Results 161 to 170 of about 1,058,270 (299)

Comparison of oral ketorolac and oral magnesium for postoperative pain management in anorectal surgery: A randomized double-blind clinical trial. [PDF]

open access: yesJ Int Med Res
Eshagh Hoseini SJ   +6 more
europepmc   +1 more source

Hyperviscous Diabetic Bone Marrow Niche Impairs BMSCs Osteogenesis via TRPV2‐Mediated Cytoskeletal‐Nuclear Mechanotransduction

open access: yesAdvanced Science, EarlyView.
Diabetic bone marrow exhibits pathological ECM hyperviscosity that activates TRPV2‐mediated Ca2⁺ influx, leading to perinuclear F‐actin disassembly, nuclear deformation, and chromatin condensation. This cytoskeletal‐nuclear decoupling suppresses osteogenic differentiation of BMSCs.
Yao Wen   +8 more
wiley   +1 more source

Cinnamic‐Hydroxamic‐Acid Derivatives Exhibit Antibiotic, Anti‐Biofilm, and Supercoiling Relaxation Properties by Targeting Bacterial Nucleoid‐Associated Protein HU

open access: yesAdvanced Science, EarlyView.
Cinnamic‐hydroxamic‐acid derivatives (CHADs) are identified as novel inhibitors of the bacterial nucleoid‐associated protein HU, exhibiting potent antibacterial, anti‐biofilm (both inhibition and eradication), and DNA relaxation (anti‐supercoiling) activities. Moreover, CHADs demonstrate strong synergistic effects with multiple antibiotics.
Huan Chen   +22 more
wiley   +1 more source

TRIM56 Aggravates Cerebral Ischemia‐Reperfusion Injury via Inhibiting KLF4‐Activated Ferroptosis Signaling

open access: yesAdvanced Science, EarlyView.
This study reveals that the E3 ubiquitin ligase TRIM56 exacerbates neuronal ferroptosis and brain damage by mediating K48‐linked ubiquitination and degradation of KLF4, leading to suppression of the xCT/GSH/GPX4 axis. Targeting TRIM56 alleviates cerebral ischemia‐reperfusion injury in vivo and in vitro, highlighting its therapeutic potential.
Qiangping Wang   +15 more
wiley   +1 more source

HRS Degradation‐Induced Nicotinamide Deficiency in Placental Extracellular Vesicles Triggers Preeclampsia by Disrupting Maternal‐Fetal Immune Homeostasis

open access: yesAdvanced Science, EarlyView.
This study shows that lower NAM levels in PE‐derived pEVs correlate with disease severity. NAM‐deficient pEVs reduce Th1 and Th17 inhibition, leading to PE‐like symptoms. NAM in pEVs inhibits Th1 via SIRT1 and Th17 via macrophages. Reduced NAM in PE‐EVs is due to decreased HRS expression in trophoblasts, resulting from elevated HSP27.
Haiyi Fei   +10 more
wiley   +1 more source

Home - About - Disclaimer - Privacy