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Almost completely homogenous gastric mucous epithelial cells of guinea pigs were grown to confluence in the presence of 10% fetal calf serum (FCS). FCS, epidermal growth factor (EGF), and insulin significantly increased 5-bromo-2'-deoxyuridine (BrdU) uptake by the cells and EGF together with insulin increased the cells' [3H] thymidine uptake. Basic fibroblast growth factor (bFGF) enhanced EGF-induced DNA synthesis by the cells, but vasoactive intestinal peptide (VIP), secretin, prostaglandin E2 (PGE2), and dibutyryl cyclic AMP (dbcAMP) neither induced DNA synthesis nor enhanced the effect of EGF on DNA synthesis by the cells. Gastrin, cholecystokinin-octapeptide (CCK8), and carbamylcholine chloride (CCh) also did not enhance the effect of EGF on DNA synthesis. 125I-EGF, 125I-bFGF, and 125I-gastrin binding to the gastric mucous cells revealed the presence of high-affinity receptors for EGF and bFGF, but not for gastrin. Northern blot analysis showed the expression of EGF receptor mRNA, but not gastrin receptor mRNA. These results suggest that EGF, insulin, and bFGF may cooperatively regulate gastric mucous cell growth, but that gastrin and other gastrointestinal hormones do not have a direct stimulatory effect on mucous cell growth in the guinea pig. [ABSTRACT FROM AUTHOR]

BACKGROUND--Left ventricular (LV) function is the most important determinant of outcome after a myocardial infarction. Global LV function after a myocardial infarction is affected not only by wall motion in the infarct zone but also by regional function in the contralateral territory. It was hypothesised that the presence of significant stenoses in coronary arteries supplying the contralateral territory might influence the ability of this region to compensate for damaged myocardium after a myocardial infarction. METHODS AND RESULTS--79 patients treated with thrombolysis for acute myocardial infarction had coronary and ventricular angiograms within 24 h and at a mean follow up of 12 months after myocardial infarction. Wall motion in the contralateral territory was analysed and scored by the centre line method and the change over time was correlated with the presence or absence of significant (> 70%) diameter stenoses in the non-infarct-related artery. Mean (SD) contralateral territory motion worsened, from 0.74 (1.78) to -1.55 (2.06) SD chord (p < 0.001) in 40 patients with stenoses, whereas contralateral territory motion improved from -0.02 (2.4) to 0.63 (2.21) SD chord (p < 0.05) in the 39 patients without coronary stenoses. The same pattern was present whether or not the infarct artery was patent. The global left ventricular ejection fraction at 12 months was also related to contralateral territory motion (r = 0.71, p < 0.001) and to the presence of coronary stenoses (54 (15)% in those with coronary stenoses and 62 (16)% in those without, p < 0.05). CONCLUSION--The results demonstrate that significant stenoses in arteries supplying the non-infarct territory adversely affect global and regional left ventricular function after a transmural infarction. Non-infarct artery anatomy should be considered in intervention strategies to improve left ventricular function after acute myocardial infarction. [ABSTRACT FROM PUBLISHER]

Twenty-two children with chronic hepatitis serologically positive for hepatitis C virus (HCV) were treated with interferon-α (IFN-α). Liver biopsy showed chronic active hepatitis in 13 and chronic persistent hepatitis in 9 patients. A sustained clearance of HCV was observed in 8/22 children 12 months after the administration of IFN-α for 26 weeks, associated with normalization of HCV core antibody. Of these eight patients six had HCV genotype III and two HCV genotype II or IV. Hepatitis relapsed in seven other patients after completion of IFN-α with an increase in HCV core antibody titre, five with HCV genotype II, and two with HCV genotype III or IV. A second course of IFN-α suppressed the reactivation of HCV in all seven patients. Three of seven responders who relapsed after the first course remained negative for HCV RNA 12 months after their second course of IFN-α. However, the remaining four patients with HCV genotype II again relapsed after completing their second course of IFN-α. Seven children with the HCV genotype II resistant to IFN, including 8 weeks of IFN-β administration, and showed no significant reduction in HCV core antibody titre.Conclusion The genotype of HCV (III) and a reduction in the core antibody titre appear to be useful parameters for predicting the response to IFN-α therapy. [ABSTRACT FROM AUTHOR]

Abstract Mutations in any of the five genes KCNQ1, KCNII2, KCNE1, KCNE2, and SCN5A can be responsible for familial long qt syndrome (LQTS), an arrhythmogenic disorder that entails a high risk of sudden death. Beta-Adrenergic blocking agents are the first therapeutic choice, and 80% of patients treated with these agents show symptomatic relief; however the remaining 20% do not respond well. We previously performed a nationwide analysis of familial long QT syndrome (LQTS) in Japan and identified 32 mutations in the KCNQ1 and KCNH2 genes. In the present retrospective study, we found that patients carrying mutations in the KCNQ1 gene responded better to Beta-adrenergic blocking agents than those with KCNII2 mutations (12 of 13 vs 1 of 5; P = 0.0077, Fisher's exact test). This is a good example of the power of genetic diagnosis to direct the selection of appropriate therapy for patients with diseases of heterogeneous genetic etiology. [ABSTRACT FROM AUTHOR]