Yi-Chou Chen

Lack of detrimental effects of nitric oxide inhibition in bile duct-ligated rats with hepatic encephalopathy.

Background  The pathogenetic mechanisms of hepatic encephalopathy (HE) are not fully understood. Vasodilatation induced by nitric oxide (NO) may be involved in the development of HE. There is no comprehensive data concerning the effects of NO inhibition on HE in chronic liver disease.

Simvastatin effects on portal‐systemic collaterals of portal hypertensive rats

Background and Aim:  Portal‐systemic collateral vascular resistance and vasoconstrictor responsiveness are crucial in portal hypertension and variceal bleeding control. Statins enhance vasodilators production, but their influence on collaterals is unknown. This study aimed to survey the effect of simvastatin on collaterals.

Detrimental effects of nitric oxide inhibition on hepatic encephalopathy in rats with thioacetamide‐induced fulminant hepatic failure: Role of nitric oxide synthase isoforms

Background:  Hepatic encephalopathy is a complex neuropsychiatric syndrome. A previous study showed that chronic nitric oxide (NO) inhibition aggravated the severity of encephalopathy in thioacetamide (TAA)‐treated rats. The present study investigated the relative contribution of NO synthase (NOS) isoforms on the severity of hepatic encephalopathy in TAA‐treated rats.

Simvastatin for rats with thioacetamide-induced liver failure and encephalopathy.

Background and Aim:  Nitric oxide (NO) inhibition aggravates hepatic damage and encephalopathy and increases mortality in rats with thioacetamide (TAA)‐induced acute liver failure. Statins enhance NO synthase expression beyond their lipid‐lowering capability, but the impact on encephalopathy remains unexplored. The aim of this study was to assess the effects of simvastatin on rats with TAA‐induced acute liver damage and hepatic encephalopathy.

Methimazole Alleviates Hepatic Encephalopathy in Bile-duct Ligated Cirrhotic Rats

Background: Acute or chronic liver damage may lead to hepatic encephalopathy. Previous studies have indicated the hemodynamic and hormonal mimicry between portal hypertension and hyperthyroidism. Furthermore, medically or surgically induced hypothyroidism has been found to be beneficial in ameliorating hyperdynamic circulation in the portal hypertensive state and in alleviating acute or chronic liver injury in rats. However, the effect of chronic thyroid hormone inhibition on chronic hepatic encephalopathy in cirrhosis remains unknown. Methods: Liver cirrhosis was induced by bile‐duct ligation (BDL) in male Sprague‐Dawley rats. Three weeks after BDL, rats were randomized to receive either tap water (control) or 0.04% methimazole in drinking water for 3 weeks. At the end of 6 weeks after BDL, severity of encephalopathy was assessed by the Opto‐Varimex animal activity meter and hemodynamic parameters were measured. Blood samples were collected for determination of thyroid stimulating hormone, ammonia and liver biochemistry. Results: The heart rate of the methimazole‐treated group was significantly lower than that of the control group (p = 0.015), whereas there were no differences in the mean arterial pressure and portal pressure. The total amount of movements were significantly increased in the methimazole group (p = 0.029). Plasma levels of ammonia, aspartate aminotransferase and alkaline phosphatase were significantly lower (p = 0.01) and thyroid stimulating hormone significantly higher (p = 0.035) in the methimazole group. Conclusion: Chronic methimazole treatment alleviates hepatic encephalopathy and liver damage in rats with BDL‐induced hepatic cirrhosis.

