NAKACHI-MIYAGI Megumi

写真a

Title

Lecturer

Researcher Number(JSPS Kakenhi)

60632015

Laboratory Address

207 Uehara,Nishihara,Okinawa

Mail Address

E-mail address

Laboratory Phone number

+81-98-895-1214

Current Affiliation Organization 【 display / non-display

  • Duty   University of the Ryukyus   Faculty of Medicine   Lecturer  

Graduate School 【 display / non-display

  • 2011.04
    -
    2015.03

    Kyushu University  Graduate School, Division of Medical Sciences  Doctor's Course  Completed

External Career 【 display / non-display

  • 2011.11
    -
    2012.12

     

  • 2012.12
    -
    2016.01

    University of the Ryukyus, Facuity of Medicine, Instructor  

  • 2016.02
     
     

    Office of Medical Education, Faculty of Medicine, University of the Ryukyus  

Research Interests 【 display / non-display

  • 医学教育

  • 食育

  • 社会疫学

  • 動脈硬化

  • シェアストレス

Published Papers 【 display / non-display

  • Age- and sex-related effects on ankle-brachial index in a screened cohort of Japanese: the Okinawa Peripheral Arterial Disease Study (OPADS).

    Ishida A, Miyagi M, Kinjo K, Ohya Y.

    Eur J Prev Cardiol.   21 ( 6 ) 712 - 718   2014.06 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

     View Summary

    AIMS: Age-related change of ankle-brachial index (ABI) within the general population, especially <40 years, has not been determined in large population studies. We evaluated the value of the ABI by age- and sex-related differences in a screened cohort. METHODS AND RESULTS: The ABI was examined in 13,211 participants (aged 21-89 years) in a health evaluation programme. The mean ABI was lower in women than in men at all ages. The ABI was lowest at <40 years, and increased with age; the maximum was at 60-69 years in both sexes. In participants <40 years, 186 (22%) of women and 108 (9.8%) of men had a borderline ABI (0.9-1.0). The prevalence of an ABI ≤0.9 in men increased with age, and sharply rose to 3.3% at ≥70 years. Conversely, women demonstrated a J-curve relationship, where the prevalence of an ABI ≤0.9 was lowest at 60-69 years (0.2%), and increased at <40 (0.9%) and ≥70 years (1.6%). The prevalence of atherosclerotic risk factors was higher in participants with an ABI ≤0.9 than those with an ABI >0.9 in men, both ≤60 and >60 years, and in women >60 years. In women ≤60 years, however, the prevalence of atherosclerotic risk factors in participants with an ABI >0.9 was as small as those with an ABI ≤0.9. CONCLUSION: The ABI increased with age until 60-69 years, and was lower in women than in men. It is unlikely that a low ABI in younger healthy women always indicate that existence of arterial stenosis.

  • Improvement of cardiac function after granulocyte-colony stimulating factor-mobilized peripheral blood mononuclear cell implantation in a patient with non-ischemic dilated cardiomyopathy associated with thromboangiitis obliterans

    Ayano Kakihana, Akio Ishida, Megumi Miyagi, Tetsuya Ishiki, Koichiro Okumura, Tomomasa Kamiyama, Yusuke Ohya, Shuichi Takishita

    Intern Med .   48 ( 12 ) 1003 - 1007   2009.06 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

     View Summary

    Cardiac involvement is a rare complication with thromboangiitis obliterans (TAO). We report a 29-year-old man with TAO accompanied with non-ischemic dilated cardiomyopathy. He had no history of heart disease, but echocardiogram demonstrated diffuse hypokinesis and dilated left ventricle. Coronary angiography revealed no organic stenotic lesion. For limb salvage, he was treated with granulocyte-colony stimulating factor (G-CSF)-mobilized peripheral blood mononuclear cell (PBMNC) implantation on his right leg. Not only ischemic leg symptoms, but also plasma level of BNP and (123)I-metaiodobenzylguanidine scintigraphic parameters improved after 24 weeks. G-CSF-mobilized PBMNC implantation could be an effective approach to treating non-ischemic cardiomyopathy.

  • Activator protein-1 mediates shear stress-induced prostaglandin d synthase gene expression in vascular endothelial cells.

    Miyagi M, Miwa Y, Takahashi-Yanaga F, Morimoto S, Sasaguri T.

    Arterioscler Thromb Vasc Biol.   25 ( 5 ) 970 - 975   2005.05 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

     View Summary

    OBJECTIVE: We attempted to determine the molecular mechanism of fluid shear stress-induced lipocalin-type prostaglandin D synthase (l-PGDS) expression in vascular endothelial cells. METHODS AND RESULTS: We examined the promoter region of the l-PGDS gene by loading laminar shear stress (20 dyne/cm2), using a parallel-plate flow chamber, on endothelial cells transfected with luciferase reporter vectors containing the 5'-flanking regions of the human l-PGDS gene. A deletion mutant analysis revealed that a shear stress-responsive element resided in the region between -2607 and -2523 bp. A mutation introduced into the putative binding site for activator protein-1 (AP-1) within this region eliminated the response to shear stress. In an electrophoretic mobility shift assay, shear stress stimulated nuclear protein binding to the AP-1 binding site, which was supershifted by antibodies to c-Fos and c-Jun. Shear stress elevated the c-Jun phosphorylation level in a time-dependent manner, similar to that of l-PGDS gene expression. SP600125, a c-Jun N-terminal kinase inhibitor, decreased the c-Jun phosphorylation, DNA binding of AP-1, and l-PGDS expression induced by shear stress. Additionally, an mRNA chase experiment using actinomycin D demonstrated that shear stress did not stabilize l-PGDS mRNA.

