Publications by authors named "Chuanyu Gao"

112 Publications

Delta QRS Distinguishes I -mediated J waves from Pseudo J waves Produced by Conduction Delay on Body Surface ECG.

Pacing Clin Electrophysiol 2021 Sep 9. Epub 2021 Sep 9.

Lankenau Medical Center, Wynnewood, PA, 19096.

Background: On surface ECGs, it is difficult to differentiate I -mediated J waves, a repolarization phenomenon seen in J wave syndromes (JWS) from terminal QRS deflections that mimic J waves (pseudo J waves) in intraventricular conduction delay (IVCD), an abnormality in depolarization. We hypothesize that the difference between the "maximum QRS duration" inclusive of J point or terminal QRS deflections and the minimum QRS duration identified across a 12-lead ECG is significantly larger in I -mediated J waves, and can serve as a marker to make this distinction.

Methods: A retrospective analysis was performed on adults with ECGs consisting of one of the four following manifestations: J waves associated with hypothermia and early repolarization, and pseudo J waves associated with RBBB and nonspecific IVCD (NS-IVCD). All ECGs were assessed individually and the maximum and minimum discrete QRS deflections on 12-lead tracings, defined as "QRS " and QRS , were identified. The difference between "QRS " and QRS , designated as ∆QRS, was calculated and compared across the studied populations.

Results: A total of 60 patients consisting of 15 patients in each arm were included in the study. ΔQRS was significantly larger in the hypothermia and early repolarization groups, compared to RBBB and NS-IVCD (p<0.0001), with the following mean ∆QRS: hypothermia 54.3±13.7 ms, early repolarization pattern 47.3±15.3 ms, RBBB 19.3±6.5 ms and NS-IVCD 16.0±6.6 ms.

Conclusion: ∆QRS may serve as a reliable ECG parameter for distinguishing I -mediated J waves from pseudo J waves produced by delayed intraventricular conduction. This article is protected by copyright. All rights reserved.
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http://dx.doi.org/10.1111/pace.14359DOI Listing
September 2021

[Association of RAGE gene polymorphisms with MHR ratio and heart rate variability among patients with coronary heart disease].

Zhonghua Yi Xue Yi Chuan Xue Za Zhi 2021 Jul;38(7):681-685

Department of Emergency, Heart Center of Henan People's Hospital, Zhengzhou, Henan 410105, China.

Objective: To assess the association of polymorphisms of receptor of advanced glycation end products (RAGE) gene, monocyte to high-density lipoprotein cholesterol ratio (MHR) and variability of heart rate among patients with coronary heart disease (CHD).

Methods: 120 patients with CHD and 120 healthy individuals were respectively selected as the observation group and the control group. Allelic and genotypic differences of -429T>C, 1704G>T, 82G>S, MHR ratio and heart rate variability between the two groups and patients with different severity were analyzed. The correlation between their genotypes and MHR ratio and heart rate variability was analyzed.

Results: The 82G>S polymorphism of the RAGE gene and the allelic difference between the two groups and patients with different severity were statistically significant (P< 0.05). Compared with the control group and patients with mild to moderate phenotype, monocyte, total cholesterol, triglyceride, low density lipoprotein, MHR, low frequency in the observation group and patients with severe symptoms were significantly higher, while their high density lipoprotein, standard deviation of NN intervals (SDNN), standard deviation average of NN intervals (SDANN), root mean square successive differences, percentage of differences exceeding 50ms between adjacent normal number of intervals (PMN50), high frequency (HF) were significantly lower. The gene frequencies of G-Gly-T, T-Gly-T, G-Ser-T and G-Gly-C were correlated with SDNN, SDANN, rMSSD, PMN50, HF and MHR, but negatively correlated with low frequency.

Conclusion: Polymorphisms of the RAGE gene in patients with coronary heart disease are associated with the MHR ratio and heart rate variability, which can be used as markers for the diagnosis and efficacy evaluation.
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http://dx.doi.org/10.3760/cma.j.cn511374-20200430-00318DOI Listing
July 2021

MicroRNA-532-5p-programmed cell death protein 4 (PDCD4) axis regulates angiotensin II-induced human umbilical vein endothelial cell apoptosis and proliferation.

Microvasc Res 2021 Nov 8;138:104195. Epub 2021 Jun 8.

Department of Neonatology, Kaifeng Maternity and Children Health Hospital, Kaifeng City, Henan Province 475002, PR China.

Background: This study was carried out to investigate the effect of microRNA miR-532-5p on the proliferation of hypertension endothelial cells.

Methods: Angiotensin II (Ang II)-treated human umbilical vein endothelial cells (HUVECs) and primary human aortic endothelial cells (HAECs) were used as cell models to imitate the pathological changes in endothelial cells under hypertensive conditions. The expression levels of miR-532-5p and programmed cell death protein 4 (PDCD4) were detected by Quantitative Real-time PCR (qRT-PCR). The effects of miR-532-5p and PDCD4 on the proliferation of HUVECs and HAECs treated with Ang II were detected by Methyl Thiazolyl Tetrazolium (MTT) assay. The effects of miR-532-5p and PDCD4 on the apoptosis and cell cycle of HUVECs and HAECs treated with Ang II were detected by flow cytometry. Western blot was used to detect the expression levels of PDCD4, apoptosis-related proteins and cycle-related proteins in HUVECs and HAECs treated with Ang II. Bioinformatics analysis and Luciferase gene reporter assay were used to assess the relationship between miR-532-5p and PDCD4.

Results: The expression levels of miR-532-5p were reduced, while the expression levels of PDCD4 were raised in Ang II-treated HUVECs and HAECs. MiR-532-5p mimic and si-PDCD4 restrained the apoptosis, promoted the proliferation of Ang II-treated HUVECs and HAECs and caused S-phase arrest of cells. PDCD4 was identified as a potential target for miR-532-5p. Knockdown of PDCD4 significantly affected apoptosis and proliferation of Ang II-treated HUVECs. MiR-532-5p regulates apoptosis and proliferation of Ang II-induced HUVECs and HAECs. In addition, overexpression of PDCD4 attenuated the effect of miR-532-5p on the proliferation of Ang II-treated HUVECs and HAECs.

Conclusion: MiR-532-5p inhibited the expression of PDCD4, thereby inhibiting apoptosis and promoting proliferation of Ang II-treated HUVECs and HAECs.
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http://dx.doi.org/10.1016/j.mvr.2021.104195DOI Listing
November 2021

The IDENTIFY study: the investigation and detection of urological neoplasia in patients referred with suspected urinary tract cancer - a multicentre observational study.

BJU Int 2021 May 14. Epub 2021 May 14.

Great Western Hospitals NHS Foundation Trust, Swindon, UK.

Objective: To evaluate the contemporary prevalence of urinary tract cancer (bladder cancer, upper tract urothelial cancer [UTUC] and renal cancer) in patients referred to secondary care with haematuria, adjusted for established patient risk markers and geographical variation.

