Objective To explore the effect of HIPK2 on apoptosis of human kidney tubular epithelial cells (HKC) induced by cisplatin.Methods Apoptosis of HKC cells was induced by cisplatin and the expression of HIPK2 was detected by RT-qPCR and Western blot.Two HIPK2 siRNAs were designed according to gene sequence of HIPK2 and cell lines with HIPK2 knockdown were established through transfecting the HIPK2 siRNAs into HKC cells by liposome.The expression of HIPK2 mRNA and protein was detected by RT-qPCR and Western blot after induced by cisplatin.Then cell apoptosis was detected by Annexin V/PI after the HIPK2-knockdown cells were treated with cisplatin.Moreover,the expression of pro-apoptotic protein bax was detected by Western blot after HIPK2 was knockdown.Results The expression of HIPK2 mRNA and protein was down-regulated obviously on the process of HKC apoptosis which induced by dose-dependent cisplatin (P＜0.05).The transfection of siRNA could significantly reduce the expression of HIPK2 mRNA and protein in HKC (P＜0.05),which promotes the HKC cells apoptosis induced by cisplatin.Conclusions HIPK2 can suppress the HKC cells apoptosis induced by cisplatin.

Hepatocellular carcinoma is one of the most common malignancies in the worldwide.Selected patients with hepatocellular carcinoma are candidates for curative resection,but nevertheless there is a high risk of tumor recurrence.Microvascular invasion (MVI) is an aggressive biological behavior and has repeatedly been identified as a risk factor for prognosis after curative treatment,meanwhile,it is now becoming increasingly concerned.It would be of great significance to distinguish MVI in an early stage and choose an appropriate treatment timely to get a definite improvement for the long-term survival in patients with hepatocellular carcinoma after curative treatment.This review focuses on some certain issues of MVI.

Objective To study the effects of russel viper venom X(RVV X)on blood coagulation protein.Methods We divide diluted protein into control and RVV-X groups,then use chromogenic substract assay to detect the activation effect of RVV-Ⅹ on coagulation factor Ⅶ,Ⅸ,Ⅹ and antithrombin,plasminogen,with or without activator.Results In RVV-Ⅹ group,the coagulation factor Ⅶ, Ⅸ and plasminogen displayed weakly enhanced chromogenesis,all P

Objective To study the therapeutic effects of intermittent hypoxia therapy(IHT)in isolated systolic hypertension(ISH)patients with elevated cerebral blood flow velocity(Vp),and to explore the mechanisms involved.Methods Seventy-six ISH patients with increasing Vp and normal pulsatility index(PI)of the middle ce- rebral artery(MCA)were randomly divided into a therapy group and a control group.IHT was administrated in the therapy group,and air in the control group.The Vp and PI of the MCA and blood pressure(BP)were observed be- fore and after treatment.Results Vp and systolic blood pressure(SBP)were significantly reduced after IHT(P＜0.01)compared with the therapy group's scores betore treatment,but PI and diastolic blood pressure showed no sig- nificant difference.There was no significant change in BP,Vp or PI in the control group before or after treatment. Conclusion IHT has therapeutic effects on ISH by reducing Vp and moderating SBP.

