In this study, Albis (containing ranitidine, sucralfate, and bismuth) prevented the gastric mucosal injury provoked by long-term use of ASA. There was no development of peptic ulcer in either of the groups during the study period. This might be due to the study period being too short to allow peptic ulcer to develop by the use of low-dose ASA. However, gastric mucosal injury measured by the MLS developed, but was reduced by concomitant use of Albis. Although several studies have reported the efficacy of PPIs or H2RAs in the prevention of peptic ulcer and gastric mucosal injury caused by ASA, there is no report of the efficacy of fixed-dose combination of H2RA, sucralfate, and bismuth [3,7,11,14-17]. This is the first prospective trial to evaluate the efficacy of combination of H2RA, sucralfate, and bismuth for the prevention of peptic ulcer or gastric mucosal injury due to long-term use of lowdose ASA ...

TY - JOUR. T1 - Ii-CS on gastric epithelial cells interacts with CD44 on T cells and induces their proliferation. AU - Barrera, C. A.. AU - Chan, T.. AU - Crowe, S. E.. AU - Ernst, P. B.. AU - Reyes, Victor. PY - 2003. Y1 - 2003. KW - CD44. KW - Gastric epithelial cell. KW - H. pylori. UR - http://www.scopus.com/inward/record.url?scp=0038579613&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0038579613&partnerID=8YFLogxK. M3 - Article. VL - 987. SP - 285. EP - 287. JO - Annals of the New York Academy of Sciences. JF - Annals of the New York Academy of Sciences. SN - 0077-8923. ER - ...

We have shown that contact with H. pylori rapidly activates ERK1, ERK2, p38, JNK p46, and JNK p54 MAP kinases in AGS gastric epithelial cells. We also find that H. pylori cag+ strains are more potent than cag− strains in inducing MAP kinase activation. Differential MAP kinase activation by cag+ and cag−H. pylori strains is particularly evident for JNK phosphorylation and appears to be dependent upon genes within the cag pathogenicity island. Inhibitors of p38 and MEK1 MAP kinases prevent H. pylori-induced IL-8 production. However, p38 and MEK1 MAP kinase activity do not appear to be essential for H. pylori-induced NF-κB activation.. H. pylori has adapted to interact specifically with gastric-type epithelial cells. H. pylori infection is limited to areas of the gastrointestinal tract that are lined by gastric epithelium, and the bacterium is known to activate several gastric epithelial cell signaling events. Previous studies have shown that adherence of H. pylori to AGS gastric epithelial ...

The HGT-1 human gastric cell line is similar to acid secreting parietal cells in that it possesses H2 receptors, histamine sensitive adenyl cyclase, and Cl- channels, which are activated by histamine by a cyclic adenosine monophosphate (cAMP) dependent mechanism. To discover if HGT-1 cells have additional properties found in parietal cells, [3H]omeprazole and patch clamp recording techniques were used to evaluate specific omeprazole binding sites and K+ channels in the plasma membrane. HGT-1 cells exhibited [3H]omeprazole binding in the non-stimulated state, which increased 100% in the presence of 1 mM histamine. High conductance (about 155 pS) K+ channels were active spontaneously in 17% of cell attached or excised inside out patches in non-stimulated subconfluent HGT-1 cells. In inside out patches, channel activity increased fivefold during depolarisation, ion substitution experiments confirmed that the channels were highly selective for K+, and channel activity was almost abolished by removal ...

The isolation of Helicobacter pylori from the human gastric mucosa in 1982 and the demonstration of its involvement in gastritis, peptic ulcer disease and gastric adenocarcinomas have radically changed our perception of these diseases. H. pylori is a small, spiral, gram-negative bacillus that appears to inhabit the mucous layer overlying the gastric epithelial cells in humans. It produces a potent urease, which, by producing ammonia, may help to neutralize gastric acid, but the mechanism by which the bacteria produces gastric inflammation is not clear as it does not invade the mucosa. Development of atrophy and metaplasia of the gastric mucosa are strongly associated with H. pylori infection. Oxidative and nitrosative stress in combination with inflammation plays an important role in gastric carcinogenesis. More. Last updated: 25 Janury 2008. ...

