Publications by authors named "Jianzhong Zhao"

15 Publications

  • Page 1 of 1

Delayed specific IgM antibody responses observed among COVID-19 patients with severe progression.

Emerg Microbes Infect 2020 Dec;9(1):1096-1101

Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, People's Republic of China.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread rapidly worldwide since it was confirmed as the causative agent of COVID-19. Molecular diagnosis of the disease is typically performed via nucleic acid-based detection of the virus from swabs, sputum or bronchoalveolar lavage fluid (BALF). However, the positive rate from the commonly used specimens (swabs or sputum) was less than 75%. Immunological assays for SARS-CoV-2 are needed to accurately diagnose COVID-19. Sera were collected from patients or healthy people in a local hospital in Xiangyang, Hubei Province, China. The SARS-CoV-2 specific IgM antibodies were then detected using a SARS-CoV-2 IgM colloidal gold immunochromatographic assay (GICA). Results were analysed in combination with sera collection date and clinical information. The GICA was found to be positive with the detected 82.2% (37/45) of RT-qPCR confirmed COVID-19 cases, as well as 32.0% (8/25) of clinically confirmed, RT-qPCR negative patients (4-14 days after symptom onset). Investigation of IgM-negative, RT-qPCR-positive COVID-19 patients showed that half of them developed severe disease. The GICA was found to be a useful test to complement existing PCR-based assays for confirmation of COVID-19, and a delayed specific IgM antibody response was observed among COVID-19 patients with severe progression.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1080/22221751.2020.1766382DOI Listing
December 2020

Small-size effect on wrinkle and fracture of monolayer graphene subjected to in-plane shear.

Nanotechnology 2017 Nov;28(45):455702

Shanghai Institute of Applied Mathematics and Mechanics, Shanghai Key Laboratory of Mechanics in Energy Engineering, Shanghai University, Shanghai 200072, People's Republic of China.

Controlling surface patterns are useful in a wide range of applications including flexible electronics, biological templates, microelectromechanical systems and device fabrication. The present paper investigates the wrinkling and fracture of graphene subjected to in-plane shear. It is found that the size of a graphene sheet has significant effect on the wrinkle and fracture based on both molecular dynamics simulation and nonlocal plate theory. The analytical expressions for wrinkle amplitude and wavelength are deduced. The nonlocal parameter of nonlocal plate theory is evaluated. Furthermore, the higher aspect ratio has enhanced the wrinkle resistance and shear strength of graphene. Temperature and chirality have insignificant impact on the wrinkling, but significantly influence the fracture of the graphene sheet. This work is expected to provide a better understanding of the mechanism of nanometer scale wrinkles.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1088/1361-6528/aa8f6dDOI Listing
November 2017

Adiponectin is required for cardiac MEF2 activation during pressure overload induced hypertrophy.

J Mol Cell Cardiol 2015 Sep 19;86:102-9. Epub 2015 Jul 19.

Department of Biology, York University, Toronto, Canada. Electronic address:

