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Heiko Braak - One of the best experts on this subject based on the ideXlab platform.
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gastric alpha synuclein immunoreactive inclusions in meissner s and auerbach s plexuses in cases staged for parkinson s disease related brain pathology
Neuroscience Letters, 2006Co-Authors: Heiko Braak, Rob A I De Vos, Jurgen Bohl, Kelly Del TrediciAbstract:The progressive degenerative process associated with sporadic Parkinson's disease (sPD) is characterized by formation of alpha-synuclein-containing inclusion bodies in a few types of projection neurons in both the enteric and central nervous systems (ENS and CNS). In the brain, the process apparently begins in the brainstem (dorsal motor nucleus of the vagal nerve) and advances through susceptible regions of the basal mid-and forebrain until it reaches the cerebral cortex. Anatomically, all of the vulnerable brain regions are closely interconnected. Whether the pathological process begins in the brain or elsewhere in the nervous system, however, is still unknown. We therefore used immunocytochemisty to investigate the gastric myenteric and submucosal plexuses in 150 microm cryosections and 8 microm paraffin sections from five autopsy individuals, whose brains were also staged for Parkinson-associated synucleinopathy. alpha-synuclein immunoreactive inclusions were found in neurons of the submucosal Meissner plexus, whose axons project into the gastric mucosa and terminate in direct proximity to Fundic Glands. These elements could provide the first link in an uninterrupted series of susceptible neurons that extend from the enteric to the central nervous system. The existence of such an unbroken neuronal chain lends support to the hypothesis that a putative environmental pathogen capable of passing the gastric epithelial lining might induce alpha-synuclein misfolding and aggregation in specific cell types of the submucosal plexus and reach the brain via a consecutive series of projection neurons.
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gastric α synuclein immunoreactive inclusions in meissner s and auerbach s plexuses in cases staged for parkinson s disease related brain pathology
Neuroscience Letters, 2006Co-Authors: Heiko Braak, Jurgen Bohl, Kelly Del TrediciAbstract:Abstract The progressive degenerative process associated with sporadic Parkinson's disease (sPD) is characterized by formation of α-synuclein-containing inclusion bodies in a few types of projection neurons in both the enteric and central nervous systems (ENS and CNS). In the brain, the process apparently begins in the brainstem (dorsal motor nucleus of the vagal nerve) and advances through susceptible regions of the basal mid-and forebrain until it reaches the cerebral cortex. Anatomically, all of the vulnerable brain regions are closely interconnected. Whether the pathological process begins in the brain or elsewhere in the nervous system, however, is still unknown. We therefore used immunocytochemisty to investigate the gastric myenteric and submucosal plexuses in 150 μm cryosections and 8 μm paraffin sections from five autopsy individuals, whose brains were also staged for Parkinson-associated synucleinopathy. α-synuclein immunoreactive inclusions were found in neurons of the submucosal Meissner plexus, whose axons project into the gastric mucosa and terminate in direct proximity to Fundic Glands. These elements could provide the first link in an uninterrupted series of susceptible neurons that extend from the enteric to the central nervous system. The existence of such an unbroken neuronal chain lends support to the hypothesis that a putative environmental pathogen capable of passing the gastric epithelial lining might induce α-synuclein misfolding and aggregation in specific cell types of the submucosal plexus and reach the brain via a consecutive series of projection neurons.
Scillitani G - One of the best experts on this subject based on the ideXlab platform.