Patients And Methods: This was an international multicentre prospective observational study. We included patients aged ≥16 years, referred to secondary care with suspected urinary tract cancer. Patients with a known or previous urological malignancy were excluded. We estimated the prevalence of bladder cancer, UTUC, renal cancer and prostate cancer; stratified by age, type of haematuria, sex, and smoking. We used a multivariable mixed-effects logistic regression to adjust cancer prevalence for age, type of haematuria, sex, smoking, hospitals, and countries.

Results: Of the 11 059 patients assessed for eligibility, 10 896 were included from 110 hospitals across 26 countries. The overall adjusted cancer prevalence (n = 2257) was 28.2% (95% confidence interval [CI] 22.3-34.1), bladder cancer (n = 1951) 24.7% (95% CI 19.1-30.2), UTUC (n = 128) 1.14% (95% CI 0.77-1.52), renal cancer (n = 107) 1.05% (95% CI 0.80-1.29), and prostate cancer (n = 124) 1.75% (95% CI 1.32-2.18). The odds ratios for patient risk markers in the model for all cancers were: age 1.04 (95% CI 1.03-1.05; P < 0.001), visible haematuria 3.47 (95% CI 2.90-4.15; P < 0.001), male sex 1.30 (95% CI 1.14-1.50; P < 0.001), and smoking 2.70 (95% CI 2.30-3.18; P < 0.001).

Conclusions: A better understanding of cancer prevalence across an international population is required to inform clinical guidelines. We are the first to report urinary tract cancer prevalence across an international population in patients referred to secondary care, adjusted for patient risk markers and geographical variation. Bladder cancer was the most prevalent disease. Visible haematuria was the strongest predictor for urinary tract cancer.
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http://dx.doi.org/10.1111/bju.15483DOI Listing
May 2021

COVID-19 and its impact on the clinical specialty training recruitment process: lessons learned and the shape of future specialty recruitment in the UK.

J R Soc Med 2021 Jun 5;114(6):323-326. Epub 2021 May 5.

William Harvey Hospital, East Kent Hospitals University NHS Foundation Trust, Kennington Road, Willesborough, Ashford, Kent TN24 0LZ.

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http://dx.doi.org/10.1177/01410768211008860DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8212549PMC
June 2021

Silencing of SNHG6 alleviates hypoxia/reoxygenation-induced cardiomyocyte apoptosis by modulating miR-135a-5p/HIF1AN to activate Shh/Gli1 signalling pathway.

J Pharm Pharmacol 2021 Mar;73(1):22-31

Department of Cardiology, People's Hospital of Zhengzhou University, Henan Provincial People's Hospital, Fuwai Central China Cardiovascular Hospital, Zhengzhou, China.

Objectives: To examine the effects of small nucleolar RNA host gene 6 (SNHG6) on apoptosis during myocardial ischemic/reperfusion (I/R) injury and its potential molecular mechanisms.

Methods: In vitro model of I/R was built through exposing mouse HL-1 cardiomyocytes to hypoxia/reoxygenation (H/R) treatment. Quantitative real-time polymerase chain reaction assays were performed to determine gene expression. Cell Counting Kit-8, flow cytometric and western blot assays were conducted to detect cell viability, apoptosis and protein expression. Lactate dehydrogenase (LDH) activity was examined by a commercial detection kit. Dual-luciferase gene reporter and RNA immunoprecipitation experiments were applied for determining the interaction between the molecules.

Key Findings: SNHG6 expression was increased in H/R-challenged cardiomyocytes. Depletion of SNHG6 protected against H/R-induced cardiomyocytes apoptosis. SNHG6 could sponge miR-135a-5p to inhibit its expression. Down-regulation of miR-135a-5p reversed the anti-apoptotic effect caused by SNHG6 knockdown in H/R-induced cardiomyocytes. Hypoxia inducible factor 1 subunit alpha inhibitor (HIF1AN) was identified as a direct target of miR-135a-5p, and knockdown of HIF1AN relieved H/R-induced cardiomyocytes apoptosis. Silencing of SNHG6 activated Shh/Gli1 signalling pathway by regulating miR-135a-5p/HIF1AN. Furthermore, inactivation of Shh/Gli signalling abolished the anti-apoptotic effects of SNHG6 knockdown in H/R-induced cardiomyocytes.

Conclusions: SNHG6 serves as a sponge for miR-135a-5p to promote HIF1AN expression and inactivate Shh/Gli1 signalling, eventually aggravating H/R-induced apoptosis in cardiomyocytes.
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http://dx.doi.org/10.1093/jpp/rgaa064DOI Listing
March 2021

Thirty-six-month results of laparoscopic-based renal denervation plus unilateral laparoscopic adrenalectomy for the treatment of patients with resistant hypertension caused by unilateral aldosterone-producing adenoma.

J Clin Hypertens (Greenwich) 2021 05 16;23(5):946-953. Epub 2021 Feb 16.

Department of Cardiology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Zhengzhou, China.

The aim of this study was to explore the long-term clinical results of Renal denervation (RDN) from the adventitia of the renal artery plus unilateral laparoscopic adrenalectomy to treat patients with resistant hypertension caused by unilateral aldosterone-producing adenoma (APA). Sixty patients with resistant hypertension caused by APA who were treated at Henan Provincial People's Hospital from December 2016 to March 2018 were selected and randomly assigned to undergo RDN from the adventitia of the renal artery plus adrenalectomy (RDN group, n = 30) or adrenalectomy alone (control group, n = 30). Office blood pressure (BP), antihypertensive medication usage and other laboratory characteristics were followed every 6 months through 36 months. Follow-up data were available at 36 months for 23 of 30 subjects in the RDN group and for 21 of 30 subjects who were in the control group. At 36 months postprocedure, the reduction in the RDN group was 42.2 ± 21.6 mmHg and that in the control group was 29.8 ± 13.5 mmHg (p = .029 between the groups). During the follow-up to 36 months postprocedure, no patients in either the RDN group or the control group died due to surgical complications, and the RDN group had no procedural complications, including renal artery dissection, perforation, and renal artery stenosis. There was no change in the mean eGFR of the two groups, and no serious adverse events were reported. In conclusion, RDN from the adventitia of the renal artery plus unilateral laparoscopic adrenalectomy resulted in sustained lowering of BP at 3 years in a selected population of subjects with resistant hypertension caused by unilateral APA without serious safety concerns.
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http://dx.doi.org/10.1111/jch.14223DOI Listing
May 2021

Understanding angiogenesis and the role of angiogenic growth factors in the vascularisation of engineered tissues.

Mol Biol Rep 2021 Jan 3;48(1):941-950. Epub 2021 Jan 3.

Division of Surgery and Interventional Science, Centre for Nanotechnology and Tissue Engineering, Royal Free Campus, UCL, London, NW3 2PF, UK.

