Thesis (Ph.D.)--Memorial University of Newfoundland, Faculty of Medicine, 2000. / Typescript. Bibliography: p. 137-164.

Thesis (Ph. D.)--University of Washington, 1999. / Vita. Includes bibliographical references (leaves 95-109).

Thesis (Ph. D.)--Cornell University, May, 2008. / Vita. Includes bibliographical references (leaves 104-122).

Thesis (doctoral)--Lund University, 1995. / Added t.p. with thesis statement inserted.

FundaÃÃo de Amparo à Pesquisa do Estado do Cearà / O estudo mostrou os efeitos do extrato padronizado de Erythrina velutina (EPEV), na atividade motora, na memÃria e nas concentraÃÃes de aminoÃcidos cerebrais de camundongos submetidos à isquemia cerebral global (ISQ). Os animais (camundongos swiss, machos, 30-35g) foram submetidos à isquemia cerebral transitÃria pela oclusÃo de ambas as artÃrias carÃtidas durante 30 minutos e tratados durante 5 dias com EPEV 200 ou 400 mg/kg e Memantina (MEM), controle positivo, 10mg/kg, 2 ou 24 h apÃs a isquemia. O mesmo procedimento foi feito no grupo Falso-operado + DMSO (FO) com exceÃÃo do clampeamento das artÃrias carÃtidas. No 6Âdia apÃs a induÃÃo da isquemia, os animais foram submetidos aos testes de atividade locomotora, rota rod e memÃria (step down, Y-maze e reconhecimento de objetos), a seguir foram sacrificados e as Ãreas cerebrais dissecadas como (cÃrtex prÃ-frontal âCPF; hipocampo- HC e corpo estriado- CE) para determinaÃÃo das concentraÃÃes de aspartato (ASP), glutamato (GLU), glicina (GLI), taurina (TAU) e Ãcido gama-amino-butirico (GABA). Nenhuma alteraÃÃo na atividade exploratÃria vertical foi detectada entre os grupos FO e ISQ tratados com os diluentes, bem como entre os grupos tratados com EPEV ou MEM. PorÃm, um aumento na atividade exploratÃria horizontal (rearing) foi observado no grupo EPEV 200mg 2H quando comparado com o grupo ISQ. No teste de rota rod nenhuma alteraÃÃo significativa foi detectada entre os grupos. No teste de memÃria step down a ISQ afetou os processos de aquisiÃÃo e retenÃÃo de memÃria tanto na fase imediata (memÃria recente - MR), quanto na fase de consolidaÃÃo (memÃria tardia - MT) quando comparado ao grupo FO. Comparando os tratamentos de EPEV 200 ou 400 mg/kg observamos um aumento significativo, no tempo de permanÃncia na plataforma, nos animais tratados apÃs a isquemia quando avaliados na MR e na MT. No teste Y-maze a ISQ promoveu um dano na retenÃÃo da memÃria dos animais em relaÃÃo ao grupo controle (FO), porÃm o EPEV e a MEM conseguiram reverter esse dano em ambas as doses. Os animais submetidos a ISQ mostraram dÃficit na memÃria tambÃm no teste de reconhecimento de objetos. Esse dÃficit foi revertido pelo grupo EPEV 400mg (2 ou 24H) e por MEM . A dosagem de aminoÃcidos apÃs o teste de comportamento no CPF, HC e CE apresentou aumento nas concentraÃÃes dos aminoÃcidos excitatÃrios (ASP, GLU) nos animais ISQ +DMSO quando comparados ao FO. No CPF esse aumento pode ser revertido pelos animais tratados com EPEV 24H em ambas as doses e MEM 24H. Jà no HC esse aumento foi revertido por todos os grupos tratados. No CE houve reduÃÃo das concentraÃÃes de GLU nos grupos EPEV 200mg (2 ou 24H) e MEM 2H. A respeito das concentraÃÃes de GABA, GLI e TAU, no CPF, houve reversÃo dos valores nos grupos EPEV 200mg 2H e no grupo 400mg em ambos os horÃrios de tratamento como tambÃm no grupo MEM 24H quando comparados ao controle isquemiado. No HC um aumento nas concentraÃÃes de GLI e TAU pode ser visto nos grupos EPEV 200mg 24H, EPEV 400mg 2H e MEM 24H. Jà as concentraÃÃes de GABA foram revertidas nos grupos EPEV 400mg e MEM no tempo de 24H. O CE apresentou concentraÃÃes elevadas de TAU e GABA nos animais ISQ quando comparados com o controle. O valor de GABA sà foi revertido pelo grupo EPEV 200mg 2H. Diante do exposto, concluÃmos que o EPEV em ambas as doses desenvolveu uma aÃÃo neuroprotetora, possivelmente pela reduÃÃo das concentraÃÃes de aminoÃcidos excitatÃrios e aumento dos inibitÃrios apÃs a isquemia. Possibilitando, assim, a perspectiva de um uso futuro do EPEV em doenÃas isquÃmicas no Sistema Nervoso Central. / The study shows the effects of standardized extract of Erythrina velutina (EPEV) in motor activity, in memory and in the determination of amino acids in mice brain undergoing global cerebral ischemia (ISQ). Animals (swiss mice, males, 30-35 g) were subjected to transient cerebral ischemia by occlusion of both carotid arteries during 30 minutes and treated for 5 days with EPEV 200 or 400 mg/kg and Memantine (MEM) 10 mg/kg, 2 or 24 hours