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Quantitative determination of stress status and its clinical applications

Research Project

Project/Area Number 13670694
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Circulatory organs internal medicine
Research InstitutionThe University of Tokyo

Principal Investigator

UEHARA Yoshio  The University of Tokyo, Health Service Center, Associate Professor, 保健管理センター, 助教授 (40184965)

Co-Investigator(Kenkyū-buntansha) NEGORO Hideyuki  The University of Tokyo, Health Service Center, Staff, 医学部附属病院, 非常勤医師
TAGUCHI Rie  The University of Tokyo, Health Service Center, Instructor, 保健管理センター, 助手 (90301126)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥2,100,000 (Direct Cost: ¥2,100,000)
Keywordsstress / prostaglandin / cognitive function / exercise loading / excessive salt intake / cerebrospinal fluid / adrenergic nervous system / organ damage / 臓器障害
Research Abstract

To determine factors that predict quantitatively stress status in human, we assessed the lipocaline-type prostaglandin D synthase (PGDS). PGDS is biosyntheslzed in the choroidal plexus in the brain and released in the circulating blood. Urinary PGDS excretion well reflects he concentrations in the blood. In various stress-related diseases, we firstly investigated urinary PGDS excretion in primary renal diseases in humans and in adriamycin-induced glomerulosclerosis with enhanced adrenergic nerve activity. Urinary PGDS excretion is increased in chronic renal dysfunction and this parallels the advance of renal injury. Moreover, urinary PGDS excretion is increased in early stage of essential hypertension without apparent renal injury, suggesting that the PGDS is related to the onset of hypertension in humans. In over-weight stress followed by type 2 diabetes in both rats and humans, urinary PGDS excretion is increased before the renal injury. When the normal rats are challenged for 52 weeks with sensory stress of excessive salt intake, urinary PGDS excretion is significantly increased. These data clearly indicate that urinary PGDS excretion is potentially a predictor of stress status and the forthcoming stress-induced systemic diseases. We need to expand our study to elucidate the relationship between PGDS status and psychiatric stress like fear or aching like sever inflammation.

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • Research Products

    (18 results)

All Other

All Publications (18 results)

  • [Publications] Hirawa N et al.: "Urinary prostaglandin D synthase (b-trace) excretion increases in the early stage of diabetes mellitus"Nephron. 87・3. 321-327 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Hirawa N et al.: "Lipocalin-type prostaglandin D synthase in essential hypertension"Hypertension. 39・2. 449-454 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Hamano K et al.: "Blood sugar control reverses the increase in urinary excretion of prostaglandin D synthase in diabetic patients"Nephron. 92・1. 77-85 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Negoro H et al.: "Endogenous prostaglandin D2 synthesis is associated with an increase in plasminogen activator inhibitor-1 generation in bovine endothelial cells"J Hypertens. 20・7. 1347-1354 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Tsuchida T et al.: "Lipocaline-type prostaglandin D synthase in urine in adriamycin-induced nephropathy of mice"Nephron in submission.

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Hirawa N: "Urinary prostaglandin D synthase (β-trace) excretion increases in the early stage of diabetes mellitus"Nephron. 87-3. 321 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Hirawa N: "Lipocalin-type prostaglandin D synthase in essential hypertension"Hypertension. 39-part 2. 449 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Hamano K: "Blood sugar control reverses the increase in urinary excretion of prostaglandin D synthase in diabetic patients"Nephron. 92-1. 77 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Negoro H: "Endogenous prostaglandin D_2 synthesis is associated with an increase in plasminogen activator inhibitor-1 generation in bovine endothelial cells"Journal of Hypertension. 20-7. 1347 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Tsuchida T: "Lipocaline-type prostaglandin D synthase in urine in adriamycin-induced nephropathy of mice"Nephron. in submission.

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Hirawa N et al.: "Urinary prostaglandin D synthase (b-trace) excretion increases in the early stage of diabetes mellitus"Nephron. 87・3. 321-327 (2001)

    • Related Report
      2002 Annual Research Report
  • [Publications] Hirawa N et al.: "Lipocalin-type prostaglandin D synthase in essential hypertension"Hypertension. 39・2. 449-454 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Hamano K et al.: "Blood sugar control reverses the increase in urinary excretion of prostaglandin D synthase in diabetic patients"Nephron. 92・1. 77-85 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Negoro H et al.: "Endogenous prostaglandin D2 synthesis is associated with an increase in plasminogen activator inhibitor-1 generation in bovine endothelial cells"J Hypertens. 20・7. 1347-1354 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Hirawa N, et al.: "Urinary prostaglandin D synthase(b-trace)excretion increases in the early stage of diabetes mellitus"Nephron. 87. 321-327 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Hirawa N, et al.: "Lipocalin-type prostaglandin D synthase in essential hypertension"Hypertension. 39・2. 449-454 (2002)

    • Related Report
      2001 Annual Research Report
  • [Publications] Hamano K, et al.: "Excretion of prostaglandin D synthase in diabetic patients"Nephron. (印刷中). (2002)

    • Related Report
      2001 Annual Research Report
  • [Publications] Negoro H, et al.: "Endogenous prostaglandin D_2 synthesis is associated with an increase in plasminogen activator inhibitor-1 generation in bovine endothelial cells"J Hypertens. (印刷中). (2002)

    • Related Report
      2001 Annual Research Report

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Published: 2001-04-01   Modified: 2016-04-21  

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