• The Journal of Internal Korean Medicine
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• v.40 no.4
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• pp.697-708
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• 2019

Objective: The aim of this study was to introduce gastric dysmotility as a common cause in patients with concurrent functional dyspepsia and chronic atrophic gastritis. Method: Dyspeptic symptoms, the Rydoraku score, gastric motility (electrogastrography, bowel sound analysis), gastric mucosa (gastroendoscopy), and blood and blood chemistry were all evaluated. For the treatment method, Pyengwi-san (solution) and Banwhasashim-tang (extract) were used as herbal drugs. Both ST36 electrical stimulation and simple immersion stimulation of CV11, 12, and 13 in the abdomen were applied. Results: Dyspeptic symptoms including indigestion, headache, and insomnia were all relieved. Gastric myoelectrical activity and gastric pyloric function were additionally improved. The condition of the gastric mucosa was changed from atrophic to erosive. Other side-effects of the treatment were not noted. Conclusion: The traditional Korean treatment showed effectiveness in the relief of dyspeptic symptoms and mucosal improvement of chronic atrophic gastritis. Gastric dysmotility is a common cause of the condition being concurrent with both functional dyspepsia and chronic atrophic gastritis without Helicobacter pylori infection.

• Journal of Physiology & Pathology in Korean Medicine
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• v.31 no.5
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• pp.255-263
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• 2017

This article is for understanding relations between the classifications of gastritis and syndrome differentiation types of Korean Medicine through research on syndrome differentiations of clinically applied gastritis and literature of Korean Medicine. Clinical papers were searched in China Academic Journals(CAJ) of China National Knowledge Infrastructure(CNKI) from 1995 to 2015. Conclusions are as follows. First, disease mechanism of chronic gastritis are qi stagnation, damp stagnation, heat obstruction, blood stasis obstruction, yin damage, damage to collaterals with healthy qi deficiency and pathogenic qi. And qi movement stagnation is shown through the status of chronic gastritis. Second, chronic superficial gastritis belongs to qi aspect syndrome and mainly pathogen excess syndrome. And the key mechanisms are congestion and disharmony of stomach qi sometimes combined with liver depression, food accumulation and dampness-heat. Third, chronic atrophic gastritis belongs to qi-blood syndrome and deficiency-excess complex syndrome with the root of spleen qi deficiency and stomach yin deficiency and the tip of blood stasis, qi stagnation. And key mechanism is damage to collaterals with healthy qi deficiency and toxin-blood stasis. Forth, pathogen excess syndromes are shown at the early stage of chronic gastritis and healthy qi deficiency syndromes after the middle stage. Qi deficiency is shown at the beginning of the disease and yin deficiency at the late stage. And qi deficiency is related with superficial gastritis and yin deficiency with atrophic gastritis.

• Journal of Veterinary Clinics
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• v.33 no.5
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• pp.286-289
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• 2016

Two dogs (Case 1: Poodle, 4 years old, spayed female; Case 2: Bulldog, 3 years old, intact female) were referred to us for treatment of vomiting; Case 1 had a history of acute vomiting that started 1 day prior to presentation, and Case 2 had a history of chronic vomiting that started 2 years prior to presentation. The vomiting did not respond to medication in the local animal hospital. Results from abdominal ultrasound examinations showed that case 1 had gastric wall thickening, and case 2 had no remarkable findings. For both cases, we performed gastrointestinal endoscopic examinations, and several biopsy samples were obtained from different gastric areas. On the basis of the results of histopathological examinations, both dogs were diagnosed with atrophic gastritis concurrent with a Helicobacter infection. Clinical signs improved after antibiotic therapy. This case report describes the clinical, endoscopic, and histopathological findings of atrophic gastritis concurrent with a Helicobacter infection.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.7
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• pp.2999-3001
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• 2015

