https://www.selleckchem.com/JAK.html 1 mutant root has increased root meristem growth with lower NOS-like activity and NO accumulation than wild type upon Cd exposure, and exogenous NO donors sodium nitroprusside or nitrosoglutathione can restore its reduced Cd sensitivity. In addition, Cd activates WDR5a expression in roots, and overexpressing WDR5a results in increased NO accumulation and suppressed root meristem growth similar to Cd-stressed wild-type roots, while scavenging NO or inhibiting NOS-like activity significantly reverts these effects of Cd. Furthermore, WDR5a acts in Cd-repressed auxin accumulation through reducing the levels of auxin efflux carriers PIN1/3/7 and biosynthetic enzyme TAA1, and reduced sensitivity of wdr5a-1 root meristem to Cd can be partially reverted by inhibiting TAA1 activity pharmaceutically or mutating TAA1 genetically. This study identified WDR5a as a key factor modulating NO accumulation and root meristem growth in plant response to Cd. This narrative review makes the case for greater efforts to reduce cardiovascular disease (CVD) risk in women with diabetes. In a recent meta-analysis including five CVOTs of diabetes medications with 46,606 subjects, women (vs men) with type 2 diabetes had a higher relative risk for stroke (RR 1.28; 95% CI 1.09, 1.50) and heart failure (1.30; 1.21, 1.40). Prior studies found higher "within-gender" RR for CVD mortality in women with diabetes although men have an absolute higher risk. Women with prior gestational diabetes mellitus (GDM) have a 2-fold higher CVD risk than the background population. Worse CVD and CVD risk factor management in women, as well as lower female therapy adherence, contribute further to these disparities. The mechanism behind this excess risk includes biological, hormonal, socioeconomic, clinical, and behavioral factors that still require further investigation. The need for more intensive CVD reduction in women now includes more attention to screening for both incident dia