anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
All AIDS principal mysteries are resolved. “One step” AIDS is successive contaminations.(with low [anti-env]). Strong sole lethal animal doses are confirming. Mobility macrophage (mφ) receptors contaminate at 1st stage with nonproductive entry with nonintegrated and heterogenous (due to nef) HIV DNA and proteins and preudoinfectious A particles. Such heterogeneity is obligatory for 2nd productive contamination with heterogenous anti-env, with integrated DNA and homologous proteins. Encephalites are due to moving into brain myp due to locally liberated cyto and chemokines Nongenetic factors are determining: at general persistent seronegativity (contact regularity) or absence of 2nd contamination due to different Fc receptor carbohydrates (babies before 3 months, chimpanzee). Minor genetic factors (as CCR5-2) only modify. AIDS in explaining all dangerous vaccinations. Carbohydrate origin of NK-cell mechanism. Artificial. virus culture contaminations. HIV signallings are resolved with general laws of functional recognitions and foldings with help of Universalest “Du-2T”-like peptides and 2 prolyl-isomerases (coupled trans-cis transitions). Chaperons protect proteins against intercarbohydrate aggregations. Prione “scarpie” state is artificial dissociation of their “Du-2T”. MHC and TRC allbtypes are due to their carbohydrates. Hearts of any cell functionning: “PKC” transporting vesicle cycle and independent direct DNA activation. Apoptosis: irreversibility of preparation of next signal with stock exhaustions. Ribosome cycles. Key proprotein primary structures confirm above data. Consequences of profoundest bases: mφ mobility stopping against encephalites; charged antibodies eliminate viruses, cancer cells and harmful antibody clones (anti-viral ,anti-auto); “Du-2T” eliminates viruses and “Mad Cow”; vaccines from homogenous viruses with one neutralizing epitope and correct virus titres; ribosomal protein synthesis; means against clinical death and coma; perfectest hypnotics.
Before starting the elimination diet (time 0, T0), intervention patients will be evaluated by experienced dermatologists, as well as by physicians with expertise in the field of food intolerance about GI and extraintestinal symptoms related to foods intake. Moreover, all these subjects will be subjected to blood, urine, and stools collections, and to a dietary consult, and a food and symptom's diary will be provided to all patients, which must be filled-in daily. After 2 months of elimination diet (time 1, T1), intervention patients will be evaluated again both clinically and by laboratory techniques, identically to T0. At this time-point, intervention patients will go to an open challenge, with reintroduction of wheat. After 2 weeks of open diet or whenever dermatologic, intestinal and/or extraintestinal symptoms should return or intensify (T2int), patients will be valued again both clinically and by laboratory techniques, identically to T0 and T1, and then will end the study.
Novel modified hemoglobins comprising polyalkylene glycols and novel methods for making those hemoglobins are provided. One group of modified hemoglobins comprise polyalkylene glycols bonded to the hemoglobin with an amide linkage at Glu-43(β). Additional polyalkylene glycols can also be bonded to the Glu-22(β) and/or the Asp-47(β). These hemoglobins are made by a novel amidation procedure. A second group of modified hemoglobins comprise a polyalkylene glycol covalently bonded to the hemoglobin at the α-amino of a Val-1(β) or a Val-1(α). Additional polyalkylene glycols can optionally be covalently bonded to a limited number of ⊂-amino groups. This second group of hemoglobins is made using a novel reductive alkylation procedure. A third group of modified hemoglobins comprise a polyalkylene glycol bonded to a thiol group of the hemoglobin through a phenylsuccinimido linkage, wherein no polyalkylene glycol is bonded to a Cys-93(β). This third group of modified hemoglobins is made by an improvement in a hemoglobin-polyalkylene linkage procedure utilizing thiolation-mediated maleimide chemistry.
INTRODUCTION: One-third of people with epilepsy continue to experience seizures despite treatment with existing anti-seizure medications (ASMs). The failure of modern ASMs to substantially improve epilepsy prognosis has been partly attributed to overreliance on acute rodent models in preclinical drug development as they do not adequately recapitulate the mechanisms of human epilepsy, are labor-intensive and unsuitable for high-throughput screening (HTS). There is an urgent need to find human-relevant HTS models in preclinical drug development to identify novel anti-seizure compounds.
