• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.6 no.2
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• pp.183-186
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• 2003

Prolapse gastropathy is not uncommon in adult, but is not reported yet in previously healthy children. A 3-year-old child came to our emergency room after a 1-day history of emesis episodes with coffee-ground hematemesis. During the endoscopic procedure, and the process of retching and vomiting was observed and a tense knuckle of gastric mucosa was seen to be forcefully and repeated prolapsed into the distal esophageal mucosa, and mucosal hematoma was found in the gastric fundus. Upper gastrointestinal study revealed no abnormality and 24 hour pH monitoring revealed no pathologic gastroesophageal reflux. Retching is thought to cause the forceful prolapse and induce subsequent trauma of gastric mucosa. This case illustrates that the episodes of vigorous retching and resultant gastric mucosa are now considered to be the cause of the hematemesis and epigastric pain in children.

• Korean Journal of Veterinary Pathology
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• v.5 no.1
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• pp.5-8
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• 2001

Prevalence of Helicobacter infection in pet dogs and positive relations between the presence of Helicobacter app. and gastritis were studied. Twenty-one dogs, which died of various disease, were referred from three animal hospitals and necropsied. Upon histopathological examination, Helicobacter-like organisms (HLO) were observed only in the gastric mucosa of 5 (23.5%) out of the 21 stomachs. The bacteria mainly colonized in the mucus, gastric pits, and the lumen of gastric glands. Regardless of HLO infection, there was mild to moderate lymphocytic infiltration in fundic and pyloric mucosa. Average gastritis scores of the group infected with HLO were 1.250${\pm}$0.214 and 1.833${\pm}$0.167 in the fundic and pyloric mucosa, whereas those of uninfected group were 1.000${\pm}$0.165 and 1.625${\pm}$0.239, respectively. Accordingly, we concluded that no association exists between HLO infection and gastritis.

• The Journal of Internal Korean Medicine
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• v.22 no.4
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• pp.589-599
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• 2001

Objective: This study was carried out to investigate the effects of Hyangsayukgunja-tang extract on indomethacin-induced gastric mucosal lesions of mice. Methods: To evaluate the effects of Hyangsayukgunja-tang extract and Misoprostol, the morphology of gastric mucosa, and the distribution of mucose cells, PNA(Peanut Agglutinin), ICAM(intercellular adhesion molecule), and apoptotic cells were observed. Hyangsayukgunja-tang extract and Misoprostol were intragastric injected to the test groups at hour 72 before and just before indomethacin treatment(HYT-J, HYT-72, M-J, M-72), while the INDO group was injected only with indomethacin and the control group was subcutaneously injected only with saline. Results: The gastric mucosal lesions incresed in the fundus and body of INDO group, but softened in HYT group and M group, the effects were more excellent in the HYT-72, M-72 groups than the HYT-J, M-J groups and in the HYT group than M group. The disappearance of surface and neck mucose cells were shown in INDO group, but softened in HYT group and M group. The mucosal configuration of HYT-72 group was the same as control group. The numerical increase of PNA positive reaction in cytoplasm of perietal cells were appeared in INDO group. The PNA positive reaction in HYT group and Miso-group were shown in surface mucous cells and microvilli of apical surface in chief cells as control group, and were the same as control group in all mucosa of HYT-72 group. The distribution of ICAM positive cells, increased in INDO group, but decreased in M-72 group, and were the same as control group in HYT-72 group. The apoptotic cells, increased noticeably in gastric mucosa of INDO group, decreased in HYT group and M group, and decreased noticeably in HYT-72 group. Conclusions: Hyangsayukgunja-tang extract had excellent effects on indomethacin-induced gastric mucosal lesions.

• Journal of Pharmaceutical Investigation
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• v.31 no.1
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• pp.27-35
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• 2001

