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Carbon Monoxide Poisoning - PubMed

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Last Updated: 28 September 2022

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Cerebrospinal Fluid Biomarkers for Monitoring Delayed Neurologic Sequelae after Carbon Monoxide Poisoning.

Delayed neuropsychiatric sequelae, which are related to neuropsychiatric signs and severe sequelae, occur within a few days of re-accumulation from acute poisoning. With corticosteroid therapy, a 29-year-old man with DNS who experienced carbon monoxide poisoning underwent corticosteroid therapy, including concomitant tests of MBP, IL-6, and pNF-H. Corticosteroid therapy and monitoring can be used to treat and monitor DNS.

Source link: https://doi.org/10.4103/0028-3886.355093


Rare Causes of Acute Coronary Syndrome: Carbon Monoxide Poisoning.

CO poisoning can cause a variety of cardiac disorders, particularly ACS. The Toxicology Department of Saint Spiridon Emergency University Hospital, including all patients admitted through the emergency department with CO poisoning, has been reviewed by a retrospective review. Compared to the non-event group, Cardiac enzyme markers showed a statistically significant rise in the event group. Any type of poisoning can result in CO poisoning, and it can be temporary, reversible, or permanent. Our study, which is mainly focused on the ACS, brings new information on adverse cardiac events in patients with CO poisoning. We found that the severity of CO poisoning plays a significant role in myocardial disease in the event group, as 50% of patients in the event group were heavily impaired.

Source link: https://doi.org/10.3390/life12081158


Effects of hyperbaric oxygen on Notch signaling pathway after severe carbon monoxide poisoning in mice.

The most common pathological condition after carbon monoxide poisoning is demyelination of the cerebral white matter. HBO treated male C57 BL/6 mice with severe CO poisoning. After CO poisoning, HBO therapy also greatly reduced protein and mRNA levels of Notch1 and Hes5 (notch1 and Hes5). Our results showed that HBO could deactivate Notch signaling pathway after CO poisoning, which is the mechanism responsible for HBO's neuroprotection against demyelination after severe CO poisoning.

Source link: https://doi.org/10.4103/2045-9912.344971


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

The most severe comading sequel to acute CO poisoning is a delayed encephalopathy caused by extensive brain injury, with tissue or organ damage in the brain. The mechanism of CRNDE in DEACMP remains unclear, according to LncRNA colorectal neoplasia who differentially expressed aberrant expression in nerve cell injury; however, the mechanism of CRNDE in DEACMP remains unclear; The Sprague-Dawley rats were the first CO poisoning model. According to similar detection assays, Oxidative damage and apoptosis markers were determined. Cell apoptosis were determined by flow cytometry analysis. To determine the binding relationship between CRNDE and miR-212-5p, a combination of CRNDE and miR-212-5p and RNA immunoprecipitation assays was used. In the CO poisoning animal model and oxygen-glucose deprivation group, CRNDE was significant higher, while miR-212-5p was reduced. The hippocampus and brain tissue tissues were destroyed by the CRNDE knockdown, which culminated in increased histopathological injury and apoptosis. In addition, the protective effects of CRNDE silencing on brain tissue damage and apoptosis were reversed by the reduction of miR-212-5p in the CO poisoning model, as shown by the inhibition of miR-212-5p.

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

* 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