Cardiomyocyte (CM) hypertrophy and increased heart mass in response to pressure overload are associated with hyper-activation of the myocyte enhancer factor-2 (MEF2) family of transcriptional regulators, and concomitant initiation of the fetal gene program. Adiponectin, an adipokine that is reduced in individuals with obesity and diabetes, has been characterized both as a negative regulator or permissive factor in cardiac hypertrophy. We therefore sought to analyze temporal regulation of MEF2 activity in response to pressure overload (PO) and changes in adiponectin status. To address this we crossed a well characterized transgenic MEF2 "sensor" mouse (MEF2-lacZ) with adiponectin null mice (Ad-KO) to create compound MEF2 lacZ/Ad-KO mice. Initially, we established that transverse aortic banding induced PO in wild-type (WT) mice increased heart mass and CM hypertrophy from 1 to 4weeks following surgery, indicated by increased CM diameter and heart weight/tibia length ratio. This was associated with cardiac dysfunction determined by echocardiography. Hypertrophic changes and dysfunction were observed in Ad-KO mice 4weeks following surgery. MEF2 lacZ activity and endogenous ANF mRNA levels, used as indicators of hypertrophic gene activation, were both robustly increased in WT mice after MTAB but attenuated in the Ad-KO background. Furthermore, activation of the pro-hypertrophic molecule p38 was increased following MTAB surgery in WT mice, but not in Ad-KO animals, and treatment of primary isolated CM with recombinant adiponectin induced p38 phosphorylation in a time dependent manner. Adiponectin also increased MEF2 activation in primary cardiomyocytes, an effect attenuated by p38 MAPK inhibition. In conclusion, our data indicate that robust hypertrophic MEF2 activation in the heart in vivo requires a background of adiponectin signaling and that adiponectin signaling in primary isolated CM directly enhances MEF2 activity through activation of p38 MAPK. We conclude that adiponectin is required for full induction of cardiomyocyte MEF2 activation, thus contributing to the myocardial hypertrophic gene expression program in response to PO.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.yjmcc.2015.06.020DOI Listing
September 2015

One-dose vaccination associated with attenuated disease severity of adolescent and adult varicella cases in Beijing's Fengtai District.

Hum Vaccin Immunother 2014 ;10(8):2417-20

Department of Epidemiology and Biostatistics; School of Public Health; Capital Medical University; 2. Fengtai Center for Disease Control and Prevention; Beijing, China.

Background: In recent years, the number of varicella cases in adults has significantly increased in Beijing. However, the effect of the vaccination on varicella-related characteristics among adults has not been studied.

Methods And Results: Using data from the Infectious Disease Reporting System and the Immunization Information System, we compared the epidemiology and disease severity in breakthrough and unvaccinated varicella cases in adolescents and adults (≥ 15 year-old) from 2008 to 2011 in Beijing's Fengtai district, China. The results showed that the age (P = 0.003),contact history (90% vs. 73%, P = 0.019) and outbreak cases (10% vs. 1%, P < 0.0001) were significantly differently distributed between the two groups and that both the incidence of moderate-to-severe cases (26% vs. 45%, P = 0.035, OR = 0.446) and varicella-associated fever (49% vs. 66%, P = 0.068, OR = 0.534) were either significantly lower or trended to be lower in the breakthrough group than in the unvaccinated group. Additionally,vaccine effectiveness against moderate-to-severe cases of varicella was 55.4%.

Conclusion: Altogether, these results indicate that vaccination against varicella among adolescents and adults affected the epidemiology and attenuated the disease severity of the cases. The Results from this study will provide useful information for the prevention of varicella in adolescents and adults.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.4161/hv.29140DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4896792PMC
July 2015

Phenomics of Vascular Disease: The Systematic Approach to the Combination Therapy.

Curr Vasc Pharmacol 2015 ;13(4):433-40

Laboratory of Cardiovascular Phenomics, Department of Pharmacology, University of Nevada School of Medicine, Center for Molecular Medicine 303F, 1664 N Virginia Street/MS 318, Reno, Nevada 89557-0318, USA.