after ischemia. The same procedure was done in false-operated group + DMSO (FO) with the exception of clamping the carotid arteries. On day 6 after induction of ischemia, the animals were subjected to tests of locomotor activity, rota rod and memory (step down, Y-maze and object recognition), then were sacrificed and dissected brains on ice the prefrontal cortex (PFC), Hippocampus (HC) and striatum (ST) determination of aspartic acid (ASP), glutamate (GLU), glycine (GLY), taurine (TAU) and gamma-amino-butirico acid (GABA). No change in exploratory activity was detected between the groups vertical FO and ISQ treated with solvents, as well as between the groups treated with EPEV or MEM, however, an increase in exploration activity across (rearing) was observed on EPEV 200 mg 2H group when compared to the ISQ. In rota rod test no substantial modification has been detected between the groups FO and ISQ treated with DMSO and in the groups treated with EPEV and MEM. Memory test step down the ISQ has affected the processes of acquisition and retention of memory both in the immediate phase (recent memory-RM), and the consolidation phase (late memory-LM) when compared with the group FO. Comparing the treatments we observed a significant increase in the length of stay in the non-electrified platform, in the animals treated after ischemia when evaluated in RM, and in LM. Y-maze test the ISQ promoted a retention damage in memory of animals compared to the control group (FO), however the EPEV and MEM managed to revert the damage on the acquisition of memory induced by ISQ at both doses. Animals subjected to ISQ showed deficit in memory also in object recognition test, this deficit was reversed by EPEV 400 mg 2 or 24 H group and by MEM 10 mg. The dosage of amino acids after testing behavior on PFC, HC and ST presented an increase in concentration of excitatory amino acids (ASP, GLU) in animals ISQ + DMSO when compared to FO. In the CPF that increase can be reversed by the animals treated with EPEV 24H at both doses and MEM 10 mg 24H in HC this increase was reversed by all treated groups. In CE there was a reduction in levels of GLU on EPEV 200 mg 2 or 24H and MEM 10 mg 2H. Regarding the levels of GABA, GLY and TAU in the CPF, there was reversal of values in the Group EPEV 200 mg 2H and 400 mg in both treatment schedules as well as group MEM 10 mg 24H when compared to the control that suffered ischemia. In the HC an increase in levels of GLY and TAU can be seen in EPEV 200 mg 24H, EPEV 400 mg 2H and MEM 10 mg 24H groups. GABA levels were already reverted on EPEV 400 mg and MEM 10 mg groups at the time of 24H. The ST presented high levels of TAU and GABA in the ISQ animals when compared with the control. The value of GABA was only reversed by EPEV 200 mg 2H group. With this, we concluded that the EPEV at both doses developed a neuroprotective action, possibly by reducing the levels of excitatory amino acids and inhibitory increase after ischemia.

京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第22040号 / 医博第4525号 / 新制||医||1038(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 高橋 淳, 教授 伊佐 正, 教授 渡邉 大 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

No description available.

Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 5 uppsatser.

Background. Carotid stenosis is an important cause of stroke. Carotid endarterectomy is a means of reducing the burden of stroke but is of marginal benefit in individuals with asymptomatic carotid stenosis. The identification of factors associated with increased risk of cerebral ischemic events would help select individuals who may obtain a greater benefit. / Methods. A comprehensive search was performed to identify studies examining risk factors for cerebral ischemic events in patients with asymptomatic carotid stenosis. Inclusion criteria were defined a priori. Relevant studies were reviewed, assessed for quality, and data were extracted. / Results. Thirty-four studies met the inclusion criteria. There was a suggestion of increasing neurological events with increasing severity and progression of carotid stenosis. There was some evidence for an association with carotid plaque morphology. No consistent association was found with clinical factors, impaired cerebral vasoreactivity, or cerebral embolic signals. / Conclusions. The evidence is insufficient to reliably identify individuals with asymptomatic carotid stenosis who are at a higher risk of cerebral ischemic events.

No description available.