RESUMO
A combined experimental and theoretical study of quantum state-resolved rotational energy transfer kinetics of optically centrifuged CO molecules is presented. In the experiments, inverted rotational distributions of CO in rotational states up to J = 80 were prepared using two different optical centrifuge traps, one with the full spectral bandwidth of the optical centrifuge pulses, and one with reduced bandwidth. The relaxation kinetics of the high-J tail of the inverted distribution from each optical trap was determined based on high-resolution transient IR absorption measurements. In parallel studies, master equation simulations were performed using state-to-state rate constants for CO-CO collisions in states up to J = 90, based on data from double-resonance experiments for CO with J = 0-29 and a fit to a statistical power exponential gap model. The model is in qualitative agreement with the observed relaxation profiles, but the observed decay rate constants are smaller than the simulated values by as much as a factor of 10. The observed decay rate constants also have a stronger J-dependence than predicted by the model. The results are discussed in terms of angular momentum and energy conservation, and compared to the observed orientational anisotropy decay kinetics of optically centrifuged CO molecules. Models for rotational energy transfer could be improved by including angular momentum effects.
RESUMO
Both aberrant vascular reactivity to acute cardiovascular stress and epigenetic mechanisms such as microRNA (miR) may underlie the increased propensity for African Americans (AA) to develop cardiovascular disease. This study assessed racial differences in acute induced endothelial inflammation and related miRs. Cultured human umbilical vein endothelial cells (HUVECs) derived from AA and Caucasian Americans (CA) were exposed to influenza vaccine to determine changes in inflammatory markers, endothelial nitric oxide synthase (eNOS), and miR expression/release. Endothelial function [flow-mediated dilation (FMD)], circulating IL-6, and circulating miR were also measured in young, healthy AA and CA individuals before and after receiving the influenza vaccine. There were no significant racial differences in any parameters at baseline. The vaccine induced increases in IL-6 release (24%, P = 0.02) and ICAM-1 mRNA (40%, P = 0.03), as well as reduced eNOS mRNA (24%, P = 0.04) in AA HUVECs, but not in CA HUVECs (all P > 0.05). Intracellular levels of anti-inflammatory miR-221-3p and miR-222-3p increased specifically in CA HUVECs (72% and 53%, P = 0.04 and P = 0.06), whereas others did not change in either race. HUVEC secretion of several miRs decreased in both races, whereas the release of anti-inflammatory miR-150-5p was decreased only by AA cells (-30%, P = 0.03). In individuals of both races, circulating IL-6 increased approximately twofold 24 h after vaccination (both P < 0.01) and returned to baseline levels by 48 h, whereas FMD remained unchanged. Although macrovascular function was unaffected by acute inflammation in AA and CA individuals, AA endothelial cells exhibited increased susceptibility to acute inflammation and unique changes in related miR.NEW & NOTEWORTHY Used as an acute inflammatory stimulus, the influenza vaccine induced an inflammatory response and decreased eNOS gene expression in endothelial cells derived from African Americans, but not Caucasian Americans. Race-specific changes in intracellular expression and release of specific microRNAs also occurred and may contribute to an exaggerated inflammatory response in African Americans. In vivo, the vaccine caused similar systemic inflammation but had no effect on endothelial function or circulating microRNAs in individuals of either race.