At the present time, endovascular occlusion of the dissected site is a safe, minimally invasive, and reliable treatment for dissecting aneurysms when a test occlusion is tolerated and adequate collateral circulation is present.
Summary:We developed an antibody specific to f3-amy loid precursor protein (f3APP) fragments possessing the exact amino terminus of the f3-amyloid peptide and ex amined its induction in postischemic hippocampus, In control hippocampus, this APP fragment was lightly ob served in pyramidal neurons of CA sectors and dentate granule cells, Transient forebrain ischemia enhanced ac cumulation of the APP fragment in CAl pyramidal neu rons, Seven days after the ischemia, while the APP frag ment was still observed in dentate granule cells and CA3Transient global forebrain ischemia in rodents in duces selective degeneration affecting hippocampal CAl and CA4 neurons with relative sparing of CA3 neurons and dentate granule cells. Although the de generation of CA4 neurons begins within hours after the ischemic insult, CAl neurons remain intact for up to 2 days and then degenerate (delayed neuronal death) (Kirino, 1982). The molecular mechanisms responsible for differential neuronal vulnerability to ischemic injury are incompletely understood (Schmidt-Kastner and Freund, 1991). In the previ ous study, we showed that an amyloidogenic pro cess was induced in the early phase of postischemic hippocampus (Saido et ai., 1994). Here we exam ined the detailed distribution of the cytotoxic frag ment of the (3-amyloid precursor protein «(3APP) in Received June 12, 1995; final revision received September 22. 1995; accepted March 5, 1996. Address correspondence and reprint requests to Dr. M. Yokota at Department of Neurosurgery, Hyogo College of Med icine, Mukogawa-cho I-I, Nishinomiya, Hyogo 663, Japan.Abbreviations used: AI3. l3-amyloid peptide; I3APP, l3-amyJoid precursor protein; CCA. common carotid artery; DAB, diami nobenzidine tetrahydrochloride; GFAP, glial fibrillary acidic protein; PBS, phosphate-buffered saline.
1219neurons, it disappeared in dead CAl neurons. While as trocytes did not show in any immunoreactivity through out the experiment. those in the CAl sector showed mod erate immunoreactivity 7 days after the ischemia. The APP fragment has a cytotoxic effect on cultured neurons. These results suggest that the accumulation of the cyto toxic APP fragment in CAl neurons may play a role in the development of delayed neuronal death after the ischemic insult.
BackgroundEndovascular therapy has been shown to be effective in patients with acute cerebral large‐vessel occlusion, but real‐world efficacies are unknown.Methods and ResultsWe conducted a prospective registry at 46 centers between October 2014 and January 2017. Eligible patients were those who were aged 20 years or older, with acute cerebral large‐vessel occlusion, and who were hospitalized within 24 hours of the onset. We enrolled both consecutive patients who were treated with or without endovascular therapy. Endovascular therapy included thrombectomy, balloon angioplasty, stenting, local fibrinolysis, and piercing. The primary outcome was a favorable outcome as defined by a modified Rankin Scale of 0 to 2 at 90 days after onset. Secondary outcomes were modified Rankin Scale of 0 to 1 and mortality. Safety outcomes were intracerebral hemorrhage or a recurrence of ischemic stroke. We constructed the 2242 (1121 each) propensity score–matched patients cohort based on a propensity score for endovascular therapy and estimated the adjusted odds ratio, followed by sensitivity analyses on original 2399 (1278 in endovascular therapy versus 1121 in no endovascular therapy) patients. In the propensity score–matched cohort, favorable outcomes were observed in 35.3% and 30.7% of patients in the endovascular therapy and no endovascular therapy groups, respectively (P=0.02). The adjusted odds ratio for the favorable outcome was 1.44 (95% confidence interval, 1.10–1.86, P=0.007). The efficacy of endovascular therapy in achieving favorable outcomes did not differ between our subgroups and in the sensitivity analyses.ConclusionsEndovascular therapy decreased disabilities at 90 days in real‐world patients with acute cerebral large‐vessel occlusion.Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT02419794.
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