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The cerebral white matter's demyelination of the cerebral white matter is the most common pathological change after carbon monoxide poisoning. HBO treated male C57 BL/6 mice with severe CO poisoning. Since CO poisoning, HBO therapy also significantly reduced protein and mRNA levels of Notch1 and Hes5 in Notch1 and Hes5. Our findings indicated that HBO could delay the release of Notch signaling pathway after CO poisoning, which is the mechanism behind HBO's neuroprotection against denyelination after severe CO poisoning.
Source link: https://europepmc.org/article/MED/35946219
Objective Carbon monoxide activates intravascular neutrophils by platelet-neutrophil aggregates, which lead to neutrophil degranulation. The MPO index is a recently published inflammation marker that measures the MPO level in neutrophils. The MPXI in conditions associated with neutrophil activation are dependent on the net effect of azurophil degranulation. This study was conducted to see if the MPXI could predict neurocognitive prognosis 1 month after acute CO poisoning. Methods We included patients aged u226516 years with acute CO poisoning from a cohort at a joint tertiary academic hospital in Wonju, Korea, between January 2010 and May 2021. The patients' median MPXI of the poor outcome group was higher than that of the favorable outcome group. Conclusion 1 month after acute CO poisoning, the MPXI evaluated in the emergency department did not differ based on neurocognitive results at 1 month.
Source link: https://europepmc.org/article/MED/36116774
Purpose: The aim is to investigate early neurological deficits-related change patterns in gray matter volume in patients with carbon monoxide poisoning and GM volume differences between patients with and without delayed neurological sequelae, as well as those with and without T2 hyperintense lesions after COP. Compared to the HC group, the COP group had statistically significant GM atrophy in the bilateral prefrontal and temporal lobes, anterior cingulate, thalamus, posterior cerebellum, and right hippocampus. The DNS subgroup had greater GM atrophy in the limbic system than the non-DNS subgroup. In the subgroup with T2 hyperintense lesions, significant GM atrophy in the limbic system, motor, and visual cortex, and a default network were found in the subgroup with T2 hyperintense lesions.
Source link: https://europepmc.org/article/MED/36036278
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