http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : ( Kentaro Sugano ) (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
-
Should We Still Subcategorize Helicobacter pylori-Associated Dyspepsia as Functional Disease?
( Kentaro Sugano ) 대한소화기기능성질환·운동학회(구 대한소화관운동학회) 2011 Journal of Neurogastroenterology and Motility (JNM Vol.17 No.4
Functional dyspepsia is a group of disorders featuring symptoms believed to be derived from the stomach and duodenum such as upper abdominal discomfort, pain, postprandial fullness and early satiety. A key diagnostic requisite is the absence of organic, metabolic, or systemic disorders to explain "dyspeptic symptoms." Therefore, when peptic ulcer diseases (including scars), erosive esophagitis and upper gastrointestinal malignancies are found at endoscopic examinations, the diagnosis of functional dyspepsia is excluded. One notable exception, however, is Helicobacter pylori infection. According to the Rome III definition, H. pylori infection is included in functional dyspepsia. This is an obvious deviation from the diagnostic principle of functional dyspepsia, since H. pylori infection is a definite cause of mucosal inflammation, which affects a number of important gastric physiologies such as acid secretion, gastric endocrine function and motility. The chronic persistent nature of infection also results in more dramatic mucosal changes such as atrophy or intestinal metaplasia, the presence of which in the esophagus (Barrett`s esophagus) precludes the diagnosis of functional dyspepsia. Since careful endoscopic examination can diagnose reliably H. pylori infection not only in Japan but also in Western contries, it is now feasible and more logical to exclude patients with chronic gastritis caused by H. pylori infection as having dyspeptic symptoms. It is time to establish the Asian consensus to declare that H. pylori infection should be separated from functional dyspepsia. (J Neurogastroenterol Motil 2011;17:366-371)
-
( Hirotsugu Sakamoto ),( Hiroyuki Mutoh ),( Yoshimasa Miura ),( Miho Sashikawa ),( Hironori Yamamoto ),( Kentaro Sugano ) The Editorial Office of Gut and Liver 2013 Gut and Liver Vol.7 No.5
Background/Aims: SOX9 is a marker for stem cells in the intestine, and overexpression of SOX9 is found in gastric and colon cancer; however, the expression of SOX9 in non-ampullary duodenal adenoma and adenocarcinoma has not yet been evaluated. This study aimed to investigate SOX9 expression in nonampullary duodenal adenoma and adenocarcinoma by immunohistochemistry. Methods: We evaluated SOX9 expression in 43 clinical samples (nonam-pullary duodenal adenoma in 22 lesions and nonampullary duodenal adenocarcinoma in 21 lesions) resected under endoscopic mucosal resection or endoscopic submucosal dissection. Results: SOX9 was expressed in part of the base of the normal duodenal mucosa surrounding adenomas and adenocarcinomas. In contrast, SOX9-positive cells were found in more than half of the crypts from the bottom part of the crypt in all of the 43 samples. Moreover, in 15 adenoma samples (68.2%) and 19 carcinoma samples (90.5%), SOX9 was expressed in more than three-quarters of the crypts from the bottom part of the crypt. Conclusions: SOX9 is over-expressed in nonampullary duodenal adenoma and adeno-carcinoma in humans. (Gut Liver 2013;7:513-518)
-
( Hirotsugu Sakamoto ),( Takashi Asahara ),( Osamu Chonan ),( Norikatsu Yuki ),( Hiroyuki Mutoh ),( Shunji Hayashi ),( Hironori Yamamoto ),( Kentaro Sugano ) 대한장연구학회 2015 Intestinal Research Vol.13 No.1
Background/Aims: Caudal-related homeobox 2 (Cdx2) is expressed in the human intestinal metaplastic mucosa and induces intestinal metaplastic mucosa in the Cdx2 transgenic mouse stomach. Atrophic gastritis and intestinal metaplasia commonly lead to gastric achlorhydria, which predisposes the stomach to bacterial overgrowth. In the present study, we determined the differences in gut microbiota between normal and Cdx2 transgenic mice, using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Methods: Twelve normal (control) and 12 Cdx2 transgenic mice were sacrificed, and the gastric, jejunal, ileac, cecal and colonic mucosa, and feces were collected. To quantitate bacterial microbiota, we used real-time qRT-PCR with 16S rRNA gene-targeted, species-specific primers. Results: The total numbers of bacteria in the gastric, jejunal, ileac, cecal, and colonic mucosa of the Cdx2 transgenic mice were significantly higher than those of the normal mice. The Bacteroi-des fragilis group and also Prevotella were not detected in the stomach of the normal mice, although they were detected in the Cdx2 transgenic mice. Moreover, the Clostridium coccoides group, Clostridium leptum subgroup, Bacteroides fragilis group, and Prevotella were not detected in the jejunum or ileum of the normal mice, although they were detected in the Cdx2 transgenic mice. The fecal microbiota of the normal mice was similar to that of the Cdx2 transgenic mice. Conclusions: Our results showed the differences in composition of gut microbiota between normal and Cdx2 transgenic mice, which may be caused by the development of gastric achlorhydria and intestinal metaplasia in Cdx2 transgenic mice. (Intest Res 2015;13:39-49)
KCI연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
