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백서 대뇌 피질에서 허혈에 의한 [^3H]5-Hydroxytryptamine의 유리
장영문,송은석,노시운,김성수,김재천,김기원 의과학연구소 1995 全北醫大論文集 Vol.19 No.1
In an attempt to elucidate the mechanisms for ischemia-induced release of neurotransmitters in vitro. I examined the ischemia-induced release of [^3H]5-hydroxytryptamine(5-HT) from cerebral cortex of the rat. Ischemia, deprivation of oxygen and glucose, induced significant release of [^3H]5-HT(about 6% of total tissue content) from the cerebral cortex in vitro. This ischemia-induced release of [^3H]5-HT from the cerebral cortex was significantly attenuated by TTX(1μM), Mg^2+(1.2mM), MK-801(10μM), ketamine(10μM), NMDA receptor antagonists, DNQX(30μM), a kainate/AMPA receptor antagonist, or carbetapentane(30μM), an inhibitor of glutamate release. Dantrolene(30μM) and ryanodine(100μM), inhibitors of intracellular Ca^2+ release, flunarizine(5μM) and ω-conotxin(100μM), inihbitors of N-type Ca^2+ channels, signficantly attenuated the ischemia-induced release of [^3H]5-HT, but verapamil(5μM), and inhibitor of L-type Ca^2+ chnnels, did not. Fluoxetine(1μM), a relatively selective 5-HT transporter blocker, significantly inhibited the ischemia-induced release of [^3H]5-HT. These results suggest that ischemia-evoked release of norepinephrine was caused by release of glutamate via activation of NMDA and non-NMDA receptors, and that CA^2+-dependent and -independent release processes are underlying in this phenomenon.
장영문,장문영,김종훈,황용 의과학연구소 1997 全北醫大論文集 Vol.21 No.2
Familial adenomatous polyposis is autosomal dominant inherited, not sex linked disease, which caused by a mutation in adenomatous poyposis coli gene in chromosome 5q21 and is diagnosed when a patient has more than 100 adenomatous polyps in a colon or when a member of FAP family has any number of colo-nic adenomatous discovered. Patients with FAP have no symptoms, which are bloody stool, diarrhea, lower abdominal pain, anemia and weight loss until postadolescence, at which time the first polyps may appear and polyps are developed to cancer before 40 years old. Early detection is essential to prevent the development of metastaic cancer. Diagnosis of FAP is established by rectal examination, sigmoidoscopy or colonoscopy, identification of greater than 100 polyps on air contrast barium enema and gene test of a suspected member of FAP fa-mily. Treatment is total colectomy and permanent ileostomy, total colectomy and ileorectal anastomosis, and total colectomy, mucosal proctectomy and ileal poch-anal anastomosis. We experienced 4 cases of familial adenomatous polyposis and reported with review of literatures. (Key word : familial adenomatous polyposis)