Objective To investigate the efficacy and safety of the postoperative analgesia after thoracotomy with different patient-controlled intravenous analgesia (PCIA)medication.Methods One hundred and twenty ASA Ⅰ or Ⅱ patients scheduled for elective thoracic surgery were randomly di-vided into four groups according to different PCIA formula:group S received sufentanil 3 μg/kg;group SD received sufentanil 1.5 μg/kg plus dezocine 0.3 mg/kg;group SF received sufentanil 1.5μg/kg plus flurbiprofen axetil 3 mg/kg;group DF received dezocine 0.3 mg/kg plus flurbiprofen ax-etil 3 mg/kg.For all four goups,the applied medicine was diluted with 0.9% saline to 300 ml,and was infused at 5 ml/h with a bolus dose of 3 ml.The lockout time was set at 1 5 min.The VAS and Ramsay sedation scale were recorded 2,4,8,24,48 h after surgery,respectively.Total pressing times and the side effects were also recorded for the 24 h period after the surgery.Results There were no significant differences of the VAS score at the time 2,4,8,24 and 48 h post surgery of press num-bers within 24 h postoperatively among all groups.The Ramsay sedation scale was significantly high-er at the time 2,4,8,24 h after surgery in group S than those in other three groups (P <0.05).The side effects were more in group S than those in other three groups (P <0.05).Conclusion Compared with sufentanil alone,combination therapy is safer and more effective for analgesia after thoracic sur-gery.With good outcomes and less side effects,it deserves more consideration in clinics.

Microglia play a crucial role in inflammation after cerebral ischemia.A large number of studies have shown that microglia are highly plastic cells that can assume different phenotypes and functions in response to specific microenvironmental signals.Microglia can be polarized into the classically activated proinflammatory M1 phenotype or the alternatively activated anti-inflammatory M2 phenotype,and play different roles in ischemic injury.Irnhibiting M1 while stimulating M2 may be a new approach for the treatment of ischemic stroke.

Inflammation plays an important role in the pathophysiological mechanism of acute ischemic stroke.CD200 expressed in neurons interacts with CD200 receptor (CD200R) on microglia cells.It can inhibit microglia activation and alleviate the inflammation after cerebral ischemic injury.This article reviews the roles of CD200 and CD200R in the activation of microglia after cerebral ischemia.

Selective estrogen receptor modulators tamoxifen,raloxifene,and bazedoxifene reduce neuronal death through the mechanisms of anti-inflammation,antioxidant stress,and inhibition of glutamate excitotoxicity.They play a neuroprotective role in cerebral ischemia and may become a new neuroprotective agent for the treatment of ischemic stroke.