Wang Z.-G.,Jilin University |
Jia M.-K.,Jilin University |
Cao H.,Jilin University |
Bian P.,Changchun Childrens Hospital |
Fang X.-D.,Jilin University
Oncology Reports | Year: 2013
Coronin-1C is an important F-actin binding protein which is critical for cell motility. Furthermore, the expression of this protein was found to be increased in diffuse tumors and was correlated with the degree of tumor malignancy. However, the mechanism(s) through which this protein enhances malignancy in hepatocellular carcinoma (HCC) is poorly understood. In this study, we found that Coronin-1C was overexpressed in human HCC tissues compared with the adjacent non-tumor tissues. Overexpression of Coronin-1C enhanced the cell migration in the human HCC cell line BEL-7402, whereas suppressed cell migration and proliferation were observed in Coronin-1C-knockdown BEL-7402 cells together with impaired cell polarity, disrupted cytoskeleton and decreased Rac-1 activation. Moreover, the Coronin-1C knockdown cells displayed a lower degree of malignancy by inducing smaller tumors in nude mice. Thus, we demonstrated a relationship between Coronin-1C overexpression and human HCC growth through enhancement of tumor cell proliferation and migration, which are correlated with Rac-1 activation.
Zhang Y.,Chinese National Institute for Viral Disease Control and Prevention |
Xu S.,Chinese National Institute for Viral Disease Control and Prevention |
Wang H.,Chinese National Institute for Viral Disease Control and Prevention |
Zhu Z.,Chinese National Institute for Viral Disease Control and Prevention |
And 37 more authors.
PLoS ONE | Year: 2012
The incidence of measles in China from 1991 to 2008 was reviewed, and the nucleotide sequences from 1507 measles viruses (MeV) isolated during 1993 to 2008 were phylogenetically analyzed. The results showed that measles epidemics peaked approximately every 3 to 5 years with the range of measles cases detected between 56,850 and 140,048 per year. The Chinese MeV strains represented three genotypes; 1501 H1, 1 H2 and 5 A. Genotype H1 was the predominant genotype throughout China continuously circulating for at least 16 years. Genotype H1 sequences could be divided into two distinct clusters, H1a and H1b. A 4.2% average nucleotide divergence was found between the H1a and H1b clusters, and the nucleotide sequence and predicted amino acid homologies of H1a viruses were 92.3%-100% and 84.7%-100%, H1b were 97.1%-100% and 95.3%-100%, respectively. Viruses from both clusters were distributed throughout China with no apparent geographic restriction and multiple co-circulating lineages were present in many provinces. Cluster H1a and H1b viruses were co-circulating during 1993 to 2005, while no H1b viruses were detected after 2005 and the transmission of that cluster has presumably been interrupted. Analysis of the nucleotide and predicted amino acid changes in the N proteins of H1a and H1b viruses showed no evidence of selective pressure. This study investigated the genotype and cluster distribution of MeV in China over a 16-year period to establish a genetic baseline before MeV elimination in Western Pacific Region (WPR). Continuous and extensive MeV surveillance and the ability to quickly identify imported cases of measles will become more critical as measles elimination goals are achieved in China in the near future. This is the first report that a single endemic genotype of measles virus has been found to be continuously circulating in one country for at least 16 years. © 2012 Zhang et al.
Dong G.,Changchun University of Science and Technology |
Shi W.,Changchun University of Science and Technology |
Liu J.,Changchun Childrens Hospital |
Hu Y.,Changchun University of Science and Technology
Przeglad Elektrotechniczny | Year: 2012
According to the requirement of data intercommunication, this paper presents a solution of community health and the hospital information system intercommunication. Based on the ESB, SOA and XML technology, we construct a exchange platform of community health service center and medical and health institutions. In addition, we design the message middleware and data exchange adapter based on HL7 and DICOM3.0 standard. Consequently, this paper realizes the information exchange of the resident healthy records and hospital medical record system.
Yan H.,Jilin University |
Liu N.,Jilin University |
Zhao Z.,Changchun Childrens Hospital |
Zhang X.,Jilin University |
And 3 more authors.
