Y0, then the diagnosis of hypertension with liver cirrhosis obtained. The positive rate of diagnosis is 95% and the specificity is 96% and 91% respectively, much better than those in type B ultrasonography or gastric endoscopy, 78% or 75% respectively (P

The risk of cardiovascular diseases is significantly increased in cancer patients receiving chemotherapy or radiotherapy. Recent evidences suggested that cardiac dysfunction and subsequent heart failure are mainly caused by vascular toxicity rather than myocardial toxicity. However, not all of the vascular toxicity of cancer therapies can be explained by obstructive coronary artery disease. In the past few decades, it has been found that myocardial ischemia may be caused by structural or functional disorders of the complex vascular network that cannot be seen by coronary angiography, known as coronary microvascular dysfunction (CMD). There is growing evidences that cancer therapy-related cardiovascular dysfunction (CTRCD) and CMD have many common pathophysiological mechanisms. This paper elucidates the relationship between CTRCD and CMD from the pathophysiological perspective, providing reference for exploring new diagnostic methods and treatment strategies of cardiovascular diseases.

Objective: To investigate the relation between ser um hyaluronic acid (HA) concentration and cryopreservation-reperfusion injury. Methods: The animals were randomly assigned to 3 groups: (1 ) group A: the control; (2) group B: liver allografts were stored in lactated R inger's solution (0℃) for 2 h before implantation; (3) group C:liver allografts were stored in lactated Ringer's solution (0℃) for 4 h before implantation. Th e serum sample and liver specimen were taken up at 2 h and 4 h after transplanta tion to detect the concentration of HA, AST and LDH, and to get pathologic obser vation. Results: Serum HA increased earlier and decreased more s hortly than AST and LDH after transplantation in group A. Serum HA increased sig nificantly in group B and C, much higher than that in group A(P<0.01). The i njury of vascular endothelium and the disorder of hepatic sinuses and hepatic lo b ules were observed in group B and C. In the specimen of 4 h in group C, evident infiltration of inflammatory cell was present. Conclusion: Cryopreservation leads to injury of endothelial cell and reperfusion aggravat es this injury. The serum HA concentration indicates the degree of cold ischemia -reperfusion injury.

Objective： To investigate the effect of oxLDL and VitE on the expression of CD40 and CD40 ligand(CD40L) in cultured human monoc ytes. Methods： The expression of CD40 and CD40L on monocytes su rface were measured by indirect immunorescence technique in combination with flo w cytometry. Results： Low concentration of oxLDL（≤200 μg/L） significantly increased the expression of CD40 and CD40L in a dose and time dep endent manner. High concentration (>200 μg/L）of oxLDL markedly reduced the exp ression of CD40 and CD40L. When VitE was added, it significantly reduced the ex pression of CD40 and CD40L on monocytes surface induced by oxLDL in a dose-depe ndent manner. Conclusion：It is an important mechanism that the high expression of CD40 and CD40L induced by oxLDL may be contributed to the for mation of atherosclerosis. Antioxidan VitE can partially inhibit the high expres sion of CD40 and CD40L on monocytes surface induced by oxLDL.

Objective: To study the prevalence and pathogenesis of TT virus (TTV) in hemodialysis patients. Methods: Serum TTV DNA was tested in 69 hemodialysis patients from our hospital by nested-PCR using primers from a conservative region of TTV genenome, genetic analysis and detection of hepatitis C virus antibody (anti-HCV) and the levels of alanine aminotransferase (ALT) were also carried out simultaneously. Results: The overall prevalence of TTV viremia was 27.5%. The PCR-amplified gene fragment from one patient was sequenced, and its gene sequence homologies with GH1,TA278, TTVCHN1 and TTVCHN2 ranged from 89% to 100%, its deduced amino acid sequence ranged from 87% to 100%. There was no significant difference of TTV prevalence between anti-HCV positive and negative patients. No significant elevation of ALT was found in all patients. Conclusion: High prevalence of TTV infection is found among hemodialysis patients, and TTV infection has no significant association with HCV infection or elevation of ALT.

Objective：To investigate the mechanism of increased glucose uptake, the expression of myoc ardial glucose transporter1 (GLUT1) was determined after low-flow myocardial is chemia. Methods： An in vivo open-chest canine model of low -flow myocardial ischemia was used to correlate myocardial glucose uptake with the number of GLUT1. The expression of myocardial GLUT1 glucose transporter was determined by semiquantitative Northern blotting and immunoblotting. Res ults： GLUT1 mRNA and GLUT1 polypeptide expression was substantially inc reased in ischemic region from the experimental hearts when compared to normal h earts. There was no significant regional difference in GLUT1 expression in eith er normal or ischemic hearts.Conclusion：Myocardial ischemia ind uces a factor or factors which stimulate GLUT1 expression in ischemic myocardial regions. Enhanced GLUT1 expression may be an important protective mechanism by which myocardial cells enhance glucose uptake and metabolism during low-flow my ocardial ischemia.