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Lectin histochemistry of gastrointestinal glycoconjugates in the greater horseshoe bat, Rhinolophus ferrumequinum (Schreber, 1774)
2007Co-Authors: Scillitani G, Zizza S., Liquori G.e. Ferri E D.Abstract:Mucins in the gastrointestinal tract of Rhinolophus ferrumequinum were investigated by histochemistry and lectin histochemistry to evaluate morphofunctional variations of different regions and their possible physiological and evolutionary implications. Histochemical methods included periodic acid-Schiff (PAS), Alcian blue (AB) at pH 2.5 and 1.0 and high-iron-diamine AB pH 2.5. Binding of lectins Con A, DBA, WGA, LTA, LFA, PNA and SBA; LFA, PNA and SBA with prior sialidase treatment; and paradoxical Con A were evaluated. The oesophagus lacked Glands. The stomach was divided into a short cardias, a wide fundus and a brief pylorus. The surface muciparous cells secreted sulpho- and sialomucins with N-acetylgalactosamine (GalNAc) residues, N-acetyllactosamine and (b1,4 N-acetylglucosamine)n chains. Towards the pylorus, N-acetylgalactosamine residues disappeared and acidity decreased. Cardiac Glands, neck cells in the Fundic Glands, pyloric and duodenal Brunner’s Glands all shared neutral, stable class-III mucins, mainly with N-acetylgalactosamine sequences. The intestine was divided into a duodenum, a jejuno-ileum and a short rectum. The goblet cells produced sulpho- and sialomucins with sialylated N-acetylgalactosamine sequences, (b1,4 N-acetylglucosamine)n and N-acetyllactosamine, whose sialylation increased towards the rectum. The main features of the mucins are probably associated with the requirements of fast absorption and food passage and in protection against mechanical and pathogenic injuries
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Histochemical and immunohistochemical evidence for a gradient in gastric juice production in the greater horseshoe bat, Rhinolophus ferrumequinum (Schreber, 1774)
'Museum and Institute of Zoology at the Polish Academy of Sciences', 2005Co-Authors: Scillitani G, Zizza S., Liquori G.e. Ferri E D.Abstract:Histochemical and immunohistochemical investigations were performed on the gastric mucosa of the greater horseshoe bat, Rhinolophus ferrumequinum (Schreber, 1774) to estimate the presence of a gradient of pepsinogen and hydrochloric acid along an oro-aboral axis of the stomach, similar to that found in some non-mammals. Paraffin sections were stained with DBA-lectin binding, Bowie and fluorescent anti-H+/K+- ATPase α-subunit immunostaining to detect the chief and parietal cells in the gastric mucosa. The stomach of the bat presents a short cardias, a wide fundus and a small pylorus. Chief and parietal cells were found in the Fundic Glands and their number varied from the oral to the aboral region of fundus. In the oral region several chief cells with Bowie-positive pepsinogen granules were observed in the basal part of Glands, whereas parietal cells positive to DBA-lectin binding and immuroreactive with anti-H+/K+-ATPase α-subunit were concentrated in the the upper part of the Glands. In the aboral fundus chief cells were lacking, whereas the number of parietal cells increased and they were distributed along the Glands. A gradient of pepsinogen and hydrochloric acid secretion similar to that found in some non-mammals can be hypothesised. The possibility that this gradient is the ancestral condition in Chiroptera and Eutheria and its functional meaning are discussed
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Pepsinogen and H,K,ATPase mediate acid secretion in gastric Glands of Triturus carnifex (Amphibia, Caudata)
'Elsevier BV', 2005Co-Authors: Liquori G.e., Scillitani G, Zizza S., Mastrodonato M, Calamita G., Ferri D.Abstract:The gastric Glands of Triturus carnifex (Amphibia, Caudata) have been examined by histochemical and immunohistochemical methods with particular regard to hydrochloric acid and pepsinogen secretion. Fundic Glands consist of mucous neck cells, endocrine cells and oxynticopeptic cells producing both pepsinogen and hydrochloric acid. The neck cells showed an unexpected distribution pattern which was only observed in the oral fundus, and produced neutral mucins with glycosidic residues of GalNAc and Gal b1,3GalNAc, and in this respect they differ from the neck cells of anuran amphibians. The secretion of pepsinogen and hydrochloric acid as demonstrated by immunolabelling with anti-H,K-ATPase and with anti-pepsinogen, respectively, seems not to vary significantly along the longitudinal axis of the stomach. The mechanism of gastric acid secretion seems to be mediated by an ATPase, having similar features to the mammalian gastric H,K-ATPase, and is localised in the luminal membrane and in the subapical cytoplasm of the oxynticopeptic cells. Unusually, the same cytoplasmic areas revealed binding specificity for the winged pea lectin (WPA) from Lotus tetragonolobus, even after b elimination, indicating the presence of fucosyl residues in N-linked oligosaccharidic chains in glycoproteins of b-H,K-ATPase subunits
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Fine structure of the oxynticopeptic cells in the gastric Glands of the ruin lizard, Podarcis sicula campestris (De Betta, 1857)
'Wiley', 2000Co-Authors: Liquori G.e., Ferri D., Scillitani GAbstract:The results of an ultrastructural investigation of the gastric Glands of the ruin lizard are reported. In this reptile the stomach can be divided into a larger fundus and a smaller pars pilorica. Fundic Glands are characterized by three main kinds of cells: mucous, endocrine, and oxynticopeptic; the latter were not observed in the pyloric Glands. The morphological features of the oxynticopeptic cells change from the proximal to the distal region of the Fundic mucosa. In the proximal region, numerous electron-dense secretory granules, a well-developed granular endoplasmic reticulum, an evident Golgi complex, and a reduced system of smooth-surfaced vesicles and tubules in the apical cytoplasm characterize these cells. In the distal Fundic region, oxynticopeptic cells possessed numerous mitochondria and a well-developed smooth-surfaced endoplasmic reticulum, but secretory granules were rare. These data suggest the existence of a gradient in the production of proteolytic enzymes, and perhaps also of hydrochloric acid, along the oral-aboral axis of the stomach. The results are discussed with regard to the evolution of the gastric Glands and of the digestive mechanism in vertebrates
Liquori G.e. Ferri E D. - One of the best experts on this subject based on the ideXlab platform.
