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Author

Shokei Kim-Mitsuyama

Other affiliations: Osaka City University
Bio: Shokei Kim-Mitsuyama is an academic researcher from Kumamoto University. The author has contributed to research in topics: Angiotensin II & Angiotensin II receptor type 1. The author has an hindex of 41, co-authored 123 publications receiving 7954 citations. Previous affiliations of Shokei Kim-Mitsuyama include Osaka City University.


Papers
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Journal ArticleDOI
TL;DR: The Japanese Society of Hypertension Guidelines for the Management ofhypertension (JSH 2009) provide guidelines for the management ofpertension in patients with high blood pressure.
Abstract: The Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2009)

1,409 citations

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TL;DR: Kazuaki SHIMAMOTO, Katsuyuki ANDO, Toshiro FUJITA, Naoyuki HASEBE, Jitsuo HIGAKI, Masatsugu HORIUCHI, Yutaka IMAI, Tsutomu IMAIZUMI, Toshihiko ISHIMITSU, Masaaki ITO, Sadayoshi ITO and Hiroshi ITOH are presented.
Abstract: Kazuaki SHIMAMOTO, Katsuyuki ANDO, Toshiro FUJITA, Naoyuki HASEBE, Jitsuo HIGAKI, Masatsugu HORIUCHI, Yutaka IMAI, Tsutomu IMAIZUMI, Toshihiko ISHIMITSU, Masaaki ITO, Sadayoshi ITO, Hiroshi ITOH, Hiroshi IWAO, Hisashi KAI, Kazuomi KARIO, Naoki KASHIHARA, Yuhei KAWANO, Shokei KIM-MITSUYAMA, Genjiro KIMURA, Katsuhiko KOHARA, Issei KOMURO, Hiroo KUMAGAI, Hideo MATSUURA, Katsuyuki MIURA, Ryuichi MORISHITA, Mitsuhide NARUSE, Koichi NODE, Yusuke OHYA, Hiromi RAKUGI, Ikuo SAITO, Shigeyuki SAITOH, Kazuyuki SHIMADA, Tatsuo SHIMOSAWA, Hiromichi SUZUKI, Kouichi TAMURA, Norio TANAHASHI, Takuya TSUCHIHASHI, Makoto UCHIYAMA, Shinichiro UEDA, Satoshi UMEMURA, on behalf of The Japanese Society of Hypertension Committee for Guidelines for the Management of Hypertension

1,061 citations

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TL;DR: IL-22 derived from activated T cells acts on SEMFs to elicit expression of proinflammatory cytokines and matrix-degrading molecules indicating proinflammatory/remodeling roles in IBD.

474 citations

Journal ArticleDOI
TL;DR: In the paragraph referring to the measurement of central blood pressure and augmentation index (AI) from radial artery pulse waves, the device ‘Omron Healthcare HEM7000AI’ was stated as being used.
Abstract: Correction to: Hypertension Research (2009) 32, 11–23; doi:10.1038/hr.2008.2 A machine number specified in the JSH Guidelines (Chapter 2, page 15) was incorrect. On page 15, in the paragraph referring to the measurement of central blood pressure and augmentation index (AI) from radial artery pulse waves, the device ‘Omron Healthcare HEM7000AI’ was stated as being used.

405 citations

Journal ArticleDOI
TL;DR: Glycemic control with empagliflozin significantly ameliorated cardiovascular injury and remodeling, vascular dysfunction, and cognitive decline in obese and type 2 diabetic mice and seems to be potentially a promising therapeutic agent for diabetic macrovascular disease and Cognitive decline.
Abstract: There has been uncertainty regarding the benefit of glycemic control with antidiabetic agents in prevention of diabetic macrovascular disease. Further development of novel antidiabetic agents is essential for overcoming the burden of diabetic macrovascular disease. The renal sodium glucose co-transporter 2 (SGLT2) inhibitor is a novel antihyperglycemic agent for treatment of type 2 diabetes. This work was performed to determine whether empagliflozin, a novel SGLT2 inhibitor, can ameliorate cardiovascular injury and cognitive decline in db/db mouse, a model of obesity and type 2 diabetes. (1) Short-term experiment: The first experiment was performed to examine the effect of 7 days of empagliflozin treatment on urinary glucose excretion and urinary electrolyte excretion in db/db mice. (2) Long-term experiment: The second experiment was undertaken to examine the effect of 10 weeks of empagliflozin treatment on cardiovascular injury, vascular dysfunction, cognitive decline, and renal injury in db/db mice. (1) Short-term experiment: Empagliflozin administration significantly increased urinary glucose excretion, urine volume, and urinary sodium excretion in db/db mice on day 1, but did not increase these parameters from day 2. However, blood glucose levels in db/db mice were continuously decreased by empagliflozin throughout 7 days of the treatment. (2) Long-term experiment: Empagliflozin treatment caused sustained decrease in blood glucose in db/db mice throughout 10 weeks of the treatment and significantly slowed the progression of type 2 diabetes. Empagliflozin significantly ameliorated cardiac interstitial fibrosis, pericoronary arterial fibrosis, coronary arterial thickening, cardiac macrophage infiltration, and the impairment of vascular dilating function in db/db mice, and these beneficial effects of empagliflozin were associated with attenuation of oxidative stress in cardiovascular tissue of db/db mice. Furthermore, empagliflozin significantly prevented the impairment of cognitive function in db/db mice, which was associated with the attenuation of cerebral oxidative stress and the increase in cerebral brain-derived neurotrophic factor. Empagliflozin ameliorated albuminuria, and glomerular injury in db/db mice. Glycemic control with empagliflozin significantly ameliorated cardiovascular injury and remodeling, vascular dysfunction, and cognitive decline in obese and type 2 diabetic mice. Thus, empagliflozin seems to be potentially a promising therapeutic agent for diabetic macrovascular disease and cognitive decline.

