Objective To investigate the relationship between the expressions of TMPRSS4 and clinical pathologi-cal parameters in gastric carcinoma. To explore its significance in judging the prognosis of patients. To analyze the expression of TMPRSS4 in the epithelial-mesenchymal transition. Methods The expressions of TMPRSS4, E-cad-herin and Vimentin were detected by immunohistochemistry ( SABC) in 100 cases of gastric carcinoma specimens and corresponding adjacent normal tissue. Results In gastric carcinoma, TMPRSS4, E-cadherin and Vimentin positive rate was 47%,45%,37%. In adjacent tissues,their positive rate was 9%,30%,4%. The differences be-tween tumor tissues and adjacent tissues had statistical significance ( P<0.05 ) . High expression of TMPRSS4 cor-related significantly with lymph node metastases and TNM stage (P<0.05), but not with gender, age, size, tumor histological type,depth of invasion (P>0.05). The 5-year survival rate of patients with high TMPRSS4 expression was significantly lower than that in patients with low expression. The high TMPRSS4 expression was significantly correlated in gastric carcinoma accompanied by low expression of E-cadherin (rs = -0.207,P=0.038) and high Vimentin expression (rs=0.233,P=0.020). Conclusion The expression of TMPRSS4 is closely related to the biological characteristics in gastric carcinoma,detection the expression of TMPRSS4 is valuable in predicting tumor prognosis,invasion and metastasis. TMPRSS4 may promote invasion, metastasis of human gastric carcinoma through epithelial-mesenchymal transition by reduce the expession of E-cadherin.

Objective To observe the changes of brain oxygenation in patients with extremely severe craniocerebral injury and the therapeutic effect of early normobaric hyperoxia.Methods Sixtyeight patients with extremely severe craniocerebral injury treated from January 2011 to January 2013 were assigned to two groups according to the random number table:50％ oxygen breathing for one week in control group (34 cases) and 80％ oxygen breathing for one week in treatment group (34 cases).Blood samples from jugular vein and radial artery were collected at 1,3,5,and 7 days to measure indices of blood gas analysis,i.e.,PaO2,PjvO2,CaO2,CjvO2,Da-jvO2,CERO2 and Djv-a Lac.GCS and content of neuron-specific enolase (NSE) were recorded as well.Results Values of PaO2 at each time point and GCS at 5 and 7 days were significantly higher in treatment group than in control group (P ＜0.05).Djv-a Lac at 3,5 and 7 days and NSE at 7 days revealed significantly higher levels in treatment group than in control group(P ＜ 0.05).Whereas at each time point,there were no significant differences between the two groups in aspects of PjvO2,CaO2,CjvO2,Da-jvO2 and CERO2 (P ＞ 0.05).Conclusion Early use of 100％ oxygen in patients with extremely severe craniocerebral injury may be beneficial to the prognosis.

Amyloid beta-peptides (Aβ) are known to undergo active transport across the blood-brain barrier, and cerebral amyloid angiopathy has been shown to be a prominent feature in the majority of Alzheimer׳s disease. Quercetin is a natural flavonoid molecule and has been demonstrated to have potent neuroprotective effects, but its protective effect on endothelial cells under Aβ-damaged condition is unclear. In the present study, the protective effects of quercetin on brain microvascular endothelial cells injured by fibrillar Aβ 1-40 (fAβ 1-40) were observed. The results show that fAβ 1-40-induced cytotoxicity in human brain microvascular endothelial cells (hBMECs) can be relieved by quercetin treatment. Quercetin increases cell viability, reduces the release of lactate dehydrogenase, and relieves nuclear condensation. Quercetin also alleviates intracellular reactive oxygen species generation and increases superoxide dismutase activity. Moreover, it strengthens the barrier integrity through the preservation of the transendothelial electrical resistance value, the relief of aggravated permeability, and the increase of characteristic enzyme levels after being exposed to fAβ 1-40. In conclusion, quercetin protects hBMECs from fAβ 1-40-induced toxicity.