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Lectin histochemistry of gastrointestinal glycoconjugates in the greater horseshoe bat, Rhinolophus ferrumequinum (Schreber, 1774)
2007Co-Authors: Scillitani G, Zizza S., Liquori G.e. Ferri E D.Abstract:Mucins in the gastrointestinal tract of Rhinolophus ferrumequinum were investigated by histochemistry and lectin histochemistry to evaluate morphofunctional variations of different regions and their possible physiological and evolutionary implications. Histochemical methods included periodic acid-Schiff (PAS), Alcian blue (AB) at pH 2.5 and 1.0 and high-iron-diamine AB pH 2.5. Binding of lectins Con A, DBA, WGA, LTA, LFA, PNA and SBA; LFA, PNA and SBA with prior sialidase treatment; and paradoxical Con A were evaluated. The oesophagus lacked Glands. The stomach was divided into a short cardias, a wide fundus and a brief pylorus. The surface muciparous cells secreted sulpho- and sialomucins with N-acetylgalactosamine (GalNAc) residues, N-acetyllactosamine and (b1,4 N-acetylglucosamine)n chains. Towards the pylorus, N-acetylgalactosamine residues disappeared and acidity decreased. Cardiac Glands, neck cells in the Fundic Glands, pyloric and duodenal Brunner’s Glands all shared neutral, stable class-III mucins, mainly with N-acetylgalactosamine sequences. The intestine was divided into a duodenum, a jejuno-ileum and a short rectum. The goblet cells produced sulpho- and sialomucins with sialylated N-acetylgalactosamine sequences, (b1,4 N-acetylglucosamine)n and N-acetyllactosamine, whose sialylation increased towards the rectum. The main features of the mucins are probably associated with the requirements of fast absorption and food passage and in protection against mechanical and pathogenic injuries
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Histochemical and immunohistochemical evidence for a gradient in gastric juice production in the greater horseshoe bat, Rhinolophus ferrumequinum (Schreber, 1774)
'Museum and Institute of Zoology at the Polish Academy of Sciences', 2005Co-Authors: Scillitani G, Zizza S., Liquori G.e. Ferri E D.Abstract:Histochemical and immunohistochemical investigations were performed on the gastric mucosa of the greater horseshoe bat, Rhinolophus ferrumequinum (Schreber, 1774) to estimate the presence of a gradient of pepsinogen and hydrochloric acid along an oro-aboral axis of the stomach, similar to that found in some non-mammals. Paraffin sections were stained with DBA-lectin binding, Bowie and fluorescent anti-H+/K+- ATPase α-subunit immunostaining to detect the chief and parietal cells in the gastric mucosa. The stomach of the bat presents a short cardias, a wide fundus and a small pylorus. Chief and parietal cells were found in the Fundic Glands and their number varied from the oral to the aboral region of fundus. In the oral region several chief cells with Bowie-positive pepsinogen granules were observed in the basal part of Glands, whereas parietal cells positive to DBA-lectin binding and immuroreactive with anti-H+/K+-ATPase α-subunit were concentrated in the the upper part of the Glands. In the aboral fundus chief cells were lacking, whereas the number of parietal cells increased and they were distributed along the Glands. A gradient of pepsinogen and hydrochloric acid secretion similar to that found in some non-mammals can be hypothesised. The possibility that this gradient is the ancestral condition in Chiroptera and Eutheria and its functional meaning are discussed
Andre Bado - One of the best experts on this subject based on the ideXlab platform.
