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Objective To examine the expression of scinderin in primary hepatocellular carcinoma (HCC) and its paired portal vein tumor thrombus (PVTT) tissues; and to explore its role in the development of HCC and its relationship with prognosis of HCC.Methods Immunohistochemistry was used to detect the expressions of scinderin in tumor-adjacent normal liver tissues,HCC tissues and PVTT tissues from 33 patients.Results The positive expression rates of scinderin in tumor-adjacent normal tissues,HCC tissues and PVTT tissues were 69.7％ (23/33),45.5％ (15/33) and 24.2％ (8/33) respectively.A significantly lower scinderin expression was found in HCC tissues when compared with tumor-adjacent normal tissues (P ＜ 0.05).Also,the expression of scinderin in PVTT tissues was significantly lower than in HCC tissues (P ＜ 0.05).The expression of scinderin in HCC tissues significantly correlated with tumor size,absence of tumor capsule and serum AFP (P ＜0.05).The recurrence-free survival (RFS) and overall survival (OS) of Scinderin-positive patients were significantly longer than Scinderin-negative patients (P ＜ 0.05).Multivariate analysis revealed scinderin expression level to be an independent risk factor affecting RFS and OS after curative resection.Conclusions Scinderin was down-regulated in HCC tissues and PVTT tissues when compared with its paired tumor-adjacent normal liver tissues.The expression level of scinderin correlated with HCC recurrence and prognosis.Scinderin can be used as an indicator of prognosis of HCC patients with PVTT.
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Objective: To observe the protective roll of atorvastatin on post-operative cardiac remodeling induced by transverse aortic constriction (TAC) in experimental mice with its possible mechanism. Methods: A total of 48 C57BL/6 mice were randomly divided into 4 groups: Sham group, TAC group, TAC + valsartan group and TAC + atorvastatin group,n=12 in each group. Myocardial hypertrophy model was successfully established at 4 weeks after the operation, and then the animals were further treated by normal saline, valsartan 5mg/kg and atorvastatin 10mg/kg respectively for 8 weeks. Left ventricular anterior wall thickness at diastole (LVAWd), left ventricular posterior wall thickness at diastole (LVPWd), LVEF and left ventricular fractional shortening (FS) were examined by echocardiography, cardiac hypertrophy indexes were calculated. Protein expression of NF-κB was detected by Western blot analysis, cardiac tissue hydroxyproline (Hyp) level was measured by alkaline hydrolysis, serum levels of TNF-α, IL-1β were determined by ELISA, cardiac collagen deposition was identiifed by HE and Masson staining. Results: Compared with Sham group, TAC group had increased LVAWd, LVPWd, cardiac hypertrophy indexes and increased area of cardiac fibrosis, allP Conclusion: Atorvastatin had protective roll on myocardial hypertrophy induced by pressure overload in experimental mice, which might be related to its anti-inlfammatory effect.
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The incidence of hepatocellular carcinoma (HCC) with portal vein tumor thrombosis (PVTT) is very high,and the prognosis is often unsatisfactory.Currently,some therapy such as radiotherapy or radiation combined with interventional therapy are effective and worth attention.Radiation therapy was divided into external beam radiation therapy and internal beam radiation therapy according to different administration pathway.This article summarized the current situation and prospect of radiotherapy.
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Objective To investigate the expression of peroxiredoxin 1 (Prx 1) in hepatocellular carcinoma (HCC) with portal vein tumor thrombosis (PVTT) and to evaluate the relationship between the expressions of Prx 1 and the postoperative recurrence of this disease. Methods Immunohisto chemistry and Western blotting were performed to examine the expression of Prx 1 protein in 40 patients with HCC with PVTT. Experiments on Sprague Dawley (SD) rat hepatoma model were further carried out to observe the pathological changes of Prx 1 by immunohistochemistry. Clinical outcomes were analyzed to find a correlation between the recurrence and positive rate of Prx 1. Results The expression level of Prx 1 was significantly up-regulated in primary tumor tissues than in tumor thrombosis samples (P＜0.01). Immunohistochemistry results showed that the positive rate of Prx 1 in primary tumor tissues were higher than that in tumor thrombosis. Western blotting confirmed a same trend in the level of Prx 1, the average luminosity of the blots were 1534.2 and 735.6, respectively. There was a significant difference in SD rat hepatoma model, the 4, 8, 12, 16, 20 and 24-week positive rates of Prx 1 in liver tumor tissues were 60%, 80%, 75% ,65%, 40% and 25% respectively. Clinical outcomes showed that the time to first postoperative recurrence of Prx 1 in the primary tumor positive group was significantly higher than that in the negative group (6. 3 vs 3. 7 months, P＜0. 01). Conclusions Prx 1 protein was down-regulated in HCC with PVTT. There was a negative correlation between the expression of Prx 1 and recurrence.
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Myocardial protection has been the subject of intensive investigation. Several studies have suggested that Ginsenosides may protect against ischemia/reperfusion injury. The isolated, working rat heart model was used in this study to evaluate the effects of St. Thomas' Hospital Cardioplegic Solution containing various concentrations of Ginsenosides on the enhancement of myocardial protection following hypothermic ischemic arrest (20 ℃, 120 min). The added concentration of Ginsenosides in cardioplegic solution was 0(control), 50, 100 150?g/ml, respectively. Recoveries of aortic flow, cardiac output, and minute work were markedly improved by adding Ginsenosides to cardioplegia. Dose-response study indicated that 100?g/ml in cardioplegia had the best protective effects, in which group the generation of thiobarbituric acid reactive materials (MDA) was markedly reduced. Our results indicated that Ginsenosides provides additional myocardial protection in St. Thomas' Hospital Cardioplegia. Addition of Ginsenosides to cardioplegia may protect the ischsmic myocardium from free-radical injury also.