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Runlin Xing

Researcher at Nanjing University of Chinese Medicine

Publications -  18
Citations -  377

Runlin Xing is an academic researcher from Nanjing University of Chinese Medicine. The author has contributed to research in topics: Fibrosis & Osteoarthritis. The author has an hindex of 7, co-authored 16 publications receiving 148 citations.

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Increased HIF-1α in Knee Osteoarthritis Aggravate Synovial Fibrosis via Fibroblast-Like Synoviocyte Pyroptosis.

TL;DR: An elevated hypoxia-inducible factor-1 α (HIF-1α) level is found in the synovial tissue of KOA model rats, and inhibiting the increase of HIF- 1α could improvesynovial fibrosis in rats, indicating that increased HIF -1α is highly involved in the KOA synovia fibrosis.
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Inhibition of Synovial Macrophage Pyroptosis Alleviates Synovitis and Fibrosis in Knee Osteoarthritis.

TL;DR: Investigating whether synovial macrophage pyroptosis did occur and whether this form of cell death should be related to synovitis and fibrosis of KOA concluded that it may occur in the pathological processes ofKOA and inhibition of synovials pyroPTosis alleviates synovococcalitis and Fibrosis in KOA model rats.
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Effect of intramedullary nail and locking plate in the treatment of proximal humerus fracture: an update systematic review and meta-analysis.

TL;DR: The intramedullary nail is superior to locking plate in reducing the total complication, intraoperative blood loss, operative time, postoperative fracture healing time and postoperative humeral head necrosis rate of PHF.
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Bisphosphonates therapy for osteoarthritis: a meta-analysis of randomized controlled trials

TL;DR: Bisphosphonates therapy is effective in relieving pain, stiffness and accelerating functional recovery in OA, and no significant differences were found in subjective improvement, osteoarthritis progression, the number of required acetaminophen treatment or joint replacement.
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Excessive mechanical stress induces chondrocyte apoptosis through TRPV4 in an anterior cruciate ligament-transected rat osteoarthritis model.

TL;DR: Results indicated that TRPV4 was upregulated in OA articular cartilage, and that excessive mechanical stress might induce chondrocyte apoptosis via TRP V4-mediated Ca2+ influx, suggesting TRPv4 as a potential drug target in Oa.