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出 处:《Journal of Medical Colleges of PLA(China)》2001年第3期161-164,共4页中国人民解放军军医大学学报(英文版)
摘 要:Objective:Theaimof thisstudywas to determinethepatternsof heat-shockprotein70(HSP 70 )biosynthesis followingtraumaticbraininjury,andobservetheeffectof HSP 70 inductionon thefunctionof thevitalcenterinthebrain stem.Methods:Ratmodelsof suddendeathresultedformtraumaticbraininjurywereproduced,andHSP 70 expressionin theratbrainstemwasdeterminedby immunohistochemistry,theinductionof HSP 70 mRNAdetectedby RT-PCR.Re -sults: Thelevelof HSP 70 mRNAwasprominentlyelevatedinthebrainstemas earlyas15minfollowingtheimpactin-jury,whileHSP 70 expressionwasonlyobserved3to6h aftertheinjury.Itwasalsoobservedthatthelevelsof HSP 70 mR-NAbutnottheproteinwereelevatedinthebrainstemof suddendeathrats.Conclusion:Thesynthesisof HSP 70 wassig-nificantlyenhancedinthebrainstemfollowingtraumaticinjury,andtheexpressionof HSP 70 is beneficialto eliminatethe stressagents,andto sustainthecellularproteinhomeostasis.Whentheinjurydisturbsthesynthesisof HSP 70 to disarmthe protectivemechanismof heat-shockproteins,dysfunctionof thevitalcenterinthebrainstem,andconsequentlydeathmay occur.Breachinthesynchronizationof HSP 70 mRNA-proteincanbeindicativeof fataldamageto thenervecells.Objective:Theaimof thisstudywas to determinethepatternsof heat-shockprotein70(HSP 70 )biosynthesis followingtraumaticbraininjury,andobservetheeffectof HSP 70 inductionon thefunctionof thevitalcenterinthebrain stem.Methods:Ratmodelsof suddendeathresultedformtraumaticbraininjurywereproduced,andHSP 70 expressionin theratbrainstemwasdeterminedby immunohistochemistry,theinductionof HSP 70 mRNAdetectedby RT-PCR.Re -sults: Thelevelof HSP 70 mRNAwasprominentlyelevatedinthebrainstemas earlyas15minfollowingtheimpactin-jury,whileHSP 70 expressionwasonlyobserved3to6h aftertheinjury.Itwasalsoobservedthatthelevelsof HSP 70 mR-NAbutnottheproteinwereelevatedinthebrainstemof suddendeathrats.Conclusion:Thesynthesisof HSP 70 wassig-nificantlyenhancedinthebrainstemfollowingtraumaticinjury,andtheexpressionof HSP 70 is beneficialto eliminatethe stressagents,andto sustainthecellularproteinhomeostasis.Whentheinjurydisturbsthesynthesisof HSP 70 to disarmthe protectivemechanismof heat-shockproteins,dysfunctionof thevitalcenterinthebrainstem,andconsequentlydeathmay occur.Breachinthesynchronizationof HSP 70 mRNA-proteincanbeindicativeof fataldamageto thenervecells.
关 键 词:heat shock protein TRAUMATIC BRAIN INJURY immunohistochemistry RT-PCR
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