BACKGROUND/AIMS: Hepatic fibrosis in rat induced by thioacet amide shares similar morphological and biochemical characteristics with human liver cirrhosis. Thioacetamide (T AA) initially induces accumulation of collagen in Disse space and eventually leads to macro- and micronodular cirrhos is. Ito cell was believed to play a main role in hepatic fibrosis. And it s activity was known to be regulated by the expression of various genes. But little has been discovered about the upstream signal trans duction pathway of these genes in hepatic fibrosis. The expression of genesrelated to Ito cell activity was regulated by many transcription factors , the activity of which was regulated by protein kinase C( PKC) is oforms. So it is s upposed that PKC could be as s ociated with fibrosis in liver. METHODS: We investigated the correlation of PKC is oforms and It ocell activity in the course of hepatic fibrosis using TAA induced rat liver cirrhosis model. We used six week- old male rats , and administered 0.03% TAA in drinking water. The animals were sacrificed at 9, 20, and 30 weeks after TAA administration. The degree of hepatic fibrosis was evaluated by measuring the total amount of collagen.-SMA immunohist ochemical st aining of liver tissue was done to determine the Ito cell activity. The expression pattern of PKC isoforms was investigated by West ern blotting. RESULTS: In TAA- treated group, collagen cont ent and Ito cell activity did not increase until 30 weeks and 20 weeks of treatment , respectively, while in control group collagen cont ent and Ito cell activity were not detected. Collagen content showed linear correlation with Ito cell activity. This implied that the proliferation of activated Ito cells was prior to the increase of collagen content. In view of expression pattern of PKC is oforms, PKC alpha showed no difference in TAA- treated group and control group. In TAA-treated group, PKCbeta1 exhibited increased level of expression in both particulate and cytosolic forms at 9 weeks, while PKCdelta and PKC epsilon showed striking shift to particulated form. After 20 weeks, all of the PKC beta1, delta, and epsilon degenerated and showed remarkably decreased level of expression. This suggested PKC alpha had no relation to hepatic fibrosis,while PKC beta1, delta, and epsilon, showing activity at 9 weeks, were related to fibrosis og liver. In response to fibrogenic factors, molecules engaged in intracellular signal transduction pathway like PKC beta1, delta, and epsilon, began to change prior to the increase of Ito cell activity, morphologic changes and alterations of collagen content. CONCLUSION: Our results strongly suggest that the activity of PKC isoforms play an important role in early step of hepatic fibrosis, while accompanying Ito cell activity do in later step.
Animals ; Collagen ; Cytosol ; Drinking Water ; Fibrosis ; Hepatic Stellate Cells ; Humans ; Liver Cirrhosis* ; Liver* ; Male ; Protein Isoforms ; Protein Kinase C-epsilon ; Protein Kinases ; Rats ; Signal Transduction ; Strikes, Employee ; Thioacetamide ; Transcription Factors

PURPOSE: A pancreatic ductal adenocarcinoma is one of the most fatal cancers, as the majority of the patients present with locally advanced or metastatic tumors in the late stages of the disease. However, there is no simple, sensitive, noninvasive, and inexpensive test for the early detection of pancreatic ductal adenocarcinomas. In recent studies, S100A4 has emerged as an important protein in the tumorgenesis of pancreatic adenocarcinomas. METHODS: The possibility of the expression of S100A4 as a new tumor marker of pancreatic adenocarcinomas was confirmed using immunohistochemistry to 32-pancreatic ductal adenocarcinomas, 20 IPMN (intraductal papillary mucinous neoplasm), 8 serous cystadenomas, 5 chronic pancreatitis and 3 neuroendocrine tumors. RESULTS: Thirty-one (96.9%) ductal adenocarcinoma cases and 11 (55.5%) IPMN expressed S100A4, whereas all normal pancreatic tissues (47 cases), chronic pancreatitis and endocrine tumors did not. The expression of S100A4 was associated with the degree of dysplasia in IPMN, but not with the differentiation of ductal adenocarcinomas. CONCLUSION: The overexpression of S100A4 in adenocarcinomas and early emerging IPMN may suggest its potential as a diagnostic marker for the early detection of pancreatic ductal adenocarcinomas.
Adenocarcinoma* ; Carcinoma, Pancreatic Ductal ; Cystadenoma, Serous ; Humans ; Immunohistochemistry ; Mucins* ; Neuroendocrine Tumors ; Pancreas* ; Pancreatic Ducts ; Pancreatitis, Chronic ; Biomarkers, Tumor

Cytomegalovirus (CMV) infections are usually reported in immunocompromised patients. However, it occurs rarely in immunocompetent individuals. A case of CMV associated with stomach ulcers and mucosal nodules is reported in a immunocompetent host. A previously healthy 27-year-old man visited our hospital with a thirty-day history of epigastric pain and a nine-day history of vomiting. The demonstration of intranuclear inclusion bodies in a few gastric glandular epithelial cells contributed to the diagnosis of CMV gastritis. Treatment with a proton pump inhibitor and ganciclovir was successful to mitigate the epigastric pain and vomiting.
Adult* ; Cytomegalovirus ; Diagnosis ; Epithelial Cells ; Ganciclovir ; Gastritis* ; Humans ; Immunocompromised Host ; Intranuclear Inclusion Bodies ; Proton Pumps ; Stomach Ulcer ; Vomiting