound). The client computing device may be authenticated by the medical information system by matching information in a client computing device authentication request with information in a device database accessible by the medical information system. Once authenticated, the client computing device may send an upload request to the medical information system including medical information. The medical information system may store the medical information in an associated patient profile in a patient database.
The objective of the study is to evaluate the evolving phenotype and genetic spectrum of patients with succinic semialdehyde dehydrogenase deficiency (SSADHD) in long-term follow-up. Longitudinal clinical and biochemical data of 22 pediatric and 9 adult individuals with SSADHD from the patient registry of the International Working Group on Neurotransmitter related Disorders (iNTD) were studied with in silico analyses, pathogenicity scores and molecular modeling of ALDH5A1 variants. Leading initial symptoms, with onset in infancy, were developmental delay and hypotonia. Year of birth and specific initial symptoms influenced the diagnostic delay. Clinical phenotype of 26 individuals (median 12 years, range 1.8-33.4 years) showed a diversifying course in follow-up: 77% behavioral problems, 76% coordination problems, 73% speech disorders, 58% epileptic seizures and 40% movement disorders. After ataxia, dystonia (19%), chorea (11%) and hypokinesia (15%) were the most frequent movement disorders. Involvement of the dentate nucleus in brain imaging was observed together with movement disorders or coordination problems. Short attention span (78.6%) and distractibility (71.4%) were the most frequently behavior traits mentioned by parents while impulsiveness, problems communicating wishes or needs and compulsive behavior were addressed as strongly interfering with family life. Treatment was mainly aimed to control epileptic seizures and psychiatric symptoms. Four new pathogenic variants were identified. In silico scoring system, protein activity and pathogenicity score revealed a high correlation. A genotype/phenotype correlation was not observed, even in siblings. This study presents the diversifying characteristics of disease phenotype during the disease course, highlighting movement disorders, widens the knowledge on the genotypic spectrum of SSADHD and emphasizes a reliable application of in silico approaches.