Objective To research the expression change and the sense of histone acetylation and p21WAF1 protein in breast cancer. Methods Pathological morphologic changes of breast cancer were identified by H. E. staining. Immunohistochemical study for p21WAF1 protein expression was performed on 80 breast cancers and 80 normal breast tissues. The expressions of acetylated histone H3, H4 and p21WAF1 protein in 80 breast cancers and 80 normal breast tissues were analyzed by Western blot. Results H.E. staining discovered that the tissue structure and cell morphous of breast cancer had visible atypia, compared with normal breast tissues. The immunohistochemical results displayed that the positive expression of p21 WAF1 in 80 breast cancers and 80 normal breast tissues was 49 cases(61.25 %) or 3 cases (3.75%), respectively. There was significantly difference in the expression level between the 80 breast cancers and 80 normal breast tissues (P ＜ 0. 05). The expression levels of p21WAF1 protein in breast cancer tissues were higher than that in normal breast tissues, 0. 78 ± 0. 095 or 0. 65 ± 0. 055, respectively. The expression levels of acetylated histone H3, H4 protein in normal breast tissues were higher than those in breast cancer tissues. H3 was 2. 35 ± 0. 340 or 1.07 ± 0. 067, respectively, H4 was 3.44 ± 0. 202 or 1.11 ± 0. 086, respectively. There was significantly difference in the expression levels between the 80 breast cancers and 80 normal breast tissues (P ＜0. 01). Conclusions The occurrence and development of breast cancers may be related to the expression change of histone acetylation and p21WAF1 protein.

Objective: To investigate the effects of oxLDL and HMG CoA reductase inhibitor simvastatin on PKC activity, and level of cytosolic free Ca 2+ in cultured human umbilical vein endothelial cells. Methods: The activity of PKC was determined by its ability to transfer phosphate from 32 P ATP to lysine rich histone and level of cytosolic free calcium[Ca 2+ ]i was measured by flow cytometric analysis loading with the Ca 2+ dye Fluo 3/Am. Results: oxLDL increased PKC total activity in a dose dependent manner and peaked after 12 min, then decreased slowly and maintained for at least 30 min, while oxLDL induced biphasic [Ca 2+ ]i responses including the rapid initial transient phase and the sustained phase. Removal of extracellular Ca 2+ did not inhibit the rapid transient phase, but abolished the sustained phase. When simvastatin was added, the activity of PKC wasmarkedly decreased with no impairment to the initial peak response, but significantly reduced the sustained phase. Conclusion: oxLDL can induced dynamic changes of signal transduction of PKC and level of cytosolic free Ca 2+ in HUVEC, these 2 events are closely linked. The change of rapid initial transient phase is the result of mobilization of Ca 2+ from intracellular pool and the change of sustained phase is from the influx of extracellular Ca 2+ . The inhibition of PKC activity induced by simvastatin may contribute to the changes of [Ca 2+ ]i. [

Objective: To investigate the effects of oxLDL and HMG-CoA reductase inhibitor simvastatin on PKC activity, and level of cytosol ic free Ca 2+ in cultured human umbilical vein endothelial cells. Methods: Th e activity of PKC was determined by its ability to transfer phosphate from 32P-ATP to lysine-rich histone and level of cytosolic free calcium［Ca2+ ］i was measured by flow cytometric analysis loading with the Ca2+ dye F luo-3/Am. Results: oxLDL increased PKC total activity in a dose-de pendent manner and peaked after 12 min, then decreased slowly and maintained for at least 30 min, while oxLDL induced biphasic ［Ca2+］i responses includ ing the rapid initial transient phase and the sustained phase. Removal of extrac ellular Ca2+ did not inhibit the rapid transient phase, but abolished the sustained phase. When simvastatin was added, the activity of PKC wasmarkedly dec reased with no impairment to the initial peak response, but significantly reduce d the sustained phase. Conclusion: oxLDL can induced dynamic changes of signal transduction of PKC and level of cytosolic free Ca2+ in HUVEC, these 2 events are closely linked. The change of rapid initial transient phase i s the result of mobilization of Ca2+ from intracellular pool and the chang e of sustained phase is from the influx of extracellular Ca2+. The inhibit ion of PKC activity induced by simvastatin may contribute to the changes of ［Ca 2+］i.

