Additivity of the proliferative effects of HGF/SF and EGF on hepatocytes.

The additivity of DNA synthesis induced by hepatocyte growth factor/scatter factor (HGF/SF) and epidermal growth factor (EGF) was revealed in periportal hepatocytes (PPH), perivenous hepatocytes (PVH), and primary hepatocytes. Furthermore, additivity of the signal transduction pathway of HGF/SF and EGF was investigated (i.e., the activity of mitogen-activated protein kinase (MAPK) induced by HGF/SF and EGF), but it was not seen in PPH, PVH, or primary hepatocytes, although wortomannin, a PI 3-kinase inhibitor, abolished the additivity. The additivity of DNA synthesis induced by HGF/SF and EGF was not related to hepatocyte heterogeneity, but to a difference in the signal transduction pathway, probably another pathway that is different from the classical MAPK (MAPK/ERK1,2) path.

The effect of lansoprazole treatment on the healing and relapse of peptic ulcer and serum levels of IgG anti-Helicobacter pylori antibody.

In the present study, the effects of short-term treatment with lansoprazole on healing and recurrence of peptic ulcer were investigated. Complete healing (change to the S2 stage) after 3 or 4 weeks of treatment with lansoprazole was observed in 9.9% of gastric ulcers and 38.3% of duodenal ulcers. Complete healing was observed after 3 or 4 weeks of treatment with lansoprazole in gastric ulcers and was significantly related to the serum titer of IgG anti-Helicobacter pylori antibodies. This was not the case in duodenal ulcers. Complete healing after 6 or 8 weeks of treatment with lansoprazole was not dependent on serum levels of IgG anti-H. pylori antibodies. Short-term treatment by lansoprazole did not affect serum levels of IgG anti-H. pylori antibodies immediately after the end of lansoprazole treatment, but significantly reduced serum levels of IgG anti-H. pylori antibodies were found 9 months after treatment.