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Changchun, China

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

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. Source

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

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. Source

Yan H.,Jilin University | Liu N.,Jilin University | Zhao Z.,Changchun Childrens Hospital | Zhang X.,Jilin University | And 3 more authors.
Biotechnology Letters

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. Source

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

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. Source

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.

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. Source

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