AIM:To determine the effects of posthepatic manipulative bleeding on the lung injury induced by hepatic ischemia-reperfusion (HIR)in rat model. METHODS:Rat 35 min total hepatic ischemia model was used in this study. We treated the experimental rats by posthepatic manipulative bleeding or IH-CV manipulative bleeding at 10 min after reperfusion. RESULTS:Two percent of body weight posthepatic manipulative bleeding with blood transfusion at 10 min after reperfusion significantly decreased circulating malondialdehyde(MDA). Tissue edema,myeloperoxidase(MPO) and MDA concentrations in lung were significantly decreased 6 h after treatments. The 7 d survival rate was remarkably improved in experimental group. CONCLUSION:Two percent of body weight posthepatic manipulative bleeding with blood transfusion at 10 min after reperfusion significantly protects the rats from lung injury induced by HIR.

100 d),and the histological grade of rejection was significantly lower than that in group Ⅱ(P

AIM: To study the molecular mechanism of EGCG on inhibiting the growth of hepatic carcinoma. METHODS: The proliferation of hepatic cell line HepG2 cultured with different doses of EGCG was studied by MTT and suspension/adherence methods. The effect of EGCG on the expression of HIF-1α/VEGF at mRNA and protein levels in vitro and in vivo was evaluated by RT-PCR and Western blotting, respectively. The inhibition of EGCG on the growth of tumor implanted into athymic nude mice was also observed. RESULTS: The proliferation of hepatic cell line HepG2 was inhibited by EGCG in a dose-dependent manner. The expression of HIF-1α/VEGF was suppressed markedly by EGCG at protein level. However, the inhibitory effect of EGCG on the mRNA expression was only observed on VEGF, not on HIF-1α. In the animal experiment, the implanted tumor growth was inhibited by 39.8%±5.1%. CONCLUSION: EGCG suppresses the hepatic carcinoma cell growth, and interrupts the HIF-1α/VEGF signaling pathway significantly, indicating a fundamental mechanism of EGCG for inhibiting tumor growth.

Anatomic hepatic resection not only enables enough tumor-free resection margin,but also guarantee the maximal remnant of normal liver tissue.A 61-year-old male patient with hepatic cancer was admitted to the Affiliated Hospital of Hainan Medical College in February 2012.Multiple space-occupying lesions were found in segment Ⅵ,Ⅶ and Ⅷ by computed tomography (CT).The results of CT volumetry analysis showed that the left hemihepatic volume was lesser than the minimal limit of survival,so anatomic hepatic segmentectomy of Ⅵ,Ⅶ and Ⅷ with preservation of segment Ⅴ was designed to guarantee the maximal remaining of normal liver tissue.Glisson's pedicle transection was used twice to divide the right hemihepatic Glisson's pedicle,segment Ⅵ and Ⅶ Glisson's pedicle,respectivley,then the resection line was determined,and anatomical hepatic segmentectomy of Ⅵ,Ⅶ and Ⅷ was completed.With the procedures adopted,the hepatic ischemia reperfusion injury and hemodynamic instability were maximally reduced during operation.

Objective To explore the treatment of primary hepatic neuroendocrine tumors (PHNET).Methods The therapeutic treatments of 9 PHNET patients from January 2003 to January 2010 in 3 hospitals were retrospective analyzed and followed up.Results Diagnosis of PHNET was confirmed immunohistochemically and by excluding extrahepatic primary sites.The survival is significantly dependent on tumor resectability.One patient received only radiotherapy and one with only chemotherapy,one with radiofrequency ablation.Six patients received R0 resection,one received postoperative radiotherapy,one with TACE perioperatively and internal radiotherapy.Two patients were lost to follow up 3 patients died and 4 were alive.Intrahepatic recurrence was found in 1 patient and metastasis to bone in 2 patients.Survival time ranged from 11 days to 66 months.Conclusions PHNET is an extremely rare entity with difficulty in early diagnosis.Curative liver resection integrated with transarterial chemoembolization or radiotherapy is considered to be an effective modality.