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vagal stimulation rapidly increases leptin secretion in human stomach
Gastroenterology, 2002Co-Authors: Iradj Sobhani, Marion Buyse, J P Laigneau, Dominique Henin, Healene Goiot, Nina Weber, Jean Claude Soule, Andre BadoAbstract:Abstract Background & Aims: Leptin production has been reported in the rat and in human stomach. It initiates intestinal nutrient absorption. In this study, we analyzed the effect of vagal stimulation on leptin release in the human stomach. Methods: We studied the secretion of gastric acid and leptin on stimulation with insulin (a stimulant of vagal pathways via hypoglycemia) and pentagastrin in 11 healthy men (normal endoscopy and normal histological gastric mucosa), 5 with previous highly selective vagotomy (HSV), and 6 without HSV. Fundic biopsies were performed for immunostaining of leptin. Results: There was no difference between the 2 groups with respect to age, body mass index, basal leptin (4.8 ± 1.2 ng/15 minutes) and gastric acid (0.7 ± 0.2 mmol/15 minutes) outputs. Leptin-immunoreactivity was found in the Fundic Glands, and its distribution and density were similar in 2 groups. Insulin caused a rapid (15-minute) increase in leptin output in men without HSV (31 ± 9 ng/15 minutes), but not in those with HSV (7.7 ± 3.2 ng/15 minutes). Insulin-stimulated gastric leptin was biphasic, with a rapid increase (15 minutes after injection) followed by a second steady and sustained increase (39.9 ± 7.6 ng/15 minutes at 120 minutes after injection). Pentagastrin increased gastric leptin output in individuals with (30 ± 4.9 ng/15 minutes) and without (26 ± 3.2 ng/15 minutes) HSV. Insulin and pentagastrin did not modify plasma leptin, whatever HSV status. Conclusions: Vagal stimulation of leptin release in the human stomach suggests that leptin is released during the cephalic phase of gastric secretion. Luminal leptin may be involved in vagus-mediated intestinal functions. GASTROENTEROLOGY 2002;122:259-263
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leptin secretion and leptin receptor in the human stomach
Gut, 2000Co-Authors: Iradj Sobhani, Andre Bado, C Vissuzaine, Marion Buyse, Stephanie Kermorgant, J P Laigneau, T Lehy, Dominique Henin, Samir Attoub, Maxime Le MignonAbstract:BACKGROUND AND AIM The circulating peptide leptin produced by fat cells acts on central receptors to control food intake and body weight homeostasis. Contrary to initial reports, leptin expression has also been detected in the human placenta, muscles, and recently, in rat gastric chief cells. Here we investigate the possible presence of leptin and leptin receptor in the human stomach. METHODS Leptin and leptin receptor expression were assessed by immunohistochemistry, reverse transcriptase-polymerase chain reaction (RT-PCR), and western blot analysis on biopsy samples from 24 normal individuals. Fourteen (10 healthy volunteers and four patients with non-ulcer dyspepsia and normal gastric mucosa histology) were analysed for gastric secretions. Plasma and Fundic mucosa leptin content was determined by radioimmunoassay. RESULTS In Fundic biopsies from normal individuals, immunoreactive leptin cells were found in the lower half of the Fundic Glands. mRNA encoding ob protein was detected in the corpus of the human stomach. The amount of Fundic leptin was 10.4 (3.7) ng leptin/g mucosa, as determined by radioimmunoassay. Intravenous infusions of pentagastrin or secretin caused an increase in circulating leptin levels and leptin release into the gastric juice. The leptin receptor was present in the basolateral membranes of Fundic and antral gastric cells. mRNA encoding Ob-RL was detected in both the corpus and antrum, consistent with a protein of ∼120 kDa detected by immunoblotting. CONCLUSION These data provide the first evidence of the presence of leptin and leptin receptor proteins in the human stomach and suggest that gastric epithelial cells may be direct targets for leptin. Therefore, we conclude that leptin may have a physiological role in the human stomach, although much work is required to establish this.