OBJECTIVES: This paper developed high-throughput preclinical screening models to identify new ASMs.
METHODS: 14 natural compounds (α-asarone, curcumin, vinpocetine, magnolol, ligustrazine, osthole, tanshinone IIA, piperine, gastrodin, quercetin, berberine, chrysin, schizandrin A and resveratrol) were assessed for their ability to suppress epileptiform activity as measured by multi-electrode arrays (MEA) in neural cultures derived from human induced pluripotent stem cells (iPSCs). In parallel, they were tested for anti-seizure effects in zebrafish and mouse models, which have been widely used in development of modern ASMs. The effects of the compounds in these models were compared. Two approved ASMs were used as positive controls.
RESULTS: Epileptiform activity could be induced in iPSCs-derived neurons following treatment with 4-aminopyridine (4-AP) and inhibited by standard ASMs, carbamazepine, and phenytoin. Eight of the 14 natural compounds significantly inhibited the epileptiform activity in iPSCs-derived neurons. Among them, piperine, magnolol, α-asarone, and osthole showed significant anti-seizure effects both in zebrafish and mice. Comparative analysis showed that compounds ineffective in the iPSCs-derived neural model also showed no anti-seizure effects in the zebrafish or mouse models.
CONCLUSION: Our findings support the use of iPSCs-derived human neurons for first-line high-throughput screening to identify compounds with anti-seizure properties and exclude ineffective compounds. Effective compounds may then be selected for animal evaluation before clinical testing. This integrated approach may improve the efficiency of developing novel ASMs.
The present invention relates to an anti-cancer slow-release preparation containing glucocorticoid. It is a slow-release injection formed from slow-release microsphere and solvent. The slow-release microsphere includes anti-cancer effective component and slow-release auxiliary material, the solvent is a special solvent containing suspension adjuvant. The anti-cancer effective component is combination of glucocorticoid selected from cortisone, prednisone, clobetasone, dexamethasone, betamethasone, triamcinolone, triamcinolone acetonide, halometasone monohyudrate and fluocinonide, etc. and anti-cancer medicine selected from anti-tumor antibiotic and/or antimetabolite medicine. The slow-release auxiliary material is selected from bio-degradable absorbable high-molecular multimer and its polymer or mixture, and the viscosity of suspension adjuvant is 80 cp-3000 cp. Said anti-cance preparation also can be made into slow-release implantation preparation.
Arterial access is the key step during the endovascular treatment of cardiovascular diseases. However, failure in hemostasis of the arterial access sites is associated with high risk of complications such as bleeding, pseudoaneurysm, and arteriovenous fistula. Major bleeding events after percutaneous coronary intervention has been shown be associated with poor short-term as well as long-term prognosis. Thus, there have been a variety of approaches to quickly and effectively achieve hemostasis of the puncture site. The traditional method was to apply manual compression followed by simple dressing directly on the puncture site. Despite a long history and economic advantage, this method required prolonged hemostasis time, substantial efforts by trained practitioner, and patients' discomfort.

Use of hemostasis pad that accelerates blood clotting has become an effective alternative. The ezClot pad is a new product that uses chitosan, a deacetylated complex carbohydrate derived from the naturally occurring substance chitin. The positively charged chitosan molecules attract the negatively charged blood cells and platelets, thus promoting clots. The ability to hemostasis of chitosan has been proven with the HemCon® pad (HemCon Medical Technologies, Inc., Portland, OR, USA). This study was designed to confirm the safety and efficacy of the ezClot pad in patients undergoing percutaneous procedures with arterial approach. Two cohorts will be included in this study: transradial and transfemoral cohort. Among the transfemoral cohort, the safety and efficacy of the ezClot pad will be compared with the BloodSTOP® pad (LifeScience PLUS, Palo Alto, CA, USA). The BloodSTOP® pad is an etherized and oxidized regenerated cellulose matrix that achieves hemostasis by activating the intrinsic coagulation pathway.

Transradial approach is increasing used during coronary procedures. The most important benefit of transradial approach compared to transfemoral approach is low risk of major bleeding. Widely used method for hemostasis of radial puncture sites were manual or device-assisted compression. There is yet only a limited data regarding the use of hemostasis pad after transradial approach. The hypothesis will be tested in the transradial cohort that the combined use of a hemostasis pad and a compression device is superior to that of a compression device only in terms of hemostasis in patients who underwent transradial coronary procedures.