Ethanol, after intragastric administration, penetrates deeply into the gastric mucosa because of high lipid solubility and, at concentrations of 50-100%, causes microvascular damage and hemorrhagic lesions (23, 34, 37, 38, 41). Ethanol-induced injury to the gastric mucosa is a time-related process in which disruption or exfoliation of the gastric surface epithelium is followed by necrosis of deeper mucosal layers, including the mucosal proliferative zone and the microvasculature (23,37, 38, 41). Angiogenesis is a prerequisite for the healing of ethanol-induced deep gastric mucosal damage. Our previous study has shown that ethanol-induced injury to gastric mucosa triggers an angiogenic response as well as an increase in bFGF, a known angiogenic factor, in the mucosa bordering necrosis (36, 39).. The present study demonstrates for the first time that ethanol-induced injury to the gastric mucosa activates VEGF gene expression as reflected by increases in VEGF at both the transcriptional and ...

Visualizing the mucosal surface may require using forceps to hold the specimen open (Fig. 19), unlike the specimens pictured in the other gross photographs. Histology shows marked thickening and fibrosis of the lamina propria, submucosa, and muscularis propria (Fig. 20). (Compare the normal histology in Fig. ) Fig. 19 Stricture of the esophagus, fresh specimen 44 Fig. 20 Histology of stricture (H & E, ×20) B. Gorman 2 Histologic Anatomy 45 Inlet Patch The inlet patch is characterized by ectopic gastric mucosa that is surrounded by normal squamous mucosa (Fig. A b Fig. 21 (a) Inlet patch (H & E, ×40). The mucosa on the left side of this photomicrograph shows essentially normal gastric mucosa with foveolar and glandular epithelium. The mucosa on the right shows normal esophageal squamous epithelium. (b) Inlet patch (H & E, ×200). On higher power, the gastric mucosa of the inlet patch is identical to that seen in the stomach, with foveolar epithelium overlying gastric glands composed of mucus ...

Bullfrog tadpole stomachs of various metamorphic stages were examined to determine the fine-structural development of oxyntic cells and to correlate observed morphological development with the capacity to secrete HCl. It was found that in vitro tadpole stomachs can consistently be stimulated to secrete acid by stage XXIV of metamorphosis, when tail reabsorption is nearly complete. Concomitant with the appearance of HCl secretion, identifiable oxyntic cells were found in the gastric glands.. Prior to stage XXIV (stages XXI and XXII) the majority of cells present in the developing gastric glands exhibit features of cytological organization characteristic of undifferentiated cells: large nuclei, relatively scantry cytoplasm, and numerous ribosomal particles within the cytoplasmic matrix. The newly differentiated oxyntic cells of stage XXIV tadpole stomachs are recognizable by the accumulation of tubular members of the smooth-surfaced endoplasmic reticulum in the apical portion of the cells. These ...

Lawson R. Thoracoabdominal duplication cyst containing heterotopic gastric mucosa: report of a case. J Am Osteopath Assoc 1968;67(11):1292. doi: .. Download citation file:. ...

