Publications by authors named "Jianquan Liao"

8 Publications

  • Page 1 of 1

Early Goal-Directed Renal Replacement Therapy in Acute Decompensated Heart Failure Patients with Cardiorenal Syndrome.

Blood Purif 2021 Jun 15:1-9. Epub 2021 Jun 15.

Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.

Introduction: The aim of this study was to clarify the efficacy of early goal-directed renal replacement therapy (GDRRT) for treatment of cardiorenal syndrome (CRS) patients after acute decompensated heart failure (ADHF).

Methods: In the retrospective, observational study, we enrolled 54 patients in the early GDRRT group and 63 patients in the late GDRRT group. Baseline characteristics, clinical data at initiation renal replacement therapy time, and the clinical outcome were collected and several parameters were compared and analyzed between 2 groups.

Results: The urine volume at GDRRT initiation time in the early group was higher than that in the late GDRRT group (1,060.3 ± 332.1 vs. 300.5 ± 148.3 mL, p < 0.001). Hemodynamic parameters such as mean artery pressure were higher (70.06 ± 32.99 vs. 54.34 ± 40.88 mm Hg, p = 0.012), the heart rate was slower (80.17 ± 15.26 vs. 99.21 ± 25.45 bpm, p = 0.002), and the diameter of inferior vena cava was narrower (22.00 ± 1.91 vs. 25.77 ± 5.5 mm, p = 0.04) in early GDRRT. Primary end point was inhospital all-cause mortality and cardiovascular mortality, which was obviously lower in the early GDRRT group (respectively 24.1 vs. 60.3%, p = 0.002 and 20.3 vs. 50.8%, p = 0.005). The second end point of kidney recovery in the early GDRRT group was much better than that in the latter GDRRT group (p = 0.018). Moreover, urine volume after GDRRT of the early group was more significant than that of the late group (1,432 ± 172 vs. 702 ± 183 mL, p = 0.005).

Conclusion: This study clarified the effectiveness of the early GDRRT strategy in ADHF patients suffered from CRS, which reduced inhospital mortality and improved the urine output and clinical kidney recovery outcome.
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http://dx.doi.org/10.1159/000515826DOI Listing
June 2021

A reverse Mulholland-type inequality in the whole plane.

J Inequal Appl 2018 10;2018(1):79. Epub 2018 Apr 10.

Department of Mathematics, Guangdong University of Education, Guangzhou, P.R. China.

We present a new reverse Mulholland-type inequality in the whole plane with a best possible constant factor by introducing multiparameters, applying weight coefficients, and using the Hermite-Hadamard inequality. Moreover, we consider equivalent forms and some particular cases.
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http://dx.doi.org/10.1186/s13660-018-1669-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5891574PMC
April 2018

Endothelial‑to‑mesenchymal transition in human idiopathic dilated cardiomyopathy.

Mol Med Rep 2018 Jan 8;17(1):961-969. Epub 2017 Nov 8.

Key Laboratory of Viral Heart Diseases, Ministry of Public Health, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.

Dilated cardiomyopathy (DCM) is characterized by left ventricular dilation and cardiac fibrosis. Emerging evidence indicated that endothelial‑to‑mesenchymal transition (Endo‑MT) is a crucial event during organ fibrosis. This study was performed to clarify whether Endo‑MT contributed to the progression of cardiac fibrosis in DCM. Cardiac samples from patients with DCM and control were obtained. The presence of endothelial markers, cluster of differentiation (CD)31 and vascular endothelial (VE)‑cadherin, and mesenchymal markers, α smooth muscle actin (SMA) and fibroblast‑specific protein 1 (FSP1) was performed using immunohistochemistry. Co‑localization of endothelial markers and mesenchymal markers were identified using confocal immunofluorescence staining. Serum procollagen type I carboxy‑terminal propeptide (PICP) and procollagen type III amino‑terminal propeptide (PIIINP) were measured by ELISA. Protein levels of Wnt, β‑catenin and Snail were determined using western blot analysis. Immunohistochemistry and double‑immunofluorescence staining demonstrated that the expression of CD31 and VE‑cadherin were significantly decreased in DCM samples, whereas the FSP‑1, and αSMA were significantly increased. CD31 and VE‑cadherin labeling indexes were respectively negatively correlated with left ventricular end‑diastolic diameter (LVEDD) (CD31 r=‑0.82, P<0.01; VE‑cadherin r=-0.73, P<0.01), while FSP‑1 and αSMA were positively associated with LVEDD (αSMA r=0.65, P<0.01, FSP1 r=0.53, P<0.01) and left ventricular ejection fraction (αSMA r=‑0.18, P<0.05; FSP1 r=‑0.21, P<0.05). Furthermore, PICP and PIIINP levels were positively associated with the co‑expression labeling indexes (CD31/SMA co‑labeling index and PICP r=0.727, P<0.01; CD31/SMA co‑labeling index and PIIINP r=0.741, P<0.01; VE‑Cadherin/FSP‑1 co‑labeling index and PICP r=0.716, P<0.01; VE‑cadherin/FSP‑1 co‑labeling index and PIIINP r=0.648, P<0.05). Western blot analysis indicated that proteins levels of Wnt signaling and snail were significantly increased in DCM samples. These results suggested that Endo‑MT is potentially implicated in the pathogenesis of myocardial fibrosis and remodeling during the development of DCM, indicating a potential therapeutic target for DCM treatment.
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http://dx.doi.org/10.3892/mmr.2017.8013DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5780177PMC
January 2018

