Objective To investigate the efficacy of different radical surgical procedures for the treatment of hilar cholangiocarcinoma.Methods The clinical data of 207 patients with hilar cholangiocarcinoma who were treated at the Southwest Hospital from June 2007 to June 2012 were retrospectively analyzed.Local resection or hemihepatectomy combined with caudate lobectomy was applied to patients with Bismuth type Ⅰ hilar cholangiocarcinoma; dumbbell type radical resection was applied to patients with Bismuth type Ⅱ hilar cholangiocarcinoma or some patients with type Ⅲ a,Ⅲ b and Ⅳ hilar cholangiocarcinoma; hemihepatectomy or extended hemihepatectomy combined with caudate lobectomy was applied to patients with Bismuth type Ⅲ a,Ⅲ b and Ⅳ hilar cholangiocarcinoma.The patients were followed up every 3 months postoperatively till December 2012.All data were analyzed using the chi-square test or Fisher exact probability test,the survival curve was drawn by Kaplan-Meier method,and the survival was analyzed using the Log-rank test.Results Of the 207 patients,124 received radical resection,including 14 received local resection,23 received dumbbell type resection,87 received lobectomy + caudate lobectomy,49 received palliative resection; 34 received biliary drainage.Four patients died perioperatively.The incidences of complications of dumbbell type radical resection,left hemihepatectomy + caudate lobectomy,right hemihepatectomy + caudate lobectomy were 21.7％ (5/23),46.6％ (27/58) and 48.3％ (14/29),respectively.The incidence of complications after dumbbell type radical resection was significantly lower than left hemihepatectomy + caudate lobectomy and right hemihepatectomy + caudate lobectomy (x2 =4.42,3.90,P ＜ 0.05).One hundred and seventy patients were followed up.The median survival time of the 112 patients who received radical radical resection was 26.5 months,and the 1-,3-,5-year survival rates were 75.9％ (85/112),42.9％ (24/56) and 28.9％ (11/38),respectively.The median survival time of the 38 patients who received palliative resection was 8.5 months,and the 1-,3-year survival rates were 31.6％ (12/38) and 0.The survival time of 20 patients who received biliary drainage was 4.0 months,and the l-year survival rate was 0.The survival rate of patients who received radical resection was significantly higher than those who received palliative resection (x2=65.32,P ＜ 0.05).There was a significant difference in the survival rate between patients who received surgical treatment and those who received biliary drainage (x2=99.97,P ＜ 0.05).Of the 112 patients who received radical resection,the median survival time of 10 patients who received local resection of tumor was 47.0 months,the 1-year survival rate was 10/10,and 4 patients survived at the end of the follow-up; the median survival time of 23 patients who received dumbbell type radical resection was 32.0 months,and the 1-,3-year survival rates were 95.7％ (22/23) and 7/15,and the survival time of 6 patients was longer than 5 years; the median survival time of 54 patients who received left hemihepatectomy or extended left hemihepatectomy + caudate lobectomy was 27.6 months,and the 1-,3-year survival rates were 42.1％ (24/57) and 38.7％ (12/32),and the survival time of 9 patients was longer than 5 years,3 patients survived at the end of the follow-up ; the median survival time of 25 patients who received right hemihepatectomy or extended right hemihepatectomy + caudate lobectomy was 28.3 months,and the 1-,3-year survival rates were 45.8％ (11/24) and 6/15,and the survival time of 6 patients was longer than 5 years,2 patients survived at the end of follow-up.The median survival time of 35 patients (patients with Bismuth type Ⅰ,Ⅱ hilar cholangiocarcinoma and Bismuth Ⅲ a and Ⅲ b hilar cholangiocarcinoma which did not invade the secondary bile duct) who received hemihepatectomy + caudate lobectomy was 32.0 months,and the 1-,3-,5-year survival rates were 91.4％ (32/35),45.8％ (11/24) and 5/16,which were not different from the survival rate of patients who received dumbbell type radical resection (x2 =0.17,P ＞ 0.05).The 5-year survival rate of patients with lymph node metastasis was 4/19,which was significantly lower than 30.4％ (7/23) of patients without lymph node metastasis (x2 =23.40,P ＜ 0.05).Conclusion Joint lobectomy and standardized lymph node dissection could help to improve the efficacy of surgical treatment for patients with hilar cholangiocarcinoma.

