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Aim: To evaluate the association of glutathione S-transferases gene polymorphisms with the risk of gastric cancer, with reference to smoking and Helicobacter pylori infection. Methods: We conducted a 1:1 matched casecontrol study with 410 gastric cancer cases and 410 cancer-free controls. Polymorphisms of GSTM1, GSTT1 and GSTP1 were determined using PCR-CTPP. Results: The GSTM1 and GSTT1 null genotypes were significantly associated with the risk of gastric cancer after adjusting for potential confounding factors (OR=1.68, 95% CI=1.32-2.23 for null GSTM1, OR=1.73; 95% CI=1.24-2.13 for null GSTT1). The combination of null GSTM1 and null GSTT1 conferred an elevated risk (OR=2.54, 95% CI=1.55-3.39). However, no association was found for GSTP1 polymorphism The smoking modified the association of GSTM1 and GSTT1 null genotypes with the risk of gastric cancer. Conclusion: GSTM1 and GSTT1 null genotypes are associated with increased risk of gastric cancer, and smoking modifies the association.

Objective To examine atrial natriuretic peptide(ANP) and endothelin-1(ET-1) and ultrastructural pathologic changes in myocardial tissues in rabbits after severe crush injury and to investigate the secondary damage to myocardial tissues after severe injury and its mechanism.Methods A crush injury model was established in rabbits.Forty-two rabbits were randomly assigned into one control group(n=6) and one crush injury group(n=36).The crush injury group was further divided to six subgroups based on the time after crush release,i.e.,immediately after release and at 6,12,24,48,and 72h after release;each subgroup has six rabbits.The level of blood urea nitrogen,Cr,K+,and CK in serum is detected with an automatic biochemical analyzer.Myoglobin(MYO),cardiac troponin I(c-TnI),and CK-MB in the serum were measured using the chemiluminescence method.The myocardial tissues were collected from the same part of rabbit in each group and the content of ANP and ET-1 was determined by radio-immunoassay and the morphologic changes(at different times after the injury) in hematoxylin and eosin-stained myocardial tissue samples were observed under light microscopy and electron microscopy.Results The levels of CK,CK-MB and c-TnI in serum 12-24h after crush are apparently higher than that before crush(P < 0.05),whereas the content of ANP and ET-1 in the myocardial tissue drops(P < 0.05).Observation under light microscopy and electron microscopy revealed progressive pathologic changes in the myocytes,with the most severe myocardial damage observed within 12-24h after crush injury.The damage subsequently decreased and eventually disappears.Conclusions Severe crush injury may induce secondary damage to myocardial tissues and cardiac function.The changing trend in the cardiac markers ANP and ET-1 is consistent with the pathologic changes in myocytes during crush injury.

Objective To explore the mechanism of myocardial secondary injury and cardiac dysfunction after crush injury in rabbits. Methods Forty-two New Zealand rabbits were randomly divided into control group (6 rabbits) and crush injury group (36 rabbits that received pressure of 20kg for 6h), and crush injury group were subdivided into instant group, 6, 12, 24, 48 and 72h group after pressure relief with 6 rabbits in each group according to pressure relief time. The cardiac function changes in different time periods were detected by the multi-functional composite echocardiography, and the myocardial ultrastructural changes in different time periods were observed under electron microscope. Results The systolic indexes such as left ventricular ejection fraction (EF), left ventricular circumference shortening (CS), ventricular wall thickening and cardiac output per minute and diastolic function indexes such as peak flow velocity during rapid filling phase, peak flow velocity during slow filling phase, E/A ratio and diastolic filling rate were progressively reduced at respective time points after pressure relief, especially EF and CS. All the indexes for cardiac function were reduced to negative peak level 12-24h after pressure relief (P < 0.01); the myocardial ultrastructural changes were obvious, particularly 24h after injury. Conclusions Crush injury may result in secondary injury to the myocardium and cardiac dysfunction, and the peak phase of cardiac injury was during 12-24h after pressure relief. Multi-functional composite cardiac echocardiography can accurately, objectively and rapidly assess the myocardium damage after crush injury.