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Harbin, China

Harbin Medical University is a public university located in Harbin, Heilongjiang, China. Wikipedia.

Zhao Y.,Harbin Medical University
American Journal of Epidemiology | Year: 2013

Adenomatous polyposis coli gene (APC) polymorphisms may influence the risk for colorectal neoplasia. However, results thus far have been inconclusive. We performed a systematic literature search of the Medline, Embase, Cochrane Collaboration, and HuGE databases and reviewed the references of pertinent articles through May 2012. Odds ratios with 95% confidence intervals were used to estimate the association between 3 APC polymorphisms (D1822V, E1317Q, and I1307K) and colorectal neoplasia. In total, 40 studies from 1997 to 2010 were included in this meta-analysis, and individuals with the D1822V variant homozygote VV genotype had a slight decrease in the risk for colorectal neoplasia compared with the wild-type homozygote DD genotype (pooled odds ratio = 0.87, 95% confidence interval: 0.77, 0.99). There was a small association between the APC E1317Q polymorphism and a risk for colorectal neoplasia (variant vs. wild-type: pooled odds ratio = 1.41, 95% confidence interval: 1.14, 1.76), particularly for colorectal adenomas (variant vs. wild-type: odds ratio = 2.89, 95% confidence interval: 1.83, 4.56). Compared with those who carried the wild-type I1307K, Ashkenazi Jews who carried the I1307K variant were at a significantly increased risk for colorectal neoplasia, with a pooled odds ratio of 2.17 (95% confidence interval: 1.64, 2.86). Our study suggests that APC is a candidate gene for colorectal neoplasia susceptibility. © 2013 © The Author 2013. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. Source

He Y.H.,Harbin Medical University
Molecular and cellular biochemistry | Year: 2012

Adipocyte differentiation and adipogenesis are closely related to obesity and obesity-induced metabolic disorders. The calcium-sensing receptor (CaSR) has been reported to play an antilipolytic role in human adipocyte and regulate cell differentiation in many tissues. However, the effects of CaSR on adipocyte differentiation and adipogenesis have not been clarified. In the study, we observed that activation of CaSR significantly promoted adipocyte differentiation and adipogenesis in human SW872 adipocytes. Gene expression analysis revealed that the CaSR activation increased the transcription factor proliferator-activated receptor γ (PPARγ) and its downstream genes including CCAAT element binding protein α (C/EBPα), adipose fatty acid-binding protein (aP2), and lipoprotein lipase. The activity of glycerol-3-phosphate dehydrogenase was also increased after the stimulation of CaSR. In addition, levels of cyclic AMP and calcium which have been shown to regulate PPARγ gene expression were significantly affected by the activation of CaSR. These effects could be suppressed by CaSR small interfering RNA (CaSR-siRNA). In conclusion, our findings suggest that activation of CaSR promotes differentiation and adipogenesis in adipocytes, which might be achieved by upregulating PPARγ and its downstream gene expressions. Therefore, CaSR in adipocytes may be involved in the pathogenesis of obesity by promoting adipocyte differentiation and adipogenesis. Source

Tang J.,Harbin Medical University
International journal of nanomedicine | Year: 2011

Genistein, one of the major isoflavones, has received great attention as a phytoestrogen and potential cancer chemoprevention agent. However, the dissolution and bioavailability of genistein from solid oral preparations is low due to its poor water solubility. In order to improve the oral bioavailability of genistein, genistein nanoparticles were prepared by the nanoprecipitation technique using Eudragit(®) E100 as carriers and an optimized formulation of mass ratio (genistein:Eudragit E100, 1:10). The mean particle size of genistein nanoparticles was approximately 120 nm when diluted 100 times with distilled water. The drug-loaded nanoparticles were spherical on observation by transmission electric microscopy. Encapsulation efficiency and drug loading of the genistein nanoparticles were approximately 50.61% and 5.02%, respectively. Release of drug from the genistein nanoparticles was two times greater than that from the conventional capsules. After administration of genistein suspension or genistein nanoparticles at a single dose of 100 mg/kg to fasted rats, the relative bioavailability of genistein from the nanoparticles compared with the reference suspension was 241.8%. These results suggested that a nanoparticle system is a potentially promising formulation for the efficient delivery of poorly water-soluble drugs by oral administration. Source

Cao M.,Harbin Medical University
Journal of cancer research and clinical oncology | Year: 2014

To determine the interaction between insulin receptor substrate-1 (IRS-1) and miR-23a on the migration and invasion of non-small cell lung cancer (NSCLC) cells, and to examine IRS-1 expression in NSCLC tissues and its correlation with clinicopathologic characteristics. The migration and invasion of A549 cells were measured using transwell assay. miR-23a levels were examined by quantitative reverse transcription-PCR and IRS-1 expression by Western blotting. The interaction between miR-23a and IRS-1 was examined by luciferase reporter assay. IRS-1 expression in 105 NSCLC specimens was determined by immunohistochemistry and its correlation with patient clinicopathologic characteristics was evaluated. Transwell assay revealed that miR-23a significantly promoted the migration and invasion of A549 cells with a 44.0 and 44.6 % increase in the number of migrated and invading cells, respectively. Luciferase assay showed that miR-23a markedly reduced luciferase activities of A549 cells co-transfected with plasmids overexpressing the 3' UTR of IRS-1 mRNA (P < 0.05). Co-transfection of A549 cells with miR-23a and plasmids overexpressing IRS-1 significantly reduced the increase in the number of migrated and invading cells mediated by miR-23a. Immunohistochemistry showed low IRS-1 expression in 26.7 % and high IRS-1 expression in 73.3 % of the NSCLC specimens. Kaplan-Meier analysis revealed that the overall survival and disease-free survival of NSCLC were markedly longer in patients with high IRS-1 expression than those with low IRS-1 expression (P = 0.002). Multivariate Cox regression analysis showed that IRS-1 was an independent prognostic factor for the overall survival of NSCLC patients (RR 0.413 CI 0.238-0.718, P = 0.002). There is an interaction between miR-23a and IRS-1 in the modulation of the migration and invasion of NSCLC cells. IRS-1 is variably expressed in NSCLC patients and correlates with NSCLC patient survival. Source

Yin J.J.,Harbin Medical University
Autophagy | Year: 2012

In pancreatic β-cells, the endoplasmic reticulum (ER) is the crucial site for insulin biosynthesis, as this is where the protein-folding machinery for secretory proteins is localized. Perturbations to ER function of the β-cell, such as those caused by high levels of free fatty acid and insulin resistance, can lead to an imbalance in protein homeostasis and ER stress, which has been recognized as an important mechanism for type 2 diabetes. Macroautophagy (hereafter referred to as autophagy) is activated as a novel signaling pathway in response to ER stress. In this review, we outline the mechanism of ER stress-mediated β-cell death and focus on the role of autophagy in ameliorating ER stress. The development of drugs to take advantage of the potential protective effect of autophagy in ER stress, such as glucagon like peptide-1, will be a promising avenue of investigation. Source

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