Vascular diseases are usually caused by multifactorial pathogeneses involving genetic and environmental factors. Our current understanding of vascular disease is, however, based on the focused genotype/phenotype studies driven by the "one-gene/one-phenotype" hypothesis. Drugs with "pure target" at individual molecules involved in the pathophysiological pathways are the mainstream of current clinical treatments and the basis of combination therapy of vascular diseases. Recently, the combination of genomics, proteomics, and metabolomics has unraveled the etiology and pathophysiology of vascular disease in a big-data fashion and also revealed unmatched relationships between the omic variability and the much narrower definition of various clinical phenotypes of vascular disease in individual patients. Here, we introduce the phenomics strategy that will change the conventional focused phenotype/genotype/genome study to a new systematic phenome/genome/proteome approach to the understanding of pathophysiology and combination therapy of vascular disease. A phenome is the sum total of an organism's phenotypic traits that signify the expression of genome and specific environmental influence. Phenomics is the study of phenome to quantitatively correlate complex traits to variability not only in genome, but also in transcriptome, proteome, metabolome, interactome, and environmental factors by exploring the systems biology that links the genomic and phenomic spaces. The application of phenomics and the phenome-wide associated study (PheWAS) will not only identify a systemically-integrated set of biomarkers for diagnosis and prognosis of vascular disease but also provide novel treatment targets for combination therapy and thus make a revolutionary paradigm shift in the clinical treatment of these devastating diseases.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397150PMC
http://dx.doi.org/10.2174/1570161112666141014144829DOI Listing
May 2016

The epidemiology of varicella cases among children in Beijing's Fengtai District from 2008 to 2012.

Vaccine 2014 Jun 2;32(29):3569-72. Epub 2014 May 2.

Department of Epidemiology and Biostatistics, School of Public Health, Capital Medical University, Beijing 100069, China; Municipal Key Laboratory of Clinical Epidemiology, Beijing 100069, China. Electronic address:

In recent years, the number of breakthrough cases of varicella (onset >42 days after vaccination) increased each year, and varicella outbreaks continue to occur in Beijing. Data from the Immunization Information System and the Infectious Disease Reporting System demonstrated that in Beijing's Fengtai District, the varicella breakthrough rate increased from 0.7% in 2008 to 2.5% in 2012 and showed an increased trend (P<0.001). Among the varicella cases in children (age of 3-15 years), the number of breakthrough cases increased from 167 in 2008 to 622 in 2012, which was 45.2% (n=1735) of the total child cases (n=3842). From 2008 to 2012, a total of 62 outbreaks occurred; among the 787 affected child outbreak cases, 61% were vaccinated. Altogether, the results from this study indicated that 1-dose vaccination cannot sufficiently prevent the occurrence of breakthrough cases of varicella or control varicella outbreaks in Beijing's Fengtai District.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.vaccine.2014.04.069DOI Listing
June 2014

Expression of CagL from Helicobacter pylori and Preliminary Study of its Biological Function.

Indian J Microbiol 2013 Mar 15;53(1):36-40. Epub 2012 Dec 15.

School of Medical Science and Laboratory Medicine, Jiangsu University, 301 Xuefu Road, Zhenjiang, 212013 Jiangsu People's Republic of China.

Helicobacter pylori (H. pylori) is a highly successful human-specific gastric pathogen, infecting over half the world's population. Virulent H. pylori isolates harbour the cytotoxin-associated genes pathogenicity island (cag-PAI), the majority of which have no known function. In this study, we used cell infection assay and reverse transcriptase PCR, identified that CagL recombinant protein, one of the cag-PAI proteins, induced GES-1 cells to express cytokine IL-8. Then we performed western blot and translocation assay. Our result showed CagL polyclonal antibody counteracted translocation of CagA. This will provide a foundation for the further studies on its biological function.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12088-012-0341-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587514PMC
March 2013

Predominant role of vasoconstrictors over dilatators derived from arachidonic acid in hypoxic pulmonary vasoconstriction.

Mol Med Rep 2013 Oct 19;8(4):1263-71. Epub 2013 Aug 19.

Department of Anesthesiology, Changzhou No. 2 People's Hospital, Changzhou, Jiangsu 213003, P.R. China.

