[Development and research progress of suture button fixation Latarjet procedure].

Objective: To review the development and research progress of suture button fixation Latarjet procedure. Methods: A comprehensive literature review was conducted to summarize the development and related modified techniques of the suture button fixation Latarjet procedure. Results: Since the Latarjet procedure was first introduced by French scholar Latarjet in 1954, it has undergone three key transformations, resulting in suture button fixation Latarjet procedure, which has shown satisfactory outcomes in treatment of recurrent shoulder dislocation. However, there are still drawbacks such as the risk of impingement of the graft on surrounding tissues, and the surgical disruption of anatomical structures like the coracoclavicular ligament and the pectoralis minor muscle. The scholars have proposed several modified techniques based on the suture button fixation Latarjet procedure to further reduce complications from impingement of the graft, to lower the glenohumeral contact pressure, and to eliminate the impact of surgery on the physiological structures of the shoulder joint. The modified techniques include the arthroscopic suture button fixation Latarjet procedure using FiberTape Cerclage, reconstruction of the coracoacromial ligament during congruent-arc Latarjet procedures, and limit unique coracoid osteotomy suture button Latarjet procedure (LU-tarjet procedure). These modified techniques have also shown good clinical outcomes. Additionally, other related modified techniques for reconstruction of the glenoid, such as Chinese unique Inlay Bristow procedure (Cuistow procedure), arthroscopic glenoid bone grafting with soft fixation, and all-arthroscopic modified Eden-Hybinette procedure, have also demonstrated favorable efficacy. However, there is still a lack of long-term follow-up results for these techniques and comparative studies between them. Conclusion: Suture button fixation Latarjet procedure is an effective method for the treatment of recurrent shoulder dislocation. There are various techniques, but there is no recognized gold standard, and further clinical and basic research is needed.

HIMF deletion ameliorates acute myocardial ischemic injury by promoting macrophage transformation to reparative subtype.

Appropriately manipulating macrophage M1/M2 phenotypic transition is a promising therapeutic strategy for tissue repair after myocardial infarction (MI). Here we showed that gene ablation of hypoxia-induced mitogenic factor (HIMF) in mice (Himf-/- and HIMFflox/flox;Lyz2-Cre) attenuated M1 macrophage-dominated inflammatory response and promoted M2 macrophage accumulation in infarcted hearts. This in turn reduced myocardial infarct size and improved cardiac function after MI. Correspondingly, expression of HIMF in macrophages induced expression of pro-inflammatory cytokines; the culturing medium of HIMF-overexpressing macrophages impaired the cardiac fibroblast viability and function. Furthermore, macrophage HIMF was found to up-regulate C/EBP-homologous protein (CHOP) expression, which exaggerated the release of pro-inflammatory cytokines via activating signal transducer of activator of transcription 1 (STAT1) and 3 (STAT3) signaling. Together these data suggested that HIMF promotes M1-type and prohibits M2-type macrophage polarization by activating the CHOP-STAT1/STAT3 signaling pathway to negatively regulate myocardial repair. HIMF might thus constitute a novel target to treat MI.