  • Physiology and pharmacology of the prostaglandin J2 family.

    Miwa Y, Taba Y, Miyagi M, Sasaguri T.

    Nihon Yakurigaku Zasshi   123 ( 1 ) 34 - 40   2004.01

    Type of publication: Research paper (scientific journal)

     View Summary

    The prostaglandin (PG) J(2) family including PGJ(2), Delta(12)-PGJ(2), and 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)) are metabolites of PGD(2). They had been known as powerful inhibitors of cell proliferation and viral replication until 15d-PGJ(2) was found to be a natural ligand for peroxisome proliferator-activated receptor gamma (PPAR gamma). Since then, several new pharmacological actions of the PGJ(2) family have been found, such as pro- and anti-apoptotic effects, cell differentiation-inducing effects, and inhibitory effects on inflammatory processes, whether they depend on PPAR gamma or not. We reported that the PGJ(2) family, particularly 15d-PGJ(2), inhibits cell proliferation by reducing the expression of G(1) cyclins and inducing the expression of cyclin-dependent kinase inhibitor p21 and moreover, induces cell differentiation in vascular smooth muscle cells. In vascular endothelial cells, we found that 15d-PGJ(2) inhibits apoptotic cell death at least in part by the induction of the inhibitor of apoptosis protein c-IAP1. More importantly, physiological levels of laminar fluid shear stress loaded on endothelial cells upregulate the expression of lipocalin-type PGD(2) synthase, which converts PGH(2) to PGD(2), the precursor of the PGJ(2) family. Based on these results, we have hypothesized that the PGJ(2) family synthesized in vascular wall plays an important physiological role to protect vascular cells from atherogenic stimuli.

  • 15-deoxy-delta 12,14-prostaglandin J2 and laminar fluid shear stress stabilize c-IAP1 in vascular endothelial cells.

    Taba Y, Miyagi M, Miwa Y, Inoue H, Takahashi-Yanaga F, Morimoto S, Sasaguri T.

    Am J Physiol Heart Circ Physiol.   285 ( 1 ) 38 - 46   2003.06 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

     View Summary

    Laminar shear stress strongly inhibits vascular endothelial cell apoptosis by unknown mechanisms. We reported that shear stress stimulates endothelial cells to produce 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2) by elevating the expression level of lipocalin-type prostaglandin D synthase. To investigate the role of 15d-PGJ2 produced in the vascular wall, we examined the effect of 15d-PGJ2 on endothelial cell apoptosis. We induced apoptosis in human umbilical vein endothelial cells (HUVECs) by growth factor deprivation. 15d-PGJ2 strongly inhibited DNA ladder formation, nuclear fragmentation, and caspase-3-like activity in HUVECs. To elucidate the mechanism by which 15d-PGJ2 inhibits endothelial cell apoptosis, we examined expression of the inhibitor of apoptosis proteins (IAP) cellular-IAP1 (c-IAP1), c-IAP2, x-linked IAP, and survivin in HUVECs. In parallel with the inhibition of apoptosis, 15d-PGJ2 elevated the expression level of c-IAP1 protein in a dose- and time-dependent manner without changing the mRNA level. Laminar shear stress also induced c-IAP1 expression. Chase experiments with the use of cycloheximide revealed that 15d-PGJ2 and shear stress both inhibited the proteolytic degradation of c-IAP1 protein. These results suggested that 15d-PGJ2 inhibits endothelial cell apoptosis through, at least in part, c-IAP1 protein stabilization. This mechanism might be involved in the antiapoptotic effect of laminar shear stress.

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Presentations 【 display / non-display

  • Current status of clinical-clerkship at University of the Ryukyus and student questionnaire results

    The 52nd Annual Meeting of the Japan Society for Medical Education  (Kagoshima)  2020.07  -  2020.07 

  • Current status of clinical-clerkship at University of the Ryukyus and student questionnaire results

    MEGUMI NAKACHI

    The 51st Annual Meeting of the Japan Society for Medical Education  (Kyoto)  2019.07  -  2019.07 

  • Experience of the fieldwork organized by health care students for community health seminar

    The 51st Annual Meeting of the Japan Society for Medical Education  (Kyoto)  2019.07  -  2019.07 

  • Individual interview with the medical students on the poor academic results and learning support

    MEGUMI NAKACHI

    The 50th Annual Meeting of the Japan Society for Medical Education  2018  -  2018 

  • Efforts of clinical-clerkship reform in University of the Ryukyus and its effect

    MEGUMI NAKACHI

    The 49th Annual Meeting of the Japan Society for Medical Education  2017  -  2017 

Grant-in-Aid for Scientific Research 【 display / non-display

  • Challenging research (sprout)

    Project Year: 2013.04  -  2016.03 

    Direct: 22,000,000 (YEN)  Overheads: 660,000 (YEN)  Total: 2,860,000 (YEN)