D. Graham

Publications469
h-index93
Citations32,200
Highly Influential Citations907
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Diffuse axonal injury and traumatic coma in the primate
TLDR
It is concluded that axonal damage produced by coronal head acceleration is a major cause of prolonged traumatic coma and its sequelae and is identical to that seen in severe head injury in humans.
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Diffuse axonal injury in head injury: Definition, diagnosis and grading
TLDR
Diffuse axonal injury was identified in 122 of a series of 434 fatal non‐missile head injuries–‐10 grade 1, 29 grade 2 and 83 grade 3; in 24 of these cases the diagnosis could not have been made without microscope examination, while in a further 31 microscopical examination was required to establish its severity.
View on Wiley
Lateral fluid percussion brain injury: a 15-year review and evaluation.
TLDR
It is concluded that the LFP brain injury model is an appropriate tool to study the cellular and mechanistic aspects of human TBI that cannot be addressed in the clinical setting, as well as for the development and characterization of novel therapeutic interventions.
View on PubMed
Diffuse axonal injury due to nonmissile head injury in humans: An analysis of 45 cases
TLDR
The available evidence indicates that DAI in human beings occurs at the time of head injury and is not due to complicating factors such as hypoxia, brain swelling, or raised intracranial pressure.
View on Wiley
Focal Cerebral Ischaemia in the Rat: 1. Description of Technique and Early Neuropathological Consequences following Middle Cerebral Artery Occlusion
TLDR
The ability to produce a consistent focal ischaemic lesion in the rodent brain provides a technical approach that is sufficiently reproducible to enable investigation of the pathophysiology of ischaemia using recently developed autoradiographic and neurochemical methods.
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Multiple proteins implicated in neurodegenerative diseases accumulate in axons after brain trauma in humans
View on Elsevier
Recent Advances in Neurotrauma
TLDR
TBI in humans is heterogeneous, reflecting various pathologies in differing proportions in patients whose genetic background (APOE gene polymorphisms) contributes to the outcome at 6 months, although considerable progress has been made in the understanding of TBI.
View on Wolters Kluwer
Beta amyloid protein deposition in the brain after severe head injury: implications for the pathogenesis of Alzheimer's disease.
TLDR
The data from this study support proposals that increased expression of beta APP is part of an acute phase response to neuronal injury in the human brain, that extensive overexpression ofbeta APP can lead to deposition of beta AP and the initiation of an Alzheimer disease-type process within days, and that head injury may be an important aetiological factor in Alzheimer's disease.
View on BMJ
Neuropathological sequelae of traumatic brain injury: relationship to neurochemical and biomechanical mechanisms.
TLDR
The laboratory investigations linking experimental models of brain injury to clinical diagnosis and treatment are reviewed and the role of neurochemical alterations in contributing to the development of secondary or delayed cellular death and damage is studied.
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Apoptosis after traumatic brain injury.
TLDR
The regional and temporal patterns of apoptosis following TBI and the possible mechanisms underlying trauma-induced apoptosis are reviewed, and whether apoptosis may serve a protective role in the injured brain is considered.
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