Publications by authors named "Shengkai Xu"

8 Publications

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Circular RNA circ_0090231 promotes atherosclerosis in vitro by enhancing NLR family pyrin domain containing 3-mediated pyroptosis of endothelial cells.

Bioengineered 2021 Oct 12. Epub 2021 Oct 12.

Department of Cardiology, Affiliated Suzhou Science and Technology City Hospital of Nanjing Medical University, Suzhou, China.

Atherosclerosis (AS) is an inflammatory disease caused by multiple factors. Multiple circRNAs are involved in the development of AS. The present study focusses on delineating the role of circ_0090231 in AS. Human aortic endothelial cells (HAECs) were treated with oxidized low-density lipoprotein (ox-LDL) to construct an AS model. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the levels of circ_0090231, IL-1β, and IL-18 transcripts. CircRNA/ target gene interactions were predicted using StarBase and TargetScan and confirmed using an RNA pull-down assay and dual luciferase reporter assay. Further, 3-(4,5)-dimethylthiahiazo(-2)-3,5-diphenytetrazoliumromide (MTT) and lactate dehydrogenase (LDH) release assays were performed to evaluate cell viability and damage in the AS model, respectively. Cell pyroptosis and protein expression were determined using flow cytometry and western blotting respectively. The treatment of HAECs with ox-LDL not only led to significant increase in the levels of circ_0090231 but also resulted in improved cell viability as well as reduced cell injury and pyroptosis as compared to that in non-treated cells. The circ_0090231 was also identified to function as a sponge for miR-635, knockdown of which reverses the effects of circ_0090231 inhibition. Furthermore, our results revealed that levels of NLRP3, a miR-635 target, are not only augmented in the AS model but its overexpression also weakens the miR-635 regulatory effects in the AS development. Taken together, the circ_0090231/miR-635/NLRP3 axis affects the development of AS by regulating cell pyroptosis, thus providing new insights into the mechanism of AS development.
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http://dx.doi.org/10.1080/21655979.2021.1989260DOI Listing
October 2021

Blood pressure assessment with in-ear photoplethysmography.

Physiol Meas 2021 Sep 27. Epub 2021 Sep 27.

Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, Suzhou, CHINA.

Objective: In this study, we aimed to estimate blood pressure (BP) from in-ear photoplethysmography (PPG). This novel implementation provided an unobtrusive and steady way of recording PPG, whereas previous PPG measurements were mostly performed at the wrist, finger, or earlobe.

Methods: The time between forward and reflected PPG waves was very short at the ear site. To minimize errors introduced by feature extraction, a multi-Gaussian decomposition of in-ear PPG was performed. Both hand-crafted and whole-based features were extracted and the best combination of features was selected using a backward-search wrapper method and evaluated by the Akaike information criteria. Hemodynamic parameters such as compliance and inertance were estimated from a four-element Windkessel (WK4) model, which was used to pre-classify PPG signals and generate different BP estimation algorithms. Calibration was done by using previous measurements from the same class. To validate this novel approach, 53 subjects were recruited for a one-month follow-up study, and 17 subjects were recruited for a two-month follow-up study. Calibrated systolic BP estimation accuracy was significantly improved with inertance-based pre-classification, while diastolic BP showed less improvement.

Results: With proper feature selection, pre-classification and calibration, we have achieved a mean absolute error (MAE) of 5.35mmHg for SBP estimation, compared to 6.16mmHg if no pre-classification was carried out. The performance didn't deteriorate in two months, showing a decent BP trend-tracking ability.

Conclusion: The study demonstrated the feasibility of in-ear PPG to reliably measure BP, which represents an important technological advancement in terms of unobtrusiveness and steadiness.
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http://dx.doi.org/10.1088/1361-6579/ac2a71DOI Listing
September 2021

Heterogeneous ozonation of ofloxacin using MnO -CeO /γ-Al O as a catalyst: Performances, degradation kinetics and possible degradation pathways.

Water Environ Res 2021 Aug 16;93(8):1361-1369. Epub 2021 Feb 16.

College of Chemical Engineering, Beijing University of Chemical Technology, Beijing, China.