Chem Biol Interact. 2009 Aug 14;180(3):499-505. doi: 10.1016/j.cbi.2009.04.006. Epub 2009 May 3. Research Support, Non-U.S. Govt

Helicobacter pylori (H. pylori) is implicated in human gastric mucosa. Fork head box M1 (FoxM1), the key positive regulator of cell proliferation is overexpressed in gastric cancer. MicroRNAs are important post-transcriptional regulators of gene expression. In this study, we explored the effect of H. pylori infection on FoxM1 expression and possible mechanisms. The expression of FoxM1 was gradually increased in human gastric specimens from inflammation to cancer. FoxM1 was time- and concentration-dependently upregulated in gastric epithelial-derived cell lines infected with H. pylori. CagA, the key virulence factor of H. pylori, was associated with increasing FoxM1 expression. H. pylori and CagA inhibited the expression of P27Kip1 (cylcin-dependent kinase inhibitor 1B, CDKN1B) and promoted cell proliferation by upregulating FoxM1. The expression of hsa-miR-370 was decreased in human gastritis and gastric cancer. FoxM1 was directly downregulated by hsa-miR-370 in gastric cell lines. H. pylori and ...

Indomethacin (IND) is an extensively used drug. However, it provokes aggressive ulcerogenic potential. Chamomile is a widely used as natural herb with a powerful antioxidant activity. This study aims to assess the effects of chamomile flowers extract (CFE) in IND induced peptic ulcer (PU). Fifty rats classified to five groups; control, ulcer, and pretreated groups with CFE (200 mg/kg), pretreated with ranitidine RAN (50 mg/kg), and pretreated with CFE+RAN for 14 days pre-ulcer induction. Pretreatment with CFE and/or RAN significantly decreased ulcer index, gastric acidity, pepsin activity, gastric oxidative stress biomarkers, serum anti-inflammatory cytokines, and histopathological changes induced by IND. The pretreated groups significantly elevated gastric enzyme antioxidant activity, mucin content and gastric mucosal prostaglandin E2 with comparison to IND group. Pretreatment with CFE+RAN displayed the most gastroprotective effects compared with pretreated with either CFE or RAN alone. ...

Wound-healing of the gastric mucosa is suggested to be stimulated by hepatocyte growth factor (HGF). Polyamines are shown to contribute to repair after damage in the gastric mucosa. The present study was designed to elucidate whether HGF can stimulate wound-healing of the gastric mucosa via polyamin …

Investigations on gastric mucosal protective mechanisms are focused mainly on the local mucosal processes. Much less is known about how the central nervous system may influence the gastric mucosal defense. However, gastric mucosal protection induced by a central mechanism was described recently (Tache et al., 1994; Gyires, 1997;Guidobono et al., 1998; Kaneko et al., 1998; Yang et al., 1999). In our present study, the role of central opioid receptors was analyzed by means of selective δ- and μ-opioid receptor agonists. It was found that both the selective δ- and μ-opioid receptor agonists injected either i.c.v. or i.c. exerted protective effect against acidified ethanol-induced lesions; the rank order of potency was β-endorphin , DAGO , DADLE , deltorphin II , DPDPE following i.c.v. injection and deltorphin II , β endorphin , DPDPE , DAGO , DADLE following i.c. administration. The results suggest that activation of supraspinal δ- and μ-opioid receptors may induce gastric mucosal ...

Dr. Donald Colantino answered: Gastritis: This should resolve with the taking of prolosec type medication. However I feel that its...

Academic Journals Database is a universal index of periodical literature covering basic research from all fields of knowledge, and is particularly strong in medical research, humanities and social sciences. Full-text from most of the articles is available. Academic Journals Database contains complete bibliographic citations, precise indexing, and informative abstracts for papers from a wide range of periodicals.

Endothelial nitric oxide synthase (eNOS) has previously been detected in the glandular part of the human gastric mucosa. Furthermore, nitric oxide (NO) has been shown to influence gastric secretion in various animal models. The present study was cond

