Global longitudinal LA epsilon/SR parameters determined by 2D speckle tracking echocardiography are feasible and reproducible indices for the evaluation of LA function.
The purpose of this study was to evaluate the effects of aroma massage applied to middle-aged women with hypertension. The research study had a nonequivalent control group, nonsynchronized design to investigate the effect on home blood pressure (BP), ambulatory BP, and sleep. The hypertensive patients were allocated into the aroma massage group (n = 28), the placebo group (n = 28), and the no-treatment control group (n = 27). To evaluate the effects of aroma massage, the experimental group received a massage with essential oils prescribed by an aromatherapist once a week and body cream once a day. The placebo group received a massage using artificial fragrance oil once a week and body cream once a day. BP, pulse rate, sleep conditions, and 24-hour ambulatory BP were monitored before and after the experiment. There was a significant difference in home systolic blood pressure (SBP) (F = 6.71, P = 0.002) between groups after intervention. There was also a significant difference in SBP (F = 13.34, P = 0.001) and diastolic blood pressure (DBP) (F = 8.46, P = 0.005) in the laboratory between aroma massage and placebo groups. In sleep quality, there was a significant difference between groups (F = 6.75, P = 0.002). In conclusion, aroma massage may help improve patient quality of life and maintain health as a nursing intervention in daily life.
In vascular smooth muscle cells, reactive oxygen species (ROS) were known to mediate platelet-derived growth factor (PDGF)-induced cell proliferation and NADH/NADPH oxidase is the major source of ROS. NADH/NADPH oxidase is controlled by rac1 in non-phagocytic cells. In this study, we examined whether the inhibition of rac1 by adenoviral-mediated gene transfer of a dominant negative rac1 gene product (Ad.N17rac1) could reduce the proliferation of rat aortic vascular smooth muscle cells (RASMC) stimulated by PDGF via decreasing intracellular ROS. RASMC were stimulated by PDGF (80 ng/mL) with or without N-acetylcysteine 1 mM or infected with 100 mutiplicity of infection of Ad.N17rac1. Intracellular ROS levels were measured at 12 hr using carboxyl-2', 7'-dichlorodihydrofluorescein diacetate confocal microscopy. At 72 hr, cellular proliferation was evaluated by cell number counting and XTT assay. Compared with control, ROS levels were increased by 2-folds by PDGF. NAC and Ad.N17rac1 inhibited PDGF-induced increase of ROS by 77% and 65%, respectively. Cell number was increased by PDGF by 1.6-folds compared with control. NAC and Ad.N17rac1 inhibited PDGF-induced cellular growth by 45% and 87%, respectively. XTT assay also showed similar results. We concluded that inhibition of rac1 in RASMCs could reduce intracellular ROS levels and cellular proliferation induced by PDGF.
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