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The cellular inflammatory response in human spinal cords after injury.
TLDR
Data indicate that potentially destructive neutrophils and activated microglia, replete with oxidative and proteolytic enzymes, appear within the first few days of SCI, suggesting that anti-inflammatory 'neuroprotective' strategies should be directed at preventing early neutrophil influx and modifying microglial activation.
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Induction of reproducible brain infarction by photochemically initiated thrombosis
TLDR
The fact that the main pathological features of stroke are consistently reproduced should permit its use in assessing treatment regimens, and the capability of producing infarction in preselected cortiacal regions may facilitate the study of behavioral, functional, and structural consequences of acute and chronic stroke.
View on Wiley
Small Differences in Intraischemic Brain Temperature Critically Determine the Extent of Ischemic Neuronal Injury
TLDR
Results demonstrate that rectal temperature unreliably reflects brain temperature during ischemia, and that despite severe depletion of brain energy metabolites at all temperatures, small increments of intraischemic brain temperature markedly accentuate histopathological changes following 3-day survival.
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Inflammatory Mechanisms after Ischemia and Stroke
TLDR
Data is summarized regarding the role of the vasculature, leukocytes, blood-brain barrier, macrophages, and microglia after experimental and clinical stroke.
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Glutamate Release and Free Radical Production Following Brain Injury: Effects of Posttraumatic Hypothermia
TLDR
The present data indicate that TBI is followed by prompt increases in both glutamate release and hydroxyl radical production from cortical regions adjacent to the impact site, suggesting a mechanism by which hypothermia confers protection following TBI.
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Early microvascular and neuronal consequences of traumatic brain injury: a light and electron microscopic study in rats.
TLDR
A consistent pattern of microvascular and neuronal abnormalities can be documented in the early posttraumatic period of TBI in anesthetized Sprague-Dawley rats, and ultrastructural studies obtained evidence for irreversible neuronal injury and mechanical damage to vessel walls at this early post traumatic period.
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Effect of mild hypothermia on ischemia-induced release of neurotransmitters and free fatty acids in rat brain.
TLDR
The results suggest that mild intraischemic hypothermia does not affect the ischemia-induced local cerebral blood flow reduction or free fatty acid accumulation.
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Effect of Ischemia on the In Vivo Release of Striatal Dopamine, Glutamate, and γ‐Aminobutyric Acid Studied by Intracerebral Microdialysis
TLDR
Levels of 1CBF, energy metabolites, and energy metabolites were uniformly reduced in both the ipsi‐ and contralateral striata at the end of the ischemic period, a finding implying that the lesion did not affect the severity of theIschemic insult itself, and suggests that excessive release of DA is important for the development of isChemic cell damage in the striatum.
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Therapeutic modulation of brain temperature: relevance to ischemic brain injury.
TLDR
The importance of monitoring and regulating the brain temperature during experimental studies of cerebral ischemia to insure a consistent pathologic outcome and to avoid the false attribution of "pharmacoprotection" to drugs that reduce the body temperature is underscored.
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Temporal and Regional Patterns of Axonal Damage following Traumatic Brain Injury: A Beta‐amyloid Precursor Protein Immunocytochemical Study in Rats
TLDR
Data indicate that parasagittal F-P brain injury results in widespread axonalDamage, that axonal damage includes both reversible and delayed patterns, and that injury severity is an important factor in determining the severity of the axonal response to TBI.
View on Wolters Kluwer
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