Effects of physical activity on subjective well-being: the mediating role of social support and self-efficacy

ObjectiveSubjective well-being is an essential component of college students' mental health, and the purpose of this study was to investigate the relationship between physical activity and subjective well-being among college students and to examine the mediating role of social support and self-efficacy between the physical activity and subjective well-being.MethodsThis study utilized a cross-sectional design with a stratified whole group sample of 989 college students (Mage = 19.65 years, SD = 1.1) from three universities in Guangdong Province, China, and used the Physical Activity Scale, Subjective Well-Being Scale, Social Support Scale, and Self-Efficacy Scale for data collection. In this study, SPSS 26.0 was used for descriptive statistical analysis and correlation analysis of the collected data. Harman's one-way method was used to test for common method bias.Results(1) Physical activity, subjective well-being, social support and self-efficacy were significantly correlated with each other. Among them, physical activity was significantly and positively correlated with subjective well-being (r = 0.36), physical activity directly predicted subjective well-being (β = 0.125, t = 3.992, p < 0.01). (2) Physical activity positively predicted social support (β = 0.386, t = 12.505, p < 0.01) and self-efficacy (β = 0.358, t = 11.793, p < 0.01), social support significantly positively predicted subjective well-being (β = 0.332, t = 11.370, p < 0.01) and self-efficacy (β = 0.254, t = 8.744, p < 0.01), self-efficacy significantly and positively predicted subjective well-being (β = 0.255, t = 8.251, p < 0.01). (3) Not only did social support and self-efficacy play an independent mediating role between physical activity and subjective well-being, but social support and self-efficacy played a chain mediating role between physical activity and subjective well-being.ConclusionThis study enriched the theoretical guidance for physical activity in promoting college students' subjective well-being. In the practical teaching of promoting college students' subjective well-being, in addition to paying attention to stimulating physical activity, special attention should be paid to the promotion of social support and self-efficacy

Endothelial-derived APT1-mediated macrophage-endothelial cell interactions participate in the development of atherosclerosis by regulating the Ras/MAPK signaling pathway

Acyl-protein thioesterase 1 (APT1) can affect H-Ras localization and function by promoting its depalmitoylation. However, relatively little attention has been paid to the effects of APT1 on H-Ras in the cardiovascular system. In this study, we revealed its roles in atherosclerosis development using oxidative low-density lipoprotein (ox-LDL)-induced endothelial dysfunction models and a Western diet-induced ApoE−/− mouse model. The results showed that APT1 expression was up-regulated, while that of miR-138-5p (miR-138) was down-regulated (p < 0.05) in this model. In the meantime, APT1 and H-Ras were translocated from the cytoplasm to the plasma membrane. Bioinformatic analysis and double fluorescence identified miR-138 as the upstream regulator of APT1. APT1 knockdown regulated H-Ras localization and expression, which subsequently affected the MAPK signaling pathway and the expression of its downstream factors. Further research indicated that human umbilical vein endothelial cells (HUVECs)-derived biogenic nanoparticles (BiNPs), hBPs secretion, and RNA expression of hBP-loaded APT1 were increased (p < 0.05) in the ox-LDL induced endothelial dysfunction model. Meanwhile, the HUVECs-derived APT1 could further affect macrophage function through hBP transportation. Altogether, this study demonstrated that the miR-138-APT1 axis may be partially responsible for atherosclerosis development by regulating the H-Ras-MAPK signaling pathway and hBP transportation. The results also shed novel insight on the underlying mechanisms of, and identify potential diagnostic and therapeutic targets for, atherosclerotic cardiovascular diseases in the future

Impaired atrial electromechanical function and atrial fibrillation promotion in alloxan-induced diabetic rabbits

Background: Diabetes mellitus (DM) is an independent risk factor for atrial fibrillation (AF). However, the underlying mechanisms are still not clearly elucidated. The aim of this study was to evaluate the atrial electromechanical function, atrial electrophysiological changes and AF inducibility in alloxan-induced diabetic rabbits. Methods: In 8 alloxan-induced diabetic rabbits and 8 controls, we evaluated atrial electromechanical function by tissue Doppler imaging. Isolated Langendorff-perfused rabbit hearts were prepared to measure atrial refractory effective period (AERP) and its dispersion (AERPD), interatrial conduction time (IACT) and vulnerability to AF. Atrial interstitial fibrosis was evaluated by Sirius-Red staining. Results: Compared with controls, left atrial lateral wall Pa’-start interval (Pastart) and right atrial wall Pastart were increased in diabetic rabbits. AERPD was increased and IACT was prolonged in diabetic rabbits. Inducibility of AF in diabetic group was significant higher than controls (6/8 vs. 1/8, p < 0.05). Extensive interstitial fibrosis was observed in the DM group (p < 0.01). Correlation analysis showed that right atrial wall Pastart, Pa’-peak interval (Papeak) and total electromechanical activity (TEMA); left atrial lateral wall Papeak and TEMA, left atrial posterior wall TEMA, and IACT were correlated with atrial areas of fibrosis. Conclusions: Atrial electromechanical function is impaired in diabetic rabbits, and is associated with atrial fibrosis and interatrial electrical conduction delay

Renin–angiotensin system inhibition is associated with reduced risk of left atrial appendage thrombosis formation in patients with atrial fibrillation

