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The influence of inflammatory mediators on the pathophysiology of delayed paraplegia after spinal cord ischemia.

Research Project

Project/Area Number 20791075
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeSingle-year Grants
Research Field Anesthesiology/Resuscitation studies
Research InstitutionYamaguchi University

Principal Investigator

YAMASHITA Atsuo  Yamaguchi University, 医学部附属病院, 助教 (50379971)

Research Collaborator MATSUMOTO Mishiya  山口大学, 医学部, 教授 (60243664)
Project Period (FY) 2008 – 2009
Project Status Completed (Fiscal Year 2009)
Budget Amount *help
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Keywords脳・神経科学 / 脊髄 / 虚血 / 麻酔科学 / 脳・神経 / 神経科学
Research Abstract

Recently, high mobility group box 1 protein (HMGB1) related to cytokine gets into the limelight. We investigated whether the ischemic spinal cord injury in rabbits was reduced to inhibit the activation of HMGB1. We assigned rabbits to three groups (n=5 in each); a control group, low dose anti- HMGB1 antibody group (segmental administration of 1000μg anti- HMGB1 antibody), high dose anti- HMGB1 antibody group (segmental administration of 2000μg anti- HMGB1 antibody). Spinal cord ischemia was produced by occluding the abdominal aorta for 13 min. After the reperfusion, hindlimb motor function (score range: 4, normal to 0, paraplegia) was assessed daily for 7 days, and then the number of normal neurons in the anterior spinal cord was counted. There were no significant intergroup differences in neurological scores and the numbers of normal neurons. The ischemic spinal cord injury in rabbits was not reduced to inhibit the activation of HMGB1.

Report

(3 results)
  • 2009 Annual Research Report   Final Research Report ( PDF )
  • 2008 Annual Research Report

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Published: 2008-04-01   Modified: 2016-04-21  

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