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Carbon Monoxide Poisoning - Springer Nature

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Last Updated: 28 September 2022

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LncRNA CRNDE Deteriorates Delayed Encephalopathy After Acute Carbon Monoxide Poisoning to Inactivate AKT/GSK3β/β-catenin Pathway via miR-212-5p

The most severe sequel to acute CO poisoning is acute carbon monoxide poisoning, with structural or function disruption of the brain. However, the mechanism of CRNDE in DEACMP remains unclear, according to LncRNA colorectal neoplasia with a differentially expressed aberrant expression; however, the mechanism of CRNDE in DEACMP remains elusive; The Spragueu2013Dawley rats were the first CO poisoning model. Histopathological disease of brain and hippocampus tissue was detected by hematoxylin and eosin, Nissl, and TUNEL staining. Cell apoptosis was determined by flow cytometry analysis, resulting in cell apoptosis. To determine the binding relationship between CRNDE and miR-212-5p, Luciferase's review and RNA immunoprecipitation assays were used. In the CO poisoning animal model and oxygen-u2013glucose deprivation group, CRNDE was significantly enhanced, though the MiR-212-5p was decreased. Furthermore, the protective effects of CRNDE slencing on brain tissue damage and apoptosis were reversed by inhibition of miR-212-5p in the CO poisoning scheme, as shown by a decrease in miR-212-5p.

Source link: https://doi.org/10.1007/s12640-022-00518-2


Early gray matter atrophy and neurological deficits in patients with carbon monoxide poisoning

Objectives: To investigate early neurological deficits-related change patterns in gray matter volume in patients with and without delayed neurologic sequelae, and those with and without T2 hyperintense lesions after COP. Lower Mini-Mental State Examination results and improved Unified Parkinson's Disease Rating Scale subsection III and neuropsychiatric inventory results were attributed to lower left medial orbital superior frontal gyrus, bilateral ACC, and bilateral thalamus thalamus. The DNS subgroup had higher GM atrophy in the limbic system than the non-DNS subgroup. In the subgroup with T2 hyperintense lesions, the subgroup without T2 hyperintense lesions, increased GM atrophy in the limbic system, motor and visual cortex, and default network were observed in the subgroup with T2 hyperintense lesions. GM atrophy in the medial orbital SFG, ACC, thalamus, hippocampus, and posterior cerebellum is associated with early neurological declines in patients with COP.

Source link: https://doi.org/10.1007/s00234-022-03041-5

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions