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Go Hasegawa

Researcher at Niigata University

Publications -  317
Citations -  5726

Go Hasegawa is an academic researcher from Niigata University. The author has contributed to research in topics: TCP acceleration & TCP global synchronization. The author has an hindex of 29, co-authored 307 publications receiving 5397 citations. Previous affiliations of Go Hasegawa include Osaka University & Tohoku University.

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Constitutive Regulation of Cardiac Fatty Acid Metabolism through Peroxisome Proliferator-activated Receptor α Associated with Age-dependent Cardiac Toxicity

TL;DR: The results presented here indicate that PPARα controls constitutive fatty acid oxidation, thus establishing a role for the receptor in cardiac fatty acid homeostasis and altered expression of fatty acid-metabolizing proteins seems to lead to myocardial damage and fibrosis.
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The PTEN/PI3K pathway governs normal vascular development and tumor angiogenesis

TL;DR: PTEN is an important tumor suppressor gene and hereditary mutation of PTEN causes tumor-susceptibility diseases such as Cowden disease, and the Cre-loxP system is used to generate an endothelial cell-specific mutation of Pten (Tie2CrePten) in mice to show enhanced tumorigenesis due to an increase in angiogenesis driven by vascular growth factors.
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Regulation by Chemokines of Circulating Dendritic Cell Precursors, and the Formation of Portal Tract–Associated Lymphoid Tissue, in a Granulomatous Liver Disease

TL;DR: Circulating DC precursors can migrate into a solid organ like liver, and participate in the granulomatous reaction in response to specific chemokines, and Anti-SLC antibody diminished PALT expansion while exacerbating granuloma formation.
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Expression of pentraxin 3 (PTX3) in human atherosclerotic lesions

TL;DR: Analysis of coronary arterial thrombi containing an atherosclerotic plaque component removed from patients with acute myocardial infarction and human aortic tissues with various degrees of atherosclerosis sampled from autopsy cases indicated that macrophages, mainly foam cells, expressed PTX3 in advanced atherosolic lesions, andPTX3 derived from neutrophils as well as macrophage plays an important role in atherogenesis.