Mannose binding lectin gene deficiency increases susceptibility to traumatic brain injury in mice.
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Molecular mechanisms of inflammation and tissue injury after major trauma--is complement the "bad guy"?Mannose-binding lectin and the balance between immune protection and complicationLow-level laser light therapy improves cognitive deficits and inhibits microglial activation after controlled cortical impact in miceGenetic analysis of the role of tumor necrosis factor receptors in functional outcome after traumatic brain injury in mice.Versatility of the complement system in neuroinflammation, neurodegeneration and brain homeostasisSpinal cord trauma and the molecular point of no returnThe contribution of mannose binding lectin to reperfusion injury after ischemic stroke.Concussive injury before or after controlled cortical impact exacerbates histopathology and functional outcome in a mixed traumatic brain injury model in mice.Mannose-Binding Lectin: Biologic Characteristics and Role in the Susceptibility to Infections and Ischemia-Reperfusion Related Injury in Critically Ill Neonates.Low levels of mannose-binding lectin at admission increase the risk of adverse neurological outcome in preterm infants: a 1-year follow-up study.Thrombospondin-1 Gene Deficiency Worsens the Neurological Outcomes of Traumatic Brain Injury in MiceAbsence of the complement regulatory molecule CD59a leads to exacerbated neuropathology after traumatic brain injury in mice.The pharmacokinetics and pharmacodynamics of Kollidon VA64 dissociate its protective effects from membrane resealing after controlled cortical impact in mice.Mannose-binding lectin binds to amyloid β protein and modulates inflammation.Tumor necrosis factor alpha and Fas receptor contribute to cognitive deficits independent of cell death after concussive traumatic brain injury in mice.Pharmacological inhibition of mannose-binding lectin ameliorates neurobehavioral dysfunction following experimental traumatic brain injury.The role of the complement system in traumatic brain injury: a review.Intraventricular apolipoprotein ApoJ infusion acts protectively in Traumatic Brain Injury.Autosomal dominant mannose-binding lectin deficiency is associated with worse neurodevelopmental outcomes after cardiac surgery in infants.
P2860
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P2860
Mannose binding lectin gene deficiency increases susceptibility to traumatic brain injury in mice.
description
2008 nî lūn-bûn
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2008年の論文
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2008年学术文章
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name
Mannose binding lectin gene de ...... raumatic brain injury in mice.
@en
Mannose binding lectin gene de ...... raumatic brain injury in mice.
@nl
type
label
Mannose binding lectin gene de ...... raumatic brain injury in mice.
@en
Mannose binding lectin gene de ...... raumatic brain injury in mice.
@nl
prefLabel
Mannose binding lectin gene de ...... raumatic brain injury in mice.
@en
Mannose binding lectin gene de ...... raumatic brain injury in mice.
@nl
P2093
P2860
P356
P1476
Mannose binding lectin gene de ...... raumatic brain injury in mice.
@en
P2093
Alan B Ezekowitz
Gregory L Stahl
Hyung-Hwan Kim
Kazue Takahashi
Michael C Carroll
Michael J Whalen
Phoebe H Yager
Zerong You
P2860
P304
P356
10.1038/SJ.JCBFM.9600605
P577
2008-01-09T00:00:00Z