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Cerebral inflammatory reaction is discussed as a contributor to adverse cerebral outcome after cardiac surgery with cardiopulmonary bypass.
The intracerebral administration of bacterial endotoxin resulted in cerebral inflammatory state evidenced by increased malondialdehyde (MDA), decreased reduced glutathione (GSH) level, increased nitric oxide as well as increased acetylcholinesterase (AChE) activity in the brain.
In summary, our data suggest that attenuation of postischemic cerebral inflammatory processes decrease secondary neurotoxic cell death, decrease infarct size and ameliorate clinical neurological impairment.
Mild hypothermia after cardiac arrest attenuates cerebral inflammatory response.
So far, most association studies have focused on the presence or absence of cerebral inflammatory demyelination.
The cerebral inflammatory demyelinating form of X-ALD is independent of AMN.
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Altered eicosanoid metabolism at specific times after brain injuries contributes to dynamic local changes in the cerebral vasculature, inflammatory status, neural cell death, as well as neurophysiologic functions.
On the other hand, in a total of about 60% of male X-ALD patients, rapidly progressive, inflammatory cerebral demyelination (cerebral X-ALD, CALD) occurs independent of AMN.
In CALD, rapidly progressive, inflammatory cerebral demyelination occurs independently of AMN.
Inversely, neurotransmitters and neurohormones also modulate cerebral expression of inflammatory mediators [ 85, 86].
The broad clinical presentation can be grouped into two major phenotypes, adrenomyeloneuropathy (AMN) and inflammatory cerebral adrenoleukodystrophy (CALD).
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