Background: This study aimed to evaluate upper gastrointestinal polyps detected during esophago-gastroduodenoscopy tests. Materials and Methods: We conducted a retrospective analysis on data regarding 55,987 upper gastrointestinal endoscopy tests performed at the endoscopy unit of Istanbul Education and Research Hospital between January 2006 and June 2012. Results: A total of 66 upper gastrointestinal polyps from 59 patients were analyzed. The most common clinical symptom was dyspepsia, observed in 41 cases (69.5%). The localizations of the polyps were as follows: 29 in the antrum (43.9%), 15 in the corpus (22.7%), 11 in the cardia (16.7%), 3 in the fundus (4.54%), 3 in the second portion of the duodenum (4.54%), 2 in the bulbus (3.03%) and 3 in the lower end of the esophagus (4.54%). Histopathological types of polyps included hyperplastic polyps (44) (66.7%), faveolar hyperplasia (8) (12.1%), fundic gland polyps (4) (6.06%), squamous cell polyps (4) (6.06%), hamartomatous polyps (3) (4.54%), and pyloric gland adenoma (3) (4.54%). Histopathological analysis of the gastric mucosa showed chronic atrophic gastritis in 30 cases (50.84%), HP infection in 33 cases (55.9%) and intestinal metaplasia in 19 cases (32.20%). In 3 cases with multiple polyps, adenocarcinoma was detected in hyperplastic polyps. Conclusions: Among polypoid lesions of the upper gastrointestinal tract, the most common histological type is hyperplastic polyps. Generally, HP infection is associated with chronic atrophic gastritis and intestinal metaplasia. The incidence of adenocarcinoma tends to be higher in patients with multiple hyperplastic polyps.

• Journal of Gastric Cancer
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• v.2 no.2
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• pp.73-80
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• 2002

In spite the fact that H. pylori infection might be the causative organisms of acute and chronic gastritis, peptic ulcer diseases and the definition as the class I carcinogen by WHO IARC, still debates exist about the relationship between H. pylori and gastric carcinogenesis. Epidemiological and animal studies demonstrated a link between gastric cancer and chronic infection with H, pylori, but the exact mechanism responsible for the development of gastric cancer in H. pylori-infected patients still remain obscure. In order to declare the clear association, definate evidences like that decrement in the incidence of gastric cancer after the eradication of H. pylori in designated area compared to noneradicated region or the blockade of specific mechanism acting on the carcinogenesis by H. pylori infection. The other way is to identify the upregulating oncogenes or downregulating tumor suppressor genes specifically invovled in H. pylori-associated carcinogenesis. For that, we established the animal models using C57BL/6 mice strain. Already gastric carcinogenesis was developed in Mongolian gerbils infected with H. pylori, but there has been no development of gastric cancer in mice model infected with H. pylori after long-term evaluation. Significant changes such as atrophic gastritis were observed in mice model. However, we could observe the development of mucosal carcinoma in the stomach of transgenic mice featuring the loss of TGF-beta sig naling by the expressions of dominant negative forms of type II receptor specifically in the stomach. Moreover, the incidence of gastric adenocarcinoma was significantly increased in group administered with both MNU and H. pylori infection than MNU alone, signifying that H. pylori promoted the gastric carcinogenesis and there might be host susceptibility genes in H. pylori-associated gastric carcinogenesis. Based on the assumption that chronic, uncontrolled inflammation might predispose to carcinogenesis, there have been several evidences showing chronic atrophic gastritis predisposed to gastric carcinogenesis in H. pylori infection. Although definite outcome of chemoprevention was not drawn after the longterm administration of anti-inflammatory drug in H. pylori infection, the actual incidence of atrophic gastritis and molecular evidence of chemoprevention could be obtained. Selective COX-2 inhibitor was effective in decreasing the development of gastric carcinogenesis provoked by H. pylori infection and carcinogen like in chemoprevention of colon carcinogenesis.

• Journal of Gastric Cancer
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• v.7 no.1
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• pp.38-41
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• 2007

Increased risk of gastric cancer has been reported in patients with chronic atrophic gastritis that develops in conjunction with pernicious anemia. We report here a case of a gastric adenocarcinoma associated with pernicious anemia. A 40-year-old female patient had been diagnosed with anemia 6 years earlier at a local hospital. One month ago, she visited our hospital for aggravated dizziness and newly developed epigastric soreness. Her blood hemoglobin level was 4.2 g/dl, and a gastroscopic work-up for anemia discovered a 2.5-cm-sized, slightly elevated mucosal lesion at the anterior wall of the high body in the stomach. The biopsy of this lesion revealed a moderately-differentiated adenocarcinoma. She underwent a total gastrectomy with a Roux en Y esophagojejunostomy with D2 lymph node dissection. The final stage of the gastric carcinoma was identified as T1N0M0. Based on this experience, we recommend that a follow-up gastroscopy be performed in patients with pernicious anemia with atrophic gastritis because of the increased risk of gastric cancer in patients with pernicious anemia.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.9
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• pp.5199-5205
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• 2013