285 citations


Cited by
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Journal ArticleDOI
TL;DR: Molecular mechanisms of factors related to the EPR effect, the unique anatomy of tumor vessels, limitations and techniques to avoid such limitations, augmenting tumor drug delivery, and experimental and clinical findings are discussed.

3,034 citations

Journal ArticleDOI
TL;DR: In this article, a systematic review and meta-analysis of large-scale blood pressure lowering trials, published between Jan 1, 1966, and July 7, 2015, was performed.

2,296 citations

Journal ArticleDOI
TL;DR: In this article, a new paradigm for heart failure with preserved ejection fraction (HFPEF) development is proposed, which identifies a systemic proinflammatory state induced by comorbidities as the cause of myocardial structural and functional alterations.

2,246 citations

Journal ArticleDOI
TL;DR: IL-22 is identified as a new cytokine expressed by Th17 cells that synergizes with IL- 17A or IL-17F to regulate genes associated with skin innate immunity.
Abstract: Th17 cells are a distinct lineage of effector CD4+ T cells characterized by their production of interleukin (IL)-17. We demonstrate that Th17 cells also expressed IL-22, an IL-10 family member, at substantially higher amounts than T helper (Th)1 or Th2 cells. Similar to IL-17A, IL-22 expression was initiated by transforming growth factor β signaling in the context of IL-6 and other proinflammatory cytokines. The subsequent expansion of IL-22–producing cells was dependent on IL-23. We further demonstrate that IL-22 was coexpressed in vitro and in vivo with both IL-17A and IL-17F. To study a functional relationship among these cytokines, we examined the expression of antimicrobial peptides by primary keratinocytes treated with combinations of IL-22, IL-17A, and IL-17F. IL-22 in conjunction with IL-17A or IL-17F synergistically induced the expression of β-defensin 2 and S100A9 and additively enhanced the expression of S100A7 and S100A8. Collectively, we have identified IL-22 as a new cytokine expressed by Th17 cells that synergizes with IL-17A or IL-17F to regulate genes associated with skin innate immunity.

2,225 citations

Journal ArticleDOI
TL;DR: This work shows that interleukin-22 (IL-22) has a crucial role in the early phase of host defense against C. rodentium and identifies a new innate immune function for IL-22 in regulating early defense mechanisms against A/E bacterial pathogens.
Abstract: Infections by attaching and effacing (A/E) bacterial pathogens, such as Escherichia coli O157:H7, pose a serious threat to public health. Using a mouse A/E pathogen, Citrobacter rodentium, we show that interleukin-22 (IL-22) has a crucial role in the early phase of host defense against C. rodentium. Infection of IL-22 knockout mice results in increased intestinal epithelial damage, systemic bacterial burden and mortality. We also find that IL-23 is required for the early induction of IL-22 during C. rodentium infection, and adaptive immunity is not essential for the protective role of IL-22 in this model. Instead, IL-22 is required for the direct induction of the Reg family of antimicrobial proteins, including RegIIIbeta and RegIIIgamma, in colonic epithelial cells. Exogenous mouse or human RegIIIgamma substantially improves survival of IL-22 knockout mice after C. rodentium infection. Together, our data identify a new innate immune function for IL-22 in regulating early defense mechanisms against A/E bacterial pathogens.

1,780 citations