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Hiroaki Okabe

Researcher at Kumamoto University

Publications -  153
Citations -  5036

Hiroaki Okabe is an academic researcher from Kumamoto University. The author has contributed to research in topics: Antithrombin & Thrombin. The author has an hindex of 38, co-authored 153 publications receiving 4919 citations. Previous affiliations of Hiroaki Okabe include Fukuoka University.

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Direct measurement of high-density lipoprotein cholesterol in serum with polyethylene glycol-modified enzymes and sulfated alpha-cyclodextrin.

TL;DR: The combination of PEG-modified enzymes with alpha-cyclodextrin sulfate provided selectivity for the determination of HDL-cholesterol in serum in the presence of a small amount of dextran sulfate without the need for precipitation of lipoprotein aggregates.
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Role of neutrophils in spinal cord injury in the rat

TL;DR: Histological examination revealed that intramedullary hemorrhages observed 24 h after compression at the 12th thoracic vertebra of the spinal cord were significantly attenuated in leukocytopenic animals and those which received the anti-P-selectin monoclonal antibody, suggesting that activated neutrophils play an important role in compression-inducedThoracic spinal cord injury.
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Activated protein C attenuates endotoxin-induced pulmonary vascular injury by inhibiting activated leukocytes in rats.

TL;DR: The results suggest that the mechanism of APC inhibition of LPS-induced pulmonary vascular injury was independent of its anticoagulant activity and was related to its ability to inhibit accumulation of leukocytes.
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A new colorimetric micro-determination of free fatty acids in serum

TL;DR: A colorimetric micromethod, based on the formation of FFA-Cu soaps, was described for the determination of free fatty acids (FFA) in 100 μl of serum, and 2-(2-thiozolylazo)-p-cresol was chosen for the colorIMetric determination of copper.
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Activated protein C prevents LPS-induced pulmonary vascular injury by inhibiting cytokine production

TL;DR: It is suggested that APC prevented LPS-induced pulmonary vascular injury by inhibiting TNF production by monocytes and not via its anticoagulant activity, and the serine protease activity of APC appears to be essential for inhibition of TNFProduction.