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Kaori Yoshida

Researcher at Niigata University

Publications -  19
Citations -  624

Kaori Yoshida is an academic researcher from Niigata University. The author has contributed to research in topics: Cytokine & Myocarditis. The author has an hindex of 13, co-authored 19 publications receiving 588 citations. Previous affiliations of Kaori Yoshida include RMIT University.

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Hydrodynamic-based delivery of an interleukin-22-Ig fusion gene ameliorates experimental autoimmune myocarditis in rats.

TL;DR: Results showed that the expression of immunologic molecules in IL-1-stimulated NC cells was significantly decreased by rIL-22 or serum containing IL-22-Ig, and the reason for this effectiveness may be that IL- 22 suppressed gene expression of PG synthases, IL-6, and chemokines in activated NC noninflammatory cells.
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Lipocalin-2/Neutrophil Gelatinase-B Associated Lipocalin Is Strongly Induced in Hearts of Rats With Autoimmune Myocarditis and in Human Myocarditis

TL;DR: Cardiomyocytes, vascular wall cells and fibroblasts in myocarditis strongly express Lcn2/NGAL via proinflammatory cytokines, and high levels were initially sustained during the inflammatory stage, then decreased with recovery.
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Expression of the peptide hormone hepcidin increases in cardiomyocytes under myocarditis and myocardial infarction

TL;DR: Cardiac expression of hepcidin is strongly induced in cardiomyocytes under myocarditis and MI, conditions in which inflammatory cytokine levels increase and may play an important role in iron homeostasis and free radical generation.
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Spatiotemporal changes of coxsackievirus and adenovirus receptor in rat hearts during postnatal development and in cultured cardiomyocytes of neonatal rat.

TL;DR: Examination of expression levels of CAR in rat hearts found that CAR decreased gradually during postnatal development, although CAR was detectable, even in adults, and immunohistochemistry revealed CAR on the whole surface of cardiomyocytes in immature rat hearts.
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Alteration of IL-17 related protein expressions in experimental autoimmune myocarditis and inhibition of IL-17 by IL-10-Ig fusion gene transfer.

TL;DR: IL-17 is highly produced by αβT cells in the early phase of EAM hearts and IL-17 inhibition might be a possible mechanism of the amelioration of E AM by IL-10-Ig treatment, suggesting that IL- 17 produced by Th17 plays an important role in the pathogenesis of rat EAM.