ObjectlveTo evaluate the role of cannabinoid receptor 2 (CB2 receptor) in microglial injury induced by glutamate.MethodsMicroglia cells were randomly divided into 4 grups:control group (group C),microglial injury group ( group Ⅰ),specific CB2 receptor agonist AM 1241 group ( group AM1241 ) and specific CB2 receptor antagonist AM630 group (group AM630).In group C,the cells were cultured routinely for 26 h.In group Ⅰ,the cells were incubated in the culture medium containing glutamate 10 mmol/L for 24 h.In group AM1241,the cells were incubated in the culture medium containing AM1241 2 μmol/L for 2 h,and then in the culture medium containing glutamate 10 mmol/L for 24 h.In group AM630,the cells were incubated in the culture medium containing AM630 2 μmol/L for 2 h,and then in the culture medium containing glutamate 10 mmol/L for 24 h.The cell viability and release of LDH were measured.Microglial morphology was observed under microscope.Results Compared with group C,the cell viability was significantly decreased,and the release of LDH was significantly increased in groups Ⅰ,AM1241 and AM630 (P ＜ 0.05).Compared with group Ⅰ,the cell viability was significantly increased,and the release of LDH was significantly decreased in group AM1241 ( P ＜ 0.05).There was no significant difference in the cell viability and the release of LDH between groups 1 and AM630 ( P ＞ 0.05).Conclusion Glutamate induces microglial injury through inhibiting the function of CB2 receptor.

Primary Sj?gren's syndrome(pSS)is a chronic inflammatory autoimmune disease involving a variety of exocrine glands.It is a common autoimmune disease in the department of rheumatology.However,the pathogenesis of pSS is still unclear,re-sulting in lack of treatment.While the international research on pSS is also increasing,we review the latest literature on the mecha-nism of Sj?gren's syndrome under different factors.In this paper,the process mechanism of Sj?gren's syndrome is summarized from the aspects of heredity,environment,autoimmune cells and autoantibodies.

Background:Inflammation-based indexes have been used to predict survival and recurrence in cancer patients.Systemic immune-inflammation index (SII) was reported to be associated with prognosis in some malignant tumors.In the present study,we aimed to explore the association between SII and the prognosis of patients with gastric cancer.Methods:We retrospectively analyzed data from 444 gastric cancer patients who underwent gastrectomy at the First Affiliated Hospital of Sun Yat-sen University between January 1994 and December 2005.Preoperative SII was calculated.The Chi square test or Fisher's exact test was used to determine the relationship between preoperative SII and clinicopathologic characteristics.Overall survival (OS) rates were estimated using the Kaplan-Meier method,and the effect of SII on OS was analyzed using the Cox proportional hazards model.Receiver operating characteristic (ROC) curves were used to compare the predictive ability of SII,NLR,and PLR.Results:SII equal to or higher than 660 was significantly associated with old age,large tumor size,unfavorable Borrmann classification,advanced tumor invasion,lymph node metastasis,distant metastasis,advanced TNM stage,and high carcino-embryonic antigen level,high neutrophil-lymphocyte ratio,and high platelet-lymphocyte ratio (all P ＜ 0.05).High SII was significantly associated with unfavorable prognosis (P ＜ 0.001) and SII was an independent predictor for OS (P =0.015).Subgroups analysis further showed significant associations between high SII and short OS in stage Ⅰ,Ⅱ,Ⅲ subgroups (all P ＜ 0.05).SII was superior to NLR and PLR for predicting OS in patients with gastric cancer.Conclusion:Preoperative SII level is an independent prognostic factor for OS in patients with gastric cancer.