For this reason, it should be recommended to perform endoscopic resection for high-grade dysplasia (early mucosal gastric cancer according to the Japanese criteria). To reconcile these discrepant diagnostic criteria between Japan and the West, the term “noninvasive high-grade neoplasia” was adopted in the Vienna classification. Unfortunately, however, this term has not been widely used in either side. Moreover, the term, “intraepithelial neoplasia”

was introduced in the recent World Health Organization classification. In the future, we definitely need a global consensus how to deal with such “neoplastic” lesions, for which recent BMS-354825 nmr technological advancement would be instrumental in promoting mutual understanding. This review article is the results of intensive clinical and research efforts of colleagues in Jichi Medical University. Special thanks to Dr Hiroyuki

Mutoh who contributed to the molecular mechanisms of IM and to Dr Kiichi Satoh for the histological analysis. I also thank Dr Yoshikazu Hayashi in our department and Dr Shunji Hayashi in the department of microbiology, Jichi Medical University who contributed to gastric microbiology. Endoscopic images were kindly provided by Dr Hiroyuki Osawa Carfilzomib cell line in our department. “
“We read with interest the article by Ghouri et al.,1 who reviewed the evidence regarding the link between nonalcoholic fatty liver disease (NAFLD) and cardiovascular disease (CVD). The authors concluded that the connection between NAFLD and CVD is not well supported by existing data because of the presence of confounders such as age and established cardiovascular risk factors. We agree that the main limitation of these studies is that their results make it difficult to distinguish the contribution of liver fat per se to the risk of CVD. However, we should consider that the liver is the main regulator of insulin sensitivity

and finely tunes insulin-regulated metabolic Ibrutinib pathways such as glucose and lipid homeostasis that are involved in endothelial dysfunction and atherogenesis. Studies in null mice have clearly substantiated this issue. In particular, the disruption of insulin signaling in the liver is more relevant to whole body glucose homeostasis than its disruption in adipose tissue and muscle.2 In addition, hepatic insulin signaling regulates the secretion of very low density lipoprotein and thus lipotoxicity and atherogenesis.3 Therefore, it is impossible to identify the intrahepatic triglyceride level, which precisely reflects liver insulin resistance, as an isolated variable in the generation of CVD risk.