WorldCat Identities

島田健一 1929-

Overview
Works: 8 works in 8 publications in 2 languages and 14 library holdings
Classifications: DS894.29.S27,
Publication Timeline
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Most widely held works by 島田健一
Saru-gun no Ainugo chimei by Masayasu Ōgiya( Book )

in Japanese and held by 4 WorldCat member libraries worldwide

Gaisetsu saibā hanzai : hōrei kaisetsu to sōsa kōhan no jissai( Book )

1 edition published in 2018 in Japanese and held by 2 WorldCat member libraries worldwide

Sarugun no ainugo chimei( Book )

1 edition published in 1988 in Japanese and held by 2 WorldCat member libraries worldwide

Yakuzaishi kangoshi iyakukei gakusei no tameno rinshō iyaku ryakugoshū( Book )

1 edition published in 2010 in Japanese and held by 2 WorldCat member libraries worldwide

IL-1 Signaling Is Critically Required in Stromal Cells in Kawasaki Disease Vasculitis Mouse Model( )

1 edition published in 2015 in English and held by 1 WorldCat member library worldwide

Sarugun no ainugo chimei( Book )

1 edition published in 1988 in Japanese and held by 1 WorldCat member library worldwide

TRNA synthase suppression activates de novo cysteine synthesis to compensate for cystine and glutathione deprivation during ferroptosis( )

1 edition published in 2016 in English and held by 1 WorldCat member library worldwide

ABSTRACT: Glutathione is a major endogenous reducing agent in cells, and cysteine is a limiting factor in glutathione synthesis. Cysteine is obtained by uptake or biosynthesis, and mammalian cells often rely on either one or the other pathway. Because of the scarcity of glutathione, blockade of cysteine uptake causes oxidative cell death known as ferroptosis. A new study suggests that tRNA synthetase suppression activates the endogenous biosynthesis of cysteine, compensates such cysteine loss, and thus makes cells resistant to ferroptosis
CD8+ T Cells Contribute to the Development of Coronary Arteritis in the Lactobacillus casei Cell Wall Extract–Induced Murine Model of Kawasaki Disease( )

1 edition published in 2017 in English and held by 1 WorldCat member library worldwide

Abstract : Objective: Kawasaki disease (KD) is the leading cause of acquired heart disease among children in developed countries. Coronary lesions in KD in humans are characterized by an increased presence of infiltrating CD3+ T cells; however, the specific contributions of the different T cell subpopulations in coronary arteritis development remain unknown. Therefore, we sought to investigate the function of CD4+ and CD8+ T cells, Treg cells, and natural killer (NK) T cells in the pathogenesis of KD. Methods: We addressed the function of T cell subsets in KD development by using a well‐established murine model of Lactobacillus casei cell wall extract (LCWE)–induced KD vasculitis. We determined which T cell subsets were required for development of KD vasculitis by using several knockout murine strains and depleting monoclonal antibodies. Results: LCWE‐injected mice developed coronary lesions characterized by the presence of inflammatory cell infiltrates. Frequently, this chronic inflammation resulted in complete occlusion of the coronary arteries due to luminal myofibroblast proliferation (LMP) as well as the development of coronary arteritis and aortitis. We found that CD8+ T cells, but not CD4+ T cells, NK T cells, or Treg cells, were required for development of KD vasculitis. Conclusion: The LCWE‐induced murine model of KD vasculitis mimics many histologic features of the disease in humans, such as the presence of CD8+ T cells and LMP in coronary artery lesions as well as epicardial coronary arteritis. Moreover, CD8+ T cells functionally contribute to the development of KD vasculitis in this murine model. Therapeutic strategies targeting infiltrating CD8+ T cells might be useful in the management of KD in humans
 
Audience Level
0
Audience Level
1
  Kids General Special  
Audience level: 0.90 (from 0.87 for Gaisetsu s ... to 0.94 for Yakuzaishi ...)

Alternative Names
Shimada, Ken'ichi, 1929-

シマダ, ケンイチ, 1929-

島田健一, 1929-

Languages