Objective To upgrade No.1 Military Medial Project database from Oracle8.17 to Oracle10g. Methods Through the establishment of database link, the database migration was realized based on full test's foundation. Results The database was upgraded and the system's operation speed was enhanced greatly. Conclusion Under the existing technology, it is feasible to upgrade Oracle database from Oracle8.17 in 32 bits to Oracle10g in 64 bits, and the benefit is remarkable.

Objective To assess the association of serum resistin,TNF-? and insulin resistance in type 2 diabetes mellitus.Methods 42 cases of T2DM and 40 cases of control were involved in the study.Their waist circumference(WC),the levels of fasting serum resistin,TNF-?,fasting blood glucose(FBG) and fasting insulin(FINS)were measured.Results The levels of serum resistin,TNF-? and Homa-IR in T2DM group were significantly higher than those in control group,while serum FINS level was significantly lower than that in control group[(11.76?2.72)vs(8.65?3.00)?g/L,P

The carotid initima-media thickness(CIMT)in 78 cases of type 2 diabetic patients was measured.The level of plasma endogenous secretion receptor for advanced glycation end-products(esRAGE)in patients with normal CIMT was higher than those with chickened CIMT[(0.257 3±0.165 6 vs 0.155 4±0.0701)μg/L,P<0.01].esRAGE was negatively associated with CIMT(r=-0.247,P<0.05).Logistic regression analysis showed that CIMT was negatively associated with esRAGE and hish density lipoprotein cholesterol,but was positively associated with age.

Objective: To evaluate the role of mitochondrion-dependent apoptosis in reduction of bupivacaine-induced cardiotoxicity by lipid emulsion in rats. Methods: Forty-five healthy adult male Sprague-Dawley rats, weighing 300-350 g, were divided into 3 groups by a random number table method: sham operation group (Sham group, n=5), bupivacaine group (B group, n=20), and lipid emulsion group (L group, n=20). Cardiac arrest was induced by intravenously injecting 0.4% bupivacaine 30 mg/kg over 20 s to establish the cardiotoxicity model.Twenty percent lipid emulsion was intravenously injected in a dose of 5 ml/kg during resuscitation in group L, and normal saline was intravenously injected in a loading dose of 5 ml/kg during resuscitation in group B, followed by a 3-min infusion of 1 ml·kg^-1·min^-1in two groups.The successful resuscitation and survival rate at 120 min of return of spontaneous circulation (ROSC) were recorded.Systolic blood pressure, heart rate, mean arterial pressure, rate-pressure product (RPP) and ratio of RPP at each time point after recovery of spontaneous heart beat to baseline value (RPPh) were recorded every 10 min after ROSC.The time from administration to cardiac arrest (T₀), time from beginning of cardiopulmonary resuscitation to appearance of the first spontaneous heart beat (T_s) and time from beginning of cardiopulmonary resuscitation to appearance of ROSC (T_r) were recorded.Rats were sacrificed at 120 min of ROSC, and left ventricular tissues were obtained for determination of the expression of Bax, Bcl-2, cleaved caspase-9, cleaved caspase-3, cytochrome C (Cyt c) in cytoplasm and mitochondria (by Western blot) and expression of Bax and Bcl-2 mRNA (by real-time polymerase chain reaction) and for examination of myocardial ultrastructure. Results: Compared with Sham group, the expression of Bcl-2 protein and mRNA and mitochondrial Cyt c was significantly down-regulated, and the expression of Bax protein and mRNA, cleaved caspase-9, cleaved caspase-3 and cytoplasmic Cyt c was up-regulated in B group (P<0.05). Compared with B group, the rate of successful resuscitation and survival rate were significantly increased, T_r was shortened, systolic blood pressure, heart rate, RPP and RPPh were increased after ROSC, the expression of Bcl-2 protein and mRNA and mitochondrial Cyt c was up-regulated, the expression of Bax protein and mRNA, cleaved caspase-9, cleaved caspase-3 and cytoplasmic Cyt c was down-regulated (P<0.05), no significant change was found in T_o or T_s (P>0.05), and the pathological changes of myocardium were significantly attenuated in L group. Conclusion The mechanism by which lipid emulsion reduces bupivacaine-induced cardiotoxicity may be related to inhibiting mitochondrion-dependent apoptosis in rats.