Hydrogen has been reported to relieve damage in many disease models, and is a potential additive in drinking water to provide protective effects for patients as several clinical studies revealed. However, the absence of a dose-response relationship in the application of hydrogen is puzzling. We attempted to identify the dose-response relationship of hydrogen in alkaline electrolyzed drinking water through the aspirin induced gastric injury model. In this study, hydrogen-rich alkaline water was obtained by adding H2 to electrolyzed water at one atmosphere pressure. After 2 weeks of drinking, we detected the gastric mucosal damage together with MPO, MDA and 8-OHdG in rat aspirin induced gastric injury model. Hydrogen-dose dependent inhibition was observed in stomach mucosal. Under pH 8.5, 0.07, 0.22 and 0.84 ppm hydrogen exhibited a high correlation with inhibitory effects showed by erosion area, MPO activity and MDA content in the stomach. Gastric histology also demonstrated the inhibition of damage by

Mucosal prostaglandin E2 levels in patients with the gastric ulcer before and after their ulcers were healed. Both the antral and duodenal PG E2 are significant

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The duodenal surface epithelium shown here consists of absorptive cells with scattered goblet cells, in contrast to that of stomach which consists uniformly of surface mucous cells.. Note that Brunners glands lie beneath the muscularis mucosae, in the submucosa. Click on the rectangle for a magnified image of the intestinal epithelium, or.... ...

Dystrophic lesions of the gastric mucosa were observed to be formed and the pepsinogen content was reduced by 57% in the gastric mucosa of rats exposed to various experimental stressors...

The stomach mucosas epithelial lining consists only of surface mucus cells, which secrete a protective coat of alkaline mucus. A vast number of gastric pits dot the surface of the epithelium, giving it the appearance of a well-used pincushion, and mark the entry to each gastric gland, which secretes a complex digestive fluid referred to as gastric juice ...

Non-steroidal anti-inflammatory drugs (NSAIDs) can result in peptic ulcer disease (PUD) which is a common condition worldwide. The aim of this study was to evaluate the antiulcer properties of (1-(4-hydroxy-phenyl)-3-m-tolyl-propenone) (HPTP) chalcone in rats using indomethacin as ulcerogenic agent. None of the rats showed symptoms of kidney and liver toxicity during the term of the study. Administration of HPTP had decreased the acidity, increased gastric wall mucus and flattening of gastric mucosa and reducing erosive gastric damage area. HPTP also showed dose dependent increase in SOD, GPx activity and PGE2 level and decrease MDA. H & E stain showed decreased infiltration of leucocytes with edema of submucosal layer. PAS staining showed intense uptake of magenta color of gastric wall mucus in rats fed with HPTP, and immunohistochemical staining of gastric mucosa revealed over-expression of HSP70 protein, down-expression of Bax protein and over expression of TGF-β in rats administered with HPTP. This

Gastric gland: false-colour scanning electron micrograph (SEM) of the mucous membrane lining the stomach, showing the shadowy entrances to a number of gastric glands. The glands secrete gastric juice (hydrochloric acid & the enzyme pepsin) and a protective mucous, derived from the simple, columnar cells (moss-like) that comprise the mucosa. Gastric glands are formed by simple invagination or tubular ingrowth of this mucosa into the underlying layer of tissue, the lamina propria. Magnification: x300 at 6x7cm size. - Stock Image P510/0042

Definition of Ulcer Index in the Financial Dictionary - by Free online English dictionary and encyclopedia. What is Ulcer Index? Meaning of Ulcer Index as a finance term. What does Ulcer Index mean in finance?

Positive cells in gastric mucosa of ctsz2/2 (p = 0.009) and wt mice (p = 0.001). Compared to wt animals with no further increase in F4/80 positivity, ctsz2/2

BACKGROUND Antenatal exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) has been associated with renal dysgenesis in humans. METHODS These studies characterized cyclooxygenase-2 (COX-2) versus COX-1-selective inhibition on nephrogenesis in the rodent using histomorphometry, immunohistology, and in situ hybridization. RESULTS Administration of a COX-2-selective inhibitor (SC58236), started during pregnancy until weaning, significantly impaired development of the renal cortex and reduced glomerular diameter in both mice and rats. An identical phenotype was demonstrated in COX-2 -/- mice. In contrast to its effects on the developing kidney, a COX-2 inhibitor had no effect on glomerular volume in adult mice. This effect was specific for COX-2 because maternal administration of a COX-1-selective inhibitor (SC58560) did not affect renal development despite significantly inhibiting gastric mucosal prostaglandin E2 (PGE2) synthesis in pups. The expression of COX-2 immunoreactivity peaked in the first

Background Feeding alfalfa hay is often recommended for its buffering components, like protein and calcium, to prevent lesions of the gastric mucosa in horses. Until now, there has been no information...