BACKGROUND: A retrospective cohort study was conducted to estimate associations between an ultrafine aluminum powder, McIntyre Powder (MP), and cardiovascular disease incidence in a cohort of mine workers from Ontario, Canada. Disease outcomes included ischemic heart disease (IHD), acute myocardial infarction (AMI), congestive heart failure (CHF), and strokes and transient ischemic attacks (STIA).
METHODS: Using work history records from the Ontario Mining Master File (MMF) mine workers were followed for disease incidence in administrative health records. The analysis included 25,813 mine workers who were exposed to MP between 1943 and 1979 and followed for cardiovascular disease (CVD) diagnoses between 2006 and 2018. Cardiovascular disease cases were ascertained using physician, hospital, and ambulatory care records. Poisson regression models were used to estimate age and birth-year adjusted incidence rate ratios (RR) and 95% confidence intervals (CI) for associations between MP exposure and CVD outcomes.
RESULTS: Ever-exposure to MP was positively associated with modest increases in the incidence rate of IHD, AMI, and CHF, but not STIA, using both assessment approaches. Duration of self-reported MP exposure was positively associated with monotonically increasing rates of IHD and AMI compared to never-exposed miners, with the greatest association observed among miners with >20 years of exposure (for IHD: RR 1.24, 95% CI: 0.91-1.68; and for AMI: RR 1.52, 95% CI 1.01-2.28).
CONCLUSION: Mine workers ever-exposed to MP had modestly elevated rates of CVD. The rate of CVD diagnoses appeared to increase with longer duration of exposure when assessed by both self-reported exposure and through historical records.
Dextromethorphan is an antitussive agent and, unlike the isomeric levorphanol, it has no analgesic or addictive properties.

The drug acts centrally and elevates the threshold for coughing. It is about equal to codeine in depressing the cough reflex. In therapeutic dosage dextromethorphan does not inhibit ciliary activity.

Dextromethorphan is rapidly absorbed from the gastrointestinal tract and exerts its effect in 15 to 30 minutes. The duration of action after oral administration is approximately three to six hours. Dextromethorphan is metabolized primarily by liver enzymes undergoing O-demethylation, N-demethylation, and partial conjugation with glucuronic acid and sulfate. In humans, (+)-3-hydroxy-N-methyl-morphinan, (+)-3-hydroxymorphinan, and traces of unmetabolized drug were found in urine after oral administration.
Background: To compare the effectiveness of digital phenotyping of patients diagnosed with arterial hypertension with traditional monitoring methods over a three-year period. Patients and methods: The study was conducted from January 2021 to January 2024 among 800 patients diagnosed with arterial hypertension at 6 clinics in Moscow, Russia, evenly divided into experimental (identification of digital biomarkers of disease progression for digital phenotyping) and control (standard monitoring methods) groups. The intervention included lifestyle changes focused on increasing physical activity, improving sleep quality, reducing stress, and modifying diet. Significant improvements were observed in the experimental group compared to the control group. Systolic blood pressure decreased by 10 mmHg (p<0.001), pulse by 5 beats per minute (p<0.001), and stress level by 2 points (p<0.001) in the experimental group. Additionally, physical activity increased by 15 minutes per day (p<0.001), and sleep quality improved by 2 points on a scale from 1 to 10 (p<0.001). Results: Multiple regression analysis showed a decrease in the significance of digital biomarkers over the study period, indicating a positive response to the intervention. Conclusions: The obtained results emphasize the importance of comprehensive interventions in managing arterial hypertension and its related conditions. Implementing comprehensive lifestyle changes can lead to significant health improvements and serve as an effective preventive strategy. Further research is needed to explore optimal intervention strategies for promoting societal health.