AIM: To study the effects of intrathymic inoculation of liver specific antigen (LSA) on hepatocyte apoptosis after liver allotransplantation. METHODS: Orthotopic liver transplantation was used in this study. Group Ⅰ: syngenic control (Wistar-to-Wistar); Group Ⅱ: acute rejection (SD-to-Wistar); Group Ⅲ: thymus inoculation of SD rat LSA day 7 before transplantation. The observation of general situation and survival time, hepatocyte apoptosis and LAT expression in liver transplants were used to analyze immune state of animals in different groups. RESULTS: The general situation of group Ⅰ was very well after transplantation. Recipients of groupⅡ lost body weight progressively and all died within day 9 to day 13 post transplantation. As for group Ⅲ, the general situation of recipients was remarkably better than that in group Ⅱ. The positive cells of apoptosis in group Ⅲ detected by TUNEL were not significantly different from that in group Ⅰ, but was significantly lower than that in group Ⅱ. LAT was detected at any time in group Ⅱ with peak expression at day 5 and day 7 post transplantation. In contrast, LAT was not detected in any other groups. CONCLUSION: Intrathymic inoculation of LSA protects hepatocytes from apoptosis after liver allotransplantation.

ObjectiveTo investigate the mechanism by which cyclosporine A downregulates transcription of interferon-? gene after murine orthotopic liver transplantation.Methods Orthotopic murine liver transplantation model was employed and rats were divided into 3 groups. GroupⅠ: syngeneic control (Wistar-to-Wistar); GroupⅡ: acute rejection (SD-to-Wistar). GroupⅢ: acute rejection treated with cyclosporine A (SD-to-Wistar+CsA). EMSA was employed to analyze NFAT and NF-?B DNA-binding activity of splenocytes, RT-PCR was employed to analyze IFN-? mRNA transcription intragraft on 1,3,5,7,12 day posttransplant in each group, respectively. Histopathological examination was also performed for reference.Results In comparison to groupⅠ, NFAT and NF-?B DNA-binding activity of splenocytes in groupⅡincreased significantly( P

Objective To study the role of 1,25-dihydroxyvitamin D3 in preventing allograft acute rejection in rat orthotopic liver transplantation. Method Rats receiving orthotopic liver transplantation were divided into groupⅠ: syngenic control (Wistar-to-Wistar); GroupⅡ:acute rejection (SD-to-Wistar). GroupⅢ: acute rejection treated with cyclosporine; GroupⅣ: acute rejection treated with 1,25-(OH)_ 2 D_ 3 . Liver function, rejection index and IFN-? mRNA, IL-10 mRNA expression level were monitored on d1,5,7,15,30 posttransplantation. Results Survival of recipients in group Ⅳ was significantly prolonged (vs group Ⅱ, P

AIM: To investigate the role of NFAT in cyclosporine A downregulating IFN-? gene transcription after liver transplantation. METHODS: Rat orthotopic liver transplantation model was employed and 3 groups of experiments were performed in this study. GroupⅠ: syngeneic control (Wistar-to-Wistar); GroupⅡ: acute rejection (SD-to-Wistar). GroupⅢ: acute rejection treated with cyclosporine A intramuscularly (SD-to-Wistar+CsA). EMSA and RT-PCR were used to analyze NFAT activity of splenocytes and IFN-? gene transcription intragraft of recipients with or without CsA treatment after liver transplantation. Histopathological assessment was also performed for reference. RESULTS: No noticeable rejection was detected in GroupⅠ while only low level of IFN-? mRNA transcription and faint NFAT activity were measured. In contrast, a marked rejection reaction was demonstrated from day3 postoperation in GroupⅡ. IFN-? mRNA transcription was significant and NFAT activity was intensive. In comparison to GroupⅡ, rejection grade in Group Ⅲ significantly decreased (P

AIM:To study the molecular mechanism of EGCG on inhibiting the growth of hepatic carcinoma. METHODS: The proliferation of hepatic cell line HepG2 cultured with different doses of EGCG was studied by MTT and suspension/adherence methods. The effect of EGCG on the expression of HIF-1?/VEGF at mRNA and protein levels in vitro and in vivo was evaluated by RT-PCR and Western blotting,respectively. The inhibition of EGCG on the growth of tumor implanted into athymic nude mice was also observed. RESULTS: The proliferation of hepatic cell line HepG2 was inhibited by EGCG in a dose-dependent manner. The expression of HIF-1?/VEGF was suppressed markedly by EGCG at protein level. However,the inhibitory effect of EGCG on the mRNA expression was only observed on VEGF,not on HIF-1?. In the animal experiment,the implanted tumor growth was inhibited by 39.8%?5.1%. CONCLUSION: EGCG suppresses the hepatic carcinoma cell growth,and interrupts the HIF-1?/VEGF signaling pathway significantly,indicating a fundamental mechanism of EGCG for inhibiting tumor growth.