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1. Trends and influence factors in the prevalence, awareness, treatment, and control of hypertension among US adults from 1999 to 2018.

Author

Zhixing Fan, Chaojun Yang, Jing Zhang, Yifan Huang, Ying Yang, Ping Zeng, Wanyin Cai, Zujin Xiang, Jingyi Wu, and Jian Yang

Subjects
Medicine, Science
Abstract

ObjectiveWe aimed to describe the trends and influence factors in the prevalence, awareness, treatment, and control of hypertension among US Adults from 1999 to 2018.MethodsWe utilized data from the National Health and Nutrition Examination Survey (NHANES) spanning ten survey cycles (n = 53,496). Prevalence, awareness, treatment, and control of hypertension were calculated using survey weights. Joinpoint regression and survey-weighted generalized linear models were used to analyze trends and influence factors, respectively.ResultsThe estimated prevalence of hypertension increased significantly from 33.53% to 40.58% (AAPC = 0.896, P = 0.002) during 1999-2018 with dropping rate of newly diagnosed hypertension from 8.62% to 4.82% before 2014 (APC = -4.075, P = 0.001), and then rose to 7.51% in 2018 (APC = 12.302, P = 0.126). Despite modest improvements or stability in the awareness, treatment, and control since 1999, the latter two remained inadequate in 2018 at 59.52% and 51.71%. There was an uptrend in the use of angiotensin-converting enzyme inhibitors (from 24.02% to 45.71%) and angiotensin receptor blockers (from 20.22% to 38.38%), and downtrend in β-blocker (from 12.71% to 4.21%). Men were at higher risk of incidence, un-awareness, un-treatment, and un-control for hypertension. Lower income and education were associated with susceptibility to hypertension, while being married was favorable for treatment and control. Optimal health reduced the incidence of hypertension, and increased the awareness and treatment.ConclusionAlthough the rate of newly diagnosed hypertension has declined slightly since 2010 in the US, the prevalence of hypertension is increasing, and treatment and control rates remain inadequate. To manage hypertension effectively, we need to focus on screening and prevention for high-risk populations, while advocating for optimal health to improve the burden of hypertension.

Published
2023
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2. Comparison of the Efficacy of ECMO With or Without IABP in Patients With Cardiogenic Shock: A Meta-Analysis

Author

Ping Zeng, Chaojun Yang, Jing Chen, Zhixing Fan, Wanyin Cai, Yifan Huang, Zujin Xiang, Jun Yang, Jing Zhang, and Jian Yang

Subjects
extracorporeal membrane oxygenation (ECMO), intra-aortic balloon pump (IABP), cardiogenic shock, survival (MeSH), meta-analysis, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

ObjectiveStudies on extracorporeal membrane oxygenation (ECMO) with and without an intra-aortic balloon pump (IABP) for cardiogenic shock (CS) have been published, but there have been no meta-analyses that compare the efficacy of these two cardiac support methods. This meta-analysis evaluated the outcomes of these two different treatment measures.MethodsThe PubMed, Embase, Cochrane Library, Web of Science, and Clinical Trials databases were searched until March 2022. Studies that were related to ECMO with or without IABP in patients with CS were screened. Quality assessments were evaluated with the methodological index for nonrandomized studies (MINORS). The primary outcome was in-hospital survival, while the secondary outcomes included duration of ECMO, duration of ICU stay, infection/sepsis, and bleeding. Revman 5.3 and STATA software were used for this meta-analysis.ResultsIn total, nine manuscripts with 2,573 patients were included in the systematic review. CS patients who received ECMO in combination with IABP had significantly improved in-hospital survival compared with ECMO alone (OR = 1.58, 95% CI = 1.26–1.98, P < 0.0001). However, there were no significant differences in the duration of ECMO (MD = 0.36, 95% CI = −0.12–0.84, P = 0.14), duration of ICU stay (MD = −1.95, 95% CI = −4.05–0.15, P = 0.07), incidence of infection/sepsis (OR = 1.0, 95% CI = 0.58–1.72, P = 1.0), or bleeding (OR = 1.28, 95% CI = 0.48–3.45, P = 0.62) between the two groups of patients with CS.ConclusionECMO combined with IABP can improve in-hospital survival more effectively than ECMO alone in patients with CS.

Published
2022
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3. Suv39h1 downregulation inhibits neointimal hyperplasia after vascular injury

Author

Hui Wu, Jing Zhang, Jun Yang, Qi Hu, Wenqi Gao, Chao He, Jian Yang, Chaojun Yang, Qing Guo, Changwu Xu, Jing Chen, and Wanyin Cai

Subjects
Cyclin-Dependent Kinase Inhibitor p21, Male, 0301 basic medicine, Neointima, Intimal hyperplasia, Vascular smooth muscle, Carotid Artery, Common, Myocytes, Smooth Muscle, Down-Regulation, Vascular Remodeling, 030204 cardiovascular system & hematology, Muscle, Smooth, Vascular, Rats, Sprague-Dawley, 03 medical and health sciences, 0302 clinical medicine, Restenosis, Downregulation and upregulation, Cell Movement, medicine, Animals, Cells, Cultured, Cell Proliferation, Neointimal hyperplasia, Hyperplasia, biology, Chemistry, Methyltransferases, Vascular System Injuries, medicine.disease, Angiotensin II, Proliferating cell nuclear antigen, Repressor Proteins, Disease Models, Animal, 030104 developmental biology, cardiovascular system, biology.protein, Cancer research, Inhibitor of Differentiation Proteins, Carotid Artery Injuries, Cardiology and Cardiovascular Medicine, Cyclin-Dependent Kinase Inhibitor p27, Signal Transduction
Abstract

