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排序方式: 共有5376条查询结果,搜索用时 46 毫秒
1.
Chie Teramoto PHN RN MS Satoko Nagata PhD PHN RN Reiko Okamoto PhD PHN RN Ruriko Suzuki PHN RN MS Emiko Kishi PhD PHN RN Michie Nomura DSN PHN RN Noriko Jojima PHN RN MS Masumi Nishida PhD PHN RN Keiko Koide PhD PHN RN Emiko Kusano PhD PHN RN Saori Iwamoto PhD PHN RN Sachiyo Murashima PhD PHN RN 《Public health nursing (Boston, Mass.)》2015,32(6):654-661
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Shinsuke Hamaguchi Yasuhisa Okuda Toshimitsu Kitajima Nobuhide Masawa 《Journal canadien d'anesthésie》2002,49(7):745-748
PURPOSE: To clarify the appropriate concentration and dose of hypertonic saline solution (HSS) for preventing delayed neuronal death in the hippocampal CA1 subfield after transient forebrain ischemia in gerbils. METHODS: Thirty gerbils were randomly assigned to five groups: physiological saline solution (PSS) group, ischemia/reperfusion treated with PSS 2 mL x kg(-1); 5% HSS group, treated with 5% HSS 2 mL x kg(-1); 7.5% HSS group, treated with 7.5% HSS 2 mL x kg(-1); 10% HSS group, treated with 10% HSS 2 mL x kg(-1); 20% HSS group, treated with 20% HSS 2 mL x kg(-1). Transient forebrain ischemia was induced by occluding the bilateral common carotid arteries for four minutes. Five days later, histopathological changes in the hippocampal area were examined, and the degenerative ratio of the pyramidal cells were measured according to the following formula: (number of degenerative pyramidal cells/total number of pyramidal cells per 1 mm of hippocampal CA1 subfield) x 100. RESULTS: In PSS and 20% groups, neuronal cell damage was observed five days after ischemia. In the other three groups, these changes were not observed. The degenerative ratios of pyramidal cells were as follows; PSS group: 91.6 +/- 5.6%, 5% HSS group: 7.2 +/- 1.6%, 7.5% group: 8.3 +/- 1.4%, 10% HSS group: 6.2 +/- 1.1%, 20% HSS group: 85.8 +/- 8.7% (P < 0.05; PSS and 20% HSS vs three other groups). CONCLUSION: This study demonstrates that 5, 7.5 or 10% HSS 2 mL x kg(-1) may prevent delayed neuronal death in the hippocampal CA1 subfield after cerebral ischemia/reperfusion in gerbils. 相似文献
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Y Wada H Hasegawa H Okuda K Yoshida N Yamaguchi 《The Japanese journal of psychiatry and neurology》1989,43(2):245-253
Kindling of the primary visual cortex (VC) was compared with that of the amygdala in cats. VC kindling was basically similar to kindling of the amygdala in that daily electrical stimulation can lead to the development of a generalized convulsion in most subjects, a growth of afterdischarges in their configuration and duration, and a reduction of the afterdischarge threshold. The kindling response of the VC differed from that of the amygdala in a number of respects, i.e., a high afterdischarge threshold, a different pattern of behavioral seizure development, an abrupt growth of electroclinical seizures coincident with the onset of a generalized convulsion, an intersubject variability in seizure susceptibility, and a marked seizure instability. In VC kindling the afterdischarge propagation into the amygdala was not observed until the generalized convulsion developed, and the early involvement of afterdischarge was seen in the pulvinar, lateral geniculate body, and superior colliculus. These data suggest that a neural mechanism different from amygdaloid kindling may participate in VC kindling, and that the subcortical structures of the visual system are involved in the preferential pathway for a seizure generalization from the VC. 相似文献
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K Okuda 《Nihon Geka Gakkai zasshi》1989,90(10):1697-1705
Two tumor-associated cellular proteins, 82k/6.3 (MW/pI) and 61k/7.5, which were detected by two-dimensional gel electrophoresis, were studied by biochemical and immunological methods. In two-dimensional gel electrophoresis, 82k/6.3 and 61k/7.5 were rich in colon cancer tissue compared with normal colon mucosa, and they were also detected in fetal intestines. This shows that both proteins might be involved in category of oncofetal proteins. The localization of 82k/6.3 and 61k/7.5 was investigated by subcellular fractionation. They were rich in microsomal fraction, but not found in both nuclear and mitochondrial fractions. In binding reaction with seven kinds of lectins, 82k/6.3 reacted with RCAI, DBA and WGA, where 61k/7.5 reacted with RCAI, DBA, WGA, UEAI and SBA. Transferrin reacted with only RCAI. Each hybrid producing monoclonal antibody against 82k/6.3 or 61k/7.5 was generated by fusing spleen cells of BALB/c mice immunized by the two proteins and mouse myeloma cells. Each monoclonal antibody was specified in enzyme-linked immunoassay. In indirect immuno-fluorescent studies, monoclonal antibodies against 82k/6.3 and 61k/7.5 reacted with cytoplasma and membrane of human cancer cells. This result strongly suggests the localization of the two proteins demonstrated by subcellular fractionation. 相似文献
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Toshifumi Gabata Osamu Matsui Masumi Kadoya Samon Miyata Mitsuo Fujimura Tsutomu Takashima 《Cardiovascular and interventional radiology》1995,18(5):327-329
Gross hemorrhage is the most serious complication of anticoagulant therapy. We report the discovery and treatment of a large pseudoaneurysm of the superior gluteal artery in one patient who had been receiving oral anticoagulant therapy. We diagnosed the pseudoaneurysm by contrast-enhanced computed tomography, and embolized the artery with stainless steel coils. The exact cause of the pseudoaneurysm remains unclear, however, minor trauma appears most likely. 相似文献
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The rearrangement of terminations from the bed nucleus of stria terminalis (BST) was examined in the medial amygdaloid nucleus (MAN) at 2 months following the lesion of the accessory olfactory bulb (AOB) using an electron microscopy and degeneration study. At 2 days following a BST lesion, the number of degenerating synapses was 0.7 ± 0.1 (mean±S.E.M.) per unit area (2500 μm2 in the molecular layer, and 3/0 ± 0.3 in the cellular part. At 2 months after an AOB lesion, the degenerating synapses from the AOB had completely disappeared from the MAN. The BST was then lesioned at 2 months after the AOB lesion and, 2 days following this BST lesion, the degenerating synapses were counted in MAN. The numbers observed were 3.3 ± 0.6 per unit area in the molecular layer and 4.5 ± 0.4 in the cellular part. Therefore, the number of these degenerating synapses increased significantly within the molecular layer, though, in the cellular part the number of synapses was not significantly elevated over control. No differences in postsynaptic profiles (ratio of synapses on dendritic spine to dendritic shaft) were observed after the AOB lesion. These results indicate that the BST fibers formed new synapses in the molecular layer following the denervation of AOB fibers. The possibility of new synapse formation by other afferent fibers in addition to the AOB fibers is discussed as is the relationship between lesion induced synaptic reorganization and functional recovery after injury. 相似文献