anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
INTRODUCTION: Overtreatment and frequent hospital admissions in patients at end-of-life has been shown in several studies, including in the nursing home (NH) setting. However, overtreatment in NH residents with advanced cancer has not been studied before. Our objective was to compare emergency room (ER) visits and hospital admissions in the last month of life and place of death among NH residents with or without advanced cancer.
MATERIALS AND METHODS: This retrospective study is based on Region Stockholm's administrative database from 2015 to 2019. Demographic data, ER visits, and Hospital Frailty Risk Score (HFRS) were extracted for each subject. Univariable and multivariable analyses were performed, and odds ratios (OR) calculated.
RESULTS: In total, 30,324 NH residents were identified, of which 1807 had advanced cancer. Advanced cancer was associated with more ER visits in the last month of life in the univariable analysis but not when adjusted for age, sex, and risk of frailty with an adjusted aOR of 1.07 (95 %CI 0.97-1.19). Having a cancer diagnosis was significantly associated with acute hospital admissions, although the association was rather weak with an aOR 1.13 (95 %CI 1.02-1.26). NH residents with advanced cancer were less likely to die in hospital than non-cancer residents: aOR 0.63 (95 %CI 0.54-0.73).
DISCUSSION: NH residents with advanced cancer have a slightly higher risk of hospital admissions in the last month of life compared to non-cancer residents but are less likely to die in hospital. The probability of ER visits during the last month of life was similar between NH residents with and without cancer.
Post-traumatic epilepsy (PTE) stands as one of the numerous debilitating consequences that follow traumatic brain injury (TBI). Despite its impact on many individuals, the current landscape offers only a limited array of reliable treatment options, and our understanding of the underlying mechanisms and susceptibility factors remains incomplete. Among the potential contributors to epileptogenesis, astrocytes, a type of glial cell, have garnered substantial attention as they are believed to promote hyperexcitability and the development of seizures in the brain following TBI. The current study evaluated the transcriptomic changes in cortical astrocytes derived from animals that developed seizures as a result of severe focal TBI. Using RNA-Seq and ingenuity pathway analysis (IPA), we unveil a distinct gene expression profile in astrocytes, including alterations in genes supporting inflammation, early response modifiers, and neuropeptide-amidating enzymes. The findings underscore the complex molecular dynamics in astrocytes during PTE development, offering insights into therapeutic targets and avenues for further exploration.
The participants in the SPEG will participate in the 16-style simplified Pilates exercise sessions (about 60 minutes each) in a group (about 10 participants in each group) twice a week for 12 weeks. Each participant will undertake a total of 24 exercise sessions.
A group of healthy subjects who meet the inclusion and exclusion criteria established for the study to which an imagery training and placebo observation, inspired by a rural landscape, will be given for four consecutive days. This group will carry out the observation and imagination of a landscape during 2 series of 30 seconds for each manual motor sequence to remember.
To date, earlier diagnosis of Alzheimer's disease (AD) is still challenging. Recent studies revealed the elevated expression of connective tissue growth factor (CTGF) in AD brain is an upstream regulator of amyloid-beta (Aβ) plaque, thus CTGF could be an earlier diagnostic biomarker of AD than Aβ plaque. Herein, we develop a peptide-coated gold nanocluster that specifically targets CTGF with high affinity (KD ~ 21.9 nM). The probe can well penetrate the blood-brain-barrier (BBB) of APP/PS1 transgenic mice at early-stage (earlier than 3-month-old) in vivo, allowing non-invasive NIR-II imaging of CTGF when there is no appearance of Aβ plaque deposition. Notably, this probe can also be applied to measuring CTGF on postmortem brain sections by multimodal analysis, including fluorescence imaging, peroxidase-like chromogenic imaging, and ICP-MS quantitation, which enables distinguishment between the brains of AD patients and healthy people. This probe possesses great potential for precise diagnosis of earlier AD before Aβ plaque formation.