Background: and Purpose Previous studies have revealed the diverse neuroprotective effects of GV1001. In this study, we investigated the effects of GV1001 on focal cerebral ischemia-reperfusion injury (IRI) in rats and oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury in neural stem cells (NSCs) and cortical neurons. Methods: Focal cerebral IRI was induced by transient middle cerebral artery occlusion (MCAO). Brain diffusion-weighted imaging (DWI) was performed 2 hours after occlusion, and a total of 37 rats were treated by reperfusion with GV1001 or saline 2 hours after occlusion. Fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging, immunohistochemistry, and neurobehavioral function analyses were performed. Additionally, OGD/R-injured NSCs and cortical neurons were treated with different GV1001 concentrations. Cell viability, proliferation, migration, and oxidative stress were determined by diverse molecular analyses. Results In the stroke model, GV1001 protected neural cells against IRI. The most effective dose of GV1001 was 60 μM/kg. The infarct volume on FLAIR 48 hours after MCAO compared to lesion volume on DWI showed a significantly smaller ratio in the GV1001-treated group. GV1001-treated rats exhibited better behavioral functions than the saline-treated rats. Treatment with GV1001 increased the viability, proliferation, and migration of the OGD/R-injured NSCs. Free radicals were significantly restored by treatment with GV1001. These neuroprotective effects of GV1001 have also been demonstrated in OGD/R-injured cortical neurons. Conclusions The results suggest that GV1001 has neuroprotective effects against IRI in NSCs, cortical neurons, and the rat brain. These effects are mediated through the induction of cellular proliferation, mitochondrial stabilization, and anti-apoptotic, anti-aging, and antioxidant effects.

Background: and Purpose Previous studies have revealed the diverse neuroprotective effects of GV1001. In this study, we investigated the effects of GV1001 on focal cerebral ischemia-reperfusion injury (IRI) in rats and oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury in neural stem cells (NSCs) and cortical neurons. Methods: Focal cerebral IRI was induced by transient middle cerebral artery occlusion (MCAO). Brain diffusion-weighted imaging (DWI) was performed 2 hours after occlusion, and a total of 37 rats were treated by reperfusion with GV1001 or saline 2 hours after occlusion. Fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging, immunohistochemistry, and neurobehavioral function analyses were performed. Additionally, OGD/R-injured NSCs and cortical neurons were treated with different GV1001 concentrations. Cell viability, proliferation, migration, and oxidative stress were determined by diverse molecular analyses. Results In the stroke model, GV1001 protected neural cells against IRI. The most effective dose of GV1001 was 60 μM/kg. The infarct volume on FLAIR 48 hours after MCAO compared to lesion volume on DWI showed a significantly smaller ratio in the GV1001-treated group. GV1001-treated rats exhibited better behavioral functions than the saline-treated rats. Treatment with GV1001 increased the viability, proliferation, and migration of the OGD/R-injured NSCs. Free radicals were significantly restored by treatment with GV1001. These neuroprotective effects of GV1001 have also been demonstrated in OGD/R-injured cortical neurons. Conclusions The results suggest that GV1001 has neuroprotective effects against IRI in NSCs, cortical neurons, and the rat brain. These effects are mediated through the induction of cellular proliferation, mitochondrial stabilization, and anti-apoptotic, anti-aging, and antioxidant effects.

Cirrhotic portal hypertension refers to a series of syndroms characterized by structural abnormality and dysfunction of hepatic sinusoid caused by chronic liver injury and obstructing portal-systemic blood flow, resulting in gradually increased portal venous system pressure as clinical manifestations. Increased intrahepatic resistance and portal venous system blood flow are main causes for cirrhotic portal hypertension. The structural abnormality and dysfunction of hepatic sinusoid cause not only increased intrahepatic resistance, but also substance exchange barriers between hepatic sinusoidal blood and hepatocytes, resulting in splanchnic artery dilation and increased blood flow and pressure of portal venous system. Dysfunction of splanchnic hemodynamic is an important factor for hyperdynamic circulation in cirrhotic portal hypertension. As the disease progresses, cirrhotic portal hypertension can continuously promote the activation of hyperdynamic circulation, which in turn can accelerate the development of cirrhotic portal hyperten-sion. This vicious circle is the main reason for the irreversible and untreatable end-stage liver disease. The authors review the pathophysiological mechanisms of cirrhotic portal hypertension, splanchnic hemodynamic dysfunction and hyperdynamic circulation.