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  • 1
    Electronic Resource
    Electronic Resource
    Optical measurement of interaction potentials between a single microparticle and an evanescent field (2000)
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 76 (2000), S. 2815-2817 
    Details
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Radiation pressure exerted on a single microparticle within an evanescent field has been analyzed by a three-dimensional potential measurement system. Temporal fluctuation of the particle position due to the thermal Brownian motion was sequentially measured, and the potential energy was estimated by a thermodynamical analysis. A potential profile corresponding to the evanescent-field-induced radiation pressure could be obtained as an energy difference between two potentials measured with and without illumination of the evanescent field. The exponential dependence on the longitudinal position was clearly observed. The lateral radiation force on a 4.5 μm polystyrene latex particle in water was determined to be 90 fN at the laser intensity of 1.0 kW cm−2. © 2000 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.126482
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  • 2
    Electronic Resource
    Electronic Resource
    Teprenone, but not H2-Receptor Blocker or Sucralfate, Suppresses Corpus Helicobacter pylori Colonization and Gastritis in Humans: Teprenone Inhibition of H. pylori-Induced Interleukin-8 in MKN28 Gastric Epithelial Cell Lines (2004)
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 9 (2004), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background.  The role of teprenone in Helicobacter pylori-associated gastritis has yet to be determined. To investigate the effect of teprenone on inflammatory cell infiltration, and on H. pylori colonization of the gastric mucosa in H. pylori-infected patients, we first compared the effect of teprenone with that of both histamine H2 receptor antagonists (H2-RA) and sucralfate on the histological scores of H. pylori gastritis. We then examined its in vitro effect on H. pylori-induced interleukin (IL)-8 production in MKN28 gastric epithelial cells.Materials and Methods.  A total of 68 patients were divided into three groups, each group undergoing a 3-month treatment with either teprenone (150 mg/day), H2-RA (nizatidine, 300 mg/day), or sucralfate (3 g/day). All subjects underwent endoscopic examination of the stomach before and after treatment. IL-8 production in MKN28 gastric epithelial cells was measured by enzyme-linked immunosorbent assay (ELISA).Results.  Following treatment, the teprenone group showed a significant decrease in both neutrophil infiltration and H. pylori density of the corpus (before vs. after: 2.49 ± 0.22 vs. 2.15 ± 0.23, p = .009; 2.36 ± 0.25 vs. 2.00 ± 0.24, p = .035, respectively), with no significant differences seen in either the sucralfate or H2-RA groups. Teprenone inhibited H. pylori-enhanced IL-8 production in MKN28 gastric epithelial cells in vitro, in a dose-dependent manner.Conclusions.  Teprenone may modify corpus H. pylori-associated gastritis through its effect on neutrophil infiltration and H. pylori density, in part by its inhibition of IL-8 production in the gastric mucosa.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1083-4389.2004.00209.x
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  • 3
    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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  • 4
    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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  • 5
    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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  • 6
    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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