antispasmodic/atròfia

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Association of spasmolytic polypeptide-expressing metaplasia with carcinogen administration and oxyntic atrophy in rats.

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Spasmolytic polypeptide (TFF2)-expressing metaplasia (SPEM) is a gastric metaplastic lineage associated with the development of intestinal-type gastric adenocarcinoma. To study the etiology of this potential neoplastic precursor metaplasia, we used surgical rat models of remnant gastric

Biologic profiles meet clinical priorities: incorporating pseudopyloric, and spasmolytic-expressing metaplasia in the assessment of gastric atrophy.

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Altered metaplastic response of waved-2 EGF receptor mutant mice to acute oxyntic atrophy.

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Metaplastic cell lineages are putative precursors for the development of gastric adenocarcinoma. The loss of parietal cells (oxyntic atrophy) is the initiating step in the evolution of gastric fundic mucosal lineage changes including metaplasia and hyperplasia. However, the intrinsic mucosal factors

Alterations in gastric mucosal lineages induced by acute oxyntic atrophy in wild-type and gastrin-deficient mice.

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In addition to their role in gastric acid secretion, parietal cells secrete a number of growth factors that may influence the differentiation of other gastric lineages. Indeed, oxyntic atrophy is considered the most significant correlate with increased risk for gastric adenocarcinoma. We studied the

Amphiregulin-deficient mice develop spasmolytic polypeptide expressing metaplasia and intestinal metaplasia.

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OBJECTIVE The loss of parietal cells from the fundic mucosa leads to the emergence of metaplastic lineages associated with an increased susceptibility to neoplastic transformation. Both intestinal metaplasia (IM) and spasmolytic polypeptide (TFF2/SP) expressing metaplasia (SPEM) have been identified

Spasmolytic polypeptide-expressing metaplasia (SPEM) in the gastric oxyntic mucosa does not arise from Lgr5-expressing cells.

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OBJECTIVE Metaplastic lineages in the oxyntic mucosa of the stomach are critical preneoplastic precursors of gastric cancer. Recent studies have demonstrated that spasmolytic polypeptide-expressing metaplasia (SPEM) in the mouse oxyntic mucosa arises from transdifferentiation of mature gastric chief

Potentiation of oxyntic atrophy-induced gastric metaplasia in amphiregulin-deficient mice.

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OBJECTIVE The loss of parietal cells from the gastric mucosa (oxyntic atrophy) is a critical step in the pathogenesis of chronic gastritis and gastric adenocarcinoma. Parietal cells are known to secrete epidermal growth factor receptor (EGFR) ligands, which are critical regulators of differentiation

Omeprazole treatment ameliorates oxyntic atrophy induced by DMP-777.

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Atrophic gastritis, characterized as parietal cell loss or oxyntic atrophy, is the primary event in the evolution of the spectrum of metaplastic and hyperplastic lineage changes thought to predispose to gastric neoplasia. A number of animal models have provided insights into the lineage changes

Differentiation of the gastric mucosa III. Animal models of oxyntic atrophy and metaplasia.

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Gastric cancer in humans arises in the setting of oxyntic atrophy (parietal cell loss) and attendant hyperplastic and metaplastic lineage changes within the gastric mucosa. Helicobacter infection in mice and humans leads to spasmolytic polypeptide-expressing metaplasia (SPEM). In a number of mouse

Vesicoureteric reflux deterioration in monozygotic twins.

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Primary vesicoureteric reflux (VUR) is the most common inherited structural urinary tract disorder, conforming closely to autosomal dominant transmission. A pair of monozygotic siblings is described exhibiting a remarkably parallel clinical course. VUR grade II was diagnosed in girl A during urinary

Loss of HGF activator inhibits foveolar hyperplasia induced by oxyntic atrophy without altering gastrin levels.

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Spasmolytic polypeptide/trefoil family factor 2 expressing metaplasia (SPEM) is induced by oxyntic atrophy and is known as a precancerous or paracancerous lesion. We now have sought to determine whether hepatocyte growth factor (HGF) influences the development of SPEM and oxyntic atrophy. DMP-777, a

Inducible activation of Cre recombinase in adult mice causes gastric epithelial atrophy, metaplasia, and regenerative changes in the absence of "floxed" alleles.

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The epithelium of the mammalian gastric body comprises multiple cell types replenished by a single stem cell. The adult conformation of cell lineages occurs well after birth; hence, study of genes regulating stem cell activity is facilitated by inducible systems for gene deletion. However, there is

Emergence of spasmolytic polypeptide-expressing metaplasia in Mongolian gerbils infected with Helicobacter pylori.

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Spasmolytic polypeptide (TFF2)-expressing metaplasia (SPEM) is observed in mucosa adjacent to human gastric cancer and in fundic glands showing oxyntic atrophy in Helicobacter felis-infected mice. Mongolian gerbils infected with Helicobacter pylori (Hp) develop goblet cell intestinal metaplasia and

Alterations in gastric mucosal lineages before or after acute oxyntic atrophy in gastrin receptor and H2 histamine receptor-deficient mice.

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Spasmolytic polypeptide (SP/TFF2)-expressing metaplasia (SPEM) is induced by oxyntic atrophy and is known as a precancerous or paracancerous lesion. We seek to determine whether the gastrin receptor or H(2) histamine receptor influence the development of SPEM. DMP-777 was administered to gastrin

A novel gastrokine, Gkn3, marks gastric atrophy and shows evidence of adaptive gene loss in humans.

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OBJECTIVE Gastrokines are stomach mucus cell-secreted proteins; 2 gastrokines are known, GKN1 and GKN2. Gastrokine expression is lost in gastric cancer, indicating a possible function in tumor suppression. We have identified a third gastrokine gene in mammals. METHODS Gkn3 was characterized by

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