Tissue engineering is a rapidly developing field with many potential clinical applications in tissue and organ regeneration. The development of a mature and stable vasculature within these engineered tissues (ET) remains a significant obstacle. Currently, several growth factors (GFs) have been identified to play key roles within in vivo angiogenesis, including vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF), FGF and angiopoietins. In this article we attempt to build on in vivo principles to review the single, dual and multiple GF release systems and their effects on promoting angiogenesis. We conclude that multiple GF release systems offer superior results compared to single and dual systems with more stable, mature and larger vessels produced. However, with more complex release systems this raises other problems such as increased cost and significant GF-GF interactions. Upstream regulators and pericyte-coated scaffolds could provide viable alternative to circumnavigate these issues.
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http://dx.doi.org/10.1007/s11033-020-06108-9DOI Listing
January 2021

Circ_0010729 knockdown protects cardiomyocytes against hypoxic dysfunction via miR-370-3p/TRAF6 axis.

EXCLI J 2020 11;19:1520-1532. Epub 2020 Nov 11.

Coronary Care Unit, Department of Cardiology, People's Hospital of Zhengzhou University, Zhengzhou City, Henan Procince, China.

Few studies have addressed the mechanism by which circ_0010729 regulates hypoxia-induced cell injury in cardiovascular diseases. However, its role and its regulatory mechanism in myocardial infarction remain to be explored. Cell viability, cycle, apoptosis, and migration were analyzed using cell counting kit-8 assay, flow cytometry, caspase-3 activity assay kit and transwell assay, respectively. Tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) concentrations were examined by enzyme-linked immunosorbent assay. Glucose metabolism was calculated by detecting ATP production, glucose uptake and lactate production. Levels of circ_0010729, miR-370-3p and TNF Receptor Associated Factor 6 (TRAF6) were detected using quantitative real-time polymerase chain reaction or western blot. The direct interaction between circ_0010729 and TRAF6 or miR-370-3p was verified using dual-luciferase reporter assay and RNA immunoprecipitation assay. Under hypoxia condition, cardiomyocytes suffered from cell viability suppression, cell cycle arrest, cell apoptosis promotion, migration reduction, increase of inflammatory factor IL-6 and TNF-α, as well as glycolysis inhibition. Circ_0010729 expression was up-regulated in the cardiomyocytes at different hypoxia-exposed time points. Circ_0010729 knockdown protected cardiomyocytes against hypoxic dysfunction, while circ_0010729 overexpression showed inverse effects. MiR-370-3p was confirmed to directly bind to circ_0010729 or TRAF6. MiR-370-3p inhibition attenuated the protective effects of circ_0010729 knockdown on hypoxia-modulated cardiomyocyte dysfunction. MiR-370-3p restoration protected cardiomyocytes against hypoxic injury via targeting TRAF6. Besides, circ_0010729 indirectly regulated TRAF6 expression via miR-370-3p. This study demonstrated that circ_0010729 knockdown attenuated hypoxia-induced cardiomyocyte dysfunction via miR-370-3p/TRAF6 axis, indicating a potential therapeutic target for myocardial infarction.
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http://dx.doi.org/10.17179/excli2020-2809DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7689242PMC
November 2020

A Practical Risk Score to Predict 24-Month Post-Discharge Mortality Risk in Patients With Non-ST-Segment Elevation Myocardial Infarction.

Circ J 2020 10 17;84(11):1974-1980. Epub 2020 Sep 17.

Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Science and Peking Union Medical College.

Background: Risk stratification of patients with non-ST-segment elevation myocardial infarction (NSTEMI) is important in terms of treatment strategy selection. Current efforts have focused on short-term risk prediction after discharge, but we aimed to establish a risk score to predict the 24-month mortality risk in survivors of NSTEMI.Methods and Results:A total of 5,509 patients diagnosed with NSTEMI between January 2013 and September 2014 were included. Primary endpoint was all-cause death at 24 months. A multivariable Cox regression model was used to establish a practical risk score based on independent risk factors of death. The risk score included 9 variables: age, body mass index, left ventricular ejection fraction, reperfusion therapy during hospitalization, Killip classification, prescription of diuretics at discharge, heart rate, and hemoglobin and creatinine levels. The C-statistics for the risk model were 0.83 (95% confidence interval [CI]: 0.81-0.85) and 0.83 (95% CI: 0.79-0.86) in the development and validation cohorts, respectively. Mortality risk increased significantly across groups: 1.34% in the low-risk group (score: 0-58), 5.40% in intermediate group (score: 59-93), and 23.87% in high-risk group (score: ≥94).

Conclusions: The current study established and validated a practical risk score based on 9 variables to predict 24-month mortality risk in patients who survive NSTEMI. This score could help identify patients who are at high risk for future adverse events who may benefit from good adherence to guideline-recommended secondary prevention treatment.
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http://dx.doi.org/10.1253/circj.CJ-20-0509DOI Listing
October 2020

Clinical outcomes of laparoscopic-based renal denervation plus adrenalectomy vs adrenalectomy alone for treating resistant hypertension caused by unilateral aldosterone-producing adenoma.

J Clin Hypertens (Greenwich) 2020 09 18;22(9):1606-1615. Epub 2020 Aug 18.

Department of Cardiology, Henan University People's Hospital, Henan Provincial People's Hospital, Zhengzhou, China.

Previous studies describing renal denervation (RDN) from the intima of the renal artery for the treatment of resistant hypertension have reported variable efficacies, and RDN triggers renal intimal injury and atherosclerosis. This study aimed to evaluate the efficacy and safety of RDN from the adventitia of renal artery plus unilateral laparoscopic adrenalectomy to treat patients with resistant hypertension caused by unilateral aldosterone-producing adenoma (APA). A total of 60 consecutive patients with resistant hypertension caused by unilateral APA were enrolled in this study. Patients were randomly assigned to undergo RDN from the adventitia of the renal artery plus adrenalectomy (RDN group, n = 30) or adrenalectomy alone (control group, n = 30) and were followed up for 12 months. The primary efficacy end point was the change in 24-hours mean ambulatory systolic blood pressure (SBP) from baseline to 12 months. At the 12-month follow-up, the mean reduction of 24-hours average SBP and office SBP in the RDN group was 20.7 ± 15.2 and 37.1 ± 26.0 mm Hg, respectively, which was significantly higher than the mean reduction of 24-hours average SBP (11.9 ± 11.1 mm Hg, P = .017) and the office SBP (25.9 ± 16.8 mm Hg, P = .035) in the control group. Serum potassium levels returned to normal 12 months post-procedure. Patients in the RDN group had higher proportion of cured clinical and biochemical outcomes than those in the control group (35.7% vs 17.9% in clinical outcome; 96.4% vs 89.3% in biochemical outcome, respectively). There were no procedural-, device-, or treatment-related safety events during the 12-month follow-up period between the groups. In conclusion, RDN from the adventitia of the renal artery plus unilateral laparoscopic adrenalectomy is more effective than adrenalectomy alone for treating resistant hypertension caused by unilateral APA.
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http://dx.doi.org/10.1111/jch.13963DOI Listing
September 2020

METTL14 aggravates endothelial inflammation and atherosclerosis by increasing FOXO1 N6-methyladeosine modifications.

Theranostics 2020 11;10(20):8939-8956. Epub 2020 Jul 11.

