First Hospital of Qiqihaer City

Qiqihar, China

First Hospital of Qiqihaer City

Qiqihar, China
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Zhao W.,Harbin Medical University | Zhao W.,Harbin University | Wen H.-X.,Harbin Medical University | Zheng H.-L.,First Hospital of Qiqihaer City | And 3 more authors.
Journal of Ethnopharmacology | Year: 2011

Aim of the study: Although Zuo Gui Yin Decoction has long been used in Traditional Chinese Medicine to treat menopausal symptoms, the underlying mechanism(s) by which these effects are induced remains to be defined. The aim of this study was to investigate the action mechanism of Zuo Gui Yin Decoction on estradiol production in the rat ovary during peri-menopause. Materials and methods: The peri-menopausal animal model was established by natural aging. Peri-menopausal rats were treated by intragastric administration (ig) with low (13.78 g kg-1), middle (20.67 g kg-1) or high (31 g kg-1) dose of Zuo Gui Yin Decoction per day for 8 weeks. At the 8th weekend, the rats were sacrificed for sampling. Estradiol (E2) levels in rats' serum were evaluated by radioimmunoassay (RIA). RT-PCR, in situ hybridization and immunohistochemistry were used to determine mRNA and protein expression of relevant genes. Results: Medium- and high-dose of Zuo Gui Yin Decoction could significantly increase serum estradiol concentration, ovarian CYP19 mRNA levels, and P450arom protein expression in rats during peri-menopause. Zuo Gui Yin Decoction at three different dosages all could promote FSHR expression and the effect of low-dose was the greatest. Zuo Gui Yin Decoction could elevate LRH-1 and ERα expression in a dose dependent manner. Conclusions: Taken collectively, these findings suggest that Zuo Gui Yin Decoction could promote estradiol production in rat serum during peri-menopausal period through ovarian ERα → LRH-1 → CYP19 pathway as well as the ovarian classical FSHR → CYP19 mechanism. © 2010 Elsevier Ireland Ltd.

Li L.,First Hospital of Qiqihaer City | Li L.,Dalian University | Zhao D.,China University of Political Science and Law | Jin Z.,First Hospital of Qiqihaer City | And 3 more authors.
PLoS ONE | Year: 2015

Introduction: Treatment with short hairpin RNA (shRNA) interference therapy targeting phosphodiesterase 5a after myocardial infarction (MI) has been shown to mitigate post-MI heart failure. We investigated the mechanisms that underpin the beneficial effects of PDE5a inhibition through shRNA on post-MI heart failure. Methods: An adenoviral vector with an shRNA sequence inserted was adopted for the inhibition of phosphodiesterase 5a (Ad-shPDE5a) in vivo and in vitro. Myocardial infarction (MI) was induced in male C57BL/6J mice by left coronary artery ligation, and immediately after that, the Ad-shPDE5a was injected intramyocardially around the MI region and border areas. Results: Four weeks post-MI, the Ad-shPDE5a-treated mice showed significant mitigation of the left ventricular (LV) dilatation and dysfunction compared to control mice. Infarction size and fibrosis were also significantly reduced in Ad-shPDE5a-treated mice. Additionally, AdshPDE5a treatment decreased the MI-induced inflammatory cytokines interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and transforming growth factor-β1, which was confirmed in vitro in Ad-shPDE5a transfected myofibroblasts cultured under oxygen glucose deprivation. Finally, Ad-shPDE5a treatment was found to activate the myocardial Akt signaling pathway in both in vivo and in vitro experiments. Conclusion: These findings indicate that PDE5a inhibition by Ad-shPDE5a via the Akt signal pathway could be of significant value in the design of future therapeutics for post-MI heart failure. © 2015 Li et al.This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Wang L.,University of Tennessee Health Science Center | Wang L.,Inner Mongolia University | Huang Y.,University of Tennessee Health Science Center | Jiao Y.,University of Tennessee Health Science Center | And 7 more authors.
Gene Expression | Year: 2013