On Hardy-type integral inequalities with the gamma function.

J Inequal Appl 2017 7;2017(1):131. Epub 2017 Jun 7.

Department of Mathematics, Guangdong University of Education, Guangzhou, Guangdong 51003 P.R. China.

By means of real analysis and weight functions, we obtain a few equivalent conditions of two kinds of Hardy-type integral inequalities with the non-homogeneous kernel and parameters. The constant factors related to the gamma function are proved to be the best possible. We also consider the operator expressions and some cases of homogeneous kernel.
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http://dx.doi.org/10.1186/s13660-017-1404-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5487938PMC
June 2017

Olmesartan attenuates cardiac hypertrophy and improves cardiac diastolic function in spontaneously hypertensive rats through inhibition of calcineurin pathway.

J Cardiovasc Pharmacol 2014 Mar;63(3):218-26

*Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China; †Department of Medicine, Sahlgrenska University Hospital/Sahlgrenska, Gothenburg, Sweden; and ‡Institutes of Biomedical Sciences, Fudan University, Shanghai, China.

Objective: To test whether olmesartan ameliorates cardiac diastolic dysfunction in spontaneously hypertensive rats (SHRs) through calcineurin pathway.

Methods: Twenty-four male SHRs of 6 months were divided into saline- (n = 12) and olmesartan-treated (n = 12) groups. Age-matched WKY (n = 12) rats served as controls. Saline (10 mL·kg·d) or the same volume of olmesartan liquor (2.5 mg·kg·d) was administered by gavage for 3 months. Heart rate, systolic blood pressure, cardiac structure, and function and histological studies were determined. Expression of calcineurin and downstream NFAT3 were also detected.

Results: Compared with age-matched Wistar Kyoto rats, SHRs of 6 months exhibited evident cardiac hypertrophy and diastolic dysfunction as demonstrated by elevated systolic blood pressure and E/E', decreased E/A and E'/A', while F, left ventricular ejection fraction and fractional shortening remained unimpaired. Treatment with olmesartan significantly decreased systolic blood pressure and ventricular hypertrophy, attenuated fibrosis, and improved diastolic function (all P < 0.05). Meanwhile, both calcineurin and NFAT3 expressions were downregulated in olmesartan group compared with the other 2 groups (both P < 0.05).

Conclusions: These data suggest the beneficial effect of olmesartan on cardiac structure and diastolic dysfunction, and it may be mediated through calcineurin pathway. This indicates a new therapeutic target for diastolic dysfunction.
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http://dx.doi.org/10.1097/FJC.0000000000000038DOI Listing
March 2014

Impaired cardiac microvascular endothelial cells function induced by Coxsackievirus B3 infection and its potential role in cardiac fibrosis.

Virus Res 2012 Oct 4;169(1):188-94. Epub 2012 Aug 4.

Key Laboratory of Viral Heart Diseases, Ministry of Public Health, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.

