RESUMO
The catalytic relevance of Fe(IV) species in non-heme iron catalysis has motivated synthetic advances in well-defined five- and six-coordinate Fe(IV) complexes for a better understanding of their fundamental electronic structures and reactivities. Herein, we report the syntheses of FeDipp2 and FeMes2, a pair of unusual four-coordinate non-heme formally Fe(IV) complexes with S=1 ground states supported by strongly donating bisamide ligands. By combining spectroscopic characterization and computational modeling, we found that small variations in ligand aryl substituents resulted in substantial changes in both structures and bonding. This work highlights the strong donor capabilities and modularity of the bisamide ligand set. More broadly, it is a critical contribution to the utilization of ligand design to modulate molecular geometries and electronic structures of low-coordinate, high-valent iron complexes.
RESUMO
Background: This Mendelian randomization (MR) study aimed to explore the causal relationship between the genetic predisposition to type 2 diabetes mellitus (T2DM) and aortic dissection (AD), and to assess associations with genetically predicted glycemic traits. The study sought to verify the inverse relationship between T2DM and AD using a more robust and unbiased method, building on the observational studies previously established. Materials and methods: The study employed a two-sample and multivariable MR approach to analyze genetic data from the DIAbetes Meta-ANalysis of Trans-Ethnic association studies (DIAMANTE) with 74,124 cases and 824,006 controls, and the Meta-Analyses of Glucose and Insulin-Related Traits Consortium (MAGIC) involving up to 196,991 individuals. For AD data, FinnGen Release 10 was used, including 967 cases and 381,977 controls. The research focused on three foundational MR assumptions and controlled for confounders like hypertension. Genetic instruments were selected for their genome-wide significance, and multiple MR methods and sensitivity analyses were conducted. Results: The study revealed no significant effect of genetic predisposition to T2DM on the risk of AD. Even after adjusting for potential confounders, the results were consistent, indicating no causal relationship. Additionally, glycemic traits such as fasting glucose, fasting insulin, and HbA1c levels did not show a significant impact on AD susceptibility. The findings remained stable across various MR models and sensitivity analyses. In contrast, genetic liability to T2DM and glycemic traits showed a significant association with coronary artery disease (CAD), aligning with the established understanding. Conclusion: Contrary to previous observational studies, this study concludes that genetic predisposition to T2DM does not confer protection against AD. These findings underscore the imperative for further research, particularly in exploring the preventative potential of T2DM treatments against AD and to facilitate the development of novel therapeutic interventions.