RÉSUMÉ
Background: Patients might still experience major adverse cardiovascular events even with dual antiplatelet therapy after percutaneous coronary intervention. Our study aimed to explore the impact of gene polymorphism on clinical outcomes in one-year follow-up. Methods: A total of 171 patients treated with dual antiplatelet therapy after percutaneous coronary intervention from April to December 2020 in the first hospital of Jilin University enrolled in this study. Results: PEAR1 genetic polymorphisms was associated with the arachidonic acid (AA) and adenosine diphosphate (ADP) platelet aggregation. Hyperglycemia was associated with the rate of major adverse cardiovascular events. PEAR1 GA+AA genetic genetic polymorphisms is associated with hyperglycemia. Conclusion:PEAR1 GG is a risk factor for AA and ADP platelet aggregation. Hyperglycemia can effect the one-year outcome. PEAR1 GA+AA genetic polymorphisms are associated with hyperglycemia.
Sujet(s)
Maladies cardiovasculaires , Hyperglycémie , Intervention coronarienne percutanée , ADP/pharmacologie , Acide acétylsalicylique/effets indésirables , Maladies cardiovasculaires/traitement médicamenteux , Chine , Clopidogrel/effets indésirables , Humains , Hyperglycémie/induit chimiquement , Hyperglycémie/traitement médicamenteux , Hyperglycémie/génétique , Intervention coronarienne percutanée/effets indésirables , Agrégation plaquettaire/génétique , Antiagrégants plaquettaires/effets indésirables , Polymorphisme génétique/génétique , Récepteurs de surface cellulaire/génétiqueRÉSUMÉ
Zinc pollution impairs neural processes and protein function and also effects calcium-related transcriptional regulation and enzyme activity. In this study, we investigated pathways that potentially respond to calcium signaling under Zn2+ stress. Specifically we measured relative expressions of GeCNAα, GeCNB, GeMT, GeTNF-α, GeIL-1ß, and GeHsp90 in gills, livers, and kidneys of the indicator species Gymnocypris eckloni and found wide variation in their expression between tissues during the course of Zn2+ exposure. Notably, GeCNAα, GeCNB, GeTNF-α, GeIL-1ß, and GeMT were rapidly and strongly up-regulated in gills; GeIL-1ß and GeHsp90 transcription was quickly induced in kidneys; and GeCNB, GeTNF-α, GeIL-1ß, and GeHsp90 were most rapidly up-regulated in livers. GeCNAα and GeMT showed a contrasting late transcriptional up-regulation. These results suggest independent branches for chelation and immune responses during self-protection against Zn2+ toxicity, and the immune response appears to be faster than metal chelation.