To evaluate the site-specific permeation of aspalatone (acetylsalicylic acid maltol ester, AM) through gastrointestinal tract, the enzymatic degradation and permeation studies were carried out using gastric, duodenal and jejunal mucosae of rabbits. It was found that $15.2{\pm}11.4%$, $11.6{\pm}5.2$ and $0.8{\pm}0.6%$ of the donor dose of AM, salicylmaltol (SM) and aspirin (ASA) permeated through the upper gastric mucosa after 8 hr of permeation, respectively. After 8 hr of AM permeation, SM and ASA were measured to be $15.0{\pm}1.7$ and $2.6{\pm}0.8%$ of the dose in the donor solutions, respectively, and salicylic acid (SA) was not detected even after 6 hr, suggesting a very low gastric damage. For the gastric mucosa, the increase of donor dose from 100 to $1,000\;{\mu}g/ml$ increased the permeation flux dose-dependently (r=0.9905). For the duodenal and jejunal mucosae, however, AM was fully degraded into SM and SA due to the esterase activities within 30 min. AM and ASA were not detected in the receptor solution. This result indicates that AM is not a prodrug of ASA. Addition of potassium fluoride (0.5%) into the donor solution delayed the degradation of AM, but did not allow the permeation through duodenal mucosa even by the inhibition of esterase activity. The addition of $dimethyl-{\beta}-cyclodextrin$ and $2-hydroxypropyl-{\beta}-cyclodextrin$ (5%) into the donor solutions also did not show favorable effects on the permeation of AM through various mucosae. In comparison of permeation rates of AM and ASA through the upper gastric mucosa, the flux of ASA was 4.2 times faster than AM based on the molar concentration. ASA also was fully degraded in the donor solutions faced with duodenal and jejunal mucosae within 2 hr, and was not detected in the receptor solution, suggesting a slower metabolism compared with AM.

• Journal of Ginseng Research
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• v.38 no.1
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• pp.8-15
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• 2014

Helicobacter pylori-induced gastric inflammation includes induction of inflammatory mediators interleukin (IL)-8 and inducible nitric oxide synthase (iNOS), which are mediated by oxidant-sensitive transcription factor NF-${\kappa}B$. High levels of lipid peroxide (LPO) and increased activity of myeloperoxidase (MPO), a biomarker of neutrophil infiltration, are observed in H. pylori-infected gastric mucosa. Panax ginseng Meyer, a Korean herb medicine, is widely used in Asian countries for its biological activities including anti-inflammatory efficacy. The present study aims to investigate whether Korean Red Ginseng extract (RGE) inhibits H. pylori-induced gastric inflammation in Mongolian gerbils. One wk after intragastric inoculation with H. pylori, Mongolian gerbils were fed with either the control diet or the diet containing RGE (200 mg RGE/gerbil) for 6 wk. The following were determined in gastric mucosa: the number of viable H. pylori in stomach; MPO activity; LPO level; mRNA and protein levels of keratinocyte chemoattractant factor (KC, a rodent IL-8 homolog), IL-$1{\beta}$, and iNOS; protein level of phospho-$I{\kappa}B{\alpha}$(which reflects the activation of NF-${\kappa}B$); and histology. As a result, RGE suppressed H. pylori-induced mRNA and protein levels of KC, IL-$1{\beta}$, and iNOS in gastric mucosa. RGE also inhibited H. pylori-induced phosphorylation of $I{\kappa}B{\alpha}$ and increases in LPO level and MPO activity of gastric mucosa. RGE did not affect viable H. pylori colonization in the stomach, but improved the histological grade of infiltration of poly-morphonuclear neutrophils, intestinal metaplasia, and hyperplasia. In conclusion, RGE inhibits H. pyloriinduced gastric inflammation by suppressing induction of inflammatory mediators (KC, IL-$1{\beta}$, iNOS), MPO activity, and LPO level in H. pylori-infected gastric mucosa.

• Applied Microscopy
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• v.11 no.1
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• pp.21-28
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• 1981

Gastric xanthoma which is not a true neoplasm and clinically insignificant consists of the small yellowish lesion of the gastric mucosa, frequently of multiple occurrence. Histologically the lesion shows chronic superficial gastritis with intestinal metaplasia and occasional collections of foam cells within the lamina propria. Electron microscopically. the xanthoma, cells are composed of. lipid-laden histiocytes with. many autophagocytic Iysosomes surrounding the cytoplasmic lipid vacuoles. Many residual bodies are also noted. The pathogenesis of the gastric xanthoma is obscure, however it is thought that a previous focal lesion of the gastric mucosa may have been a factor. One case of gastric xanthoma is reported here and a brief review of literature is also made.

• The Journal of Korean Medicine
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• v.22 no.2
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• pp.84-93
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• 2001