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H3-receptor activation inhibits cholinergic stimulation of acid secretion in isolated rabbit Fundic Glands.
The Journal of pharmacology and experimental therapeutics, 1995Co-Authors: Andre Bado, J P Laigneau, L. Moizo, Y. Cherifi, Michel LewinAbstract:We previously reported evidence for H3-receptor inhibition of cholinergic stimulation of acid secretion by isolated rabbit gastric Glands. Because this inhibition was unsensitive to H2 antagonists, we postulated that the parietal cell should bear a H3-receptor. In the present study, we investigated the effects of M1-M3 muscarinic receptors antagonists on carbachol- and thioperamide-induced acid secretion (14CAP uptake) by isolated rabbit gastric Glands. Furthermore, we examined whether H3-receptor ligands could affect [3H]-N-methylscopolamine binding to the isolated rabbit parietal cells. Both carbachol and thioperamide concentration-dependently stimulated 14CAP uptake in the Glands with maximal responses being achieved for 100 microM and 0.1 microM, respectively. These stimulations were concentration-dependently inhibited by the H3-receptor agonists R(alpha)-methylhistamine and imetit. Maximal inhibitions did not exceed 60% for 1 microM. The muscarinic receptor antagonists, hexa-sila-difenidol p-fluoro analog (M3), pirenzepine (M1) and gallamine (M2) inhibited carbachol-induced 14CAP uptake with IC50 of 50 nM, 10 microM and > 100 microM, respectively. Thioperamide-induced 14CAP uptake was also inhibited by hexa-sila-difenidol p-fluoro analog and pirenzepine with IC50 of 90 nM and 12 microM, respectively; whereas gallamine had no effect. [3H]-N-methylscopolamine binding to isolated parietal cells was inhibited by atropine and pFHHSiD with IC50 of 15 nM and 132 nM, respectively. Neither R(alpha)-MeHA nor thioperamide did affect this binding although a H3-receptor inhibitory effect was observed on carbachol-induced 14CAP uptake by the cells. These data support that H3-receptor activation inhibits M3-mediated cholinergic stimulation of acid secretion through mechanisms operating downstream to the receptors sites.
Sachiyo Nomura - One of the best experts on this subject based on the ideXlab platform.
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a molecular signature of gastric metaplasia arising in response to acute parietal cell loss
Gastroenterology, 2008Co-Authors: Koji Nozaki, Masako Ogawa, Janice A Williams, Bonnie Lafleur, Ronny Drapkin, Jason C Mills, Stephen F Konieczny, Sachiyo NomuraAbstract:Background & Aims: Loss of gastric parietal cells is a critical precursor to gastric metaplasia and neoplasia. However, the origin of metaplasia remains obscure. Acute parietal cell loss in gastrin-deficient mice treated with DMP-777 leads to the rapid emergence of spasmolytic polypeptide/trefoil factor family 2 (TFF2)-expressing metaplasia (SPEM) from the bases of Fundic Glands. We now sought to characterize more definitively the pathway for emergence of SPEM. Methods: Emerging SPEM lineages in gastrin-deficient mice treated with DMP-777 were examined for immunolocalization of TFF2, intrinsic factor, and Mist1, and morphologically with electron microscopy. Emerging SPEM was isolated with laser-capture microdissection and RNA was analyzed using gene microarrays. Immunohistochemistry in mouse and human samples was used to confirm up-regulated transcripts. Results: DMP-777–induced SPEM was immunoreactive for TFF2 and the differentiated chief cell markers, Mist1 and intrinsic factor, suggesting that SPEM derived from transdifferentiation of chief cells. Microarray analysis of microdissected SPEM lineages induced by DMP-777 showed up-regulation of transcripts associated with G1/S cell-cycle transition including minichromosome maintenance deficient proteins, as well as a number of secreted factors, including human epididymis 4 (HE4). HE4, which was absent in the normal stomach, was expressed in SPEM of human and mouse and in intestinal metaplasia and gastric cancer in human beings. Conclusions: Although traditionally metaplasia was thought to originate from normal mucosal progenitor cells, these studies indicate that SPEM evolves through either transdifferentiation of chief cells or activation of a basal cryptic progenitor. In addition, induction of metaplasia elicits the expression of secreted factors, such as HE4, relevant to gastric preneoplasia.