The purpose of this study is to investigate whether expression profiles of alcoholism-relevant genes in different parts of the brain are correlated differently with those in the liver. Four experiments were conducted. First, we used gene expression profiles from five parts of the brain (striatum, prefrontal cortex, nucleus accumbens, hippocampus, and cerebellum) and from liver in a population of recombinant inbred mouse strains to examine the expression association of 10 alcoholism-relevant genes. Second, we conducted the same association analysis between brain structures and the lung. Third, using five randomly selected, nonalcoholism-relevant genes, we conducted the association analysis between brain and liver. Finally, we compared the expression of 10 alcoholism-relevant genes in hippocampus and cerebellum between an alcohol preference strain and a wild-type control. We observed a difference in correlation patterns in expression levels of 10 alcoholismrelevant genes between different parts of the brain with those of liver. We then examined the association of gene expression between alcohol dehydrogenases (Adh1, Adh2, Adh5, and Adh7) and different parts of the brain. The results were similar to those of the 10 genes. Then, we found that the association of those genes between brain structures and lung was different from that of liver. Next, we found that the association patterns of five alcoholism-nonrelevant genes were different from those of 10 alcoholism-relevant genes. Finally, we found that the expression level of 10 alcohol-relevant genes is influenced more in hippocampus than in cerebellum in the alcohol preference strain. Our results show that the expression of alcoholism-relevant genes in liver is differently associated with the expression of genes in different parts of the brain. Because different structural changes in different parts of the brain in alcoholism have been reported, it is important to investigate whether those structural differences in the brains of those with alcoholism are due to the difference in the associations of gene expression between genes in liver and in different parts of the brain. Copyright © 2013 Cognizant Comm. Corp.

Jiao Y.,University of Tennessee Health Science Center | Jiao Y.,Mudanjiang Medical College | Chen H.,First Hospital of Qiqihaer City | Gu T.,University of Tennessee Health Science Center | And 4 more authors.
BMC Research Notes | Year: 2015

Background: Considerable progress has been made in illuminating the pathological events for systemic sclerosis (SSc)-related progressive lung fibrosis. The molecular events that lead to SSc-related progressive lung fibrosis need to be defined. Some important genes have been identified from a recent study in humans. We aim to construct and compare the similarities and differences of molecular pathways between SSc-related progressive lung fibrosis and normal lungs of humans and mice. Methods: We used the analytical approach of association of key genes in SSc-related progressive lung fibrosis. We first identified the probes for genes of SSc-related progressive lung fibrosis and analyzed the pathways in human lung using data generated by microarray. We then analyzed the gene pathways in mouse lung for similar sets of probes. Gene expression data from livers were used to compare with that in lung in both humans and mice. Results: Our analysis indicated that, in humans, the expression levels of genes for macrophage activation are more strongly associated with each other than that in mice. In both humans and mice, the associations of these genes are much greater in the lung than that in the liver. The association in gene expression between humans and mice are similar for IFN-regulated genes and profibrotic/Tgfβ-regulated genes. Conclusion: Our analysis reveals the differences and similarities of the network of key genes between humans and mice during the molecular processes that eventually lead to fibrosis in the lung. © 2015 Jiao et al.

Yan J.,University of Tennessee Health Science Center | Jiao Y.,University of Tennessee Health Science Center | Jiao Y.,Mudanjiang Medical College | Chen H.,First Hospital of Qiqihaer City | And 4 more authors.
Journal of Genetics and Genomics | Year: 2013