Department of Cardiology, Henan Provincial People's Hospital, Department of Cardiology of Central China Fuwai Hospital, Henan Key Laboratory for Coronary Heart Disease Prevention and Control, Central China Fuwai Hospital of Zhengzhou University, Zhengzhou, Henan, 450003, China.

The N6-methyladenosine (mA) modification plays an important role in various biological processes, but its role in atherosclerosis remains unknown. The aim of this study was to investigate the role and mechanism of mA modification in endothelial cell inflammation and its influence on atherosclerosis development. We constructed a stable TNF-α-induced endothelial cell inflammation model and assessed the changes in the expression of mA modification-related proteins to identify the major factors involved in this process. The mA-modified mRNAs were identified by methylated RNA immunoprecipitation (RIP) sequencing and forkhead box O1 (FOXO1) was selected as a potential target. Through cytological experiments, we verified whether methyltransferase-like 14 (METTL14) regulates FOXO1 expression by regulating mA-dependent mRNA and protein interaction. The effect of METTL14 on atherosclerosis development was verified using METTL14 knockout mice. These findings confirmed that METTL14 plays major roles in TNF-α-induced endothelial cell inflammation. During endothelial inflammation, mA modification of FOXO1, an important transcription factor, was remarkably increased. Moreover, METTL14 knockdown significantly decreased TNF-α-induced FOXO1 expression. RIP assay confirmed that METTL14 directly binds to FOXO1 mRNA, increases its mA modification, and enhances its translation through subsequent YTH N6-methyladenosine RNA binding protein 1 recognition. Furthermore, METTL14 was shown to interact with FOXO1 and act directly on the promoter regions of and to promote their transcription, thus mediating endothelial cell inflammatory response. experiments showed that METTL14 gene knockout significantly reduced the development of atherosclerotic plaques. METTL14 promotes FOXO1 expression by enhancing its mA modification and inducing endothelial cell inflammatory response as well as atherosclerotic plaque formation. Decreased expression of METTL14 can inhibit endothelial inflammation and atherosclerosis development. Therefore, METTL14 may serve as a potential target for the clinical treatment of atherosclerosis.
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http://dx.doi.org/10.7150/thno.45178DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7415798PMC
June 2021

Is there an app for that?

BJU Int 2020 08;126(2):312-313

Addenbrooke's Hospital, Cambridge University Hospital Foundation Trust, Cambridge, UK.

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http://dx.doi.org/10.1111/bju.15184DOI Listing
August 2020

Potential in paleoclimate reconstruction of modern pollen assemblages from natural and human-induced vegetation along the Heilongjiang River basin, NE China.

Sci Total Environ 2020 Nov 22;745:141121. Epub 2020 Jul 22.

Key Laboratory of Wetland Ecology and Environment, Northeast Institute of Geography and Agroecology, Chinese Academy of Sciences, Changchun 130102, China. Electronic address:

The relationships among modern pollen, vegetation, climate and human activities can help improving the reliability of reconstruction of past vegetation, regional climate and human activities based on fossil pollen records. We used a dataset of 114 surface soil pollen samples from natural vegetation (wetlands, forests and grasslands) and human-induced vegetation (farmlands and residences) along the Heilongjiang River basin in northeast China to explore the relationships among modern pollen, vegetation, climate and human activities. The results indicated that surface pollen assemblages differentiated modern vegetation well in natural and human-induced vegetation types. The wetlands were mainly composed of Cyperaceae, along with Artemisia, weeds Poaceae (<35 μm) and Sanguisorba. The forests were predominated by Pinus and Betula. Artemisia, weeds Poaceae (<35 μm) and Chenopodiaceae were the most important pollen taxa in grasslands. The farmlands were characterized by Artemisia, Aster, Chenopodiaceae, cereal Poaceae (>35 μm) and Taraxacum. The pollen assemblages of residences were composed of weeds Poaceae (<35 μm), Chenopodiaceae and Salix. Ordination analyses based on main pollen taxa and climatic variables were used to determine the relationships between pollen and climate, suggesting the surface pollen assemblages were primarily influenced by the mean annual temperature (Tann) in northeast China. The statistical performance of transfer function between pollen and Tann were well indicating the modern pollen assemblages could be reliably used in paleoclimate reconstruction in our study area. Furthermore, human-induced vegetation had high frequencies of human-companion pollen taxa, such as Chenopodiaceae, Aster, Taraxacum and cereal Poaceae (>35 μm). Pollen concentrations of human-induced vegetation were lower than natural vegetation types, which could be used as an indicator of human influence intensity.
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http://dx.doi.org/10.1016/j.scitotenv.2020.141121DOI Listing
November 2020

Antithrombotic therapy in coronary artery disease patients with atrial fibrillation.

BMC Cardiovasc Disord 2020 07 6;20(1):323. Epub 2020 Jul 6.

Department of Cardiology, Zhengzhou University People's Hospital, No.7 Weiwu road, Jinshui District, Zhengzhou, 450003, Henan, China.

Background: Coronary artery disease (CAD) and atrial fibrillation (AF) frequently coexist in clinical practice, making it challenging for the treating physician to choose anticoagulation and antiplatelet therapies. The aim of this study was to investigate antithrombotic strategies and assess related adverse outcomes in stable coronary artery disease (SCAD) and acute coronary syndrome (ACS) patients with AF when the CHADS-VASc score was ≥2.

Methods: We performed a retrospective study and collected data from a computer-based patient record management system in Zhengzhou University People's Hospital in China. In total, 2978 patients with a hospital discharge diagnosis of CAD and concomitant AF who met the inclusion criteria were enrolled from January 1, 2012 to December 31, 2016, and data from 2050 patients were finally analysed. The χ test was used to compare the incidences of clinical endpoints between the SCAD+AF group and the ACS + AF group. Multivariable Cox regression analysis was performed to identify independent predictive factors of adverse outcomes in both groups.

Results: Oral anticoagulant (OAC) monotherapy was the most common antithrombotic therapy in SCAD+AF patients (49.55%), while double antiplatelet therapy (DAPT) was the most common treatment in ACS + AF patients (54.19%) at discharge. OAC monotherapy significantly increased and the use of single antiplatelet therapy (SAPT) decreased during follow-up (34 ± 13 months) when compared to their use at discharge in the SCAD+AF group (all p < 0.001). In the ACS + AF group, the proportion of patients using DAPT decreased notably, while the proportions of patients using SAPT and dual therapy (DT) combining OAC with SAPT increased significantly during follow-up (all p < 0.001) compared to the proportions at discharge. According to multivariable Cox regression analysis, age, hypertension and prior stroke were independent risk factors for ischaemic stroke in the SCAD+AF group and ACS + AF group (all p < 0.05). OAC was an independent protective factor for ischaemic stroke in both groups (all p < 0.05). Previous bleeding independently increased the risk of haemorrhage in both groups (all p < 0.01).

Conclusions: In this study, the proportion of anticoagulant-antiplatelet combined therapy was low in ACS + AF patients with high stroke risk. In clinical practice, the awareness of anticoagulation needs to be strengthened regarding patients with CAD and AF.
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http://dx.doi.org/10.1186/s12872-020-01609-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7339421PMC
July 2020

Laparoscopic-based perivascular renal sympathetic nerve denervation: a feasibility study in a porcine model.