Prostanoids derived from arachidonic acid (AA) have been shown to play a permissive role in the regulation of vascular tone and wall tension. Conventionally, epoxyeicosatrienoic acids (EETs) and prostacyclin have been considered as dilatators, whereas thromboxane (TX) and hydroxyeicosatetraenoic acid (HETE) were considered as vasoconstrictors. However, the role of these prostanoids in the mediation of acute hypoxic pulmonary vasoconstriction is not yet clearly understood. In the present study, the role of prostanoids in the acute hypoxic response in rat isolated intrapulmonary arteries (IPAs) was investigated. Exogenous AA directly caused vasoconstriction, but exerted a significant inhibition on hypoxic vasoconstriction. The vasoconstriction by AA was mediated by the endothelium. AA metabolites from lipoxygenase (LOX) had no effect on vascular tone or hypoxic vasoconstriction. Consistent results from the blockage of cytochrome P450 (CYP) or CYP epoxide hydrolase showed that HETE contributed to endothelium‑independent hypoxic vasoconstriction. EET via epoxygenase exerted no effect on 80 mM KPSS‑induced vessel contraction or hypoxic vasoconstriction. In addition, prostacyclin also failed to inhibit hypoxic pulmonary vasoconstriction (HPV). However, blockage of thromboxane A2/prostanoid (TP) receptors almost eliminated hypoxic vasoconstriction, suggesting the primary role of TP receptors in the regulation of the hypoxic response in rat IPAs. In conclusion, the current data indicate the predominant role of vasoconstrictors instead of dilatators in mediating HPV. These data also highlight a pivotal role for voltage‑independent Ca2+ entry in pulmonary hypoxic response and suggest that modulation of these channels by prostanoids underlies their regulatory mechanisms.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/mmr.2013.1645DOI Listing
October 2013

The epidemiology and risk factors for breakthrough varicella in Beijing Fengtai district.

Vaccine 2012 Sep 3;30(43):6186-9. Epub 2012 Aug 3.

Department of Epidemiology and Biostatistics, School of Public Health and Family Medicine, Capital Medical University, Beijing 100069, PR China.

Using data from the Immunization Information System (IIS) and the Infectious Disease Reporting System (IDRS), we have described the epidemiology and analyzed the risk factors for breakthrough varicella in the Fengtai district of Beijing, China. From 2008 to 2011 the breakthrough varicella infection rate (BVR) was 0.65%, 0.85%, 1.08% and 1.56% respectively, thus demonstrating a distinct increasing tendency (P<0.001). We also compared the incidence of varicella-related illnesses between the breakthrough varicella cases and unvaccinated cases, and found that the severity of illness in the breakthrough cases was milder than that of unvaccinated cases. Moderate-to-severe cases (P=0.008, OR=0.676, 95% CI=0.505-0.904) were differently distributed in the breakthrough varicella cases and unvaccinated cases. In this study, we demonstrated that floating status (P=0.031, OR=1.96, 95% CI=1.06-3.62), contact history (P<0.001, OR=2.67, 95% CI=1.59-4.69), time since vaccination (P=0.006, OR=1.59, 95% CI=1.14-2.21), age at vaccination (P=0.010, OR=0.59, 95% CI=0.39-0.88) and combined vaccination (P=0.026, OR=3.99, 95% CI=1.18-13.54) were associated with the occurrence of breakthrough varicella, and among these, floating status is a novel risk factor. This study should provide useful information for the evaluation of the performance of varicella vaccination and prevention in PR China.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.vaccine.2012.07.062DOI Listing
September 2012

Assessment of CAR- or CD46-dependent adenoviral vector-mediated TRAIL gene therapy in clinical adenocarcinoma lung cancer cells.

Oncology 2009 11;77(6):366-77. Epub 2010 Jan 11.

Laboratory Center, Changzhou Second Hospital, Nanjing Medical University, Jiangsu, China.

