We investigated the relation between vitamin D status and left ventricular (LV) structure and function in community-dwelling subjects without heart disease. Design The relationship between concentrations of 25-hydroxyvitamin D [25(OH)D], a marker of vitamin D reserve, and LV transthoracic echocardiography measures was analysed in 711 participants in the Baltimore Longitudinal Study of Selleck CDK inhibitor Aging who were without cardiac disease. Results Mean 25(OH)D in the study population was 32.3 +/- 11.4ngmL1; only 15.5% of subjects had moderate or severe vitamin D deficiency [25(OH)D<20ngmL1]. Adjusting for age, body mass index, cardiovascular disease risk factors, physical
activity, calcium and parathyroid hormone, 25(OH)D
was positively correlated with LV thickness ( 0.095, SE 0.039, P<0.05) and LV mass index ( 7.5, SE 2.6, P<0.01). A significant nonlinear relation between 25(OH)D and LV concentric remodelling was observed. LV remodelling was more likely in participants with 25(OH)D levels <30ngmL1 [odds ratio (OR) 1.24; 95% confidence interval (CI) 0.831.85] or 38ngmL1 (OR 1.73; 95% CI 1.132.65), compared with those with 3037ngmL1 25(OH)D. Consistently, LV relative wall thickness was significantly PR-171 molecular weight lower (P for trend=0.05), and LV diastolic internal diameter index (P for trend<0.05) and end-diastolic volume index (P for trend<0.05) were significantly higher in subjects with 3037ngmL1 25(OH)D compared to the rest of the study population. There was a significant interaction between 25(OH)D and hypertension on the risk of LV hypertrophy (P<0.05). Conclusions In a population-based sample of predominantly vitamin D-sufficient subjects without heart disease, LV geometry was most favourable at intermediate 25(OH)D concentrations.”
“Kruppel-like
factors (KLFs) control cell differentiation and embryonic development. KLF1 (erythroid Kruppel-like factor) plays essential roles in embryonic and adult erythropoiesis. KLF2 is a positive regulator of click here the mouse and human embryonic beta-globin genes. KLF1 and KLF2 have highly homologous zinc finger DNA-binding domains. They have overlapping roles in embryonic erythropoiesis, as demonstrated using single and double KO mouse models. Ablation of the KLF1 or KLF2 gene causes embryonic lethality, but double KO embryos are more anemic and die sooner than either single KO. In this work, a dual human beta-globin locus transgenic and KLF knockout mouse model was used. The results demonstrate that the human epsilon-(embryonic) and gamma-globin (fetal) genes are positively regulated by KLF1 and KLF2 in embryos. Conditional KO mouse experiments indicate that the effect of KLF2 on embryonic globin gene regulation is at least partly erythroid cell-autonomous.