Search

Introduction: Traditional clinical risk factors are insufficient to estimate the residual risk of large-vessel ischemic stroke. Non-targeted lipidomic techniques provide an opportunity to evaluate these risks. Methods: Plasma samples were collected from 113 hypertensive individuals, including 55 individuals at high risk of ischemic stroke and 58 matched individuals, in a prospective nested case-control cohort. To identify dysregulated lipid metabolites, we conducted multivariate and univariate analyses. A classifier based on a cross-validated procedure was employed to select the optimal combination of lipid species and their ratios. Results: We identified 23 dysregulated lipid species in patients with and without ischemic stroke, including 16 (69.6%) up-regulated and 7 (30.4%) down-regulated lipid species. Through internal cross-validation, the optimal combination of two lipid features (phosphatidylcholine 34:2 and triglyceride 18:1/18:1/22:1 / phosphatidylcholine 34:2, referred to as ischemic stroke-related 2 lipid features - IS2LP) was selected, leading to a more precise prediction probability for ischemic stroke within 3.9 years. In the comparison of different risk factors, the traditional risk score, the IS2LP risk score, and the combination of the traditional risk score with IS2LP yield AUC values of 0.613(95% CI:0.509– 0.717), 0.833(95% CI:0.755– 0.911), and 0.843(95% CI:0.777– 0.916), respectively. The combination of the traditional risk score and IS2LP exhibited significantly improved discriminative performance, with an integrated discrimination improvement (IDI) of 0.31 (p< 0.001) and a continuous net reclassification improvement (NRI) of 1.06 (p < 0.001) compared to the traditional risk score. Conclusion: We identified new lipidomic biomarkers associated with the futural event of large-vessel ischemic stroke. These lipid species could serve as potential blood biomarkers for assessing the residual risk of ischemic stroke in hypertensive individuals. [ABSTRACT FROM AUTHOR]

Accumulating evidence strongly suggests that exposure to ambient air pollution is linked with increased frailty. However, little is known about the effect of improved air quality on frailty progression. We aimed to investigate whether improvements in air quality (PM1, PM2.5, PM10, NO2, and O3) can alleviate frailty progression, particularly in the aftermath of implementation of the "Clean Air Action" policy in China. The study involved 12,891 participants with geocoded environmental data from the nationwide China Health and Retirement Longitudinal Study (CHARLS) during the period from May 2011 to August 2015. Multivariate logistic regression models were used to analyze the association of air pollution improvements and frailty progression. The protective effects were noted for PM1, PM2.5, PM10, and NO2 indices, with an aOR (adjusted odds ratio) ranging from 0.72 to 0.79. Air quality improvement in PM1, PM2.5, PM10, and NO2 could alleviate the progression of frailty. The study is the first to examine the association between the improvement of air quality and the progression of frailty, setting a precedent for the importance of a nationwide clean air policy and its impact on healthy ageing. [ABSTRACT FROM AUTHOR]

Objective To prepare the endothelialization-promoting tissue-engineered blood vessels (TEBVs) with encapsulated Ginsenoside Rg1 (Rg1) to promote endothelialization, and to evaluate its patency and endothelialization after implantation into the rat common carotid artery. Methods CCK-8 assay and flow cytometry were used to detect the effects of Rg1 on the proliferation and apoptosis of endothelial cells (ECs) after 48 hours' treatment, and the optimal dose of the agent was also determined. ECs was divided into control group, Rg1 treatment group (15.63 μmol/L Rg1), and Rg1+XL184 (15.63 μmol/L Rg1+0.5 μg/mL XL184, VEGFR2 inhibitor) treatment group. Cell proliferation and wound healing of ECs were examined after the treatment for 48 h. Chitosan coated Rg1-(2-hydroxypropyl)-cyclodextrin particles (Rg1-HGC/CS NPs, abbreviated as NPs) were prepared and modified to the lumen of blood vessels (after decellularization and collagen treatment), and then Fourier transform infrared (FTIR) spectroscopy, dynamic light scattering (DLS) and scanning electron microscopy (SEM) were used to detect these obtained samples. ECs were co-cultured with acellular vessels and TEBVs for 48 h to observe the biocompatibility. For in vivo study, the acellular vessels were divided into collagen group (collagen treatment), blank CS group (collagen and chitosan treatment), and NPs group (modified with NPs). Then these vessel samples were transplanted into the left common carotid artery of SD rats respectively. Ultrasound and micro-CT scanning were performed to observe the vascular patency in 30 and 90 d after transplantation. HE and Masson staining and immunofluorescence assay for CD31 and vWF were used to observe the endothelialization in each group in 90 d after transplantation. Results Rg1 promoted the proliferation and migration of ECs via VEGFR2 (P < 0.05), and showed no significant effect on apoptosis. The prepared NPs were about 130 nm in diameter and uniform in shape (PDI < 0.3), and could be successfully modified to the lumen of blood vessels. The co-cultured study showed that endothelialization-promoting TEBVs displayed better biocompatibility for favorable of cell adhesion and growth. In 30 and 90 d after transplantation, radiological studies displayed that the NPs-treated vessels showed better vascular patency than the other groups. HE and Masson staining indicated that in 90 d after transplantation, the collagen and blank CS groups had blood vessels deformed, without normal structures and blocked due to the thrombosis and collagen fibrosis, while the NPs group had intact blood vessels and better patency. Immunofluorescence assay for CD31 and vWF showed that the lumen in the vessles from the NPs group had ECs well-covered, suggesting better endothelialization when compared with other groups. Conclusion Endothelialization-promoting TEBVs shows better promoting effect on endothelialization, and is helpful in maintenance of long-term patency of blood vessels after transplantation.