AIM　To investigate the effect of OX-LDL and HMG- CoA reductase inhibitors simvastatin on PKC activity and cytosolic free Ca2+ in cultured human monocy tes. METHOD　The activity of PKC was determined by its ability to tr ansfer phosphate from ［32P］ATP to lysine-rich histone and cytosolic free calcium［Ca2+］i was measured by flow cytometric analysis loading with the Ca2+ dye fluo3/Am. RESULTS　OX-LDL increased PKC tot al activity in a dose-dependent manner with phase peaking at 12 min, then decre ased slowly and maintained for at least 20 min, while OX-LDL induced biphasic ［Ca2+］i responses including the rapid initial transient phase and the sustained phase. Removal of extracellular Ca2+ did not inhibit the rapid i nitial transient phase of OX-LDL-induced rise in ［Ca2+］i,but abolish ed the sustained phase of ［Ca2+］i response to OX-LDL. When simvastati n was added, the activity of PKC was markedly decreased and simvastatin did not impair the initial peak response to OX-LDL but significantly reduced the subseq uent plateau phase. CONCLUSION OX-LDL can significantly activate t he activity of PKC and elevate ［Ca2+］i in monocytes. The rapid initial transient phase was the result of mobilization of ［Ca2+］i from intrac ellular pool and sustained phase resulted from the influx of extracellular Ca 2+. The inhibition of PKC activity induced by simvastatin may be contribute to the changes of intracellular Ca2+.

AIM To investigate the effect of OX- LDL and HMG-CoA reductase inhibitors simvastatin on PKC activity and cytosolic free Ca2+ in cultured human monocytes. METHOD The activity of PKC was determined by its ability to transfer phosphate fm [32P] ATP to lysine-rich histone and cytosolic free calcium[Ca2+]i was measured by flow cytometric analysis loading with the Ca2+ dye fluo3/Am.RE- SULTS OX-LDL increased PKC total activity in a dose-dependent manner with phase peaking at 12 min, then decreased slowly and maintained for at least 20 min, while OX-LDL induced biphasic [Ca2+ ], responses including the rapid initial transient phase and the sustained phase. Removal of extracellular Ca2+ did not inhibit the rapid initial transient phase of OX-LDL-induced rise. in [ Ca2+ ]i, but abol- abolished the sustained phase of [ Ca2+ ] i response to OX LDL. When simvastatin was added, the activity of PKC was markedly decreased and simvastatin did not impair the initial peak response to OX-LDL but sig- nificantly reduced the subsequent plateau phase. CONCLUSION OX-LDL can significantly activate the activity of PKC and elevate [Ca2+ ]i in monocytes. The rapid initial transient phase was the result of mobilization of [Ca2+ ], fm intracellular pool and sustained phase resulted from the influx of extracellular Ca2+. The inhibition of PKC activity induced by simvastatin may be contribute to the changes of intracellular Ca2+.

AIM: To investigate effects of OX-LDL and VitE on the levels of IL-6,IL-8 and TNF-? in human umbilical vein endothelial cells(HUVEC). METHODS: Human umbilical vein endothelial cells were obtained by in vitro culture. HUVEC treated with or without Vit E was incubated with OX-LDL, and the levels of IL-6, IL-8 and TNF-? were determined by enzyme-linked immunosorbent assy technique. RESULTS:50 ?g/L,100 ?g/L, 200 ?g/L OX-LDL induced the release of IL-6,IL-8 and TNF-? by HUVEC in a dose-dependent manner. Compared with the control group , the levels of IL-6 and IL-8 were significantly increased at 6-12 h of stimulation with OX-LDL . Maximal levels of IL-6 and IL-8 occurred after 24-36 h, reaching a plateau maintained for at least 48 h. TNF-? rose after 2-6 h in HUVEC, and reached a maximum after 12 h. In contrast to IL-6 and IL-8, TNF-? declined after 48 h. However, when VitE (50 mg/L,100 mg/L,200 mg/L)was added, it can significant inhibited the release of IL-6, IL-8 and TNF-? in a dose-dependent manner, and after 48 h these cytokines have no diference between OX-LDL+VitE groups and OX-LDL groups. CONCLUSION: OX-LDL can obviously stimulate the production of IL-6,IL-8 and TNF-? in vascular endothelial cells, which can significantly be inhibited by VitE in a short time.