A preparation method of novel medicine sustained and controlled release aqueous coating is made of ethyl cellulose and adopts a phase variation method to prepare ethyl cellulose aqueous dispersion. The ethyl cellulose and plasticizers are premixed and granulated for internal plasticization in an extruder and then adopts the phase variation method to prepare the aqueous coating. The invention has the main steps that the ethyl cellulose EC and the plasticizer dibutyl sebacate DBS are mixed in a high-power mixer with a plastication method, the plasticizer is added, the mixture is plastified through a screw extruder, and the mixture is granulated after being extruded; with the phase variation method, and the plastified ethyl cellulose granular material is put in a three mouth flask. Through constant temperature water bath, the granular material is melted completely under the action of mechanical stirring. Next, oleic acid, ammonia and distilled water are slowly added into the above system to obtain the aqueous dispersion after the phase variation. The coating has the advantages of high solid content, low viscosity, good film forming performance, favorable medicine sustained and controlled release effect and no plastication in coating medicine, the process technique is simplified, requirements to processing equipment are less, and the product price is low.
A vessel evaluation antenna device is suitable for measuring the access state of a blood vessel of a patient, and comprises an antenna unit and a fabric sleeve. The antenna unit includes a substrate having a first side surface, a circuit module, a transmitting antenna and a receiving antenna, wherein the transmitting antenna and the receiving antenna are disposed on the first side surface. The circuit module transmits a radio carrier to the blood vessel via the transmitting antenna and receives a reflected echo signal via the receiving antenna. The fabric sleeve is sleeved to the antenna unit and includes an insulating layer suitable for being sandwiched between the transmitting antenna and the patient's skin, and a protective layer cooperating with the insulating layer to define an antenna space for disposing the antenna unit. The dielectric coefficient of the insulating layer is not greater than 3. In this way, the signal leakage can be avoided to obtain the better quality of the echo signal. The insulating layer is plain woven fabric or T/C blended fabric. In the material of the insulating layer, the proportion of tetoron is between 30% and 40% and the proportion of cotton is between 60% and 70%. The thickness of the substrate is not less than 0.3 mm. The material of the substrate is polyimide or polyester. The transmitting antenna has an emission transmission line extending from the circuit module, and an emitting part extending from one end of the emission transmission line away from the circuit module. The receiving antenna has a receiving transmission line extending from the circuit module, and a receiving part extending from one end of the receiving transmission line away from the circuit module and toward the emitting part. The emitting part is separated from the receiving part by a distance.
Carcinogenesis: Sulfamethoxazole was not carcinogenic when assessed in a 26-week tumorigenic mouse (Tg-rasH2) study at doses up to 400 mg/kg/day sulfamethoxazole; equivalent to 2.4-fold the human systemic exposure (at a daily dose of 800 mg sulfamethoxazole twice a day).

Mutagenesis: In vitro reverse mutation bacterial tests according to the standard protocol have not been performed with sulfamethoxazole and trimethoprim in combination. An in vitro chromosomal aberration test in human lymphocytes with sulfamethoxazole and trimethoprim was negative. In in vitro and in vivo tests in animal species, sulfamethoxazole and trimethoprim did not damage chromosomes. In vivo micronucleus assays were positive following oral administration of sulfamethoxazole and trimethoprim. Observations of leukocytes obtained from patients treated with sulfamethoxazole and trimethoprim revealed no chromosomal abnormalities.

Sulfamethoxazole alone was positive in an in vitro reverse mutation bacterial assay and in in vitro micronucleus assays using cultured human lymphocytes.

Trimethoprim alone was negative in in vitro reverse mutation bacterial assays and in in vitro chromosomal aberration assays with Chinese Hamster ovary or lung cells with or without S9 activation. In in vitro Comet, micronucleus and chromosomal damage assays using cultured human lymphocytes, trimethoprim was positive. In mice following oral administration of trimethoprim, no DNA damage in Comet assays of liver, kidney, lung, spleen, or bone marrow was recorded.