Introduction: Malnutrition during a critical window of development in a fetus or infant can result in abnormal cardiac remodeling and function. It is uncertain whether the contribution of these effects continues to impact the cardiac remodeling and function of adults over the course of several decades of growth. Our study examined the impact of early Chinese famine exposure on cardiac remodeling, left ventricular (LV) diastolic function, and LV systolic function in adults. Methods: Participants at high risk of cardiovascular disease from the China Patient-Centered Evaluative Assessment of Cardiac Events Million Persons Project (PEACE MPP) were enrolled. The famine in China lasted from 1959 to 1962. A total of three groups were formed based on the participants' birth dates: pre-famine group, famine exposure group, and post-famine group. Logistic regression and linear mixed models were used to explore the association between famine exposure and cardiac remodeling, LV diastolic function and LV systolic function in adults. Results: The study included 2,758 participants, the mean age was 57.05 years, 62.8% were female, 26.4% had LV hypertrophy (LVH), 59.6% had LV diastolic dysfunction (LVDD), and 10.5% had reduced global longitudinal strain (GLS). Compared to post-famine exposure, participants had independently increased risk of LVH in the famine exposure group (OR: 2.02, 95% CI: 1.60–2.56) and pre-famine exposure (OR: 1.36, 95% CI: 1.06–1.76). Compared to post-famine exposure, the risk of LVDD remarkably increased in the famine exposure group (OR: 3.04, 95% CI: 2.49–3.71) and pre-famine exposure group (OR: 1.87, 95% CI: 1.52–2.31). Famine exposure had no significant impact on GLS but was associated with a significant increase in LV ejection fraction (LVEF) and LV end-diastolic diameter (LVEDD). Significant interactions were observed between the effects of famine exposure and other clinical/sociodemographic variables (gender, systolic blood pressure [SBP] ≥140 mm Hg or not, high school or above or not, and annual income <50,000 RMB or not) on these outcomes. Conclusion: Exposure to famine, particularly during fetal and infant stages, increases the risk of LVH and LVDD in adults. However, the LV systolic function remains preserved. These impacts are more pronounced in females, individuals with SBP ≥140 mm Hg, those with low income, or those with high educational status. [ABSTRACT FROM AUTHOR]

Objective: This study aims to explore the association between metabolic syndrome (MetS) and left ventricular diastolic dysfunction (LVDD) and systolic dysfunction (LVSD), defined by impaired global longitudinal strain (GLS), and assess additive and multiplicative interactions among age, sex, obesity, and MetS regarding LVDD and LVSD. Methods: We prospectively recruited 5503 participants from the China PEACE (Patient‐Centered Evaluative Assessment of Cardiac Events) Million Persons Project with complete echocardiography exam. Multivariable logistic models were used to calculate adjusted odds ratios to evaluate both additive and multiplicative interactions. Results: The mean age was 56.59 years; 59.4% were women, 46.7% had MetS, 26.6% had left ventricular hypertrophy, 46.3% had LVDD, and 12.50% had impaired GLS. Compared to the non‐MetS, the odds ratio (OR) of LVDD and impaired GLS in MetS were 1.40 (1.20–1.64) and 1.26 (1.03–1.54), respectively. For LVDD, relative excess risk due to additive interaction (RERI) for women and MetS, elderly and MetS, obesity and MetS were 0.76 (0.02–1.50), 35.65 (17.51–53.79), and 2.14 (0.66–3.62), respectively, thus suggesting additive interactions. For impaired GLS, RERI for obesity and MetS was 3.37 (0.50–6.24), thus suggesting additive interactions. Conclusions: The MetS is independently associated with LVDD and impaired GLS. From the public health implications, prevention of MetS in women, elderly, and obese individuals might result in a greater reduction of LVDD and LVSD risk in cardiovascular high‐risk population. [ABSTRACT FROM AUTHOR]