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1 bromodeoxyuridine and was attributed to the hypergastrinemia.
2 arietal cells results in hypochlorhydria and hypergastrinemia.
3 by proton pump inhibitor therapy can lead to hypergastrinemia.
4 inogenic effect in the setting of endogenous hypergastrinemia.
5 increased proliferation resulting from serum hypergastrinemia.
6 e of potent acid suppressants that can cause hypergastrinemia.
7 stic state and are associated primarily with hypergastrinemia.
8 CK-BR-mediated growth even in the absence of hypergastrinemia.
9 lcerogenic pancreatic tumor syndrome without hypergastrinemia.
10 an be accelerated by acid inhibition-induced hypergastrinemia.
11 asia are usually associated with high pH and hypergastrinemia.
12 tumors occurred as a consequence of chronic hypergastrinemia.
13 tory canaliculi, causing hypochlorhydria and hypergastrinemia.
15 ng evidence suggested an association between hypergastrinemia and colorectal cancer, we examined whet
17 e tumors, delineating the connection between hypergastrinemia and gastric carcinoids, and most import
18 described a synergistic interaction between hypergastrinemia and Helicobacter felis infection on gas
19 s studies have shown that the combination of hypergastrinemia and Helicobacter infection resulted in
20 Specifically, human and animal models of hypergastrinemia and hypogastrinemia have been described
22 enostomy with proximal gastrectomy to induce hypergastrinemia and reflux of duodenogastric juice with
23 (KO) mice developed gastric hypochlorhydria, hypergastrinemia, and a phenotype that resembled foveola
24 8(-/fl) mice developed foveolar hyperplasia, hypergastrinemia, and hypochlorhydria associated with en
26 rmal parietal cell morphology, achlorhydria, hypergastrinemia, and striking gastric glandular hyperpl
27 T helper 1 lymphocyte (Th1) immune response, hypergastrinemia, and suppressed tissue somatostatin (SO
28 , the results demonstrate that gastritis and hypergastrinemia are not specific for H. pylori but can
29 may provide insight into the pathogenesis of hypergastrinemia associated the H. pylori infection.
30 inoids are a well-recognized complication of hypergastrinemia associated with chronic atrophic gastri
32 ll-specific deletion of Shh (PC-Shh(KO)) and hypergastrinemia, crossed with gastrin-deficient (GKO) m
33 s with Zollinger-Ellison syndrome (ZES) with hypergastrinemia, each having a different increased risk
34 astric tissues from PC-Shh(KO)/GKO mice with hypergastrinemia had an expanded surface pit epithelium,
35 Evaluation showed ZES was present (fasting hypergastrinemia, hyperchlorhydria) and control of all s
36 vious studies from our group have shown that hypergastrinemia in mice can synergize with Helicobacter
37 pport the unexpected conclusion that chronic hypergastrinemia in mice can synergize with Helicobacter
38 edgehog (Shh) from parietal cells results in hypergastrinemia in mice, accompanied by increased expre
39 n by the observation that prolonged moderate hypergastrinemia in transgenic mice leads to remodelling
40 ially more important are the consequences of hypergastrinemia, including rebound hypersecretion of ac
48 cystokinin B/gastrin receptor mRNA, and thus hypergastrinemia may increase progression through the ad
52 tric carcinoid tumors, including the role of hypergastrinemia on enterochromaffin-like cell prolifera
55 ATPase alpha-subunit causes achlorhydria and hypergastrinemia, severe perturbations in the secretory
57 include: the best approach to a patient with hypergastrinemia suspected of possibly having ZES, the a
60 ugh the response to gastrin decreased during hypergastrinemia, the proliferative effect of TGF-alpha
61 amidated gastrin (INS-GAS) and mice in which hypergastrinemia was induced using omeprazole, following
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