Eur J Med Res 2020 Jun 18;25(1):22. Epub 2020 Jun 18.

Department of Cardiology, Zhengzhou University People's Hospital, Zhengzhou, 450003, People's Republic of China.

Background: This study aims to evaluate the effects and safety of laparoscopic-based perivascular renal sympathetic nerve denervation (RDN) in a porcine model fed a high-fat diet.

Method: Thirty-six high-fat diet-fed Bama minipigs were randomly divided into an RDN group (n = 18), in which minipigs received laparoscopic-based perivascular RDN, and a sham group (n = 18). All pigs were fed the high-fat diet after the operation to establish a model of obesity-induced hypertension. Bama pigs in the RDN and sham groups were killed at 3 time points [2 days after RDN (n = 6), day 90 (n = 6) and day 180 (n = 6)].

Result: The systolic blood pressure (SBP) and noradrenaline (NE) concentration in the kidney tissue were significantly lower in the RDN group than in the sham group at 2 days (113.83 ± 3.26 mmHg vs 129.67 ± 3.32 mmHg, P = 0.011, and 112.02 ± 17.34 ng/g vs 268.48 ± 20.61 ng/g, P < 0.001, respectively), 90 days (116.83 ± 3.88 mmHg vs 145.00 ± 4.22 mmHg, P = 0.001, respectively) and 180 days (129.33 ± 2.87 mmHg vs 168.57 ± 2.86 mmHg, P < 0.001, and 152.15 ± 16.61 ng/g vs 318.97 ± 24.84 ng/g, P < 0.001, respectively) after the operation. The diastolic blood pressure (DBP) was significantly lower in the RDN group than in sham group at 90 and 180 days after the operation (72.17 ± 2.7 mmHg vs 81.50 ± 2.22 mmHg, P = 0.037, and 76.83 ± 2.75 mmHg vs 86.33 ± 2.22 mmHg P = 0.021, respectively). Based on the pathological evaluation, the renal sympathetic nerve fascicles were successfully disrupted by radiofrequency energy after laparoscopic-based perivascular RDN, but the intima was intact. Tyrosine hydroxylase (TH) expression was decreased, while the expression of the S100 protein was increased in treated renal arteries after RDN.

Conclusions: Laparoscopic-based perivascular RDN prevented the occurrence and development of hypertension, and thus it may be an efficient and safe method for controlling blood pressure in an experimental model.
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http://dx.doi.org/10.1186/s40001-020-00422-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7301974PMC
June 2020

Effects of surgical septal myectomy on survival in patients with hypertrophic obstructive cardiomyopathy.

Anatol J Cardiol 2020 06;23(6):342-348

Department of Cardiology, Zhengzhou University People's Hospital; Central China Fuwai Hospital; Central China Branch of the National Cardiovascular Center; Henan Provincial People's Hospital; Henan-China.

Objective: The purpose of this study was to determine the effects of surgical resection of muscle layer on the long-term survival of patients with hypertrophic obstructive cardiomyopathy (HOCM).

Methods: The original study cohort consisted of 552 patients with hypertrophic cardiomyopathy (HCM), including 380 patients with HOCM and 172 patients with nonobstructive HCM. All these patients had a definite diagnosis in our center from October 1, 2009, to December 31, 2012. They were divided into three groups, viz., HOCM with myectomy group (n=194), nonoperated HOCM group (n=186), and nonobstructive HCM group (n=172). Median follow-up duration was 57.57±13.71 months, and the primary end point was a combination of mortality from all causes.

Results: In this survival study, we compared the prognoses of patients with HOCM after myectomy, patients with nonoperated HOCM, and patients with nonobstructive HCM. Among the three groups, the myectomy group showed a lower rate of reaching the all-cause mortality with statistically indistinguishable overall survival compared with patients with nonobstructive HCM (p=0.514). Among patients with left ventricular outflow tract (LVOT) obstruction, the overall survival in the myectomy group was noticeably better than that in the nonoperated HOCM group (log-rank p<0.001). Parameters that showed a significant univariate correlation with survival included age, previous atrial fibrillation (AF), NT-proBNP, Cr, myectomy, and LV ejection fraction. When these variables were entered in the multivariate model, the only independent predictors of survival were myotomy [hazard ratio (HR): 0.109; 95% CI: 0.013-0.877, p<0.037], age (HR: 1.047; 95% CI: 1.007-1.088, p=0.021), and previous AF (HR: 2.659; 95% CI: 1.022-6.919, p=0.021).

Conclusion: Patients with HOCM undergoing myectomy appeared to suffer from a lower risk of reaching the all-cause mortality and demonstrated statistically indistinguishable overall survival compared with patients with nonobstructive HCM. Multivariate analysis clearly demonstrated myectomy as a powerful, independent factor of survival, confirming that the differences in long-term survival recorded in this study may be due to surgical improvement in the LVOT gradient.
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http://dx.doi.org/10.14744/AnatolJCardiol.2020.05043DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7414245PMC
June 2020

Management of heart failure patients with COVID-19: a joint position paper of the Chinese Heart Failure Association & National Heart Failure Committee and the Heart Failure Association of the European Society of Cardiology.

Eur J Heart Fail 2020 Jun 13;22(6):941-956. Epub 2020 Jul 13.

Cardiology, ASST Spedali Civili di Brescia and Department of Medical and Surgical Specialties, Radiological Sciences, and Public Health, University of Brescia, Brescia, Italy.

The coronavirus disease 2019 (COVID-19) pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is causing considerable morbidity and mortality worldwide. Multiple reports have suggested that patients with heart failure (HF) are at a higher risk of severe disease and mortality with COVID-19. Moreover, evaluating and treating HF patients with comorbid COVID-19 represents a formidable clinical challenge as symptoms of both conditions may overlap and they may potentiate each other. Limited data exist regarding comprehensive management of HF patients with concomitant COVID-19. Since these issues pose serious new challenges for clinicians worldwide, HF specialists must develop a structured approach to the care of patients with COVID-19 and be included early in the care of these patients. Therefore, the Heart Failure Association of the European Society of Cardiology and the Chinese Heart Failure Association & National Heart Failure Committee conducted web-based meetings to discuss these unique clinical challenges and reach a consensus opinion to help providers worldwide deliver better patient care. The main objective of this position paper is to outline the management of HF patients with concomitant COVID-19 based on the available data and personal experiences of physicians from Asia, Europe and the United States.
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http://dx.doi.org/10.1002/ejhf.1915DOI Listing
June 2020

IDENTIFY: The investigation and detection of urological neoplasia in patients referred with suspected urinary tract cancer: A multicentre cohort study.

Int J Surg Protoc 2020 28;21:8-12. Epub 2020 Feb 28.

Division of Surgery and Interventional Science, University College London.