Biotechnology Letters | Year: 2012
P53 is an attractive target in molecular cancer therapeutics because of its critical role in regulating cell cycle arrest and apoptosis. The limitations in the development of p53-based cancer therapeutic strategy include its inefficient transmission through cell membrane of tumor cells and low protein yields in the expression system. In the present study, p53 was fused with HIV TAT protein, which can cross cell membranes, and expressed by Pichia pastoris. Stable production of Tat-p53 was achieved. After being transduced with Tat-p53 protein, the growth of cancer cell line, HepG2, was inhibited by increased apoptosis in culture. This expression system could thus be utilized to produce human Tat-p53 fusion protein. © 2012 Springer Science+Business Media B.V.
Zhu Y.-F.,Fudan University |
Xu F.,Chongqing Medical University |
Lu X.-L.,Hunan Childrens Hospital |
Wang Y.,Shanghai JiaoTong University |
And 10 more authors.
Chinese Medical Journal | Year: 2012
Background Acute hypoxemic respiratory failure (AHRF) often develops acute respiratory distress syndrome (ARDS), and its incidence and mortalities in critically ill pediatric patients in China were 2% and 40% respectively. This study aimed at prospectively investigating incidence, causes, mortality and its risk factors, and any relationship to initial tidal volume (VT) levels of mechanical ventilation, in children ≤5 years of age with AHRF and ARDS. Methods In 12 consecutive months in 23 pediatric intensive care units (PICU), AHRF and ARDS were identified in those requiring >12 hour intratracheal mechanical ventilation and followed up for 90 days or until death or discharge. ARDS was diagnosed according to the American-European Consensus definitions. The mortality and ventilation free days (VFD) were measured as the primary outcome, and major complications, initial disease severity, and burden were measured as the secondary outcome. Results In 13 491 PICU admissions, there were 439 AHRF, of which 345 (78.6%) developed ARDS, resulting in incidences of 3.3% and 2.6%, and corresponding mortalities of 30.3% and 32.8% respectively along with 8.2 and 6.7 times of relative risk of death in those with pneumonia (62.9%) and sepsis (33.7%) as major underlying diseases respectively. No association was found in VT levels during the first 7 days with mortality, nor for VT at levels <6, 6-8, 8-10, and >10 ml/kg in the first 3 days with mortality or length of VFD. By binary Logistic regression analyses, higher pediatric risk of mortality score III, higher initial oxygenation index, and age <1 year were associated with higher mortality or shorter VFD in AHRF. Conclusions The incidence and mortalities of AHRF and ARDS in children ≤5 years were similar to or lower than the previously reported rates (in age up to 15 years), associated with initial disease severity and other confounders, but causal relationship for the initial VT levels as the independent factor to the major outcome was not found.
So M.-T.,University of Hong Kong |
LeonThomas Y.-Y.,University of Hong Kong |
Cheng G.,University of Hong Kong |
TangClara S.-M.,University of Hong Kong |
And 25 more authors.
PLoS ONE | Year: 2011
Rare (RVs) and common variants of the RET gene contribute to Hirschsprung disease (HSCR; congenital aganglionosis). While RET common variants are strongly associated with the commonest manifestation of the disease (males; short-segment aganglionosis; sporadic), rare coding sequence (CDS) variants are more frequently found in the lesser common and more severe forms of the disease (females; long/total colonic aganglionosis; familial). Here we present the screening for RVs in the RET CDS and intron/exon boundaries of 601 Chinese HSCR patients, the largest number of patients ever reported. We identified 61 different heterozygous RVs (50 novel) distributed among 100 patients (16.64%). Those include 14 silent, 29 missense, 5 nonsense, 4 frame-shifts, and one in-frame amino-acid deletion in the CDS, two splice-site deletions, 4 nucleotide substitutions and a 22-bp deletion in the intron/exon boundaries and 1 single-nucleotide substitution in the 5′ untranslated region. Exonic variants were mainly clustered in RET the extracellular domain. RET RVs were more frequent among patients with the most severe phenotype (24% vs. 15% in short-HSCR). Phasing RVs with the RET HSCR-associated haplotype suggests that RVs do not underlie the undisputable association of RET common variants with HSCR. None of the variants were found in 250 Chinese controls. © 2011 So et al.