Anti-oxidative Herbs and Indomethacin-Induced Rat Gastric Mucosal Lesions: Protection by GamiHyangsa-Yukgunja Heung Mook Shin (Acce...

We previously reported that gastrin induced PAI-2 in gastric epithelial cells via activation of PKC and RhoA, which in part triggered release of an unidentified paracrine mediator (11) . The present findings therefore extend these studies both by identification of H. pylori as a regulator of PAI-2 in gastric epithelial cells and by demonstration of the role of NFκB and of IL-8 and COX-2 as mediators of the response. It is well recognized that NFκB is activated by H. pylori and in turn leads to induction of IL-8 and COX-2 (28 , 33 , 34) . Less clear, however, are putative targets within the gastric epithelium that might mediate the progression to cancer and the integrative mechanisms that might account for differential cell signaling in tissues as complex as the gastric mucosa. The present observations indicate that PAI-2 should now be considered a putative target of NFκB activation by H. pylori. It seems, however, that the role of NFκB is limited to cells exposed directly to H. pylori and ...

The mucus-secreting columnar cells lining the luminal surface and the pits are joined near their free surfaces to each other by tight junctions (Ham l974). It is surmized that this arrangement forms one of the mechanisms by which the underlying layers are protected against luminal acid. The supranuclear portions of the cells just below their free surfaces contain dense, homogeneous, spherical or ovoid granules consisting of a type of mucigen (Bloom and Fawcett l975). Upon release into the lumen, the granules give rise to the layer of mucus that covers the luminal surface of the mucosa. In the cells of the gastric pits, the granules become progressively less abundant at deeper levels, and in the bottom of the pits they from only a thin layer immediately beneath the cell surface. Cells of this kind continue into the necks of the gastric glands. Under physiological conditions, the surface mucus cells are continuously desquamated into the lumen and are completely replaced every 3 days (Ham l974; ...

Adenosine is the endogenous agonist at all adenosine receptors. Under resting physiological conditions, adenosine levels in the interstitial fluid are between 30 and 300 nM (7). This is sufficient to activate A1, A2A, and A3 adenosine receptors whenever these proteins are abundantly expressed on the cell surface. The local adenosine level increases 10-fold during hypoxia and 100- to 1,000-fold in ischemia (7, 18, 34, 72), allowing cell responses mediated via A2BR in these settings. The pharmacological and functional studies presented here have been conducted using parietal cells obtained from normal rabbit gastric mucosa, which are representative populations of native, nontransformed primary cells at rest. They provide evidence that A2B is the adenosine receptor that is preferentially, if not exclusively, expressed on the parietal cell membrane and mediates acid production via Gs activation. Moreover, activation kinetics indicate that the A2BR might act at full power to activate acid production ...

In the GC cell lines, the level ofmiR-200a/b methylation decreased and the level of expression increased after demethylation. In the human gastric mucosa, the miR-200a/b methylation levels increased in the following group order: H. pylori-negative control group, H. pylori-positive control group, and H. pylori-positive GC group. Conversely, the miR-200a/b expression levels decreased in the same order. In the H. pylori-persistence group, no significant changes were observed in the methylation and expression levels of miR-200a/b after 6 months, whereas the level of methyla-tion decreased and the level of expression of miR-200a/b increased significantly 6 months in the H. pylori-eradication group ...

