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Pathobiology of ischaemic stroke: an integrated view
Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury
It is demonstrated that necroptosis contributes to delayed mouse ischemic brain injury in vivo through a mechanism distinct from that of apoptosis and offers a new therapeutic target for stroke with an extended window for neuroprotection.
Evidence of a Cerebrovascular Postarteriole Windkessel with Delayed Compliance
A modified windkessel model was developed to describe the temporal evolution of rCBV as a rapid elastic response of capillaries and veins followed by slow venous relaxation of stress, and venous delayed compliance was suggested as the mechanism for the poststimulus undershoot in blood oxygen-sensitive magnetic resonance imaging signal.
Neurological diseases: Mechanisms, challenges and opportunities in stroke
This new research focus addresses an important need in stroke research, provides challenges and opportunities that can be used to therapeutic advantage and is focused on how blood vessels and brain cells communicate with each other.
Effects of Matrix Metalloproteinase-9 Gene Knock-Out on the Proteolysis of Blood–Brain Barrier and White Matter Components after Cerebral Ischemia
Data demonstrate that the protective effects of MMP-9 gene knock-out after transient focal ischemia may be mediated by reduced proteolytic degradation of critical blood–brain barrier and white matter components.
Mechanisms of migraine aura revealed by functional MRI in human visual cortex
High-field functional MRI with near-continuous recording during visual aura in three subjects observed blood oxygenation level-dependent signal changes that strongly suggest that an electrophysiological event such as CSD generates the aura in human visual cortex.
Hypertension in mice lacking the gene for endothelial nitric oxide synthase
Responses to NOS blockade in the mutant mice suggest that non-endothelial isoforms of NOS may be involved in maintaining blood pressure, and eNOS mediates basal vasodilation.
Activation and Cleavage of Caspase-3 in Apoptosis Induced by Experimental Cerebral Ischemia
The existence of a time-dependent evolution of ischemic injury characterized by the close correspondence between caspase-like enzyme activation and an associated increase in immunoreactive product (caspases-3p20) beginning at or before reperfusion and followed several hours later by morphological and biochemical features of apoptosis is suggested.
Suppression of cortical spreading depression in migraine prophylaxis
It is hypothesized that migraine prophylactic agents suppress CSD as a common mechanism of action.