No evidence for the presence of apolipoprotein epsilon4, interleukin-lalpha allele 2 and interleukin-1beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans.

No evidence for the presence of apolipoprotein epsilon4, interleukin-lalpha allele 2 and interleukin-1beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans. Research Abstract Details 

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No evidence for the presence of apolipoprotein epsilon4, interleukin-lalpha allele 2 and interleukin-1beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans. Abstract Text:

V E Johnson,L Murray,R Raghupathi,J Stewart,J A R Nicoll,M A MacKinnon,T K McIntosh,D I Graham,

BACKGROUND: Brain injury after trauma is an important cause of mortality and morbidity in society. There is evidence in both man and laboratory animals that in addition to necrosis, cell loss may occur as a result of programmed cell death (PCD). The cellular and molecular responses after head injury are partly influenced by genetic polymorphisms of apolipoprotein E and the pro-inflammatory cytokine IL-I. AIM: The principal aim of this study was to determine whether the presence of the ApoE epsilon4, IL- 1 alpha2 or IL- 1beta2 allele types influenced the amounts of PCD after head injury compared with controls. METHODS: Paraffin sections from the hippocampus of 38 patients (32 M : 6 F, aged 15 - 75, mean 38 years, survival 7- 576 hours; mean 36 hours) who died after a head injury were stained by Tunel histochemistry and quantified, and genotyping was undertaken by PCR "blind" to clinical detail. RESULTS: There were more Tunel+ cells (neurons and glia) after head injury than in controls with statistically increased numbers in all sectors of the hippocampus including the dentate fascia. However, there was no correlation between ApoEepsilon4, IL- 1 alpha allele 2 and IL- 1beta allele 2 and the amount of Tunel positivity. CONCLUSION: Given that both the ApoE and IL-1 influence outcome after various forms of acute brain injury, further work will be required to determine the mechanism underlying this relationship.

No evidence for the presence of apolipoprotein epsilon4, interleukin-lalpha allele 2 and interleukin-1beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans. Publishing Authors By Initials

VE Johnson,L Murray,R Raghupathi,J Stewart,JA Nicoll,MA MacKinnon,TK McIntosh,DI Graham,

For similar genetic phenomena: variation (genetics): polymorphism, genetic research abstracts see: genetic phenomena: variation (genetics): polymorphism, genetic research

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No evidence for the presence of apolipoprotein epsilon4, interleukin-lalpha allele 2 and interleukin-1beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Clinical neuropathology

VOLUME: 25

Page Numbers: 255-64

Journal Abbreviation: Clin. Neuropathol.

ISSN: 0722-5091

DAY: 3

MONTH: 12

YEAR: 2007

No evidence for the presence of apolipoprotein epsilon4, interleukin-lalpha allele 2 and interleukin-1beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8214420

No evidence for the presence of apolipoprotein epsilon4, interleukin-lalpha allele 2 and interleukin-1beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans. Keywords Mesh Terms:

KEYWORDS: Polymorphism, Genetic

MESH TERMS: genetics

Chemical & Substance for Abstract: No evidence for the presence of apolipoprotein epsilon4, interleukin-lalpha allele 2 and interleukin-1beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans. Information

Substance Name: Interleukin-1beta

Registry Number: 0

Grant and Affiliation Information for No evidence for the presence of apolipoprotein epsilon4, interleukin-lalpha allele 2 and interleukin-1beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans.

AFFILIATION: Academic Unit of Neuropathology, University of Glasgow, Glasgow, Scotland, UK.

Country: Germany

AGENCY: United States NINDS

GRANT: 5-P05-NS008803-30

ACRONYM: NS

MEDLINETA: Clin Neuropathol

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