Adenoviral vector-mediated transfer of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can be a powerful approach to lung cancer therapy. However, the efficiency of adenoviral vector gene transfer and the sensitivity to TRAIL-induced apoptosis in the context of adenoviral vector gene transfer have yet to be characterized in primary lung cancers. In this study, we investigated the expression of adenoviral receptor CD46 expression in primary lung cancer cells. In contrast to previous reports on enhanced CD46 expression in various types of cancer cells, we show a significantly higher CD46 expression in lung adenocarcinomas compared to lung squamous cell carcinomas. Using Ad5-GFP and Ad5F35-GFP vectors, we demonstrated an improved gene transfer efficiency in primary lung cancer cells by the Ad5F35 vector. The apoptosis induction effect mediated by Ad5-TRAIL and Ad5F35-TRAIL vector gene transfer was compared in cells from 10 lung adenocarcinomas. Of 5 lung cancers in which apoptosis was induced, 2 had an enhanced effect by Ad5F35-TRAIL vector gene transfer compared to Ad5-GFP. Thus, these results indicate a method to identify TRAIL-sensitive primary lung cancers, which will also facilitate the analysis of resistance mechanisms in lung cancers.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1159/000275831DOI Listing
March 2010

Protein kinase A-regulated assembly of a MEF2{middle dot}HDAC4 repressor complex controls c-Jun expression in vascular smooth muscle cells.

J Biol Chem 2009 Jul 23;284(28):19027-42. Epub 2009 Apr 23.

Department of Biology, York University, Toronto, Ontario M3J 1P3, Canada.

Vascular smooth muscle cells (VSMCs) maintain the ability to modulate their phenotype in response to changing environmental stimuli. This phenotype modulation plays a critical role in the development of most vascular disease states. In these studies, stimulation of cultured vascular smooth muscle cells with platelet-derived growth factor resulted in marked induction of c-jun expression, which was attenuated by protein kinase Cdelta and calcium/calmodulin-dependent protein kinase inhibition. Given that these signaling pathways have been shown to relieve the repressive effects of class II histone deacetylases (HDACs) on myocyte enhancer factor (MEF) 2 proteins, we ectopically expressed HDAC4 and observed repression of c-jun expression. Congruently, suppression of HDAC4 by RNA interference resulted in enhanced c-jun expression. Consistent with these findings, mutation of the MEF2 cis-element in the c-jun promoter resulted in promoter activation during quiescent conditions, suggesting that the MEF2 cis-element functions as a repressor in this context. Furthermore, we demonstrate that protein kinase A attenuates c-Jun expression by promoting the formation of a MEF2.HDAC4 repressor complex by inhibiting salt-inducible kinase 1. Finally, we document a physical interaction between c-Jun and myocardin, and we document that forced expression of c-Jun represses the ability of myocardin to activate smooth muscle gene expression. Thus, MEF2 and HDAC4 act to repress c-Jun expression in quiescent VSMCs, protein kinase A enhances this repression, and platelet-derived growth factor derepresses c-Jun expression through calcium/calmodulin-dependent protein kinases and novel protein kinase Cs. Regulation of this molecular "switch" on the c-jun promoter may thus prove critical for toggling between the activated and quiescent VSMC phenotypes.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1074/jbc.M109.000539DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2707197PMC
July 2009

Protein kinase A represses skeletal myogenesis by targeting myocyte enhancer factor 2D.

Mol Cell Biol 2008 May 25;28(9):2952-70. Epub 2008 Feb 25.

Department of Biology, York University, 4700 Keele Street, Toronto M3J 1P3, Ontario, Canada.