•IDENTIFY study: The largest prospective cohort study of haematuria in secondary care.•Contemporary urinary cancer detection rates and diagnostic strategies.•The effectiveness of diagnostic tests, e.g. ultrasound, in detecting urinary cancer.•Novel patient risk factors associated with bladder and upper tract urinary cancers.
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http://dx.doi.org/10.1016/j.isjp.2020.02.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7163317PMC
February 2020

Aggravated endothelial endocrine dysfunction and intimal thickening of renal artery in high-fat diet-induced obese pigs following renal denervation.

BMC Cardiovasc Disord 2020 04 16;20(1):176. Epub 2020 Apr 16.

Department of Cardiology, Zhengzhou University People's Hospital, No.7 Weiwu road, Jinshui District, Zhengzhou, 450003, Henan, China.

Background: Renal denervation (RDN) targeting the sympathetic nerves in the renal arterial adventitia as a treatment of resistant hypertension can cause endothelial injury and vascular wall injury. This study aims to evaluate the risk of atherosclerosis induced by RDN in renal arteries.

Methods: A total of 15 minipigs were randomly assigned to 3 groups: (1) control group, (2) sham group, and (3) RDN group (n = 5 per group). All pigs were fed a high-fat diet (HFD) for 6 months after appropriate treatment. The degree of intimal thickening of renal artery and the conversion of endothelin 1 (ET-1) receptors were evaluated by histological staining. Western blot was used to assess the expression of nitric oxide (NO) synthesis signaling pathway, ET-1 and its receptors, NADPH oxidase 2 (NOX2) and 4-hydroxynonenal (4-HNE) proteins, and the activation of NF-kappa B (NF-κB).

Results: The histological staining results suggested that compared to the sham treatment, RDN led to significant intimal thickening and significantly promoted the production of endothelin B receptor (ETR) in vascular smooth muscle cells (VSMCs). Western blotting analysis indicated that RDN significantly suppressed the expression of AMPK/Akt/eNOS signaling pathway proteins, and decreased the production of NO, and increased the expression of endothelin system proteins including endothelin-1 (ET-1), endothelin converting enzyme 1 (ECE1), endothelin A receptor (ETR) and ETR; and upregulated the expression of NOX2 and 4-HNE proteins and enhanced the activation of NF-kappa B (NF-κB) when compared with the sham treatment (all p < 0.05). There were no significant differences between the control and sham groups (all p > 0.05).

Conclusions: RDN aggravated endothelial endocrine dysfunction and intimal thickening, and increased the risk of atherosclerosis in renal arteries of HFD-fed pigs.
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http://dx.doi.org/10.1186/s12872-020-01472-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7161153PMC
April 2020

LncRNA CASC2 inhibits hypoxia-induced pulmonary artery smooth muscle cell proliferation and migration by regulating the miR-222/ING5 axis.

Cell Mol Biol Lett 2020 17;25:21. Epub 2020 Mar 17.

Department of Cardiology, Henan Province People's Hospital, Huazhongfuwai Hospital, No. 7, Weiwu Road, Jinshui area, Zhengzhou City, Henan P.R. China.

Background: Pulmonary arterial hypertension (PAH) is often characterized by cell proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs). LncRNA cancer susceptibility candidate 2 (CASC2) has been revealed to be involved in PASMC injury in hypoxia-induced pulmonary hypertension. However, the exact molecular mechanisms whereby CASC2 regulates PASMC proliferation and migration are still incompletely understood.

Methods: The expression levels of CASC2, miR-222 and inhibitor of growth 5 (ING5) were measured using quantitative real-time polymerase chain reaction (qRT-PCR) or western blot, respectively. Cell proliferation was analyzed by Cell Counting Kit-8 (CCK-8) assay. Wound healing assay was used to analyze cell migration ability. The relationship between miR-222 and CASC2 or ING5 was confirmed using bioinformatics analysis, luciferase reporter assay and RNA immunoprecipitation assay.

Results: CASC2 was down-regulated in hypoxia-induced PASMCs in a dose- and time-dependent manner. Functional experiments showed that CASC2 overexpression could reverse hypoxia-induced proliferation and migration of PASMCs. Bioinformatics analysis indicated that CASC2 acted as a competing endogenous RNA of miR-222, thereby regulating the expression of ING5, the downstream target of miR-222, in PASMCs. In addition, rescue assay suggested that the inhibition mediated by CASC2 of hypoxia-induced PASMC proliferation and migration could be attenuated by miR-222 inhibition or ING5 overexpression.

Conclusion: CASC2 attenuated hypoxia-induced PASMC proliferation and migration by regulating the miR-222/ING5 axis to prevent vascular remodeling and the development of PAH, providing a novel insight and therapeutic strategy for hypoxia-induced PAH.
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http://dx.doi.org/10.1186/s11658-020-00215-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7079380PMC
December 2020

Berberine attenuates mitochondrial dysfunction by inducing autophagic flux in myocardial hypoxia/reoxygenation injury.

Cell Stress Chaperones 2020 05 22;25(3):417-426. Epub 2020 Feb 22.

Department of Scientific Research and Discipline Construction, Henan Provincial People's Hospital, Zhengzhou university people's hospital, Henan University People's Hospital, Zhengzhou, 450003, China.

Berberine (BBR) is routinely prescribed in many Asian countries to treat diarrhea. Evidence from both animal and clinical investigations suggests that BBR exerts diverse pharmacological activities, including antidiabetic, antineoplastic, antihypertensive, and antiatherosclerotic effects. This study aimed to explore the cardioprotective mechanisms of BBR and to elucidate the modulations between autophagy and mitochondrial function during hypoxia/reoxygenation (H/R) in H9c2 cells. The degree of autophagic flux was assessed by pretreating H9c2 cells with BBR prior to H/R exposure and measuring the expression levels of Beclin-1 and green fluorescent protein (GFP)-labeled LC3B fusion proteins as well as the LC3II/LC3I ratio. The mitochondrial membrane potential (△Ψm) in H9c2 cells was evaluated by detecting rhodamine-123 fluorescence using flow cytometry. The results revealed that pretreatment with BBR upregulated autophagic flux and protected against the loss of the △Ψm in H9c2 cells subjected to H/R. We conclude that BBR attenuates mitochondrial dysfunction by inducing autophagic flux.
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http://dx.doi.org/10.1007/s12192-020-01081-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7193011PMC
May 2020

MMP9, CXCR1, TLR6, and MPO participant in the progression of coronary artery disease.

J Cell Physiol 2020 11 12;235(11):8283-8292. Epub 2020 Feb 12.

Department of Cardiology, Henan Provincial People's Hospital, Fuwai Central China Cardiovascular Hospital, People's Hospital of Zhengzhou University, Zhengzhou, Henan, China.

