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Hidehiko Konno

Researcher at Tohoku University

Publications -  59
Citations -  2346

Hidehiko Konno is an academic researcher from Tohoku University. The author has contributed to research in topics: Spinal cord & Axoplasmic transport. The author has an hindex of 32, co-authored 59 publications receiving 2202 citations. Previous affiliations of Hidehiko Konno include Yamagata University.

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Diffusion-weighted MRI abnormalities as an early diagnostic marker for Creutzfeldt-Jakob disease.

TL;DR: DWI was the most sensitive test for the early clinical diagnosis of CJD; consideration should be given to its inclusion in the clinical diagnostic criteria of CJd.
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Presence of six different lesion types suggests diverse mechanisms of tissue injury in neuromyelitis optica.

TL;DR: It is shown that active lesions in NMO display a wide spectrum of pathology even within a single tissue block of an individual patient, and that different mechanisms of tissue injury operate in parallel in the same patient and even within the same lesion.
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Loss of aquaporin-4 in active perivascular lesions in neuromyelitis optica: a case report.

TL;DR: The findings suggest that astrocytic impairment associated with humoral immunity against AQP4 may be primarily involved in the lesion formation of N MO, and that the pathomechanisms of NMO are different from those of MS in which demyelination is the primary pathology.
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Shy-Drager syndrome and amyotrophic lateral sclerosis. Cytoarchitectonic and morphometric studies of sacral autonomic neurons.

TL;DR: The results imply that these two disorders distinguished by different clinical manifestations share a common loss of somatic motor and parasympathetic motor neurons at least in the sacral cord.
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Forebrain ischemia induced by temporary bilateral common carotid occlusion in normotensive rats

TL;DR: Ischemic brain lesions were induced in adult Wistar and Fischer rats by temporary occlusion of the bilateral common carotid artery and the simplicity of procedure could make this model suitable for the study of the pathogenesis of ischemic neuronal damage in a critically low perfusion state.