The combination of an aging population and the increased prevalence of chronic diseases among the elderly presents a major public health concern. Depression acts as both a cause and a consequence of disability, and with major depressive disorder (MDD) affecting up to 25% of women and 12% of men during their lifetimes, effective treatments for people of all ages must be made available. Although antidepressant medications are available as treatments for MDD, they sometimes either do not adequately relieve depressive symptoms, or do relieve depressive symptoms, but cause undesirable side effects. These side effects may become more common or more problematic as people age. Alternative approaches to treating depression, therefore, are necessary. Research suggests that exercise positively affects the levels of certain mood-enhancing neurotransmitters in the brain. This study will evaluate the effectiveness of both center-based and home-based exercise versus the antidepressant drug sertraline in treating depression in middle-aged and older adults.

Participants in this double-blind study will be randomly assigned to one of the following four treatments for 16 weeks: supervised aerobic exercise; home-based aerobic exercise; drug therapy; or placebo. All participants assigned to an exercise condition will report to the study site for a baseline exercise stress test. Participants assigned to supervised aerobic exercise will attend study visits 3 times per week for an exercise session. Each session will entail 10 minutes of warm-up exercises, followed by 30 to 35 minutes of continuous walking, biking, or jogging, and 10 to 15 minutes of cool-down exercises. Participants assigned to home-based aerobic exercise will attend one introductory session with an exercise physiologist, who will prescribe an exercise regimen and provide instruction on how to self-monitor pulse rate. They will also receive written information about their exercise plan, tips for maintaining progress and relapse prevention, and daily activity logs. The exercise prescription will be adjusted on a bi-weekly basis. Participants will be expected to exercise 3 times per week on their own, and will perform 10 minutes of warm-up exercises, followed by 30 to 35 minutes of continuous walking, biking, or jogging, and 10 to 15 minutes of cool-down exercises. In addition, they will mail in daily activity logs weekly for the first 6 weeks and biweekly for the remaining 10 weeks. Brief telephone contacts will be made to monitor progress, answer questions, and provide individualized feedback. Additionally, the exercise physiologist will conduct home visits at Weeks 4 and 8. Participants assigned to receive sertraline or placebo will receive their medication in pill-form at baseline and Weeks 2, 4, 8, 12, and 16 study visits. All participants will receive several phone calls to assess treatment response and suicide risk. These calls will take place weekly for the first 4 weeks and biweekly for the remainder of the study. Follow-up visits will occur at Months 6 and 12 post-treatment, and will include participating in psychological interviews and filling out questionnaires.
Naproxen Oral Suspension, USP is available as a light orange suspension which readily resuspends on shaking containing 125 mg/5 mL of naproxen, USP for oral administration. 

Naproxen is a propionic acid derivative related to the arylacetic acid group of nonsteroidal anti-inflammatory drugs. The chemical name is (S)-2-(6-Methoxy-naphth-2-yl) propionic acid (2S)-2-(6-Methoxynaphthalen-2-yl)propanoic acid. The molecular weight is 230.26. Its molecular formula is C14H14O3, and it has the following chemical structure.

Naproxen, USP is a white to off-white crystalline powder. It is practically insoluble in water and soluble in alcohol and in methanol. 

Naproxen Oral Suspension, USP for oral administration contains the following inactive ingredients: FD&C Yellow No. 6, fumaric acid, magnesium aluminum silicate, methylparaben, orange flavor, pineapple flavor, purified water, sodium chloride, sorbitol solution, and sucrose. It has a sodium content of 39.3 mg/5 mL, 1.71 mEq/5 mL, with a pH range of 2.2 to 3.7.
Patients receive lurbinectedin IV over 60 minutes on day 1. Treatment repeats every 21 days in the absence of disease progression or unacceptable toxicity. Patients also undergo fine-needle aspiration on days 2-6 of cycle 1. Beginning in cycle 2, if the biopsy shows suppression of NR0B1, then patients receive irinotecan IV over 1 hour on the day of maximum NR0B1 suppression on cycle 2. If the duration of NR0B1 suppression from lurbinectedin alone exceeds 48 hours, or if the duration of NR0B1 suppression from lurbinectedin and irinotecan exceeds 48 hours and is longer than that seen with lurbinectedin alone, then patients may receive a second dose of irinotecan during the extended period of NR0B1 suppression.
Controls will be instructed to maintain their weight throughout the 12 m trial and to not change eating or physical activity habits. Controls will not receive dietary counseling. Controls will visit the research center every 3 months for outcome measurements.