Previous studies have revealed the significance of cytokine interleukin 1 (IL-1) in the onset and progression of rheumatoid arthritis (RA). The precise molecular mechanisms related to IL-1 underlying RA is still elusive. We conducted a whole genome-wide transcriptomal comparison of wild-type (WT) and arthritis-prone IL-1 receptor antagonist (IL-1rn) deficient BALB/c mice to address this issue. To refine our search efforts, gene expression profiling was also performed on paired wild-type and arthritis-resistant IL-1rn deficient DBA/1 mice as internal controls when identifying causative arthritis candidate genes. Two hundred and fifteen transcripts were found to be dysregulated greater than or equal to 2-fold in the diseased mice. The altered transcriptome in BALB/c mice revealed increased myeloid cell activities and impaired lymphocyte functionality, suggesting dual regulatory effects of IL-1 hyperactivity on immunological changes associated with arthritis development. Phase-specific gene expression changes were identified, such as early increase and late decrease of heat shock protein coding genes. Moreover, common gene expression changes were also observed, especially the upregulation of paired Ig-like receptor A (Pira) in both early and late phases of arthritis. Real-time PCR was performed to validate the expression of Pira and an intervention experiment with a major histocompatibility complex (MHC) class I inhibitor (brefeldin A) was carried out to investigate the role of suppressing Pira activity. We conclude that global pattern changes of common and distinct gene expressions may represent novel opportunities for better control of RA through early diagnosis and development of alternative therapeutic strategies. © 2013.

Liu H.,Harbin Medical University | Liu H.,Center for Infection and Genomics | Liu H.,University of Calgary | Yan Z.-Q.,Harbin Medical University | And 11 more authors.
Journal of Ovarian Research | Year: 2014

Background: Products of the SOX gene family play important roles in the life process. One of the members, SOX7, is associated with the development of a variety of cancers as a tumor suppression factor, but its relevance with ovarian cancer was unclear. In this study, we investigated the involvement of SOX7 in the progression and prognosis of epithelial ovarian cancer (EOC) and the involved mechanisms. Methods: Expression profiles in two independent microarray data sets were analyzed for SOX7 between malignant and normal tissues. The expression levels of SOX7 in EOC, borderline ovarian tumors and normal ovarian tissues were measured by immunohistochemistry. We also measured levels of COX2 and cyclin-D1 to examine their possible involvement in the same signal transduction pathway as SOX7. Results: The expression of SOX7 was significantly reduced in ovarian cancer tissues compared with normal controls, strongly indicating that SOX7 might be a negative regulator in the Wnt/β-catenin pathway in ovarian cancer. By immunohistochemistry staining, the protein expression of SOX7 showed a consistent trend with that of the gene expression microarray analysis. By contrast, the protein expression level of COX2 and cyclin-D1 increased as the tumor malignancy progressed, suggesting that SOX7 may function through the Wnt/β-catenin signaling pathway as a tumor suppressor. In comparison between the protein expression levels of SOX7 with pathological features of the cancer, we found that SOX7 was down-regulated mainly in serous cystadenocarcinoma and advanced stages of the cancers. Conclusions: The expression of SOX7 correlates with tumor progression as a tumor suppressor, possibly through the Wnt/β-catenin signaling pathway in ovarian cancers, suggesting that SOX7 may be a promising prognostic marker. © 2014 Liu et al.; licensee BioMed Central Ltd.

Fu Y.,Harbin Medical University | Zhang W.,Harbin Medical University | Wang H.,Harbin Medical University | Wang H.,First Hospital of Qiqihaer City | And 7 more authors.
BMC Infectious Diseases | Year: 2013