In this study, the performance of ofloxacin (OFX) degradation in synthetic wastewater using synthesized MnO -CeO /γ-Al O as a heterogeneous ozonation catalyst was evaluated. The removal rates of OFX and chemical oxygen demand (COD) during 15-day continuous-flow experiments were 98.2% and 76.7% on average, respectively. An ozone index (mgCOD/mgO ) of 1.09 with a high ozone utilization efficiency of 91.39% was achieved. The pseudo-first-order rate constant of ofloxacin degradation reached 15.216 × 10  min , which was five times that (3.085 × 10  min ) without catalysts. The results of gas chromatography-mass spectrometry (GC-MS) demonstrated that a variety of small-molecule organics occurred in the final oxidation products, such as 4-hydroxyl-4-methyl-2-pentanone and 2-oxoadipic acid in addition to homologs of OFX. The results of this study suggested that hydroxyl radicals played critical roles in the degradation and mineralization of OFX via four main pathways: (a) electrophilic addition of nitrogen; (b) breakdown of carbon-carbon double bonds; (c) hydrolysis of ether rings; and (d) halodecarboxylation of carboxyl groups. The biodegradability (BOD /COD) of OFX after catalytic ozonation reached 0.54. PRACTITIONER POINTS: Ofloxacin wastewater was treated using catalytic ozonation in a 15-day continuous experiment with MnO -CeO /γ-Al O as a catalyst. The ozone index reached 1.09 mgCOD/mgO during ozonation of ofloxacin. The presence of the catalyst increased the reaction rate constant by a factor of five. 4-hydroxy-4-methyl-2-pentanone was the primary ofloxacin oxidation product.
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http://dx.doi.org/10.1002/wer.1524DOI Listing
August 2021

Integration of catalytic ozonation and adsorption processes for increased efficiency of textile wastewater treatment.

Water Environ Res 2019 Jul 29;91(7):650-660. Epub 2019 Mar 29.

College of Chemical Engineering, Beijing University of Chemical Technology, Beijing, China.

Advanced and optimized textile wastewater treatment by catalytic ozonation and activated carbon (AC) adsorption was investigated. Scanning electron microscopy, X-ray diffraction, and X-ray photoelectron spectroscopy indicated that Mn and Ce oxides were successfully loaded on the γ-Al O support, and MnO , Mn O , CeO , and Ce O were the main components of the catalyst. Actual textile wastewater from biochemical effluent was used as experiment wastewater. The removal efficiencies of chemical oxygen demand (COD) and chromaticity were approximately 30.6% (414-287 mg/L on average) and 99.3% (4,033 times to 27 times on average), respectively during the 30-day on-site continuous-flow test with an ozone dosage, contact time, and gas-liquid ratio of 100 mg/L, 15.7 min, and 2.9, respectively. Following 1 g/L AC adsorption, the effluent COD concentration was reduced to 40 mg/L. By contrast, AC adsorption without catalytic ozonation as pretreatment required 10 g/L AC dosage to achieve similar treatment results. Gas chromatography-mass spectrometry analyses indicated that volatile phenols, sulfides, and aniline in wastewater were completely removed after treatment. Inductively coupled plasma results further showed that the active components of MnO -CeO in the catalyst were stable after continuous use for 60 days. PRACTITIONER POINTS: Mesoporous catalyst synthesized by impregnating MnO -CeO on γ-Al O support. Catalytic ozonation and AC adsorption were combined to degrade organics. Maximum degradation of COD and chromaticity by optimizing process variables. The efficiency of the method was compared to that of single AC adsorption.
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http://dx.doi.org/10.1002/wer.1102DOI Listing
July 2019

Slit3 regulates migration of endothelial progenitor cells by activation of the RhoA/Rho kinase pathway.

Int J Clin Exp Pathol 2018 1;11(7):3398-3404. Epub 2018 Jul 1.

Department of Cardiology, Gansu Provincial Hospital Lanzhou, China.

Nerves and blood vessels are in close proximity, indicating possible biomolecular interactions. Slit/Robo signaling pathways play critical roles in cell proliferation and motility. Endothelial progenitor cells (EPCs) participate in angiogenesis and vascular homeostasis. EPC migration induced by Slit3 has not been fully characterized. Thus, the expression of Slit and Robo in EPCs was examined, and the chemotactic functions of Slit3 and the Slit/Robo signaling pathway regulatory mechanisms were explored. We observed that EPCs express mainly the Robo4 receptor, and its ligand Slit3 plays roles in regulation of EPCs migration through activating the RhoA/Rho related kinases. Regulation of Slit3/-Robo4 signaling in EPCs may provide a new therapeutic target for ischemic disease.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6962882PMC
July 2018

Urotensin II promotes the proliferation of endothelial progenitor cells through p38 and p44/42 MAPK activation.

Mol Med Rep 2012 Jul 2;6(1):197-200. Epub 2012 May 2.

Department of Cardiology, Gansu Provincial Hospital, Lanzhou, Gansu 730000, PR China.

