Blue phases are types of liquid crystal phases that appear in a temperature range between a chiral nematic phase and an isotropic liquid phase. Because blue phases have a three-dimensional cubic structure with lattice periods of several hundred nanometres, they exhibit selective Bragg reflections in the range of visible light corresponding to the cubic lattice. From the viewpoint of applications, although blue phases are of interest for fast light modulators or tunable photonic crystals, the very narrow temperature range, usually less than a few kelvin, within which blue phases exist has always been a problem. Here we show the stabilization of blue phases over a temperature range of more than 60 K including room temperature (260-326 K). Furthermore, we demonstrate an electro-optical switching with a response time of the order of 10(-4) s for the stabilized blue phases at room temperature.

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.

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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.

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