Coronary artery disease (CAD) is the most frequent cardiovascular disease, which is induced by the decreased myocardial blood supply. The present study is conducted to understand the mechanisms of CAD. The GSE98583, GSE69587, and GSE71226 datasets from the Gene Expression Omnibus database were obtained. The differentially expressed genes (DEGs) were analyzed by the limma package, then the DEGs appeared in two or three datasets were selected as the coregulated genes using the VENNY tool, followed by enrichment analysis using DAVID tool. Protein-protein interaction (PPI) network, microRNA-transcription factor-target regulatory network, and drug-gene network were visualized. Finally, quantitative PCR and dual-luciferase reporter assay were conducted to validate the expression of key genes and the target relationship. There were 221 coregulated genes in GSE98583, GSE69587, and GSE71226. Besides, four pathways and 23 functional terms for co-upregulated genes, and 11 functional terms for co-downregulated genes were enriched. The degrees of PPI network nodes matrix metallopeptidase 9 (MMP9), C-X-C motif chemokine receptor 1 (CXCR1), toll-like receptor 6 (TLR6), and myeloperoxidase (MPO) were relatively higher. Moreover, MPO could interact with MMP9, CXCR1, and TLR6 in the PPI network. In the regulatory network, TLR6 and MMP9 separately were targeted by miR-3960 and v-rel avian reticuloendotheliosis viral oncogene homolog A (RELA). Additionally, MMP9, CXCR1, and MPO were involved in the drug-gene network. The expression of MMP9, CXCR1, TLR6, and MPO were significantly upregulated in CAD samples than control, and miR-3960 could bind to TLR6 to inhibit its expression. CXCR1 and MPO might be involved in the progression of CAD. Besides, miR-3960 might function in the pathogenesis of CAD through targeting TLR6, and RELA might exert its role in CAD via targeting MMP9.
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http://dx.doi.org/10.1002/jcp.29485DOI Listing
November 2020

Y-box protein 1 promotes hypoxia/reoxygenation- or ischemia/reperfusion-induced cardiomyocyte apoptosis via SHP-1-dependent STAT3 inactivation.

J Cell Physiol 2020 11 22;235(11):8187-8198. Epub 2020 Jan 22.

Department of Scientific Research and Discipline Construction, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Henan University People's Hospital, Zhengzhou, Henan, China.

Cardiomyocyte apoptosis induced by hypoxia and ischemia plays important roles in heart dysfunction after acute myocardial infarction (AMI). However, the mechanism of apoptosis induction remains unclear. A previous study reported that Y-box protein 1 (YB1) is upregulated after myocardial hypoxia/reoxygenation or ischemia/reperfusion (H/R or I/R, respectively) injury; however, whether YB1 is associated with H/R-induced cardiomyocyte apoptosis is completely unknown. In the present study, we investigated the roles of YB1 in H/R-induced cardiomyocyte apoptosis and the possible underlying molecular mechanisms. In vitro, H/R treatment upregulated the YB1 expression in H9C2 cells, whereas YB1 knockdown inhibited H/R-induced cardiomyocyte apoptosis and induced H9C2 cell proliferation via Src homology region 2 domain-containing phosphatase 1 (SHP-1)-mediated activation of signal transducer and activator of transcription 3 (STAT3). In vivo, YB1 knockdown ameliorated AMI, reducing infarct size, cardiomyocyte apoptosis, and oxidative stress, via SHP-1-mediated inactivation of STAT3. Additionally, YB1 knockdown inhibited H/R- or I/R-induced oxidative stress in vitro and in vivo. H/R and I/R increase YB1 expression, and YB1 knockdown ameliorates AMI injury via SHP-1-dependent STAT3 inactivation.
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http://dx.doi.org/10.1002/jcp.29474DOI Listing
November 2020

Stability of the permafrost peatlands carbon pool under climate change and wildfires during the last 150 years in the northern Great Khingan Mountains, China.

Sci Total Environ 2020 Apr 7;712:136476. Epub 2020 Jan 7.

Key Laboratory of Wetland Ecology and Environment, Northeast Institute of Geography and Agroecology, Chinese Academy of Sciences, Shengbei Street 4888, 130102 Changchun, China. Electronic address:

Peatlands store one-third of the total global soil carbon (C.) despite covering only 3-4% of the global land surface. Most peatlands are distributed in mid-high latitude regions and are even in permafrost regions, are sensitive to climate change and are disturbed by wildfire. Although several studies have focused on the impact of historical climate change and regional human activities on the C. accumulation process in these peatlands, the impact of these factors on the stability of the C. pool remains poorly understood. Here, based on the Pb age-depth model, we investigated the historical variations of C. stability during the last 150 years for five typical peatlands in the northern Great Khingan Mountains (Northeast China), an area located in a permafrost region that is sensitive to climate change and to wildfires, which have clearly increased due to regional human activities. The results showed that low C. accumulation rates (CARs) and weakly C. stability in studied peatlands before 1900. While, the increasing anthropogenic wildfire frequency and the residual products (e.g. pyrogenic carbon) increased the CARs and C. stability in peatlands from 1900 to 1980. The mean July temperature is the most important climate factor for peatlands C. stability. After 1980, due to the low wildfire frequencies influenced by human policies, increasing temperatures and decreasing precipitation not only increased the CARs but also markedly increased the C. stability of the peatlands C. pool in the northern Great Khingan Mountains, especially after 2000.
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http://dx.doi.org/10.1016/j.scitotenv.2019.136476DOI Listing
April 2020

MicroRNA-2861 and microRNA-5115 regulates myocardial ischemia-reperfusion injury through the GPR30/mTOR signaling pathway by binding to GPR30.

J Cell Physiol 2020 11 13;235(11):7791-7802. Epub 2020 Jan 13.

Department of Cardiology, Henan Provincial People's Hospital (Zhengzhou University People's Hospital), Zhengzhou, P.R. China.

Myocardial ischemia-reperfusion (I/R) injury, a major contributor to morbidity and mortality, represents a combination of intrinsic cellular response to ischemia and the extrinsic acute inflammatory response. In the present study, microarray analysis of GSE67308 and GSE50885 identified differentially expressed GPR30 and upstream regulatory miR-2861 and miR-5115 in myocardial I/R. Furthermore, GPR30 was confirmed as a common target gene of miR-2861 and miR-5115, and miR-2861 and miR-5115 inhibited GPR30 expression. Poor expression of GPR30 was identified in the myocardial I/R injury mouse model. Overexpressed GPR30 led to alleviated the pathological conditions, diminished myocardial infarct size and apoptosis of myocardial tissue in mice. Moreover, miR-2861 and miR-5115 were found to be highly expressed in the myocardial I/R injury mouse model and to subsequently accelerate the disease progression. Notably, PR30 curtailed the development of myocardial I/R injury through activation of the mTOR signaling pathway. The key findings suggested that miR-2861 and miR-5115 blocked the activation of the GPR30/mTOR signaling pathway by targeting GPR30, thereby accelerating myocardial I/R injury in mice.
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http://dx.doi.org/10.1002/jcp.29427DOI Listing
November 2020

Contribution of IL-7/7R genetic polymorphisms in coronary heart disease in Chinese Han population.

Int Immunopharmacol 2020 Feb 19;79:106084. Epub 2019 Dec 19.

