Molecular mechanism underlying the protective effects of ischemic preconditioning in total knee arthroplasty.

Propose: To investigate the molecular mechanisms underlying the protective effects of ischemic preconditioning (IPC) in patients undergoing total knee arthroplasty.

Methods: GSE21164 was extracted from an online database, followed by an investigation of differentially expressed genes (DEGs) between IPC treatment samples at 2 time points (T0T and T1T). Function and pathway enrichment analyses were performed on the DEGs.

Identification of key ferroptosis-related biomarkers in steroid-induced osteonecrosis of the femoral head based on machine learning.

Background: This study was aimed to identify key ferroptosis-related biomarkers in steroid-induced osteonecrosis of the femoral head (SONFH) based on machine learning algorithm.

Methods: The SONFH dataset GSE123568 (including 30 SONFH patients and 10 controls) was used in this study. The differentially expressed genes (DEGs) were selected between SONFH and control groups, which were subjected to WGCNA.

[REVERSED ARTHROSC OPIC SUBACROMIAL DEC OMPRESSION FOR TREATMENT OF ROTATOR CUFF TEARS].

Objective: To investigate the effectiveness of reversed arthroscopic subacromial decompression in the treatment of rotator cuff tears.

Methods: Between November 2012 and January 2015, 53 patients with rotator cuff tears were treated with reversed arthroscopic subacromial decompression and rotator cuff repair. Of 53 patients, 38 were male and 15 were female, with the age of 47-61 years (mean, 53.

Effect of hepcidin on intracellular calcium in human osteoblasts.

Hepcidin is known to increase intracellular iron through binding to and degrading ferroportin, which is a transmembrane protein that transports iron from the intracellular to the outside. However, it is not clear whether hepcidin has a similar effect on intracellular calcium. Here, we investigated the influence of hepcidin on intracellular calcium in human osteoblasts, with or without high environmental iron concentrations.

Hepcidin increases intracellular Ca2+ of osteoblast hFOB1.19 through L-type Ca2+ channels.

Hepcidin is a key player in the regulation of iron homeostasis. Several pathological conditions associated with iron overload are attributed to the depressed expression of hepcidin and are often associated with bone diseases including osteoporosis. Hepcidin was suggested to have anti-osteoporosis effects by preventing iron overload.

Increased intracellular iron and mineralization of cultured hFOB 1.19 cells following hepcidin activation through ferroportin-1.

Objective: To address whether hepcidin functions in bone metabolism.

Methods: This study was carried out in the Laboratory of Radiation Medicine and Public Health of Soochow University, and the Laboratory of the Second Affiliated Hospital of Soochow University, Suzhou, China, from September 2009 to July 2010. The positive expression of ferroportin-1 (Fpn-1) was detected by reverse transcriptase-polymerase chain reaction.