Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1001/jamaoncol.2016.3046 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Background/aims: Certain sociodemographic groups are routinely underrepresented in clinical trials, limiting generalisability. Here, we describe the extent to which enriched enrolment approaches yielded a diverse trial population enriched for older age in a randomised controlled trial of a blood-based multi-cancer early detection test (NCT05611632).
Methods: Participants aged 50-77 years were recruited from eight Cancer Alliance regions in England.
Therapeutic Effects of GDF6-Overexpressing Mesenchymal Stem Cells through Upregulation of the GDF15/SIRT1 Axis in Age-Related Hearing Loss.
Front Biosci (Landmark Ed)
January 2025
Department of Otolaryngology, Head and Neck Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, 330006 Nanchang, Jiangxi, China.
Background: It has been reported the therapeutic effects of mesenchymal stem cells (MSCs) on hearing loss. This study explored the therapeutic effects of growth differentiation factor 6 (GDF6) overexpression-induced MSCs (MSCs-GDF6) on age-related hearing loss (ARHL) and its underlying mechanisms.
Methods: Reverse transcription-quantitative PCR and western blotting were used to evaluate gene expression.
The Efficiency of Chitosan Against Tert Butylhydroquinone (TBHQ)-Induced Neurobehavioral Changes and Toxicity Effects in Male Rats.
Front Biosci (Landmark Ed)
January 2025
Department of Zoology, College of Science, King Saud University, 11451 Riyadh, Saudi Arabia.
Background: We investigated chitosan's protective effects against tertiary butylhydroquinone (TBHQ)-induced toxicity in adult male rats, focusing on cognitive functions and oxidative stress in the brain, liver, and kidneys.
Methods: Rats were divided into four groups (n = 8/group): (1) Control, (2) Chitosan only, (3) TBHQ only, and (4) Chitosan + TBHQ.
Results: TBHQ exposure led to significant cognitive impairments and increased oxidative stress, marked by elevated malondialdehyde (MDA) and decreased superoxide dismutase (SOD) and glutathione (GSH) levels.
Inhibition of p70 Ribosomal S6K1 Protects the Myocardium against Ischemia/Reperfusion-Induced Necrosis through Downregulation of RIP3.
Front Biosci (Landmark Ed)
January 2025
Department of Cardiology, Affiliated Hospital of Jiangnan University, 214122 Wuxi, Jiangsu, China.
Background: Myocardial ischemia-reperfusion (I/R) injury refers to cell damage that occurs as a consequence of the restoration of blood circulation following reperfusion therapy for cardiovascular diseases, and it is a primary cause of myocardial infarction. The search for nove therapeutic targets in the context of I/R injury is currently a highly active area of research. p70 ribosomal S6 kinase (S6K1) plays an important role in I/R induced necrosis, although the specific mechanisms remain unclear.
View Article and Find Full Text PDFInhibition of Endothelial-Mesenchymal Transition Mediated by Activin Receptor Type IIA Attenuates Valvular Injury Induced by Group A Streptococcus in Lewis Rats.
Front Biosci (Landmark Ed)
January 2025
Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, 530021 Nanning, Guangxi, China.
Background: Rheumatic heart disease (RHD), which is caused mainly by Group A Streptococcus, leads to fibrotic damage to heart valves. Recently, endothelial‒mesenchymal transition (EndMT), in which activin plays an important role, has been shown to be an important factor in RHD valvular injury. However, the mechanism of activin activity and EndMT in RHD valvular injury is not clear.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!