It must be assumed that some cause is operative in certain cases preventing the healing of defects in the gastric mucosa and is inoperative in others. Even though anhemolytic streptococci are present in practically all gastric ulcers, we cannot convince ourselves that these organisms have been proven as yet to be the factor which either initiates the ulceration or prevents healing. Nevertheless, the constant presence of streptococci in this type of lesion is a suggestive fact and further experiments to determine their significance are being undertaken. ...

The most common finding in this study is an inflammatory process of the gastric mucosa - gastritis.In fact, after 20 years it is present in almost everyone.More serious is the discovery of the plague.Its danger lies in the fact that it can bleed and even to break through the wall of the stomach completely.In the event of signs of complications held emergency EGD.Gastric ulcer, among other things, is able to regenerate a more serious disease.. Much more disturbing is the discovery in the stomach cavity of a tumor process.Unpleasant discovery is also a gastric polyp.If you find something similar or just inflamed mucous area with signs of changing the structure of the doctor, most likely, with the consent of the patient will take a biopsy.Later removal of tissue samples are sent to patotsitologicheskoe research.The result will allow to say exactly what is is one or the other a modified portion of the gastric mucosa.. ...

TYPE OF STAINING:Sialomucin that have acid and neutral mucopolysaccharides stain purple. Normal gastric mucosa will stain only with PAS(red), but intestinal metaplasia will stain purple ...

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History & Aims Gastric carcinoma is usually related mostly to infection, which disrupts the gastric mucosa turnover and elicits an epithelial-mesenchymal transition (EMT) and preneoplastic transdifferentiation. pattern, characterized by an early transient YAP1 nuclear accumulation and stimulated YAP1/TEAD transcription, followed by nuclear LATS2 up-regulation leading to YAP1 phosphorylation and targeting for degradation. LATS2 and YAP1 reciprocally positively regulate each others expression. Loss-of-function experiments showed that LATS2 restricts contamination engages a number of signaling cascades that alienate mucosa homeostasis, including the Hippo LATS2/YAP1/TEAD pathway. In the hostCpathogen conflict, which generates an inflammatory environment and perturbations Pterostilbene of the epithelial turnover and differentiation, Hippo signaling appears as a protective pathway, restricting the?lack of gastric epithelial cell identification that precedes gastric?carcinoma advancement. infections; ...

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What are the causes of gastritis?, Gastritis is a kind of inflammation of the stomach mucosa (inflammation). This means that the white blood cells accumulate i

T staging using MSCT and EUS.A. MSCT-T1 tumor: Transverse CT image shows an elevated lesion (arrow) of the gastric mucosa of the lesser curvature with a clear f

During the past decade, Helicobacter pylori has become recognized as one of the most common human pathogens, colonizing the gastric mucosa of almost all persons exposed to poor hygienic conditions from childhood. It also is often found, albeit with a ...

The Ulcer Index indicator is a TA tool that measures the risk considering both main factors, the depth and the duration of price fall.

Ulcer Index Indicator was developed by Peter Martin and Byron McCann in 1987. This is a volatility indicator that measures downside risk.

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Scientists have developed a new kind of tiny motor that can propel itself through acidic environments, such as the human stomach, without any external energy source, opening the way to a variety of medical and industrial applications.

The first complete mucosal support supplement of its kindMegaMucosa is the first complete mucosal support supplement of its kind, formulated to REBUILD a healthy mucosal barrier. MegaMucosa also contains dairy-free immunoglobulins clinically shown to support a healthy immune response in the mucosa and a state-of-the-art flavobiotic clinically shown to support microbial diversity and alleviate barr

MissD wrote:Hi all - I had my band out in 2009 - put on 30kgs. So had the sleeve done in nov 2013. Obviously there was quite a lot of time to heal in that 4 yrs

When did you all stop sleeping on your stomachs? I am 10 weeks and still do, but recently it had started to be periodically uncomfortable. I am curious when people started making the switch to a new position.