No abstract

The relationship of parasitic liver disease to cholangiocarcinoma has long been debated, and it has been reported that cholangiocarcinoma is associated with opisthorchiasis viverrini. We report herein a rare case of cholangiocarcinoma associated with schistosomiasis japonica. A 76-year-old Japanese man with jaundice was diagnosed with cholangiocarcinoma. Radical resection was not done because of hepatic arterial and portal vein invasion. Biliary microwave tissue coagulation therapy was performed with placement of a metallic stent endoprosthesis. Twenty-two months after the treatment, however, the patient died from hematemesis. Autopsy findings revealed that there was no distant metastasis, even in the area of regional lymph node metastasis. The primary tumor in the hepatic hilar region had been replaced by necrotic debris resulting from the microwave therapy, and an expandable metallic stent was located in the center of the debris. Histological findings showed schistosome eggs, which were old and microcalcified, in veins in the colonic submucosa. Glisson's fibrosis around the cancer lesion suggested that schistosomiasis japonica and cholangiocarcinoma can occur together with severe chronic inflammation of the portal vein.

No abstract

IκBNS is a nuclear IκB protein which negatively regulates nuclear factor-κB activity. We demonstrated that IκBNS deficiency accelerates atherosclerosis in LDL receptor-deficient (LDLr−/−) mice via increased interleukin (IL)-6 production by macrophages. Previous studies showed that the increase in IL-6 might contribute to the development of atherosclerotic lesions. However, whether an anti-mouse IL-6 receptor antibody (MR16-1) can protect atherosclerotic lesions in atherogenic mice remains to be elucidated. We investigated atherosclerotic lesions in LDLr−/− and IκBNS−/−/LDLr−/− mice after 16 weeks consumption of a high-fat diet. All mice received intraperitoneal injections of MR16-1 or phosphate-buffered saline (PBS) (control) once a week during a high-fat diet consumption. Treatment of MR16-1 yielded no adverse systemic effects, and we detected no significant differences in serum cholesterol levels in either group. The atherosclerotic lesions were significantly increased in IκBNS−/−/LDLr−/− compared with LDLr−/− mice (p < 0.01) under treatment of PBS. However, MR16-1 treatment abolished the significant difference of atherosclerotic lesions between IκBNS−/−/LDLr−/− and LDLr−/− mice. Interestingly, MR16-1 also significantly decreased atherosclerotic lesions in LDLr−/− mice compared with PBS treatment (p < 0.05). Immunostaining revealed percent phospho-STAT3-positive cell were significantly decreased in the atherosclerotic lesions of MR16-1 treated both IκBNS−/−/LDLr−/− and LDLr−/− mice compared with PBS-treated mice, indicating MR16-1 could suppress atherosclerotic lesions via the inhibition of IL-6–STAT3 signaling pathway. This study highlights the potential therapeutic benefit of anti-IL-6 therapy in preventing atherogenesis induced by dyslipidemia and/or inflammation.