Background/Aim: The Hippo signaling pathway is a newly discovered and conserved signaling cascade, which regulates organ size control by governing cell proliferation and apoptosis. This study aimed to investigate its effects in human gastric cancer. Methods: Tumor tissues (n=60), adjacent non-tumor tissues (n=60) and normal tissues (n=60) were obtained from the same patients with primary gastric cancer (GC). In addition, 70 samples of chronic atrophic gastritis (CAG) tissues were obtained from patients with intestinal metaplasia (IM) by endoscopic biopsy. Hippo signaling molecules, including Mst1, Lats1, YAP1, TAZ, TEAD1, Oct4 and CDX2, were determined by quantitative polymerase chain reaction (qPCR). Protein expression of Mst1, Lats1, YAP1, TEAD1 and CDX2 was assessed by immunohistochemistry and Western blotting. Results: Mst1, Lats1 and Oct4 mRNA expression showed an increasing tendency from GC tissues to normal gastric tissues, while the mRNA expression of YAP1, TAZ and TEAD1 was up-regulated (all P<0.01). Mst1 and Lats1 protein expression presented a similar trend with their mRNA expression. In addition, YAP1 and TEAD1 protein expression in GC was significantly higher than in the other groups (all P<0.01). CDX2 mRNA and protein expression in the CAG group were higher than in the other groups (all P<0.01). In GC, mRNA expression of Mst1, Lats1, Oct4, YAP1, TAZ, TEAD1 and CDX2 had a close correlation with lymphatic metastasis and tumor TNM stage (all P<0.01). Furthermore, protein expression of Mst1, Lats1, YAP1, TAZ, TEAD1 and CDX2 had a close correlation between each other (P<0.05). Conclusion: The Hippo signaling pathway is involved in the development, progression and metastasis of human gastric cancer. Therefore, manipulation of Hippo signaling molecules may be a potential therapeutic strategy for gastric cancer.

• The Korean Journal of Nuclear Medicine
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• v.39 no.6
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• pp.456-463
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• 2005

Purpose: we often find variable degrees of FDG uptake and patterns in stomach, which can make difficult to distinguish physiologic uptake from pathologic uptake on FDG PET. The purpose of this study was to find out the significant findings of stomach on FDG PET. Materials and Methods: Thirty-eight patients who underwent both FDG PET and endoscopy within one week from Jun. 2003, to Aug. 2004 were included in this study. We reviewed 38 patients (18 for medical check up, 15 for work up of other malignancies, and 5 for the evaluation of stomach lesion). Their mean age was 56 years old (range:$32{\sim}79$), men and women were 28 and 10, respectively. Two nuclear physicians evaluated five parameters on FDG PET findings of stomach with a consensus: 1) visual grades 2) maximum SUV (max.SUV) 3) focal 4) diffuse and S) asymmetric patterns. We correlated the lesions of FDG PET findings of stomach with those of endoscopy. We considered more than equivocal findings on FDG PET as positive. Results: The six of 38 patients were proven as malignant lesions by endoscopic biopsy and others were inflammatory lesions (ulcer in 3, chronic atrophic gastritis in 12, uncommon forms of gastritis in 5), non-inflammatory lesions (n=3), and normal stomach (n=9). By the visual analysis, malignant lesions had higher FDG uptake than the others. The max.SUV of malignant lesions was $7.95{\pm}4.83$ which was significantly higher than the other benign lesions ($2.9{\pm}0.69$ in ulcer, $3.08{\pm}1.2$ in chronic atrophic gastritis, $3.2{\pm}1.49$ in uncommon forms of gastritis (p=0.044)). In the appearance of stomach on FDG PET, malignant lesions were shown focal (5 of 6) and benign inflammatory lesions were shown diffuse (9 of 20) and asymmetric (14 of 20). Benign lesions and normal stomach were shown variable degrees of uptake and patterns. Some cases of benign inflammatory lesions such as ulcer and gastritis were shown focal and mimicked cancerous lesion (4 of 15). Conclusion: Gastric malignant lesions had higher FDG uptake and focal pattern. However, benign inflammatory lesions had moderate degrees of uptake and diffuse and asymmetric patterns rather than focal. It is difficult to differentiate between benign lesions including normal.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.11 no.sup1
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• pp.83-92
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• 2008