This research was to find out the protective and healing effects of both the Jiguyangwi-tang and the Gamijiguyangwi-tang on the gastric mucosa injuries by cyclophosphamide. At first, Jiguyangwi-tang and Gamijiguyangwi-tang extract were administered to the mice before one week, and then integral administration of those two drugs(each herbal extract and cyclophosphamide) were followed for another one week, respectively. After finishing those treatments, I have examined the state of the both ulcer and inflammation on the damaged gastric mucosa cell and watched the level of proliferating cell nuclear antigen(PCNA), Bcl-2, and apoptosis. These results were as follows, 1. Gastric mucosa inflammation have more significantly reduced in groups of integral administration of Jiguyangwi-tang plus cyclophosphamide, Gamijiguyangwi-tang plus cyclophosphamide and cyclophosphamide then in group of single cyclophosphamide. 2. Gastric ulcer have been reduced in groups of integral administration of Jiguyangwi-tang plus cyclophosphamide, Gamijiguyangwi-tang plus cyclophosphamide and cyclophosphamide then in group of single cyclophosphamide. But the significance have not shown. 3. PCNA level have more significantly elevated in integral administration of Jiguyangwi-tang plus cyclophosphamide and Gamijiguyangwi-tang plus cyclophosphamide and cyclophosphamide then in group of single cyclophosphamide. 4. The significance of both apoptosis induction and bcl-2level have not noticed among all groups. 5. Between Jiguyangwi-tang and Gamijiguyangwi-tang, the differance of effect was not admitted in statistically From these results, it is suggested that Jiguyangwi-tang and Gamijiguyangwi-tang are useful medicines in protecting gastric inflammation and ulcer, that is gastrointestinal side-effect of cyclophosphamide. The preventing effect of Jiguyangwi-tang and Gamijiguyangwi-tang may be through the 'affecting the period of cell division', but not the inhibition of apoptosis.

• Clinical Endoscopy
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• v.56 no.1
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• pp.75-82
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• 2023

Background/Aims: The etiology of superficial non-ampullary duodenal epithelial tumors (SNADETs) remains unclear. Recent studies have reported conflicting associations between duodenal tumor development and Helicobacter pylori infection or endoscopic gastric mucosal atrophy. As such, the present study aimed to clarify the relationship between SNADETs and H. pylori infection and/or endoscopic gastric mucosal atrophy. Methods: This retrospective case-control study reviewed data from 177 consecutive patients with SNADETs who underwent endoscopic or surgical resection at seven institutions in Japan over a three-year period. The prevalence of endoscopic gastric mucosal atrophy and the status of H. pylori infection were compared in 531 sex- and age-matched controls selected from screening endoscopies at two of the seven participating institutions. Results: For H. pylori infection, 85 of 177 (48.0%) patients exhibited SNADETs and 112 of 531 (21.1%) control patients were non-infected (p<0.001). Non-atrophic mucosa (C0 to C1) was observed in 96 of 177 (54.2%) patients with SNADETs and 112 of 531 (21.1%) control patients (p<0.001). Conditional logistic regression analysis revealed that non-atrophic gastric mucosa was an independent risk factor for SNADETs (odds ratio, 5.10; 95% confidence interval, 2.44-8.40; p<0.001). Conclusions: Non-atrophic gastric mucosa, regardless of H. pylori infection status, was a factor independently associated with SNADETs.

• Proceedings of the Korean Nutrition Society Conference
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• 2003.10a
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• pp.71-71
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• 2003

• Journal of Gastric Cancer
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• v.13 no.4
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• pp.232-241
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• 2013

Purpose: Gastrokine 1 plays an important role in gastric mucosal defense. Additionally, the Gastrokine 1-miR-185-DNMT1 axis has been shown to suppress gastric carcinogenesis through regulation of epigenetic alteration. Here, we investigated the effects of Gastrokine 1 on DNA methylation and gastritis. Materials and Methods: Expression of Gastrokine 1, DNMT1, EZH2, and c-Myc proteins, and the presence of Helicobacter pylori CagA protein were determined in 55 non-neoplastic gastric mucosal tissue samples by western blot analysis. The CpG island methylation phenotype was also examined using six markers (p16, hMLH1, CDH1, MINT1, MINT2 and MINT31) by methylation-specific polymerase chain reaction. Histological gastritis was assessed according to the updated Sydney classification system. Results: Reduced Gastrokine 1 expression was found in 20 of the 55 (36.4%) gastric mucosal tissue samples and was closely associated with miR-185 expression. The Gastrokine 1 expression level was inversely correlated with that of DNMT1, EZH2, and c-Myc, and closely associated with the degree of gastritis. The H. pylori CagA protein was detected in 26 of the 55 (47.3%) gastric mucosal tissues and was positively associated with the expression of DNMT1, EZH2, and c-Myc. In addition, 30 (54.5%) and 23 (41.9%) of the gastric mucosal tissues could be classified as CpG island methylation phenotype-low and CpG island methylation phenotype-high, respectively. Reduced expression of Gastrokine 1 and miR-185, and increased expression of DNMT1, EZH2, and c-Myc were detected in the CpG island methylation phenotype-high gastric mucosa. Conclusions: Gastrokine 1 has a crucial role in gastric inflammation and DNA methylation in gastric mucosa.