Objective To investigate the expression of human epidermal growth factor receptor?2(HER?2)and Survivin protein in gastric cancer tissue,and explore its relationship with clinicopathological characteristics. Methods Immunohistochemistry assay was used for detection of HER?2 and Survivin protein expression in 70 gastric cancer biopsy samples. The relationship with the clinicoathological parameters in patients with gas?tric cancer was analyzed. Results The expression of HER?2 and Survivin protein was correlated with tumor differentiation ,TNM stage and lymph node metastasis(all P<0.05),but not with sex,age,the diameter of tumor. The correlation analysis of positive rate and the semi?quantitative pro?tein expression showed that the expression of Survivin and HER?2 was significantly positively related(all P<0.01). Conclusion The positive ex?pression of HER?2 and Survivin protein in gastric cancer correlates with tumor differentiation ,TNM stage and lymph node metastasis. HER?2 ex?pression significantly correlates with Survivin at the protein level in gastric cancer tissues.

BACKGROUND: Hyperbaric oxygen can reduce brain ischemic-reperfusion injury, and this effect is closely related to the modulation of hyperbaric oxygen on microglias.OBJECTIVE: To explore the influence of hyperbaric oxygen on the activity of in vitro cultured brain microglias and secretion of interleukin-1, tumor necrosis factor α and nitric oxide (NO).DESIGN: Completely randomized grouping design, control experiment.SETTING: Teaching and Research Section of Diving Medicine, Teaching and Research Section of Immunity, Teaching and Research Section of Pathology, and the Experimental Animal Center, the Second Military Medical University of Chinese PLA.MATERIALS: This experiment was carried out at the laboratory of Diving Medicine as well as Teaching and Research Section of Immunity, the Second Military Medical University of Chinese PLA, between May 1999 and January 2000. Thirty neonatal SD rats of 1-day birth age were selected for the experiment.METHODS: [1] Brain microglias from newborn SD rats were cultured with digestion method, and microglias were identified with non-specific phosphodiesterase staining and cellular immunochemical staining. [2] Primary microglias were inoculated on 48-well culture board by 2×105/well and randomized into 5 groups: control group without hyperbaric oxygen pretreatment, and hyperbaric oxygen (0.2 MPa 1 hour) pretreatment 3, 7, 10,14 days groups. Cells in groups with hyperbaric oxygen pretreatment at the above various time points were then further divided into 2 subgroups, with one added with culture medium containing bacterium lipopolysaccharide of 1 mg/L (for microglia activation), but not in the other group. [3] Interleukin-1 activity was determined using thymocyte proliferation method. The activity of tumor necrosis factor-α was assessed with L929 cell toxicity test.Nitrous acid content detected by Griess method represented NO content.[4] t-test was used to compare the differences in non-paired quantitative data between the two groups.MAIN OUTCOME MEASURES: The activity of interleukin-1 and tumor necrosis factor a and NO content in resting and evoked brain microglias in rats at various time points of hyperbaric oxygen pretreatment.RESULTS: Thirty SD rats entered the result analysis. [1] The activity of interleukin-1 and tumor necrosis factor α and NO content in resting brain microglias: The two groups did not differ obviously. [2] Interleukin-1activity and NO content in lipopolysaccharide-evoked brain microglias: They were significantly lower in 10-day and 14-day hyperbaric oxygen pretreatment groups than those in control group [10-day group: 0.409±0.014,(5.21±0.77) μnol/L; 14day group: 0.381±0.004, (4.93±1.02) μmol/L, P ＜ 0.05].[3] The activity of tumor necrosis factor α in evoked brain microglias: It was obviously lower in 14day hyperbaric oxygen pretreatment group than in control group [(51.20±1.13) %, (70.10±2.26) %, P ＜ 0.05].CONCLUSION: Pretreatment with 0.2 MPa hyperbaric oxygen can suppress the secretion of interleukin-1, tumor necrosis factor α and NO by evoked microglias, but has not obvious effects on resting microglias.