Role of Hepatic Nitric Oxide Synthases in Rats with Thioacetamide-induced Acute Liver Failure and Encephalopathy

Background: Hepatic encephalopathy is neuropsychiatric derangement secondary to hepatic decompensation or portal‐systemic shunting. Nitric oxide (NO) synthase inhibition aggravates encephalopathy and increases mortality in rats with thioacetamide (TAA)‐induced acute liver failure, suggesting a protective role of NO. This study investigated the roles of endothelium‐derived constitutive NO synthase (eNOS) and inducible NOS (iNOS) in the liver of rats with fulminant hepatic failure and encephalopathy. Methods: Male Sprague‐Dawley rats (300‐350 g) were randomized to receive TAA 350 mg/kg/day, by intraperitoneal injection or normal saline for 3 days. Severity of encephalopathy was assessed with the Opto‐Varimex animal activity meter. Plasma levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, and bilirubin were measured. Hepatic iNOS and eNOS RNA and protein expressions were assessed by reverse transcription‐polymerase chain reaction and Western blot analyses, respectively. Results: The TAA group showed lower motor activity counts than the normal saline group. Hepatic eNOS, but not iNOS, mRNA and protein expressions were enhanced in the TAA group. In addition, hepatic eNOS mRNA expression was negatively correlated with total movement but positively correlated with ALT and AST. Protein expression of hepatic eNOS was positively correlated with ALT, AST and bilirubin. Conclusion: Upregulation of hepatic eNOS was observed in rats with TAA‐induced fulminant hepatic failure and encephalopa‐thy, which might play a regulatory role.

Cyclooxygenase expression in splanchnic hyposensitivity to glypressin of bleeding portal hypertensive rats.

Background Prostacyclin mediates, at least partly, the splanchnic vascular hyporesponsiveness to glypressin in bleeding portal hypertensive rats. This study investigated the relative contribution of cyclooxygenase‐1 (COX‐1) and cyclooxygenase‐2 (COX‐2) in the splanchnic hyposensitivity to glypressin in rats with portal hypertension induced by partial portal vein ligation (PVL).

Lack of detrimental or therapeutic effects of cyclooxygenase inhibition in bile duct-ligated rats with hepatic encephalopathy

Background:  The pathogenetic mechanisms of hepatic encephalopathy (HE) are not fully understood. Cerebral blood flow regulated by cyclooxygenase (COX) may be involved in the development of HE. There are no comprehensive data concerning the effects of COX inhibition on HE in chronic liver disease.

Intralesional curettage of central low-grade chondrosarcoma: A midterm follow-up study

Background The aim of this study was to review the experience of surgical treatment of low‐grade chondrosarcoma and to assess the long‐term oncological and functional outcomes between intralesional curettage and wide excision. Methods We included 11 patients with central low‐grade chondrosarcoma lesions treated with intralesional curettage or wide excision from 1998 to 2013. Seven patients were treated with intralesional curettage and local adjuvant treatment (Group A), and four patients were treated with wide excision and reconstructive surgery (Group B). The mean age of patients was 43.8 ± 17.6 years (range, 20–71 years), and the mean duration of follow‐up was 84.4 ± 47.6 months (range, 48–194 months). Results Group A had a significantly lower complication rate than Group B; three complications were documented in Group B (0% vs. 75%, p = 0.024). The operative time (177.1 hours vs. 366.3 hours, p = 0.010) and the hospital stay (6.6 days vs. 12.5 days, p = 0.010) were significantly shorter in Group A. There was one local recurrence in Group A without statistical significance. Also, there were no differences between intralesional curettage and wide excision with respect to the blood loss. No metastasis disease occurred in either group during the follow‐up period. The Musculoskeletal Tumor Society (MSTS) scores in Groups A and B were 99.0 ± 2.5 and 94.2 ± 4.2, respectively, with statistically significant difference (p = 0.048). Conclusion Extended intralesional curettage has the benefits of good MSTS score, shorter operative time, shorter hospital stay, and lower complication rate without increasing local recurrence in central low‐grade chondrosarcoma. For central low‐grade chondrosarcoma, we suggest extended curettage to decrease soft tissue damage and surgical risk.

DR‐70 immunoassay for the surveillance of hepatocellular carcinoma

Background and Aim:  Although alpha‐fetoprotein (AFP) is a widely used serological marker for hepatocellular carcinoma (HCC), its utility is limited due to its unsatisfactory sensitivity. Meanwhile, a newly developed immunoassay—DR‐70—has been reported to have a good sensitivity for HCC in a small‐scale study. The aim of this study was to determine the clinical value of DR‐70 for the surveillance of HCC.