Background and aims Neointimal hyperplasia resulting from pathological vascular smooth muscle cells (VSMCs) activation is a common pathophysiological basis for numerous proliferative vascular diseases, such as restenosis. Suv39h1, an important transcription suppressor, may be involved in this process. Herein, we investigated the role of Suv39h1 in pathological intimal hyperplasia and its possible mechanisms in vitro and in vivo . Methods An adenovirus vector for Suv39h1 overexpression and a lentiviral vector for its downregulation were constructed and used to transfect cultured VSMCs in vitro . The functional changes in VSMCs stimulated by angiotensin II (Ang II) were observed and the possible mechanism was investigated. Additionally, rat carotid arteries with balloon injury were locally transfected with these viral vectors and changes in neointima formation, proliferating cell nuclear antigen (Pcna) expression and collagen deposition were examined. Results Upon Ang II stimulation, the expression of Suv39h1 and inhibitor of DNA binding 3 (Id3) was significantly increased. Suv39h1 downregulation inhibited Ang II-stimulated migration and proliferation of VSMCs, antagonized the production of Id3 and promoted p21 and p27Kip1 expression. In contrast, Suv39h1 overexpression had the opposite effects. Suv39h1 regulated the transcription of p21 and p27Kip1 by controlling H3K9me3 in the proximal promoter regions. Consistent with the VSMCs results, Suv39h1 and Id3 expression was significantly increased in blood vessels after balloon injury. Suv39h1 downregulation inhibited intimal hyperplasia, and attenuated Pcna expression and collagen synthesis in the intima, while Suv39h1 overexpression had the opposite effects. Conclusions Suv39h1 downregulation effectively inhibited neointimal hyperplasia after vascular injury.

Published
2019

4. MicroRNA-24 inhibits the oxidative stress induced by vascular injury by activating the Nrf2/Ho-1 signaling pathway

Author

Wanyin Cai, Cong Ma, Jing Zhang, Chaojun Yang, Wei Wang, Zhixing Fan, Jian Yang, and Mengting Xiong

Subjects
0301 basic medicine, Blood Glucose, Male, Vascular smooth muscle, NF-E2-Related Factor 2, Myocytes, Smooth Muscle, 030204 cardiovascular system & hematology, Pharmacology, medicine.disease_cause, N-Acetylglucosaminyltransferases, Muscle, Smooth, Vascular, Diabetes Mellitus, Experimental, Rats, Sprague-Dawley, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Re-Epithelialization, medicine, Animals, Cells, Cultured, Cell Proliferation, chemistry.chemical_classification, Reactive oxygen species, NADPH oxidase, Kelch-Like ECH-Associated Protein 1, biology, Malondialdehyde, Streptozotocin, KEAP1, MicroRNAs, Oxidative Stress, 030104 developmental biology, chemistry, Heme Oxygenase (Decyclizing), biology.protein, Signal transduction, Cardiology and Cardiovascular Medicine, Carotid Artery Injuries, Oxidative stress, medicine.drug, Signal Transduction
Abstract

Background and aims The process of endothelial repair in diabetic patients after stent implantation was significantly delayed compared with that in non-diabetic patients, and oxidative stress is increasingly considered to be relevant to the pathogenesis of diabetic endothelial repair. However, the mechanisms linking diabetes and reendothelialization after vascular injury have not been fully elucidated. The aim of this study was to evaluate the effect of microRNA-24 (miR-24) up-regulation in delayed endothelial repair caused by oxidative stress after balloon injury in diabetic rats. Methods In vitro, vascular smooth muscle cells (VSMCs) isolated from the thoracic aorta were stimulated with high glucose (HG) after miR-24 recombinant adenovirus (Ad-miR-24-GFP) transfection for 3 days. In vivo, diabetic rats induced using high-fat diet (HFD) and low-dose streptozotocin (30 mg/kg) underwent carotid artery balloon injury followed by Ad-miR-24-GFP transfection for 20 min. Results The expression of miR-24 was decreased in HG-stimulated VSMCs and balloon-injured carotid arteries of diabetic rats, which was accompanied by increased expression of Ogt and Keap1 and decreased expression of Nrf2 and Ho-1. Up-regulation of miR-24 suppressed VSMC oxidative stress induced by HG in vitro, and miR-24 up-regulation promoted reendothelialization in balloon-injured diabetic rats. The underlying mechanism was related to the activation of the Nrf2/Ho-1 signaling pathway, which subsequently suppressed intracellular reactive oxidative species (ROS) production and malondialdehyde (MDA) and NADPH oxidase (Nox) activity, and to the restoration of Sod and Gsh-px activation. Conclusions The up-regulation of miR-24 significantly promoted endothelial repair after balloon injury through inhibition of oxidative stress by activating the Nrf2/Ho-1 signaling pathway.

Published
2019

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