Effectiveness of a regional trauma system in reducing mortality from major trauma: before and after study.

OBJECTIVE: To assess the effect of the development of an experimental trauma centre and regional trauma system on the survival of patients with major trauma. DESIGN: Controlled before and after study examining outcomes between 1990 and 1993, spanning the introduction of the system in 1991-2. SETTING: Trauma centre in North Staffordshire Royal Infirmary and five associated district general hospitals in the North West Midlands regional trauma system, and two control regions in Lancashire and Humberside. SUBJECTS: All trauma patients taken by the ambulance services serving the regions or arriving other than by ambulance with injury severity scores > 15, whether or not they had vital signs on arrival at hospital. MAIN OUTCOME MEASURES: Survival rates standardised for age, severity of injury, and revised trauma score. RESULTS: In 1990, 33% of major trauma patients in the experimental region were taken to the trauma centre, and by 1993 this had risen to only 39%. Crude death rates changed by the same amount in the control regions (46.5% in 1990-1 to 44.4% in 1992-3) as in the experimental region (44.8% to 41.3%). After standardisation, the estimated change in the probability of dying in the experimental region compared with the control regions was -0.8% per year (95% confidence interval -3.6% to 2.2%); for out of hours care, the change was 1.6% per year (-2.3% to 5.6%), and, for multiply injured patients, the change was -1.6% (-6.1% to 2.6%). CONCLUSION: Any reductions in mortality from regionalising major trauma care in shire areas of England would probably be modest compared with reports from the United States.     

凝溶胶蛋白与创伤后炎症反应

凝溶胶蛋白(gelsolin,GSN)是机体内重要的肌动蛋白结合蛋白,对肌动蛋白的聚合/解聚具有重要调节作用。其生理效应不仅在于维持细胞结构稳定,而且参与多种细胞活动的调节过程,是一种重要的细胞功能调节蛋白。血浆型GSN是血浆肌动蛋白清除系统主要成员之一,对维持内环境稳定非常重要。严重创伤后血浆中GSN水平显著而持续降低,且与患者预后密切相关。本文综述GSN与创伤后炎症反应的关系。     

Activation of ER stress signalling increases mortality after a major trauma

The endoplasmic reticulum (ER) adapts to stress by activating a signalling cascade known as the ER stress response. While ER stress signalling is a central component of the cellular defence against environmental insult, persistent activation is thought to contribute to the progression of various metabolic complications via loss of protein function and cell death. Despite its importance however, whether and how ER stress impacts morbidity and mortality in conditions of hypermetabolism remain unclear. In this study, we discovered that chronic ER stress response plays a role in mediating adverse outcomes that occur after major trauma. Using a murine model of thermal injury, we show that induction of ER stress with Tunicamycin not only increased mortality but also resulted in hepatic damage and hepatic steatosis. Importantly, post‐burn treatment with chaperone ER stress inhibitors attenuated hepatic ER stress and improved organ function following injury. Our study identifies ER stress as a potential hub of the signalling network affecting multiple aspects of metabolism after major trauma and as a novel potential molecular target to improve the clinical outcomes of severely burned patients.