Department of Cardiology, Henan Provincial People's Hospital, Zhengzhou 450003, People's Republic of China; Fuwai Central China Cardiovascular Hospital, Zhengzhou 450003, People's Republic of China; People's Hospital of Zhengzhou University, Zhengzhou 450003, People's Republic of China; Henan Provincial Key Laboratory for Control of Coronary Heart Disease, Zhengzhou 450003, People's Republic of China. Electronic address:

Background: Coronary heart disease (CHD) is a common chronic inflammatory disease. Interleukin (IL)-7/IL-7R has been reported to be involved in the development of CHD. However, the relationship between IL-7/7R genetic polymorphisms and CHD among the Han Chinese population remains unclear.

Methods: To examine whether IL-7/7R variants contributed to CHD, six single-nucleotide polymorphisms (SNPs) were genotyped by using the Agena MassARRAY platform in 499 CHD patients and 496 controls. Logistic regression was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs). The linkage disequilibrium was analyzed using Haploview software. The association between clinical parameters and IL-7/7R polymorphisms was determined by a one-way ANOVA.

Results: IL-7R rs969129 G (OR = 1.20, 95% CI: 1.00-1.43, p = 0.047) allele and GG (OR = 1.45, 95% CI: 1.01-2.08, p = 0.044) genotype carriers had a higher risk for CHD. IL-7R haplotype "ACAG" (OR = 1.43, 95% CI: 1.09-1.87, p = 0.010) conferred an increased CHD risk. Rs969129, rs6451231, and rs117173992 were related to CHD susceptibility in males and/or the subgroup of individuals aged >61 years. IL-7R rs969129, rs10053847, rs6451231, and rs118137916 variants were associated with diabetes in patients with CHD. Moreover, rs969129, rs6451231, and rs117173992 were associated with high-density lipoprotein cholesterol (HDL-C) concentrations, whereas rs118137916 and rs10053847 were associated with low-density lipoprotein cholesterol (LDL-C) levels (p < 0.05).

Conclusion: IL-7/7R variants were related to the genetic predisposition of CHD in the Chinese Han population. These findings increase our knowledge regarding the effect of IL-7/7R on CHD.
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http://dx.doi.org/10.1016/j.intimp.2019.106084DOI Listing
February 2020

Rationale and design of the Henan ST elevation myocardial infarction (STEMI) registry: a regional STEMI project in predominantly rural central China.

BMC Cardiovasc Disord 2019 11 28;19(1):271. Epub 2019 Nov 28.

Department of Cardiology, Zhengzhou University People's Hospital, No. 1 Fuwai Road, Zhengzhou, 450018, Henan, China.

Background: Cardiovascular disease including ST elevation myocardial infarction (STEMI) is increasing and the leading cause of death in China. There has been limited data available to characterize STEMI management and outcomes in rural areas of China. The Henan STEMI Registry is a regional STEMI project with the objectives to timely obtain real-world knowledge about STEMI patients in secondary and tertiary hospitals and to provide a platform for care quality improvement efforts in predominantly rural central China.

Methods: The Henan STEMI Registry is a multicentre, prospective and observational study for STEMI patients. The registry includes 66 participating hospitals (50 secondary hospitals; 16 tertiary hospitals) that cover 15 prefectures and one city direct-controlled by the province in Henan province. Patients were consecutively enrolled with a primary diagnosis of STEMI within 30 days of symptom onset. Clinical treatments, outcomes and cost are collected by local investigators and captured electronically, with a standardized set of variables and standard definitions, and rigorous data quality control. Post-discharge patient follow-up to 1 year is planned. As of August 2018, the Henan STEMI Registry has enrolled 5479 patients of STEMI.

Discussion: The Henan STEMI Registry represents the largest Chinese regional platform for clinical research and care quality improvement for STEMI. The board inclusion of secondary hospitals in Henan province will allow for the exploration of STEMI in predominantly rural central China.

Trial Registration: [NCT02641262] [29 December, 2015].
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http://dx.doi.org/10.1186/s12872-019-1250-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6883687PMC
November 2019

Atherosclerosis-associated endothelial cell apoptosis by miRNA let7-b-mediated downregulation of HAS-2.

J Cell Biochem 2019 Nov 17. Epub 2019 Nov 17.

Department of Cardiology, Henan Provincial People's Hospital, Zhengzhou, Henan, PR China.

MicroRNAs (miRNAs) play essential roles in the regulation and pathophysiology of various types of human diseases including atherosclerosis. Increasing numbers of miRNAs have been identified to be important regulators in the progression of atherosclerosis by regulating gene expression. However, functional miRNAs and the underlying mechanisms involved in atherosclerosis need fully elucidation. In the present study, the function of miRNA let-7b was investigated in human aortic endothelial cells (HAECs). The results showed that downregulation of let-7b in the high-fat diet mice and HAECs was inversely correlated with the expression level of HAS-2. upregulation of let-7b significantly reduced apoptosis of HAECs. The results also revealed that HAS-2 was a target gene of let-7b and HAS-2 reduction reversed the antiapoptotic effect of let-7b through regulation of the P13K/Akt pathway. These results together suggest the potential of regulating the let-7b expression and endothelial apoptosis against development and progression of atherosclerosis.
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http://dx.doi.org/10.1002/jcb.29537DOI Listing
November 2019

TRIM7 promotes proliferation and migration of vascular smooth muscle cells in atherosclerosis through activating c-Jun/AP-1.

IUBMB Life 2020 02 18;72(2):247-258. Epub 2019 Oct 18.

Department of Cardiology, FuWai Central China Cardiovascular Hospital, Zhengzhou, China.

Atherosclerosis (AS), with associated risk of stroke or cerebrovascular disease, is one of the most common causes of death globally. It has been well established that tripartite motif-containing protein 7 Tripartite Motif-containing 7 (Trim7), as an E3 ubiquitin protein ligase, is involved in protein ubiquitination and thus regulating cellular proliferation. Moreover, TRIM7 is upregulated in advanced carotid AS. However, the detailed mechanism of TRIM7 on regulation of AS remains unclear. In the present study, we firstly discovered that TRIM7 expression was robustly induced in platelet-derived growth factor type BB-treated vascular smooth muscle cells (VSMCs) and human atherosclerotic plaques. Functional approaches established that knockdown of TRIM7 inhibited proliferation and migration of VSMCs, as well as arrested the cell cycle at G1-S, thus suppressing AS progression. Our results also identified that c-Jun/activator protein 1 (AP-1) signaling pathway was activated by TRIM7. Moreover, gain- and loss-of-function studies revealed that TRIM7 could promote proliferation and migration of VSMCs via activation of c-Jun/AP-1 signaling pathway. Finally, by using atherogenic apolipoprotein E-deficient (apoE-/-) C57BL/6 mice with high-fat diet AS model, we demonstrated that interference of TRIM7 could effectively mitigate in vivo AS via inactivation of c-Jun/AP-1 signaling pathway. In general, activation of c-Jun/AP-1 signaling pathway via TRIM7 could be an important mechanism in AS progression, thus shedding light on the development of novel therapeutics to the treatment of the disease.
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http://dx.doi.org/10.1002/iub.2181DOI Listing
February 2020
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