Objective: To investigate whether insulin stimulates the translocation of glucose transporter-4 (GLUT4) and glucose uptak e in ischemic myocardium. Methods: Plasma concentration of gluc ose, lactate, free fatty acid and insulin were determined by autoanalyser, and G LUT4 was studied by Western blotting analysis. Results: Insulin increased GLUT4 significantly in sarcolemma of ischemic myocardium ［(25±4)% vs (40±6)%］, and GLUT4 content in intracellular membrane decreased proporti onally. The glucose uptake increased significantly in insulin-ischemic myocardi um. The uptake of insulin-ischemic myocardium was almost 2 times that of ischem ic myocardium. Conclusion: Insulin stimulation results in GLUT4 translocation and increases glucose uptake in ischemic myocardium. When myocardi al ischemia occurs, insulin is helpful in increasing myocardial glucose uptake a nd utilization.

Objective: To investigate whether there is additi ve effects of hyperinsulinemia and ischemia on expression of canine myocardial G LUT4 gene in vivo. Methods: The expression of myocardial GLU T4 was determined by semiquantitative immunoblotting.The expression of GLUT4 mRN A was determined by semiquantitative Northern blotting. Results: Dramatic changes were seen in GLUT4 mRNA and GLUT4 expression in the ischemic hearts.After infusing insulin for 8 h,regional GLUT4 mRNA and GLUT4 levels in is chemic hearts were 2.5, 2.3-fold that of expression in normal hearts(P<0.01 ). Myocardial glucose uptake in ischemic hearts was increased by 4-fold when co mpared with normal hearts(P<0.01). Conclusion: There are not only additive effects of hyperinsulinemia and low-flow ischemia on canine myoc ardial GLUT4 mRNA and GLUT4 expression in vivo, but also increase of myocar dial glucose uptake. Enhanced GLUT4 expression may be an important protective m echanism by which myocardial cells enhance glucose uptake and metabolism during low-flow ischemia.

Objective: To investigate the changes of myo cardial contractile function during myocardial stunning in calcium overload rats and the protective effects of tetrandrine. Methods: Forty-six rats were randomized into control, myocardial ischemia, myocardial stunning, low and high dose of tetrandrine groups. Another 10 rats were used to identify the calcium overload. vitamin D3 (0.3 million Unit/kg) and nicotinic acid were adm inistered. After 16 d when calcium overload occured, left anterior descending ar tery was ligated. Twenty minutes of myocardial ischemia followed by 60 min of re perfusion was induced. The contractile function parameters were determined dynam ically. At the end of experiment, myocardial cytosolic ［Ca2+］i was deter mined in various groups. In tetrandrine groups, tetrandrine (62.2 or 93.6 μmol/ kg ) was administered by gastrogavage daily.After 16 d, the rats undergone the e xperiments mentioned above. Results: Sixteen days after vitamin D3 , nicotinic acid were given, ［Ca2+］i increased by 2.6 folds (146.8±10.8 ) vs (368.5±22.6) nmol/L, (P<0.01). Whereas, ［Ca2+］i in tetrand rine groups were (210.8±16.4) and (198.6±15.3) nmol/L, which were significantl y lower than that of calcium overload group. Twenty minutes of myocardial ische mia resulted in the decrease of dp/dtmax and Vmax in all groups with the most si gnificant in stunning and calcium overload groups. The contractile function rest ored gradually after reperfusion. At all time points, dp/dtmax and Vmax in both tetrandrine groups were higher than those in both stunning and calcium overload groups. And effect with higher dose of tetrandrine were more significant than in low dose of tetrandrine. After 60 min of reperfusion, dp/dtmax in stunning, cal cium overload, low and high dose of tetrandrine groups were 49.7%, 51.5%, 71.0% and 83.4% of that in control, respectively， and Vmax were 55.0%, 49.8%, 73.9% and 77.5% of that in control, respectively. Conclusion: T he myocardial contractile function in vitamin D3-induced calcium overload gro up is impaired. On basis of myocardiocyte calcium overload, transient ischemia l eads to myocardial stunning. At the stage of ischemia, the impaired degree of my ocardial contractile function is similar to that in stunning group, suggesting a t this stage the effect of ischemia on myocardial function is greater than that of calcium overload. Tetrandrine chronically improves the myocardial function in Vitamin D3-induced calcium overload rats.

Objective： To investigate the effect of c ytokines (IFN-γ，TNF and IL-1) on the expression of CD40 and CD40 ligand (CD4 0L) in monocytes/macrophages. Methods： The mRNA expression of C D40 and CD40L was measured by RT-PCR and the CD40，CD40L expression on the mono cytes/macrophages were detected by flow cytometric analysis. Results： IFN-γ，TNF and IL-1 could not only significantly up-regulate the mRNA levels of CD40 and CD40L in cultured monocytes/macrophages, but also increase t he expression of CD40 and CD40L. Antioxidant VitE could reduce the expression o f CD40 and CD40L induced by IFN-γ，TNF and IL-1. Conclusion： IFN-γ，TNF and IL-1 can stimulate high expression of CD40 and CD40L . Antio xidant VitE can partially inhibit the expression of CD40 and CD40L induced by cy tokines in cultured monocytes/macrophages.