CVB3 virus tropism and tissue access are modulated by cardiac microvascular endothelial cells (CMVECs) in the context of microvasculature. This study was designed to examine biological behaviors of CMVECs following CVB3 infection and its possible effects on cardiac remodeling. Data demonstrated that CVB3 increased caspase-3 activities, Bax/Bcl-2 protein ratio and TGF-β1 levels in CMVECs, accompanying with elevated microvascular permeability. Double immunofluorescence revealed co-localization of endothelial markers (CD31 and VE-cadherin) and mesenchymal markers (FSP1 and αSMA) in infected CMVECs. Western blot demonstrated that CVB3 significantly decreased the expression of endothelial markers and increased the expression of mesenchymal markers, which were reversed by SB431542 (inhibitor of TGF-β1), indicating that endothelial-to-mesenchymal transition following CVB3 infection was probably induced by CMVECs-derived TGF-β1. Excess extracellular matrix was produced by myocardial cells incubated with supernatants of infected CMVECs. Our results displayed that CVB3 induced notable biological changes of CMVECs, which may contribute to cardiac fibrosis.
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http://dx.doi.org/10.1016/j.virusres.2012.07.027DOI Listing
October 2012

Transfer of bone-marrow-derived mesenchymal stem cells influences vascular remodeling and calcification after balloon injury in hyperlipidemic rats.

J Biomed Biotechnol 2012 14;2012:165296. Epub 2012 May 14.

Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.

Bone-marrow-derived mesenchymal stem cells (BM-MSCs) were found to markedly increase atherosclerotic lesion size. The aim of this paper was to investigate whether BM-MSCs contribute to vascular remodeling and calcification after balloon injury in hyperlipidemic rats. Labeled BM-MSCs were found in the lesion of hyperlipidemic rats after balloon injury. Comparing injury group, transferred BM-MSCs significantly triggered vascular negative remodeling, characterized by the changes of remodeling index (0.628 ± 0.0293 versus 0.544 ± 0.0217), neointimal area (0.078 ± 0.015 mm(2) versus 0.098 ± 0.019 mm(2)), PCNA index (23.91 ± 6.59% versus 43.11 ± 5.31%), and percentage of stenosis (18.20 ± 1.09% versus 30.58 ± 1.21%). Apparent vascular calcification was detected in medial layers at 6 weeks after balloon angioplasty, which may be associated with upregulation of bone morphogenetic protein-2 (BMP-2). Our data indicated that unselected BM-MSCs transfer may induce vascular remodeling and calcification after balloon injury in hyperlipidemic rats.
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http://dx.doi.org/10.1155/2012/165296DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3361346PMC
December 2012

Aldehyde dehydrogenase-2 deficiency aggravates cardiac dysfunction elicited by endoplasmic reticulum stress induction.

Mol Med 2012 Jul 18;18:785-93. Epub 2012 Jul 18.

Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.

Mitochondrial aldehyde dehydrogenase-2 (ALDH2) has been characterized as an important mediator of endogenous cytoprotection in the heart. This study was designed to examine the role of ALDH2 knockout (KO) in the regulation of cardiac function after endoplasmic reticulum (ER) stress. Wild-type (WT) and ALDH2 KO mice were subjected to a tunicamycin challenge, and the echocardiographic property was examined. Protein levels of six items--78 kDa glucose-regulated protein (GRP78), phosphorylation of eukaryotic initiation factor 2 subunit α (p-eIF2α), CCAAT/enhancer-binding protein homologous protein (CHOP), phosphorylation of Akt, p47(phox) nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and 4-hydroxynonenal--were determined by using Western blot analysis. Cytotoxicity and apoptosis were estimated using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide (MTT) assay and caspase-3 activity, respectively. ALDH2 deficiency exacerbated cardiac contractile dysfunction and promoted ER stress after ER stress induction, manifested by the changes of ejection fraction and fractional shortening. In vitro study revealed that tunicamycin significantly upregulated the levels of GRP78, p-eIF2α, CHOP, p47(phox) NADPH oxidase and 4-hydroxynonenal, which was exacerbated by ALDH2 knockdown and abolished by ALDH2 overexpression, respectively. Overexpression of ALDH2 abrogated tunicamycin-induced dephosphorylation Akt. Inhibition of phosphatidylinositol 3-kinase using LY294002 did not affect ALDH2-conferred protection against ER stress, although LY294002 reversed the antiapoptotic action of ALDH2 associated with p47(phox) NADPH oxidase. These results suggest a pivotal role of ALDH2 in the regulation of ER stress and ER stress-induced apoptosis. The protective role of ALDH2 against ER stress-induced cell death was probably mediated by Akt via a p47(phox) NADPH oxidase-dependent manner. These findings indicate the critical role of ALDH2 in the pathogenesis of ER stress in heart disease.
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http://dx.doi.org/10.2119/molmed.2011.00466DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3409283PMC
July 2012
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