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RISS 인기검색어
- 검색키워드
- 저자 : Shimizu Ippei (검색결과 4 건)
- 무료
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- 유료
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Variable-focal Length Lens Using IPMC
Ippei SHIMIZU,Kunitomo KIKUCHI,Shigeki TSUCHITANI 제어로봇시스템학회 2009 제어로봇시스템학회 국제학술대회 논문집 Vol.2009 No.8
We fabricated a liquid lens type variable-focal length lens(VFLL), which is composed of a container with a movable silicon plate having a pupil (diameter: 4mm) covered by a thin polydimethylsiloxane (PDMS) film, a liquid enclosed in the container and a plural IPMCs fixed above the container for pushing the silicon plate downward. By applying a force to the silicon plate by IPMCs, the PDMS film of the pupil deforms upward. As a result, the focal length of the liquid lens decreases. The proposed method for fabricating VFLL has a large potential to realized very small VFLL.
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Shimizu, Ippei,Minamino, Tohru,Toko, Haruhiro,Okada, Sho,Ikeda, Hiroyuki,Yasuda, Noritaka,Tateno, Kaoru,Moriya, Junji,Yokoyama, Masataka,Nojima, Aika,Koh, Gou Young,Akazawa, Hiroshi,Shiojima, Ichiro,K American Society for Clinical Investigation 2010 The Journal of clinical investigation Vol.120 No.5
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Cellular Senescence in Arterial Diseases
Ippei Shimizu,Tohru Minamino 한국지질동맥경화학회 2020 지질·동맥경화학회지 Vol.9 No.1
Cell-proliferation potency is limited, as cells cannot proceed through the cell cycle continually. Instead, they eventually show an irreversible arrest of proliferation, commonly referred to as cellular senescence. Following the initial discovery of this phenomenon by Hayflick et al., studies have indicated that cells are also destined to undergo aging. In addition to the irreversible termination of proliferation, senescent cells are characterized by a flattened and enlarged morphology. Senescent cells become pro-inflammatory and contribute to the initiation and maintenance of sustained chronic sterile inflammation. Aging is associated with the accumulation of senescent cells in the cardiovascular system, and in general these cells are considered to be pathogenic because they mediate vascular remodeling. Recently, genetic and pharmacological approaches have enabled researchers to eliminate senescent cells both in vitro and in vivo. The term “senolysis” is now used to refer to the depletion of senescent cells, and evidence indicates that senolysis contributes to the reversal of age-related pathogenic phenotypes without the risk of tumorigenesis. The concept of senolysis has opened new avenues in research on aging, and senolysis may be a promising therapeutic approach for combating age-related disorders, including arterial diseases.
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박남미,MARQUEZ JUBERT,Garcia Maria Victoria Faith,Shimizu Ippei,이성률,김형규,한진 한국지질동맥경화학회 2021 지질·동맥경화학회지 Vol.10 No.2
Objective: Ischemic cardiomyopathy (ICM) is the leading cause of heart failure. Proteomic and genomic studies have demonstrated ischemic preconditioning (IPC) can assert cardioprotection against ICM through mitochondrial function regulation. Considering IPC is conducted in a relatively brief period, regulation of protein expression also occurs very rapidly, highlighting the importance of protein function modulation by post-translational modifications. This study aimed to identify and analyze novel phosphorylated mitochondrial proteins that can be harnessed for therapeutic strategies for preventing ischemia/reperfusion (I/R) injury. Methods: Sprague-Dawley rat hearts were used in an ex vivo Langendorff system to simulate normal perfusion, I/R, and IPC condition, after which the samples were prepared for phosphoproteomic analysis. Employing human cardiomyocyte AC16 cells, we investigated the cardioprotective role of CKMT2 through overexpression and how site-directed mutagenesis of putative CKMT2 phosphorylation sites (Y159A, Y255A, and Y368A) can affect cardioprotection by measuring CKMT2 protein activity, mitochondrial function and protein expression changes. Results: The phosphoproteomic analysis revealed dephosphorylation of mitochondrial creatine kinase (CKMT2) during ischemia and I/R, while preserving its phosphorylated state during IPC. CKMT2 overexpression conferred cardioprotection against hypoxia/reoxygenation (H/R) by increasing cell viability and mitochondrial adenosine triphosphate level, preserving mitochondrial membrane potential, and reduced reactive oxygen species (ROS) generation, while phosphomutations, especially in Y368, nullified cardioprotection by significantly reducing cell viability and increasing ROS production during H/R. CKMT2 overexpression increased mitochondrial function by mediating the proliferator-activated receptor γ coactivator-1α/estrogen-related receptor-α pathway, and these effects were mostly inhibited by Y368A mutation. Conclusion: These results suggest that regulation of quantitative expression and phosphorylation site Y368 of CKMT2 offers a unique mechanism in future ICM therapeutics.
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