Helicobacter pylori is the causative agent of chronic gastritis and has a role in the pathogenesis of peptic ulcer diseases, and gastric cancer. There have been reports suggesting a close link between these gastroduodenal disorders and a state of vitamin C deficiency. In this paper, the past, present and future perspectives on H. pylori infection and vitamin C will be discussed under the following view points. Since the ecological niche of H. pylori is the mucus layer and intercellular junctions of the gastric epithelium, the various kinds of host inflammatory cells motivated by the local and systemic immune responses cannot eliminate the microorganisms. When the invading foreign body is not removed, despite full activation of defense mechanisms, adverse consequences of the immune responses develop on the host gastric mucosa. The reasons for the body vitamin C depletion could be explained as follows; 1) the increased vitamin C consumption by increased oxygen free radical production through the prolonged hypersensitivity reactions in the gastric mucosa, 2) the increased vitamin C oxidation by the nitrite which is formed from nitrate reduction by the intragastric bacteria proliferated in the hypochlorhydric gastric cavity, 3) the strong ${\gamma}$-glutamyltranspeptidase activity of H. pylori which depletes the glutathiones in gastric mucosa. Depletion of glutathiones in the stomach favors irreversible oxidative destruction of ascorbic acid. Both persistent inflammatory burdens in the stomach by H. pylori and resultant vitamin C depletions synergistically and uninhibitedly might aggravate the hypothetical sequence of gastric carcinogenesis: atrophic gastritis${\rightarrow}$intestinal metaplasia${\rightarrow}$dysplasia${\rightarrow}$gastric adenocarcinoma. High intake of vitamin C could reverse the hypothetical sequence of the gastric carcinogenesis via direct and indirect effects on H. pylori and host-parasite relationships.

• Journal of Gastric Cancer
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• v.5 no.3 s.19
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• pp.158-162
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• 2005

Purpose: In order to clarify the carcinogenesis mechanism from chronic atrophic gastritis toward gastric cancer, we measured the pepsinogen I and II and compared their ratio with several clinical findings. Materials and Methods: We measured the preoperative serum pepsinogen I and II by using a radio-immunoassay and compared their ratio with several clinical findings, such as tumor size, mucinous vs non-mucinous tumor, cell differentiation, tumor location, depth of invasion, lymph-node status, Lauren's classification, and peritumoral atrophy in 103 consecutive patients with gastric adenocarcinomas who had received resections at Bundang CHA Hospital during the period from July 2003 to February 2005. Results: There were significant differences in the serum pepsinogen I/II ratio between patients with mucinous vs non-mucinous tumors (n=4 vs 9 and mean pep I/II=1.29 vs. 2.99, p=0.0288), with tumor size more than and less than $10cm^2$ (n=55 vs. 48 and mean pep I/II=2.64 vs. 3.24, p=0.0491), and with or without peritumoral atrophy (n=94 vs. 9 and mean pep I/II=2.83 vs. 3.89, p=0.0466). In patients with peritomoral atrophy, the pepsinogen I/II ratio was also lower in larger tumors (n=48 vs. 46 and mean pep I/II=2.44 vs. 3.23, p=0.0083). Well-differentiated carcinomas showed significantly lower serum pep I/II ratios than signet-ring-ceil types. There was no correlation between serum pep I/II ratio and tumor location, depth of invasion, lymph-node status, or Lauren's classification Conclusion: We proved the existence of a correlation between serum pepsinogen level and musosal atrophy, but these results are not sufficient for clinical application of serum pepsinogen level as a screening tool for gastric cancer.