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10例淋巴细胞药物刺激试验呈阳性的非细胞毒性药物诱导的肺炎病例的临床研究

中华结核和呼吸杂志 1997年第Z1期20卷 77-77页

作者： Yoneyama H Yano T Kimura M okimoto n Matsushima T 刘兴荣(译) DepartmentofInternalMedicine KawasakiMedicalSchoolKawasakeHospital2—1—80NakasangeOkayamaCityJapan DepartmentofInternalMedicine KawasakiMedicalSchoolKawasakeHospit—80NakasangeOkayamaCityJapan DepartmentofInternalMedicine KawasakiMedicalSchoolKawasakeHospital0NakasangeOkayamaCityJapan

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Expression of mutant type-p53 products in H pylori-associated chronic gastritis

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World Journal of Gastroenterology 2007年第10期13卷 1541-1546页

作者： Masaaki Kodama Kazunari Murakami Tadayoshi okimoto Ryugo Sato Koichiro Watanabe Toshio Fujioka Department of Gastroenterology Faculty of MedicineOita UniversityHasama-machiOita879-5593Japan

AIM： To investigate the mutation of p53 immunohistochemically in non-tumorous gastric mucosa with H pylori infection before and aEer H pylori eradication therapy. METHODS： 53 subjects （36 male, 17 female, mean age ± SEM, 57.1 ± 12.1） undergoing endoscopic examination were included in this study. 42 of 53 patients were H pylori-positive, and 11 were H pylorinegative. All H pylori-positive patients had successful eradication therapy. Biopsy specimens were taken from five points of the stomach, as recommended by the updated Sydney system. Immunohistochemical studies were performed by using primary antibodies against p53 （DO-7 and PAb240）. RESULTS： p53 （DO-7 and PAb240） immunoreactivity was shown in the neck region of the gastric pits, however, quite a few cells were found to be immunopositive for p53 （PAb240）in the Hpylori-infected gastric mucosa. The proportion of patients immunopositive for p53 （PAb240） was significantly reduced 6 mo after eradication [28/42 （66.7%） to 6/42 （14.3%）] （P 〈 0.05）, while the biopsies taken from H pylori-negative patients showed no immunoreactivity for p53 （PAb240）. p53 （PAb240）-positive patients were divided into two groups by the number of positive cells detected： one with more than six positive cells per 10 gastric pits （group A, n = 12）, and the other with less than five positive cells per 10 gastric pits （group B, n = 30）. Atrophy scores in group A were significant higher than those in group B at the greater curvature of the antrum （group A： 2.00 ± 0.14 vs group B： 1.40 ± 0.15, P = 0.012）, the lesser curvature of the corpus （group A： 2.00 ± 0.21 vs group B： 1.07 ± 0.23, P = 0.017）, and the greater curvature of the corpus （group A： 1.20 ± 0.30 vs group B： 0.47 ±0.21, P = 0.031）. Group A showed significant higher intestinal metaplasia scores than group B only at the lesser curvature of the antrum （group A： 2.10 ± 0.41 vs group B： 1.12 ± 0.29, P = 0.035）. COnCLUSIOn： H pylori-associated chronic gastritis expressed the mutant-type p53, w

关键词： H pylori H pylori eradication Atrophic gastritis Mutant-type p53 Gastric cancer Updated Sydney system

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Helicobacter pylori-infected animal models are extremely suitable for the investigation of gastric carcinogenesis

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World Journal of Gastroenterology 2005年第45期11卷 7063-7071页

作者： Masaaki Kodama Kazunari Murakami Ryugo Sato Tadayoshi okimoto Akira nishizono Toshio Fujioka Department of Gastroenterology Department of Infectious Diseases (Microbiology)

Although various animal models have been developed to clarify gastric carcinogenesis, apparent mechanism of gastric cancer was not clarified in recent years. Since the recognition of the pathogenicity of Helocobacter pylori（H pylori）, several animal models with H pylori infection have been developed to confirm the association between Hpylori and gastric cancer. nonhuman primate and rodent models were suitable for this study. Japanese monkey model revealed atrophic gastritis and p53 mutation after long-term infection of Hpylori. Mongolian gerbil model showed the development of gastric carcinoma with H pylori infection alone, as well as with combination of chemical carcinogens, such as n-methyl- n-nitrosourea and n-methyl-n-nitro-n＇-nitrosoguanidine. The histopathological changes of these animal models after H pylori inoculation are closely similar to those in human beings with Hpylori infection. Eradication therapy attenuated the development of gastric cancer in Hpylori- infected Mongolian gerbil. Although several features of animal models differ from those seen in human beings, these experimental models provide a starting point for further studies to clarify the mechanism of gastric carcinogenesis as a result of Hpylon infection and assist the planning of eradication therapy to prevent gastric carcinoma.

关键词： Helicobacter pylori Gastric carcinoma Animal model Japanese monkey Mongolian gerbil

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