Impairment of Fertility: No adverse effects on fertility or general reproductive performance were observed in rats given oral dosages as high as 350 mg/kg/day sulfamethoxazole plus 70 mg/kg/day trimethoprim, doses roughly two times the recommended human daily dose on a body surface area basis.
Background: The COVID-19 pandemic catalyzed a renewed urgency to address the obesity pandemic and accelerated the use of technology to treat pediatric obesity. Yet, there are significant incongruities between the existing literature on technology for obesity management and the current health care system that may lead to suboptimal outcomes and increased costs. This study reviewed the types of e-health strategies currently in use, highlighted inconsistencies and overlap in terminology, and identified future research directions in e-health for childhood obesity, including gaps in implementation science. Methods: This narrative literature review synthesized seminal articles from the literature, as well as recent articles, using PubMed and Google Scholar that focused on the use of technology in treating pediatric obesity. This inclusive strategy was intended to elucidate the heterogeneity in how different disciplines are using digital health terminology in pediatric obesity research. Results: Both the prevalence of e-health interventions and its associated terminology are increasing in the peer-reviewed literature, especially since the beginning of the COVID-19 pandemic. Yet, their definitions and usage are unstandardized, leading to a lack of cohesion in the research and between disciplines. There is a gap in implementation science outcomes, including reimbursement, that may significantly impact external validity and uptake. Conclusion: A more systematic and precise approach to researching e-health that can assess specific technologies and combinations of technologies, their short-term and long-term effect sizes, and feasibility can produce the necessary data that may lead to reimbursement policies and, ultimately, improved pediatric weight management outcomes.
Robotic Assisted Gait Therapy using the GT has been shown to be effective in restoring gait to non-walking stroke patients. However, GaitTrainer rehabilitation sessions can result in fatigue, sling attachment discomfort, which can limit the duration, intensity and participation of patients. Immersive Virtual Reality (VR) via visio helmet is an innovative and playful approach that allows rehabilitation to focus on specific tasks, such as walking in controlled and environmentally friendly environments. Coupled with robotic assistance, it could promote patient adherence and active participation thanks to the presence of bio-feedback and its playful aspect. However, the GT has never been associated with a walking activity simulated by a VR system. VR can lead to adverse effects (i.e., cyberkinetosis) such as dizziness, nausea or headaches. Thus, it seems necessary to observe the tolerance of the virtual environment immersion during GT assisted walking rehabilitation sessions in stroke patients.

This protocol involves the recruitment of non-walking stroke participants who are being rehabilitated in a Physical Medicine and Rehabilitation (PMR) department and receiving Gait Trainer-assisted rehabilitation. The intervention will consist of Gait Trainer-assisted robotic walking rehabilitation sessions with and without the addition of an immersive VR device. Post-stroke patients will complete 3 conventional sessions (Gait Trainer alone) and 3 sessions with the VR device.
Placebo melt in mouth tablets (1100 mg). 1 tablet q.i.d. (three after meals, one before resting) for three consecutive weeks. After three weeks of wash-out period,patients will take either placebo or GERDOff® Plus q.i.d. (three after meals, one before resting) for another three weeks.
Those allocated to Group 2 were provided with a standardized packet of health education materials addressing the recommended items from the expert committee guidelines (e.g., dietary recommendations using the Food Guide Pyramid and the Traffic Light Diet, a general prescription to increase physical activity to 60 minutes daily). They were also given a community resource list that provides contact and program information for community-based obesity treatment activities in their area.
The intervention consisted of 8 weeks of ad libitum TRE with a 12-8 pm 8-hour eating window on weekdays. Participants received instructions to only consume water, black coffee, or black tea from 8 pm to 12 pm on weekdays and during the weekend, where there were no restrictions on eating timing. No other dietary or physical activity instructions were given.
