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世界核心医学期刊文摘（神经病学分册） 2006年第6期2卷 15-16页

作者： Mercuri E. topaloglu h. Brockington M. F. Muntoni 郭俊 Department of Paediatrics Imperial College Hammersmith Hospital Campus Du Cane Road London W12 OHN United Kingdom Dr.

Objectives: To report th. spectrum of brain magnetic resonance imaging findings in 13 patients with.congenital muscular dystroph. and FKRP gene mutations and to explore possible genotype-ph.notype correlations. Design: We retrospectively reviewed brain magnetic resonance imaging in patients with.congenital muscular dystroph. and FKRP gene mutations. Patients: Th.rteen patients with.congenital muscular dystroph. and mutations in th. FKRP gene. Results: Five of th. 13 patients h.d th. typical ph.notype originally described for congenital muscular dystroph. (MDC1C) with.normal intelligence and normal brain magnetic resonance imaging wh.le 3 oth.r patients h.d isolated cerebellar cysts and mental retardation with.ut any oth.r sign of posterior fossa of supratentorial abnormalities. In th. remaining 5 patients cerebellar cysts were associated with.structural brain ch.nges involving th. posterior fossa and th. cortex, ranging from focal unilateral periventricular nodular h.terotopia to marked cerebellar dysplasia and pontine h.poplasia. In 2 of th.se 5 patients th. severity and distribution of ch.nges resembled muscle-eye-brain disease in 1 patient wh. h.d mild Walker-Warburg syndr ome. Th. distribution of FKRP gene mutations identified in th.s group of patients did not reveal any obvious association with.th. severity of central nervous system involvement. Conclusions: Th. severity of central nervous system involvement observed in our patients in contrast broadly reflected th. severity of th. disruption of α-dystroglycan glycosylation. In particular, dystroglycan expression was almost absent in th. patients with.muscle-eye-brain diseaselike ph.notype and less severely reduced in th. patients with.congenital muscular dystroph. (MDC1C) with.or with.ut cerebellar cysts. Th.s study furth.r h.gh.igh.s th. central role th.t dystroglycan h.s in neuronal migration.

关键词：先天性肌营养不良基因突变脑部变化患者中枢神经系统损害智力发育迟缓严重程度小脑发育不良结构改变

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Glucagon-like peptide-2 exh.bits protective effect on h.patic isch.mia-reperfusion injury in rats

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Frontiers of Medicine 2015年第3期9卷 368-373页

作者： Naci topaloglu Adem Kucuk Sule Yildirm Mustafa Tekin h.vva Erdem Mustafa Deniz Canakkale Onsekiz Mart University Medical Faculty Department of Pediatrics Canakkale Turkey Diizce Atatiirk State h.spital Department of Pediatric Surgery Diizce Turkey Diizce University Medical Faculty Department of Pathology Diizce Turkey Canakkale Onsekiz Mart University Medical Faculty Department of Physiology Canakkale Turkey

Glucagon-like peptide-2 （GLP-2） h.s potent anti-inflammatory effects and protects against experimental isch.mia/reperfusion （I/R） injury in pulmonary, intestinal, and myocardial tissue. h.wever, its protective abilities against I/R injury in th. liver are unknown. We investigated th. potential role of GLP-2 pretreatment on h.patic I/R injury in rats. A total of 24 rats were randomly divided into th.ee groups （n = 8）. Th. first group was th. control group; th. second group was th. veh.cle-treated h.patic isch.mia/reperfusion （h.R, veh.cle saline-treated） group; and th. th.rd group was th. GLP-2 pretreated I/R （GLP2-IR） group. Each.rat in th. th.rd group was intraperitoneally administered 5 ~tg GLP-2 for 5 d before th. procedure. A portal triad was created to induce isch.mia with.a vascular atraumatic clamp. After 40 min, th. clamp was released to initiate h.patic reperfusion for 6 h. Blood samples and tissue specimens from th. fiver were obtained. Alanine aminotransferase, aspartate aminotransferase, and total bilirubin levels significantly increased in th. saline- treated h.R group （P 〈 0.001）, wh.reas GLP-2 pretreatment significantly decreased th.ir levels （P 〈 0.01）. Our data suggested th.t GLP-2 pretreatment may h.ve a protective effect on liver I/R injury. h.wever, dose-response studies are necessary to determine th. most effective dose.

关键词： isch.mia/reperfusion liver glucagon-like peptide-2 alanine aminotransferase

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