Objective To explore the correlations between elevated cfDNA with lupus nephritis and indentify the influencing factors of cfDNA in systemic lupus erythematosus (SLE).Methods Fifty four patients with SLE [37 patients with lupus nephritis (LN) and 43 age-and sex-matched healthy controls] were included in the study.In 37 LN patients,26 patients were at active stage,and 11 patients were in remission.cfDNA concentration was measured with Picogreen Kit and low-density granulocytes (LDGs) was tested by flowcytometer.Correlation and regression analysis were performed to discover whether cfDNA is related to LN and identify the influencing factor of cffDNA.Results The cfDNA in SLE group was (237±40) ng/ml,which was significantly higher than that in healthy control group (188±41 ng/ml,P＜0.01).cfDNA in LN group was significantly higher than that in patients without LN (NLN) (247±47 ng/ml vs 214±31 ng/ml,P=0.028).cfDNA in patients with active LN was significantly higher than that in patient with inactive LN (RLN) (254±50 ng/ml vs 216±29 ng/ml,P=0.035).In SLE group,cfDNA was positively correlated with quantitative 24-hour urinary protein (r=0.350,P=0.013) and reversely correlated with albumin (r=-0.500,P＜0.01) and endogenous creatinine clearance rate (Ccr) (r=-0.354,P=0.044).Percentage of LDGs in peripheral blood mononuclear ceils (PBMCs) of the SLE group was (8.3± 12.9)％,significantly was higher than that in healthy controls [(1.2±0.7)％,P=0.004].The cfDNA was positively correlated with LDGs (r=0.636,P=0.002) and neutrophils (r=0.599,P＜0.01).Conclusion NETs excessively released by neutrophils as well as LDGs may be one of the main reasons for elevated cfDNA level in SLE.cfDNA level is associated with LN activity,suggesting that there is a intrinsic link between NETs-related biomarkers and active LN and that more specific biomarkers of NETs may become a clinical biomarker for active LN.

Objective To establish a new murine model of experimental autoimmune myositis by immunizing with MYBPC2 protein. Methods The purified Myosin-binding protein C, fast type (MYBPC2) was emulsified with complete Freundˊs adjuvant, then C57BL/6 mice were immunized by multi-point subcutaneous injection (0, 7 days), and intraperitoneal injection of pertussis toxin 2 μg simultaneously. The pathological changes of mice with different immunizing dose at the preconceived time were ex-plored. Mean-while, mice were immunized with 600 μg each time, and the muscle endurance was tested on the 21th day. The expression of major histocompatibility complex (MHC) class-Ⅰ and the surface biomarkers of the inflammatory cells in muscle tissues were observed. Mann-Whitney U test was used for statistical analysis. Results ① With the increase of immunizing dosage, muscle damage and inflammation tended to be more serious. On the 21th and 28th day, muscle lesions were most significant. Muscle fiber degeneration and necrosis and inflammatory cell infiltration could be seen in the experimental group. ② Compared with the control group, muscle endurance of mice in the experimental group decreased significantly [(6.1 ±1.3) min versus (9.2±1.6) min, U=2.00, P=0.017]. The MHC class-Ⅰ on the muscle fiber surface of the experimental group was positive, scattered infiltration of CD4 +, CD8+ T ly-mphocytes and CD68 + macrophages between muscle fibers and around the vascular areas could be observed, and CD20+B lymphocytes mainly distributed in the area around the blood vessels, nevertheless rarely seen between muscle fibers. Conclusion Exper-imental autoimmune myositis models of mice have been successfully induced by immunizing with MYBPC2 in China for the first time, and similar clinical and pathological features of human polymyositis could be observed. This new model can be used for studying the pathogenesis of autoimmune myositis.

TSCI have dyskinesia and sensory disturbance that can cause various life-threaten complications. The patients with traumatic spinal cord injury (TSCI), seriously affecting the quality of life of patients. Based on the epidemiology of TSCI and domestic and foreign literatures as well as expert investigations, this expert consensus reviews the definition, injury classification, rehabilitation assessment, rehabilitation strategies and rehabilitation measures of TSCI so as to provide early standardized rehabilitation treatment methods for TSCI.