Background: Inhibition of the renin–angiotensin axis can reduce the likelihood of atrial fibrillation (AF). However, the effects of angiotensin-converting-enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) on thrombogenicity in AF remain incompletely elucidated. Thisretrospective case-control study was conducted to evaluate whether the use of ACEI or ARB could reduce the incidence of left atrial appendage thrombus (LAAT) and spontaneous echocardiographic contrast (SEC) in patients with AF. Methods: A total of 199 AF patients who received both transesophageal echocardiogram (TEE) and transthoracic echocardiogram (TTE) successively on the same day from 2012 to 2016 were enrolled. Left atrial dimension, maximal left atrial volume (LAVmax), left ventricular end-diastolic dimension, left ventricular ejection fraction, and the ratio of the early transmitral flow velocity and the early mitral annular velocity (E/e’) were determined. Longitudinal LA strain was evaluated using two-dimensional speckle tracking imaging at each LA segment. Peak systolic strain was calculated by averaging total segments. LAAT, LAA emptying flow velocity (LAAeV) and SEC were evaluated by TEE. Risk factors for LAAT and usage of ACEIs or ARBs were recorded. Results: The incidence of LAAT was 27.6%. Among the patients with renin–angiotensin system (RAS) inhibitors, 20.5% were demonstrated to have LAAT, compared with 33.3% in the nonuser group (p = 0.044). LA peak systolic strain and LAAeV were significantly increased in patients with RAS inhibitors compared to the nonuser group (p = 0.002, p = 0.047, respectively). Patients with LAAT had higher CHA2DS2-VASc scores and evident SEC comparedwith those without LAAT (p = 0.000, p = 0.000, respectively). Usage of ACEIs/ARBs and antiplatelet drugs were frequent in patients with LAAT than in those without LAAT (p = 0.044, p = 0.000, respectively). Even after controlling for LAAT-related risk factors (age, body mass index, AF type, hypertension, diabetes mellitus, prior stroke or transient ischemic attack, drinking history and usage of antiplatelet drugs and LAVmax), use of RAS inhibitors remained significantly associated with a lower risk of LAAT (OR = 0.222; 95% CI 0.084–0.585, p = 0.002). Conclusions: This study shows that RAS inhibitors may be effective in reducing the risk of LAAT in patients with AF through atrial reverse remodeling

A novel three-dimensional and tissue Doppler echocardiographic index for diagnosing and prognosticating heart failure with preserved ejection fraction

Introduction: The diagnosis of heart failure with preserved ejection fraction (HFpEF) remains challenging. In this study, a novel echocardiography index based on three-dimensional and tissue Doppler echocardiography for diagnosing and estimating prognosis in HFpEF. Materials and Methods: Patients with symptoms and/or signs of heart failure and normal left ventricular ejection fraction (LVEF ≥50%) who underwent right heart catheterization were screened. Patients were divided based on pulmonary capillary wedge pressure (PCWP) of ≥15 mmHg and PCWP <15 mmHg. A diagnosis of HFpEF was confirmed by PCWP of ≥15 mmHg according to ESC guidelines. A novel index was calculated by the ratio between stroke volume standardized to body surface area (SVI) and tissue Doppler mitral annulus systolic peak velocity S' (SVI/S'). Its diagnostic and prognostic values were determined. Results: A total of 104 patients (mean age 64 ± 12 years) were included. Of these, 63 had PCWP ≥15 mmHg and 41 patients had PCWP <15 mmHg. Compared to the PCWP <15 mmHg group, the ≥15 mmHg group had a significantly lower SVI/S' (P < 0.001). Logistic regression showed that SVI/S' was associated with high PCWP measured invasively. The SVI/S' had an area under the curve of 0.761 for diagnosing classifying between PCWP ≥15 mmHg and <15 mmHg. Kaplan–Meier analysis showed that the lower SVI/S' group showed a poorer prognosis. Conclusions: SVI/S' is a non-invasive index calculated by three-dimensional and tissue Doppler echocardiography. It is a surrogate measure of PCWP and can be used to diagnose and determine prognosis in HFpEF

Precision Control of Amphoteric Doping in Cu x Bi2Se3 Nanoplates.

Copper-doped Bi2Se3 (Cu x Bi2Se3) is of considerable interest for tailoring its electronic properties and inducing exotic charge correlations while retaining the unique Dirac surface states. However, the copper dopants in Cu x Bi2Se3 display complex electronic behaviors and may function as either electron donors or acceptors depending on their concentration and atomic sites within the Bi2Se3 crystal lattice. Thus, a precise understanding and control of the doping concentration and sites is of both fundamental and practical significance. Herein, we report a solution-based one-pot synthesis of Cu x Bi2Se3 nanoplates with systematically tunable Cu doping concentrations and doping sites. Our studies reveal a gradual evolution from intercalative sites to substitutional sites with increasing Cu concentrations. The Cu atoms at intercalative sites function as electron donors while those at the substitutional sites function as electron acceptors, producing distinct effects on the electronic properties of the resulting materials. We further show that Cu0.18Bi2Se3 exhibits superconducting behavior, which is not present in Bi2Se3, highlighting the essential role of Cu doping in tailoring exotic quantum properties. This study establishes an efficient methodology for precise synthesis of Cu x Bi2Se3 with tailored doping concentrations, doping sites, and electronic properties