Xue J.,Jilin University |
Zhao Z.,Jilin University |
Xie X.,Jilin University |
Zhao S.,Jilin University |
And 2 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2016
Background: By inhibiting the expression of endogenous aquaporin-4 (AQP-4), we aimed to evaluate the effects of AQP-4 on the apoptosis of human colon cancer HT-29 cells and the expression of inhibitors of apoptosis proteins (IAPs). Methods: HT-29 cells were routinely cultured in vitro. The expression of endogenous AQP-4 was inhibited by siRNA technology, and the transfection efficiency of AQP-4-siRNA was detected by Western blot. The inhibition rate of cell proliferation was detected by MTT assay. The apoptotic rate was detected by flow cytometry. The expression levels of c-IAP1, c-IAP2, XIAP, NAIP, Survivin and Livin in the IAPs family in HT-29 cells transfected with AQP-4-siRNA were detected by real-time quantitative fluorescent PCR and Western blot. Results: Western blot showed that AQP-4 expression in HT-29 cells transfected with AQP-4-siRNA was down-regulated by 80%. MTT assay showed that HT-29 cells transfected with AQP-4-siRNA had significantly higher inhibition rate ((28.5±4.34)%) than that of the cells transfected with NS-siRNA ((1.24±0.14)%) (t=12.704, P<0.01). Flow cytometry showed that the apoptotic rate of the AQP-4-siRNA group ((11.73±1.25)%) significantly exceeded that of the NS-siRNA group ((0.87±0.14)%) (t=-11.837, P<0.01). Real-time quantitative fluorescent PCR and Western blot showed that compared with the NS-siRNA group, the AQP-4-siRNA had significantly lower levels of c-IAP1 (t=-3.145, P<0.01), c-IAP2 (t=-0.665, P<0.01), XIAP (t=-9.157, P<0.01) and Livin (t=-8.12, P<0.01) mRNA as well as c-IAP1 (t=-0.557, P<0.01), c-IAP2 (t=-4.778, P<0.01), XIAP (t=-6.576, P<0.01) and Livin (t=-6.243, P<0.01) protein expressions. XIAP expression decreased most obviously, while those of Survivin and NAIP hardly changed. Conclusion: AQP-4-siRNA promoted the apoptosis of HT-29 cells in vitro, probably by down-regulating c-IAP1, c-IAP1, XIAP and Livin mRNA and protein expressions. © 2016, E-Century Publishing Corporation. All rights reserved.
Liang J.-M.,Jilin University |
Xu H.-Y.,Jilin University |
Zhang X.-J.,Changchun Childrens Hospital |
Li X.,Shandong University |
And 2 more authors.
Journal of International Medical Research | Year: 2013
Objective: To investigate the effects of ischaemic postconditioning on brain injury and mitochondria in focal ischaemia and reperfusion, in rats. Methods: Adult male Wistar rats (n=15 per group) underwent sham surgery, ischaemia (2-h middle cerebral artery occlusion), or ischaemia followed by ischaemic postconditioning (three cycles of 30 s reperfusion/30 s reocclusion). Brain infarction size, neurological function, mitochondrial reactive oxygen species (ROS) production, mitochondrial membrane potential and mitochondrial swelling were evaluated 24 h postsurgery. Results: Infarct size was significantly smaller, and neurological function was significantly better, in the ischaemic postconditioning group than in the ischaemia group. Ischaemia resulted in significant increases in mitochondrial ROS production and swelling, and a reduction in mitochondrial membrane potential, all of which were significantly reversed by postconditioning. Conclusions: The protective role of ischaemic postconditioning in focal ischaemia/reperfusion may be due to decreased mitochondrial ROS production, reduced mitochondrial membrane potential and suppressed mitochondria swelling. Mitochondria are potential targets for new therapies to prevent brain damage caused by ischaemia and reperfusion. © The Author(s) 2013.