Multiple screws versus sliding hip screws in femoral neck fractures: A protocol of cohort study.

BACKGROUND: There has been a paucity of cohort trials directly comparing multiple cannulated screws (MCS) and sliding hip screws (SHS) in femoral neck fractures at any level. Thus, a well-conducted clinical trial with an adequate sample size is urgently needed. We undertake a retrospective study to compare outcomes in patients who undertake MCS or SHS fixation for femoral neck fractures. METHODS: A retrospective review of femoral neck fractures performed with SHS or MCS between February 2016 and June 2018 was conducted with Institutional Review Board approval in the First Affiliated Hospital of Dali University of Orthopedic Trauma. All cases were performed by a single surgeon. Of these, we included 180 patients (90 hips) that were performed surgery in treatment of femoral neck fractures. All patients received the same standardized postoperative multimodal pain protocol and the same postoperative rehabilitation program. The primary endpoint was Harris Hip Score. Secondary outcome measures include operation time, length of hospital stay, incision length, patient satisfaction, and postoperative complications. Multivariate linear and regression analyses was used to identify independent predictors of outcome. A P-value of <.05 was defined as statistical significance. RESULTS: We hypothesize that both treatments provide comparable outcomes. TRIAL REGISTRATION: This study protocol was registered in Research Registry (researchregistry5638).

Dynamic regulation of CD28 conformation and signaling by charged lipids and ions.

CD28 provides an essential costimulatory signal for T cell activation, and its function is critical in antitumor immunity. However, the molecular mechanism of CD28 transmembrane signaling remains elusive. Here we show that the conformation and signaling of CD28 are regulated by two counteractive charged factors, acidic phospholipids and Ca2+ ions. NMR spectroscopy analyses showed that acidic phospholipids can sequester CD28 signaling motifs within the membrane, thereby limiting CD28 basal signaling. T cell receptor (TCR) activation induced an increase in the local Ca2+ concentration around CD28, and Ca2+ directly disrupted CD28-lipid interaction, leading to opening and signaling of CD28. We observed that the TCR, Ca2+, and CD28 together form a dual-positive-feedback circuit that substantially amplifies T cell signaling and thus increases antigen sensitivity. This work unravels a new regulatory mechanism for CD28 signaling and thus contributes to the understanding of the dependence of costimulation signaling on TCR signaling and the high sensitivity of T cells.