Urotensin II (UII) is a vasoactive peptide with many potent effects in the cardiorenovascular system and is also possibly involved in the pathogenesis of atherosclerosis. Endothelial progenitor cells (EPCs) are involved in angiogenesis and vascular homeostasis and may be important in the maintenance of endothelial integrity. The aim of this study was to investigate whether UII has an effect on the proliferation of bone marrow-derived EPCs and the possible signaling mechanisms involved. Bone marrow-derived EPCs were isolated from male Sprague-Dawley rats and cultured in medium containing 5% fetal bovine serum. Cells were incubated with UII for 24 h. The proliferation of EPCs was analyzed by MTT assay. Western blotting was performed to determine the phosphorylation levels of mitogen-activated protein kinases (MAPKs). The results demonstrated that UII promoted the proliferation of EPCs in a concentration-dependent manner in a certain range, and the proliferation was largely suppressed by inhibitors of GPR14 and MAPKs (p38 and p44/42). UII significantly increased the phosphorylation levels of p38MAPK and p44/42MAPK, and these effects were significantly inhibited by respective inhibitors. These findings indicate that UII promotes the proliferation of rat bone marrow-derived EPCs through a process that involves MAPK activation, and provides novel insights regarding the role of UII in the EPC-mediated repair of atherosclerotic injury.
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http://dx.doi.org/10.3892/mmr.2012.899DOI Listing
July 2012

Acute effects of ganglionated plexi ablation on sinoatrial nodal and atrioventricular nodal functions.

Auton Neurosci 2011 Apr;161(1-2):87-94

Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research institution of Wuhan University, Wuhan, China.

Ganglionated plexus (GP) ablation has been shown effective for eliminating atrial fibrillation (AF), the most common clinical tachyarrhythmia. However, the safety of destroying the main cardiac autonomic structures remains unclear. This study investigated the acute effects of GP ablation on the sinoatrial nodal (SAN) and atrioventricular nodal (AVN) functions in a canine model. In 10 open-chest dogs, multiple electrode catheters were sutured at both atria for recording and pacing. SAN and AVN function were evaluated. GP ablation caused no significant change of sinus rate immediately after GP ablation compared with the baseline state. After GP ablation, the sinus node recovery time (SNRT) and corrected SNRT did not show significant changes at long pacing cycle lengths (CLs), and only showed significant decrease at shorter pacing CLs. The AH interval at different pacing CLs, the Wenckebach atrioventricular block (AVB) CL, 2:1 AVB CL or the ventricular rate during AF were not significantly altered by GP ablations. Vagal suppression of SAN and AVN functions was eliminated by GP ablation. GP staining showed abundant choline acetyl transferase or tyrosine hydroxylase positive neurons. These findings suggest the functions of the SAN and AVN are mainly retained after GP ablation. These results may be partially related to destroying both parasympathetic and sympathetic elements in the GP by ablation.
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http://dx.doi.org/10.1016/j.autneu.2011.01.004DOI Listing
April 2011

Urotensin II induces migration of endothelial progenitor cells via activation of the RhoA/Rho kinase pathway.

Tohoku J Exp Med 2009 Dec;219(4):283-8

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, P.R. China.

Urotensin II (UII) is a vasoactive peptide with many potent effects in the cardiorenovascular system and may be involved in the pathogenesis of atherosclerosis. Cardiovascular risk factors are often accompanied by reduced numbers of endothelial progenitor cells (EPCs) and their impaired migratory capacity. However, the role of UII in the migration of EPCs has not been reported so far. The aim of this study was to investigate whether UII influences the chemotactic function of bone marrow-derived EPCs and the possible signaling mechanisms involved. As a ligand for the orphan G-protein coupled receptor 14 (GPR14, UT receptor), UII exerts vasoactive functions through activation of the RhoA/Rho kinase pathway. We therefore analyzed the expression of GPR14 mRNA and protein, the activation of RhoA kinase and the phosphorylation of myosin light chain (MLC) in EPCs, isolated from the rat bone marrow. EPCs of 1-4 passages expressed GPR14 mRNA and protein. Chemotaxis assays were performed using Transwell cell-culture chambers with UII (10(-10)-10(-6) M), showing that UII induced chemotaxis of EPCs in a concentration-dependent manner after 3-h treatment (all p < 0.05), with the highest value (about 3-fold increase) at 10(-8) M. UII caused rapid activation of RhoA and increased phosphorylation of MLC. Conversely, a Rho-kinase inhibitor Y-27632 prevented the UII-induced migration and the phosphorylation of MLC. In conclusion, GPR14/UT receptor is expressed in EPCs, and UII induces migration of EPCs via activation of the RhoA/Rho kinase pathway. These findings provide new insights into the actions of UII in atherosclerosis.
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http://dx.doi.org/10.1620/tjem.219.283DOI Listing
December 2009
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