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  • 1
    Electronic Resource
    Electronic Resource
    Effects of growth factors and gut hormones on proliferation of primary cultured gastric mucous cells of guinea pig (1996)
    Springer
    Journal of gastroenterology 31 (1996), S. 498-504 
    Details
    ISSN: 1435-5922
    Keywords: gastric mucous cell ; FGF ; EGF ; insulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract 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, and125I-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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02355048
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of antiulcer drugs on phosphatidylcholine synthesis in isolated guinea pig gastric glands (1992)
    Springer
    Digestive diseases and sciences 37 (1992), S. 1593-1599 
    Details
    ISSN: 1573-2568
    Keywords: ulcer ; antiulcer drugs ; phosphatidylcholine synthesis ; gastric glands
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To better understand phosphatidylcholine synthesis in the stomach, we isolated guinea pig gastric glands and examined their [3H] choline incorporation into phosphatidylcholine in response to either antiulcer drugs such as geranylgeranylacetone (GGA) and H2-receptor antagonists or agents that cause phosphatidylcholine synthesis in other tissues. [3H]Choline incorporation was stimulated by GGA, palmitate, and 12-O-tetradecanoylphorbol-13-acetate (TPA). Dibutyryl cyclic-AMP had no effect. By contrast with GGA, famotidine, ranitidine, and cimetidine equipotently inhibited [3H] choline incorporation into phosphatidylcholine. GGA, palmitate, and TPA increased phosphatidyl-[3H] choline and decreased phosphoryl-[3H] choline as compared with control in tissues that had been pulsed with [3H] choline. On the other hand, no more decrease in [3H] choline incorporation at chase periods was observed in pulse-labeled glands in response to each H2-receptor antagonist. The particulate fraction of glands that had been incubated with GGA or palmitate had more CTP-phosphocholine cytidylyltransferase activity than that of glands incubated without agents. A decrease in choline kinase activity was not observed in the cytosolic fraction of glands that had been incubated with cimetidine. These results suggest that GGA and palmitate stimulate phosphatidylcholine synthesis by activating cytidylyltransferase, and H2-receptor antagonists may affect phosphatidylcholine synthesis by inhibiting choline uptake in the gastric glands.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01296507
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  • 3
    Electronic Resource
    Electronic Resource
    Idiopathic chronic calcifying pancreatitis with diabetes mellitus (1993)
    Springer
    Digestive diseases and sciences 38 (1993), S. 963-967 
    Details
    ISSN: 1573-2568
    Keywords: chronic pancreatitis ; pancreatic stone protein gene ; polymerase chain reaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We present a case of a 27-year-old female suffering from chronic calcifying pancreatitis with diabetes mellitus. Radiographic examinations and exocrine pancreatic function tests revealed considerable dilatation of pancreatic ducts with large intraductal calculi and exocrine pancreatic insufficiency, respectively. Recent literature indicates that a decrease in the activity of pancreatic stone protein (PSP), which inhibits CaCO3 crystal formation in pancreatic juice, is closely related to the development of chronic calcifying pancreatitis. The patient had no apparent cause or family history of pancreatitis. We therefore investigated the possibility that alterations in the PSP gene might explain the chronic pancreatitis seen in this patient. Six exons of the PSP gene amplified by polymerase chain reaction were directly sequenced, but there was no apparent base mutation observed. Furthermore, Southern blot analysis revealed neither rearrangement nor deletion of the PSP gene in the genomic DNA of this case. However, this genetic approach will be useful for future study of the etiology of hereditary pancreatitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01295929
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of CCK-receptor antagonists on CCK-stimulated pepsinogen secretion and calcium increase in isolated guinea pig gastric chief cells (1990)
    Springer
    Digestive diseases and sciences 35 (1990), S. 873-878 
    Details
    ISSN: 1573-2568
    Keywords: dbcGMP ; L-364,718 ; CR1409 ; pepsinogen ; [Ca2+]i ; chief cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of CCK-receptor antagonists such as dibutyryl cyclic GMP (dbcGMP), L-364,718, and CR1409 on COOH-terminal octapeptide of CCK (CCK-8) -stimulated chief cell responses were examined using isolated guinea pig gastric chief cells. L-364,718 and CR1409 inhibited CCK-8-stimulated pepsinogen secretion over the same concentration range as they inhibited CCK-8-stimulated increases in intracellular Ca2+ concentration ([Ca2+]i), respectively. Schild analysis of the CCK dose-response curve indicates that L-364,718 and CR1409 exert their inhibitory effects on CCK-8-stimulated chief cell responses in a competitive manner. By contrast, dbcGMP inhibited not only CCK-8-but also carbachol-stimulated pepsinogen secretion. Furthermore, dbcGMP inhibited CCK-8-stimulated pepsinogen secretion more potently than the increases in [Ca2+]i. These results suggest that L-364,718 and CR1409 act as CCK-receptor antagonists, but dbcGMP has another inhibitory effect on pepsinogen secretion in addition to the effect as a CCK-receptor antagonist in guinea pig gastric chief cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01536801
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Induction of cyclooxygenase protein and stimulation of prostaglandin E2 release by epidermal growth factor in cultured guinea pig gastric mucous cells (1995)
    Springer
    Digestive diseases and sciences 40 (1995), S. 1679-1686 
    Details
    ISSN: 1573-2568
    Keywords: gastric mucosal cells ; epidermal growth factor ; prostaglandin E2 ; cyclooxygenase activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was undertaken to investigate whether epidermal growth factor (EGF) could stimulate prostaglandin E2 release, and if so, by what mechanism EGF would exert such an effect in gastric mucosal cells. In cultured guinea pig gastric mucous cells, EGF dosedependently stimulated prostaglandin E2 release, with maximal stimulation observed at 10 ng/ml. EGF stimulated an increase in cyclooxygenase activity, which was reduced by protein synthesis inhibitor, actinomycin D, and cycloheximide. EGF also stimulated the enzyme protein synthesis estimated by Western blot analysis, whereas EGF did not stimulate phospholipase A2 activity. These results suggest that such an effect of EGF onde novo synthesis of cyclooxygenase protein and prostaglandin E2 release may be involved at least in part in the mechanism of EGF-induced local regulation of gastric mucosal integrity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02212688
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    Paper (German National Licenses)
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