The present invention relates to medicine wine and a preparation technology thereof for treating rheumatoid diseases, which belongs to the field of a medicinal preparation. The medicine wine is prepared by immersing wine with traditional Chinese medicine. The traditional Chinese medicine comprises (weight shares) 5 to 50 shares of Japanese honeysuckle stem, 20 to 150 shares of suberect spatholobus stem, 10 to 60 shares of ovientvine, 9 to 150 shares of kadsura pepper stem and 9 to 30 shares of Chinese photinia stem. The ratio of the traditional Chinese medicine to the wine is 1: 1 to 1: 5. The alcoholic strength of the medicine wine is from 15 to 50%(V/V). The preparation technology has one of technologies that the traditional Chinese medicine is immersed for more than 3 days between 0 to 40DEG after the sealing by using the wine according to a formula. The medicine wine of the present invention for treating rheumatoid diseases has good curative effect and no side effect, and has little possibility of recurrence.
<P>PROBLEM TO BE SOLVED: To provide a cell therapy method for treating tumors.  <P>SOLUTION: Artificial antigen presenting cells [AAPC; (Drosophila melanogaster)] transfected with human HLA class I and defined accessory molecules are used to stimulate CD8+T cells from both normal donors and cancer patients. The class I molecules expressed to a high density on the surface of the Drosophila cells are empty, and allow for efficient addition of a plurality of peptides that brings the generation of polyclonal responses recognizing tumor cells endogenously expressing the specific peptides. The generated responses are robust, antigen-specific and reproducible when the peptide epitope is a defined immunogen. The artificial antigen expression system can be adapted to treat most cancers in a significant majority of the population.  <P>COPYRIGHT: (C)2011,JPO&INPIT
Arsenic exhibits varying degrees of toxicity depending on its many chemical forms. The carcinogenic properties of arsenic have already been established. However, the precise processes underlying the development of diseases following acute or chronic exposure to arsenic remain poorly known. Most of the existing investigation has focused on studying the occurrence of cancer following significant exposure to elevated levels of arsenic. Nevertheless, multiple investigations have documented diverse health consequences from prolonged exposure to low levels of arsenic. Inorganic arsenic commonly causes lung, bladder, and skin cancer. Some investigations have shown an association between arsenic in drinking water and prostate cancer, but few investigations have focused on exploring this connection. There is currently a lack of relevant animal models demonstrating a clear link between inorganic arsenic exposure and the development of prostate cancer. Nevertheless, studies using cellular model systems have demonstrated that arsenic can potentially promote the malignant transformation of human prostate epithelial cells in vitro. The administration of elevated levels of arsenic has been demonstrated to elicit cell death in instances of acute experimental exposure. Conversely, in cases of chronic exposure, arsenic prompts cellular proliferation and sustains cellular viability, thereby circumventing the constraints imposed by telomere shortening and apoptosis. Furthermore, cells consistently exposed to the stimulus exhibit an augmented ability to invade surrounding tissues and an enhanced potential to form tumors. This review aims to portray mechanistic insights into arsenic-induced prostate cancer.
The present invention relates to a traditional Chinese medicine powder preparation for treating AIDS, which is formed by preparing raw materials of the following weight proportion in the method: 20 to 30 portions of phoebe nanmu, 15 to 25 portions of purslane herb, 10 to 20 portions of Oberonia myosurus(Forst.)Lindl, 5 to 10 portions of cotoneaster horizontalis and 5 to 10 portions of giant knotweed rhizome, and the particular method is disclosed in the specification. The traditional Chinese medicine powder preparation of the present invention has the advantages that the raw materials are come from Chinese herbal medicine, the source of the raw materials is rich, preparation is convenient, and side effects are small through a No. FS-1 acute and poison test; the inhibition ratio of the No. FS-1 medicine in 0.2 mg/ml for HIV-1 viruses is 69.9%, and the inhibition ratio of the traditional Chinese medicine of the prior art for the HIV-1 viruses is about 40%; the living cell rate of the No. FS-1 medicine in 0.125 mg/ml is 69.33% contrasted with normal cells; the living cell rate of the No. FS-1 medicine in 0.125 mg/ml is 84.32% contrasted with poison containing cells. Products of the present invention are suitable for treating AIDS.