OBJECTIVE: As research into preclinical rheumatoid arthritis (pre-RA) has advanced, a growing body of evidence suggests that abnormalities in RA-affected joint cartilage precede the onset of arthritis. Thus, early prevention and treatment strategies are imperative. In this study, we aimed to explore the protective effects of mesenchymal stem cell (MSC)-derived microvesicles (MVs) on cartilage degradation in a collagen-induced arthritis (CIA) mouse model.
METHODS: A CIA mouse model was established to observe early pathological changes in cartilage (days 21-25) through histological and radiological examinations. On day 22, MSCs-MVs were intravenously injected into the mice with CIA. Radiological, histological, and flow cytometric examinations were conducted to observe inflammation and cartilage changes in these mice compared to the mice with CIA and the control mice. In vitro, chondrocytes were cultured with inflammatory factors such as IL-1β and TNFα to simulate inflammatory damage to cartilage. After the addition of MVs, changes in inflammatory levels and collagen expression were measured via Western blotting, immunofluorescence, enzyme-linked immunosorbent assays (ELISAs), and quantitative PCR to determine the role of MVs in maintaining chondrocytes.
RESULTS: MSC-MVs expressed vesicular membrane proteins (CD63 and Annexin V) and surface markers characteristic of MSCs (CD44, CD73, CD90, and CD105). In the early stages of CIA in mice, a notable decrease in collagen content was observed in the joint cartilage. In mice with CIA, injection of MSCs-MVs resulted in a significant reduction in the peripheral blood levels of IL-1β, TNFα, and IL-6, along with a decrease in the ratio of proinflammatory T and B cells. Additionally, MSC-MVs downregulated the expression of IL-1β, TNFα, MMP-13, and ADAMTS-5 in cartilage while maintaining the stability of type I and type II collagen. These MVs also attenuated the destruction of cartilage, which was evident on imaging. In vitro experiments demonstrated that MSC-MVs effectively suppressed the secretion of the inflammatory factors IL-1β, TNFα, and IL-6 in stimulated peripheral blood mononuclear cells (PBMCs).
CONCLUSIONS: MSCs-MVs can inhibit the decomposition of the inflammation-induced cartilage matrix by regulating immune cell inflammatory factors to attenuate cartilage destruction. MSC-MVs are promising effective treatments for the early stages of RA.
The invention relates to the field of medicines and specifically relates to a polypeptide compound for preventing or treating cerebral infarction. A transforming growth factor-beta 1 agonist polypeptide 2 is characterized in that the sequence is CAELYIDFRKDLGWKWIHEP. A solid-phase synthesis technology protected by Fmoc is adopted for preparation, Fmoc-Gly-Wang resin is taken as a carrier, 6-chloro-1-hydroxybenzotriazole is taken as a condensing agent, and trifluoroacetic acid is taken as a cutting reagent. An adjuvant can be covalently connected, and the adjuvant is bovine serum albumin, human serum albumin or polyethylene glycol. The invention further relates to application of the transforming growth factor-beta 1 agonist polypeptide 2 in prevention or treatment of cerebral infarction. The transforming growth factor-beta 1 agonist polypeptide 2 can be administrated in a variety of drug delivery ways, including subcutaneous or intramuscular injection, intravenous injection or intravenous infusion and oral administration, such as pills, capsules, nasal sprays and the like, for preventing or treating cerebral infarction. The transforming growth factor-beta 1 agonist polypeptide 2 in the invention can promote the expression of the transforming growth factor-beta 1 in a targeted manner, as well as improve the content of the transforming growth factor-beta 1 in plasma so as to achieve the effect of preventing or treating cerebral infarction.
