Abstract:Aim To explore the relationship of serum zinc, copper, copper/zinc ratio and coronary artery calcification (CAC) in patients with chronic kidney disease. Methods Using the cross-sectional analysis method, 274 patients with chronic kidney disease were studied. According to the coronary artery calcification scores, the patients were divided into calcified group and non-calcified group, and the clinical data and laboratory indicators of the two groups were compared. Spearman correlation analysis was used to analyze CAC related factors, binary Logistic regression was used to analyze CAC risk factors, and ROC curve was used to explore the predictive value of zinc, copper, and copper/zinc ratio on CAC. Results The serum zinc level of calcified group ((77.09±15.84) μmol/L) was lower than that of non-calcified group ((88.21±11.55) μmol/L). Serum copper ((13.99±3.76) μmol/L) and copper/zinc ratio (0.19±0.08) were higher in calcified group than those of non-calcified group ((12.10±3.99) μmol/L, (0.14±0.05)). Spearman correlation analysis showed that serum zinc level (r＝－0.387, P＜0.001) was negatively correlated with coronary artery calcification scores (CACS). Serum copper(r＝0.356, P＜0.001) and copper/zinc ratio (r＝0.477, P＜0.001) were positively correlated with CACS. Binary Logistic regression analysis showed age (OR＝1.085, P＜0.001), serum copper (OR＝1.114,P＜0.001) and copper/zinc ratio (OR＝1.143, P＜0.001) were risk factors for CAC. And serum zinc (OR＝0.948, P＜0.001) was protective factor for CAC. ROC curve analysis showed that the AUC of zinc, copper, and copper/zinc ratio were 0.1,0.0,0.716 in predicting CAC (P＜0.001). Conclusion Patients with chronic kidney disease with high age, high levels of copper and copper/zinc ratio, and low zinc have higher risk of CAC, and the copper/zinc ratio has better predictive value for the occurrence of CAC.

Abstract:Aim To investigate the effects of in vivo local transfection of zinc finger protein A20 gene on restenosis of balloon injured rat carotid artery and its possible mechanism. Methods Balloon catheter denudation of the endothelium of rat common carotid artery was routinely used as a model of restenosis.104 male Sprague-Dawley rats were randomly divided into 4 groups: the sham group(no injury),the model group(the simple injury),the control group(vacant transfection regent group) and the therapeutic group(A20 gene and transfection regent group).pCAGGS-GFP/A20(20 μg) with 40 μL Lipofectamine 2000 or TE buffered solution(20 μL) with 40 μL Lipofectamine 2000 was instilled into the lumen of the injured segment for 30 min after injury.The transfection efficiency of plasmid in injured vascular wall was evaluated 24 hours after transfection by using fluorescence microscope.Quantification of intimal hyperplasia was determined by pathologic examination.Proliferation index of VSMC in vivo was assessed by thymidine analogue bromodeoxyuridine(BrdU) labeling technique.The expression of nuclear factor-kappaB p65(NF-κBp65) of rat carotid arteries in different groups were confirmed by immunohistochemical staining and Western blot analysis. Results At day 14 significant intimal hyperplasia was detected after arterial injury in the model and control group.A20 gene transfection markedly reduced the neointimal area(47.8% reduction;P<0.05) and intimal to media area ratio(42.9% reduction;P<0.05) in the therapeutic group.Proliferation index of VSMC(BrdU index) at day 10 after operation was decreased significantly in the therapeutic group(9.6%±2.3%) than in the control group(26.7%±5.1%,P<0.05).A significantly lower level of NF-κBp65 positive cells ratio was observed in the therapeutic group than in the control group at 10d after operation(P<0.05).A significantly lower level of NF-κBp65 protein expression was observed in the therapeutic group than in the control group at day 7 d,14 d,28 d after operation(P<0.05).Conclusion Local transfection of A20 gene inhibits intimal hyperplasiaand VSMC proliferation after arterial injury.Its possible molecular mechanism is that A20 negative feedback inhibits NFκ-B sig-naling pathway.This study provides evidence for the inflammatory mechanism of restenosis and suggests that A20 gene therapymay serve as a novel gene therapeutic approach to inhibit restenosis.

Abstract:Aim The effect of zinc deficiency and zinc replenishment on the distribution of elements in rats. Methods SD rats were randomized into zinc-deficient diet (ZD) group, pair-fed (PF) group, zinc normal group (ZN), zinc supplemented (ZS) group and high zinc (HZ) group. ZD group, ZN group, and HZ group were fed up with zinc deficient dietary (content of zinc< 1 mg/kg), zinc-normal dietary (50 mg/kg) and high zinc dietary (150 mg/kg) for 8 weeks respectively. ZS group were fed with zinc deficient dietary for 3 weeks, then changed to be treated with high-zinc dietary for 5 weeks. PF group were fed with zinc normal dietary according to the actual quantity of ZD group at the former day. All of the rats were killed after 8 weeks. The concentration of Zn, Cu, Fe, and Ca in serum were measured with polarography and with atomic absorption spec-troscopy (AAS) in liver, kidney, spleen, and testicle. Results The concentration of Zn, Fe in serum, liver, spleen, kidney, testiele and Cu in kidney, spleen decreased significantly owing to zinc deficiency, while the concentration of triglyceride, cholesterol, high density lipoprotein and low density lipoprotein in serum remained the same. Conclusions Zinc deficiency not only decreased zinc concentration in organism directly, but also affected the metabolism and distribution of elements. However, it didn t affect serum significantly.

Abstract:The plasma lipids of 44 type Ⅱ diabetics and 30 healthy persons were compared and analysed, the diabetics were divided into two groups. Group A(n=225) treated with D860 and glucozinc, while Group B only with D860, the course of treatment of both group was one month.The plasma lipids of the diabetics in both group and the healthy persons were measured before and after the treatment respectively. The results showed that:① The triglyceride(TG)and the low-density lipoprotein cholesterol(LDL-C) of the diabetics in both group were distinctly higher than that of the healthy persons, while the high-density lipoprotein cholesterol(HDL-C) was lower than that of healthy controls, ② After the treatment, the HDL-C of Group A was remarkably raised while the TG and LDL-C remarkably reduced, as for Group B, no distinct change was found in HDL-C. This study suggests that Zincic-tonic has an effect to raise the HDL-C level of diabetics who are, at the sametime,in treatment with plasma glucose-lowering medicines.