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Elevated serum Epithelial cell adhesion molecule (EpCAM) or Platelet endothelial cell adhesion molecule (PECAM) are associated with ischemic stroke (IS), but the causality remains unclear. A two-sample Mendelian randomization (MR) study was performed to examine the causal effect of serum EpCAM or PECAM levels on the risk of IS subtypes.The study utilized GWAS datasets from European and African American populations to identify SNPs associated with serum EpCAM and PECAM levels as instrumental variables. These were then used in MR analyses for IS subtypes, employing multiple methods including IVW, weighted median, MR-Egger, and maximum likelihood. Sensitivity analyses were conducted to validate the results. No significant causal association was observed for EpCAM levels with any of three IS subtypes. Main IVW MR analysis indicated that serum PECAM levels were negatively related to the incidence of large artery stroke (LAS), small vessel stroke (SVS), and cardioembolic stroke (CES), especially CES. Sensitivity analyses confirmed the robustness of these results. Our study reveals a negative correlation between genetically predicted PECAM levels and ischemic stroke risk, particularly for cardioembolic stroke, suggesting PECAM's potential as a biomarker for risk stratification. While no clear causal relationship was found for EpCAM, these findings have significant implications for stroke prevention and treatment strategies. Further research is needed to validate these results and explore their clinical applications, potentially leading to more personalized approaches in stroke management., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: Reactive oxygen species (ROS) often promote acute brain injury after stroke, but their roles in the recovery phase have not been well studied. We tested the hypothesis that ROS activity mediated by NADPH oxidase 2 (NOX2) contributes to acute brain injury but promotes functional recovery during the delayed phase, which is linked with neuroinflammation, autophagy, angiogenesis, and the PI3K/Akt signaling pathway., Methods: We used the NOX2 inhibitor apocynin to study the role of NOX2 in brain injury and functional recovery in a middle cerebral artery occlusion (MCAO) stroke mouse model. Infarct size, neurological deficits and behavior were evaluated on days 3, 7, 10 and 14 after reperfusion. In addition, dynamic NOX2-induced ROS levels were measured by dihydroethidium (DHE) staining. Autophagy, inflammasomes, and angiogenesis were measured by immunofluorescence staining and western blotting. RNA sequencing was performed, and bioinformatics technology was used to analyze differentially expressed genes (DEGs), as well as the enrichment of biological functions and signaling pathways in ischemia penumbra at 7 days after reperfusion. Then, Akt pathway-related proteins were further evaluated by western blotting., Results: Our results showed that apocynin injection attenuated infarct size and mortality 3 days after stroke but promoted mortality and blocked functional recovery from 5 to 14 days after stroke. DHE staining showed that ROS levels were increased at 3 days after reperfusion and then gradually declined in WT mice, and these levels were significantly reduced by the NOX2 inhibitor apocynin. RNA-Seq analysis indicated that apocynin activated the immune response under hypoxic conditions. The immunofluorescence and western blot results demonstrated that apocynin inhibited the NLRP3 inflammasome and promoted angiogenesis at 3 days but promoted the NLRP3 inflammasome and inhibited angiogenesis at 7 and 14 days after stroke, which was mediated by regulating autophagy activation. Furthermore, RNA-Seq and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that apocynin injection resulted in PI3K-Akt signaling pathway enrichment after 7 days of MCAO. We then used an animal model to show that apocynin decreased the protein levels of phosphorylated PI3K and Akt and NF-κB p65, confirming that the PI3K-Akt-NF-κB pathway is involved in apocynin-mediated activation of inflammation and inhibition of angiogenesis., Conclusions: NOX2-induced ROS production is a double-edged sword that exacerbates brain injury in the acute phase but promotes functional recovery. This effect appears to be achieved by inhibiting NLRP3 inflammasome activation and promoting angiogenesis via autophagy activation., (© 2022. The Author(s).)

To recognize the specific evoked EEG signals is the popular track in biomedical signal processing. This paper mainly introduced a specific method to recognize the three specific cognitive states. By the way of computing the complexity of the evoked EEG signals, we analyzed the specific thinking-evoked EEG signal and found that there were some significant differences under the three different cognitive states. The differences were mainly located in the complexity of channel C3 and C4. This method provides an effective approach to recognize the three different states and the result of the recognition can be used as the controlling signals for extra usages.