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Hemodynamic changes are extremely important in analyzing responses from a brain subjected to a stimulus or treatment.
Therefore, the present study was designed to investigate the temporal component of the hippocampal pyramidal neuron damage in the rat brain subjected to chronic HH exposure.
Differences were considered to be significant when p < 0.05. Figure 1 shows the photomicrograph of a sagittally cut plane of goldfish brain subjected to lidocaine injection into CC.
FBD formula inhibited PMNs infiltration in ICR mouse brain subjected to repetitive 10 min of common carotid arteries occlusion followed 24 h reperfusion, and in vitro results showed that FBD formula could inhibit TNF- α-triggered PMNs adhesion to ECV304 endothelial cells.
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After completing behavioral testing and a 3-week resting period, the animals were sacrificed and their brains subjected to LTP analysis.
Nissl-stained sections from the brains subjected to 1-h MCAO and 24-h reperfusion were examined.
SEM images showed a similar increase in the density of the cerebrovasculature in the brains subjected to vascular corrosion casting.
After injury, mice were transcardially perfused to remove free-flowing blood and their brains subjected to immunofluorescence for the platelet-specific marker, integrin αIIb β3.
MCT-1 levels increased by 2-fold in neonatal rat brains subjected to hypoxic preconditioning at 24 h of recovery as compared with naïve control.
In addition, we found that OGD rapidly increased the expression of CBS in primary astrocytes and in rat brains subjected to pMCAO.
Vimentin expression in neurons has been linked temporally and spatially to dendrite repair in neurons of the cerebral cortex in AD and mouse brains subjected to traumatic injury [ 26].
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