112 research outputs found

    Simultaneous multi-elemental analysis by continuous flow analysis system equipped with ICP-MS

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    The Tenth Symposium on Polar Science/Ordinary sessions: [OM] Polar Meteorology and Glaciology, Wed. 4 Dec. / Entrance Hall (1st floor) , National Institute of Polar Researc

    Spatial variation of surface mass balance and seasonal variation of dust deposition at EGRIP, Greenland

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    The Tenth Symposium on Polar Science/Ordinary sessions: [OM] Polar Meteorology and Glaciology, Wed. 4 Dec. / Entrance Hall (1st floor) , National Institute of Polar Researc

    Seasonal variations of snow chemistry at EGRIP, Greenland

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    The Tenth Symposium on Polar Science/Ordinary sessions: [OM] Polar Meteorology and Glaciology, Thu. 5 Dec. / 2F Auditorium , National Institute of Polar Researc

    Densification of layered firn of the ice sheet at Dome Fuji, Antarctica

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    第6回極域科学シンポジウム[OM] 極域気水圏11月16日(月) 国立極地研究所1階交流アトリウ

    Ice Core Records of Antarctic Warming Events in the Last Glacial Period

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    第3回極域科学シンポジウム 横断セッション「海・陸・氷床から探る後期新生代の南極寒冷圏環境変動」11月26日(月) 国立国語研究所 2階講

    Continuous CH4 measurements with the NIPR CFA system

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    第6回極域科学シンポジウム分野横断セッション:[IA] 急変する北極気候システム及びその全球的な影響の総合的解明―GRENE北極気候変動研究事業研究成果報告2015―11月19日(木) 国立極地研究所1階交流アトリウ

    Pathophysiology and treatment of cerebral ischemia

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    This article describes the pathophysiology of, and treatment strategy for, cerebral ischemia. It is useful to think of an ischemic lesion as a densely ischemic core surrounded by better perfused “penumbra” tissue that is silent electrically but remains viable. Reperfusion plays an important role in the pathophysiology of cerebral ischemia. Magnetic resonance imaging (MRI) and histological studies in rat focal ischemia models using transient middle cerebral artery (MCA) occlusion indicate that reperfusion after an ischemic episode of 2- to 3-hour duration does not result in reduction of the size of the infarct. Brief occlusion of the MCA produces a characteristic, cell-type specific injury in the striatum where medium-sized spinous projection neurons are selectively lost ; this injury is accompanied by gliosis. Transient forebrain ischemia leads to delayed death of the CA1 neurons in the hippocampus. Immunohistochemical and biochemical investigations of Ca2+/calmodulin-dependent protein kinase II(CaM kinase II) and protein phosphatase (calcineurin) after transient forebrain ischemia demonstrated that the activity of CaM kinase II was decreased in the CA1 region of the hippocampus early (6- 12 hours) after ischemia. However, calcineurin was preserved in the CA1 region until 1.5 days after the ischemic insult and then lost ; a subsequent increase in the morphological degeneration of neurons was observed. We hypothesized that an imbalance of Ca2+/calmodulin dependent protein phosphorylation-dephosphorylation may be involved in delayed neuronal death after ischemia. In the treatment of acute ischemic stroke, immediate recanalization of the occluded artery, using systemic or local thrombolysis, is optimal for restoring the blood flow and rescuing the ischemic brain from complete infarction. However, the window of therapeutic effectiveness is very narrow. The development of effective neuroprotection methods and the establishment of reliable imaging modalities for an early and accurate diagnosis of the extent and degree of the ischemia are imperative
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