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emergence of spasmolytic polypeptide expressing metaplasia in mongolian gerbils infected with helicobacter pylori
Laboratory Investigation, 2007Co-Authors: Nao Yoshizawa, James R. Goldenring, Sachiyo Nomura, Yoshiharu Takenaka, Hirokazu Yamaguchi, Tsukamoto Tetsuya, Harunari Tanaka, Masae Tatematsu, Michio KaminishiAbstract: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 adenocarcinoma, but the presence of SPEM has not been studied in gerbils. We therefore have sought to examine the development of metaplastic mucosal changes in Hp-infected Mongolian gerbils. Mongolian gerbils were assigned to either uninfected controls or infected with Hp at 17 weeks of age. The animals were killed at 17, 20, 26, 31, 41 and 56 weeks of age. Stomach sections were stained using antibodies for TFF2, intrinsic factor, H/K-ATPase, BrdU and MUC2. Dual immunofluorescence staining for TFF2 with intrinsic factor and for TFF2 with MUC2 was performed. In uninfected animals, no SPEM or intestinal metaplasia was observed. Infected gerbils developed SPEM initially in the intermediate zone along the lesser curvature and subsequently spread out towards the greater curvature. In the earlier stages of infection, SPEM Glands demonstrated TFF2 and intrinsic factor double staining cells. However, after 35 weeks of infection, the number of double staining SPEM cells decreased. While early in infection SPEM organized in straight Glands, in the later stages of infections, SPEM Glands became distorted or dilated along with the development of gastritis cystica profunda that was TFF2 positive. Goblet cell intestinal metaplasia developed only late in the infection. Dual staining for TFF2 and MUC2 showed Glands containing both SPEM- and MUC2-positive goblet cell intestinal metaplasia. SPEM develops early in Hp infection in Mongolian gerbils, and alterations in gland morphology arise from SPEM Glands during the course of gastric infection with goblet cell intestinal metaplasia developing subsequent to SPEM.
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evidence for repatterning of the gastric Fundic epithelium associated with menetrier s disease and tgfα overexpression
Gastroenterology, 2005Co-Authors: Robert J. Coffey, Sachiyo Nomura, Stephen H. Settle, Charles M. Leys, Anna L. Means, Richard M. Peek, Steven D. Leach, James R. GoldenringAbstract:Background & Aims: Increase of intramucosal transforming growth factor α (TGFα) levels in the gastric fundus leads to oxyntic atrophy and massive foveolar hyperplasia in both metallothionein (MT)-TGFα mice and patients with Menetrier's disease. We have evaluated the hypothesis that increased levels of TGFα in the fundus induces an antral pattern of cell differentiation in Fundic Glands by studying Pdx1, a transcription factor whose expression normally is confined to the gastric antrum. Methods: Induction of Pdx1 expression was evaluated in Pdx1 lacZ/+ /MT-TGFα bigenic mice treated with zinc. The distribution of Pdx1 in MT-TGFα mice and Menetrier's disease patients was evaluated with anti-Pdx1 antibodies. Transcript levels were evaluated by quantitative polymerase chain reaction in mouse and human tissues and AGS cells. Results: In Pdx1 lacZ/+ mice, Pdx1 was expressed in antral mucosal cells including gastrin cells and TFF2-expressing deep glandular mucous cells. Zinc treatment for 2 to 8 weeks in Pdx1 lacZ/+ /MT-TGFα transgenic mice resulted in expression of Pdx1 throughout the fundus. No ectopic Fundic Pdx1 expression was observed in either H felis -infected or DMP777-treated mice. In MT-TGFα mice, 8 weeks of zinc treatment elicited nuclear Pdx1 staining throughout the Fundic mucosa. TGFα treatment in AGS cells led to increases in Pdx1 and gastrin messenger RNA expression. Fundic sections from Menetrier's disease patients showed nuclear Pdx1 staining throughout the Fundic Glands. Treatment of a Menetrier's disease patient with an anti-epidermal growth factor receptor monoclonal antibody reduced Fundic expression of both Pdx1 and gastrin. Conclusions: Overexpression of TGFα in MT-TGFα mice and Menetrier's disease patients elicits ectopic expression in the fundus of Pdx1, consistent with the phenotype of antralization.
