Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1001/jama.248.1.53 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Same plane, different target: aiming for proximal origins of the subscapular and axillary nerves.
Reg Anesth Pain Med
January 2025
Anesthesiology, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA.
Effectively alleviate rheumatoid arthritis via maintaining redox balance, inducing macrophage repolarization and restoring homeostasis of fibroblast-like synoviocytes by metformin-derived carbon dots.
J Nanobiotechnology
January 2025
Department of Orthopedic Surgery, Fujian Medical University Union Hospital, Fuzhou, 350001, China.
Overproduction of reactive oxygen species (ROS), elevated synovial inflammation, synovial hyperplasia and fibrosis are the main characteristic of microenvironment in rheumatoid arthritis (RA). Macrophages and fibroblast-like synoviocytes (FLSs) play crucial roles in the progression of RA. Hence, synergistic combination of ROS scavenging, macrophage polarization from pro-inflammatory M1 phenotype towards M2 anti-inflammatory phenotype, and restoring homeostasis of FLSs will provide a promising therapeutic strategy for RA.
View Article and Find Full Text PDFSP-1-activated LINC01016 overexpression promotes gastric cancer invasion and metastasis through inhibiting EIF4A3-mediated MMP9 mRNA decay.
Cell Death Dis
January 2025
Department of Pathology, Qilu Hospital and School of Basic Medical Sciences Shandong University, Jinan, Shandong, PR China.
Long noncoding RNAs (lncRNAs) are key regulators during gastric cancer (GC) development and may be viable treatment targets. In the present study, we showed that the expression of the long intergenic noncoding RNA 01016 (LINC01016) is significantly higher in GC tissues with lymph node metastasis (LNM) than those without LNM. LINC01016 overexpression predicts a poorer relapse-free survival (RFS) and overall survival (OS).
View Article and Find Full Text PDFBryostatin-1 enhances the proliferation and functionality of exhausted CD8+ T cells by upregulating MAP Kinase 11.
Front Immunol
January 2025
Department of Immunology, Erasmus University Medical Center, Rotterdam, Netherlands.
Introduction: Bryostatin-1, a potent agonist of the protein kinase C, has been studied for HIV and cancer therapies. In HIV research, it has shown anti-HIV effects during acute infection and reactivation of latent HIV in chronic infection. As effective CD8+ T cell responses are essential for eliminating reactivated virus and achieving a cure, it is important to investigate how bryostatin-1 affects HIV-specific CD8+ T cells.
View Article and Find Full Text PDFUnlocking hexafluoroisopropanol as a practical anion-binding catalyst for living cationic polymerization.
Angew Chem Int Ed Engl
January 2025
Chang Chun Institute of Applied Chemistry Chinese Academy of Sciences, Key Laboratory of Polymer Ecomaterials, 5625 Renmin Street, Changchun, , 130022, Changchun, CHINA.
Living cationic polymerization (LCP) is a classical technique for precision polymer synthesis; however, due to the high sensitivity of cationic active species towards chain-transfer/termination events, it is notoriously difficult to control polymerization under mild conditions, which inhibits its progress in advanced materials engineering. Here, we unlock a practical anion-binding catalytic strategy to address the historical dilemma in LCP. Our experimental and mechanistic studies demonstrate that commercially accessible hexafluoroisopropanol (HFIP), when used in high loading, can create higher-order HFIP aggregates to tame dormant-active species equilibrium via non-covalent anion-binding principle, in turn inducing distinctive polymerization kinetics behaviors that grant efficient chain propagation while minimizing competitive side reactions.
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!