Activation of protein kinase A (PKA) by elevation of the intracellular cyclic AMP (cAMP) level inhibits skeletal myogenesis. Previously, an indirect modulation of the myogenic regulatory factors (MRFs) was implicated as the mechanism. Because myocyte enhancer factor 2 (MEF2) proteins are key regulators of myogenesis and obligatory partners for the MRFs, here we assessed whether these proteins could be involved in PKA-mediated myogenic repression. Initially, in silico analysis revealed several consensus PKA phosphoacceptor sites on MEF2, and subsequent analysis by in vitro kinase assays indicated that PKA directly and efficiently phosphorylates MEF2D. Using mass spectrometric determination of phosphorylated residues, we document that MEF2D serine 121 and serine 190 are targeted by PKA. Transcriptional reporter gene assays to assess MEF2D function revealed that PKA potently represses the transactivation properties of MEF2D. Furthermore, engineered mutation of MEF2D PKA phosphoacceptor sites (serines 121 and 190 to alanine) rendered a PKA-resistant MEF2D protein, which efficiently rescues myogenesis from PKA-mediated repression. Concomitantly, increased intracellular cAMP-mediated PKA activation also resulted in an enhanced nuclear accumulation of histone deacetylase 4 (HDAC4) and a subsequent increase in the MEF2D-HDAC4 repressor complex. Collectively, these data identify MEF2D as a primary target of PKA signaling in myoblasts that leads to inhibition of the skeletal muscle differentiation program.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1128/MCB.00248-08DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2293079PMC
May 2008

Coxsackievirus and adenovirus receptor expression in non-malignant lung tissues and clinical lung cancers.

J Mol Histol 2006 May 22;37(3-4):153-60. Epub 2006 Sep 22.

Changzhou Second Hospital, Nanjing Medical University, Jiangsu, China.

Adenoviral vector mediated gene delivery has been applied in clinical trials and mechanistic studies to explore new treatment approaches for lung cancers. The expression of coxsackievirus adenovirus receptor (CAR), the primary receptor for the most commonly used adenovirus serotype 5 (Ad5)-based vectors, predominantly determines the permissiveness of lung cancer cells. CAR expression is also suggested to modulate tumor cell proliferation capacity. Here, we studied CAR expression in archival lung cancer specimens by using well-characterized CAR 72 antibodies. High levels of CAR expression were observed in most of the 32 cases of squamous cell carcinoma lung cancers and in all the five cases of small cell lung cancers investigated. In contrast, high levels of CAR expression were detected only in 6 of 22 adenocarcinoma lung cancers. The relative levels of CAR expression did not correlate with the pathologic grade in lung cancers, and was thus inconsistent with a role of modulating cancer cell proliferation. Of note, CAR expression was not detected in non-malignant alveolar cells. Our data suggest a preferred utility of Ad5 vector mediated gene delivery to squamous cell carcinoma lung cancers, small cell lung cancers, but not to the majority of adenocarcinoma lung cancers.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10735-006-9055-4DOI Listing
May 2006

Regulation of vertebrate myotome development by the p38 MAP kinase-MEF2 signaling pathway.

Dev Biol 2005 Jul;283(1):171-9

Istituto di Istologia ed Embriologia Generale, Universita di Roma La Sapienza, Via A. Scarpa 14, 00161 Rome, Italy.

Biochemical and cell culture studies have characterized the myocyte enhancer factor 2 (MEF2) transcriptional regulatory proteins as obligatory partners for the myogenic regulatory factors (MRFs) in the differentiation of myogenic cells in culture. However, the role of MEF2 activation in somitic myogenesis has not been fully characterized. Here, we report a critical interaction between the p38 mitogen-activated protein kinase (p38 MAPK) and MEF2 in the developing somite myotome. We document expression of MEF2A and p38 MAPK proteins in the somite of 9.5 dpc mouse embryos concurrent with Myf 5 protein expression. We also observed that abrogation of p38 MAPK signaling blocks MEF2 activation using a MEF2 transgenic 'sensor' mouse. Inhibition of p38 MAPK signaling concurrently inhibited myogenic differentiation in somite cultures and in embryos in vivo using transplacental injection of a p38 inhibitor (SB203580). Finally, we document that commitment to the myogenic lineage is not appreciably affected by p38 MAPK inhibition since the activation of an early marker of myogenic commitment (Myf 5) occurs normally when p38 MAPK signaling is inhibited. Thus, we present novel evidence indicating a crucial role for p38 MAPK signaling to the MEF2 transcriptional regulators during early mammalian somite development and myotome formation.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ydbio.2005.04.009DOI Listing
July 2005