Anti-IL-17A antibodies, such as secukinumab and ixekizumab, are effective proinflammatory cytokine inhibitors for autoimmune disorders, including psoriasis. However, anti-IL-17A small molecule treatments are yet to be commercialized. Celastrol, a natural compound extracted from the roots of traditional Chinese medicinal plants, has anti-inflammatory and antioxidant properties. However, the binding of celastrol to IL-17A and the associated anti-inflammatory mechanisms remain unclear. This study investigated whether celastrol could directly bind to IL-17A and regulate inflammation in psoriatic in vitro and in vivo models. The results showed that celastrol directly binds to IL-17A and inhibits its downstream signaling, including the NF-kB and MAPK pathways. Interestingly, celastrol restored autophagy dysfunction and reduced proinflammatory cytokine secretion in keratinocytes. In addition, celastrol increased autophagy in the epidermis of a mouse model of psoriasis. Celastrol decreased Th17 cell populations and proinflammatory cytokine levels in mice. Thus, IL-17A-targeting celastrol reduced inflammation by rescuing impaired autophagy in in vitro and in vivo models of psoriasis, demonstrating its potential as a substitute for anti-IL-17A antibodies for treating psoriasis.
PCT No. PCT/GB95/00579 Sec. 371 Date Apr. 4, 1996 Sec. 102(e) Date Apr. 4, 1996 PCT Filed Mar. 22, 1994 PCT Pub. No. WO94/22849 PCT Pub. Date Oct. 13, 1994Compounds having utility in medicine in countering cellular malfunction e.g. in conditions embraced by the general term "cancer", which compounds normally exist us a keto-enol tautomeric pair, the racetalc keto form of which is rapresented by formula (Ia), wherein R is a hydrogen, lower alkyl, acyl, or another functional group of up to 6 carbons including at least one hetero atom, which atom may be directly bonded to the  beta -carbon, which compound may be in the acylic form shown or in a cyclic form as equilibrium keto-enol tautomer derivatives and anomeric forms thereof, including enantiomers when R is hydrogen and diastereoisomers when R is another group. A method of obtaining such a compound comprises selecting an appropriate dihydrofuran having a protected primary alcohol side chain in the 2-position, subjecting the said protected alcohol side chain-substituted dihydrofuran to oxidation using a chromium-based reagent to yield the corresponding acid, subjecting said acid to iodolaetonisation conditions to yield the cis,cis,trans-trisubstituted iodo-lactone which upon displacement of the iodine provides the cis,cis,cis-tri-substituted hydroxylacetone which is capable of being reduced to obtain a lactol which is in equilibrium with the corresponding open chain aldehyde.
BACKGROUND: Dialysis-related amyloidosis (DRA) is a severe complication in end-stage kidney disease (ESKD) patients undergoing long-term dialysis treatment, characterized by the deposition of β2-microglobulin-related amyloids (Aβ2M amyloid). To inhibit DRA progression, hexadecyl-immobilized cellulose bead (HICB) columns are employed to adsorb circulating β2-microglobulin (β2M). However, it is possible that the HICB also adsorbs other molecules involved in amyloidogenesis.
METHODS: We enrolled 14 ESKD patients using HICB columns for DRA treatment; proteins were extracted from HICBs following treatment and identified using liquid chromatography-linked mass spectrometry. We measured the removal rate of these proteins and examined the effect of those molecules on Aβ2M amyloid fibril formation in vitro.
RESULTS: We identified 200 proteins adsorbed by HICBs. Of these, 21 were also detected in the amyloid deposits in the carpal tunnels of patients with DRA. After passing through the HICB column and hemodialyzer, the serum levels of proteins such as β2M, lysozyme, angiogenin, complement factor D and matrix Gla protein were reduced. These proteins acted in the Aβ2M amyloid fibril formation.
CONCLUSIONS: HICBs adsorbed diverse proteins in ESKD patients with DRA, including those detected in amyloid lesions. Direct hemoperfusion utilizing HICBs may play a role in acting Aβ2M amyloidogenesis by reducing the amyloid-related proteins.