Background: Wide use of ciprofloxacin and levofloxacin has often led to increased resistance. The resistance rate to these two agents varies in different clinical isolates of Enterobacteriaceae. Mutations of GyrA within the quinolone resistance-determining regions have been found to be the main mechanism for quinolone resistance in Enterobacteriaceae. It has been shown that only some of the mutations in the gyrA gene identified from clinical sources were involved in fluoroquinolone resistance. Whether different patterns of gyrA mutation are related to antimicrobial resistance against ciprofloxacin and levofloxacin is unclear.Methods: The minimum inhibitory concentration (MIC) of ciprofloxacin and levofloxacin were determined by the agar dilution method followed by PCR amplification and sequencing of the quinolone resistance determining region of gyrA to identify all the mutation types. The correlation between fluoroquinolone resistance and the individual mutation type was analyzed.Results: Resistance differences between ciprofloxacin and levofloxacin were found in 327 isolates of K. pneumoniae and E. coli in Harbin, China and in the isolates reported in PubMed publications. GyrA mutations were found in both susceptible and resistant isolates. For the isolates with QRDR mutations, the resistance rates to ciprofloxacin and levofloxacin were also statistically different. Among the 14 patterns of alterations, two single mutations (Ser83Tyr and Ser83Ile), and three double mutations (Ser83Leu+Asp87Asn, Ser83Leu+Asp87Tyr and Ser83Phe+Asp87Asn) were associated with both ciprofloxacin and levofloxacin resistance. Two single mutations (Ser83Phe and Ser83Leu) were related with ciprofloxacin resistance but not to levofloxacin. Resistance difference between ciprofloxacin and levofloxacin in isolates harboring mutation Ser83Leu+Asp87Asn were of statistical significance among all Enterobacteriaceae (P<0.001).Conclusions: Resistance rate to ciprofloxacin and levofloxacin were statistically different among clinical isolates of Enterobacteriaceae harboring GyrA mutations. Ser83Leu+Asp87Asn may account for the antimicrobial resistance difference between ciprofloxacin and levofloxacin. © 2013 Fu et al.; licensee BioMed Central Ltd.

Hu Y.-Z.,Harbin Medical University | Hu Y.-Z.,First Hospital of Qiqihaer City | Wang D.-H.,Harbin Medical University | Gong H.-D.,Harbin Medical University | And 5 more authors.
Chinese Journal of Cancer Prevention and Treatment | Year: 2013

OBJECTIVE: To investigate the relationship between the polymorphism of XRCC1 and MGMT and susceptibility to glioma in Han population northeastern China. METHODS: A hospital-based case-control study with glioma and none cancer or outpatients as a control group (matched for ages±5 years and sex) in Han population northeastern China was conducted to analyze XRCC1 polymorphism at Arg399Gln(included 366 glioma patients and 377 healthy controls) and MGMT polymorphism at Leu84Phe(included 543 glioma patients and 495 healthy controls), Ile143Val(included 369 glioma patients and 441 healthy controls). Genetyped by PCR-based restriction fragment length polymorphism(PCR-RFLP) techniques. RESULTS: The frequencies of 399Gln allele gene in the glioma patients was 0.35, which was significantly higher than that in controls 0.27(χ2=7.485, P=0.006). Compared with individuals with the Arg/Arg genetype, individuals with the Gln genotype, the Arg/Gln individual increased the glioma risk (OR=1.36, 95%CI=1.01-1.85, P=0.045); Gln/Gln individual increased the glioma risk(OR=1.83, 95%CI=1.10-3.05, P=0.019); Arg/Gln + Gln/Gln individual increased the glioma risk(OR =1.44, 95%CI=1.08-1.93, P=0.013); allele Gln individual increased the glioma risk(OR=1.36, 95%CI=1.09-1.69, P=0.006). The frequencies of 84Phe allele gene in the glioma patients was 0.16, which was significantly higher than that in controls 0.10(χ2=20.253, P<0.001). Compared with individuals with the Leu/Leu genetype, individuals with the Leu/Phe increased the glioma risk(OR =1.61, 95%CI=1.18-2.19, P=0.002); Phe/Phe individual increased the glioma risk(OR=4.16, 95%CI=1.68-10.30, P=0.001); Leu/Phe + Phe/Phe individual increased the glioma risk(OR=1.78, 95%CI=1.33-2.39, P<0.001); allele Phe individual increased the glioma risk(OR=1.83, 95%CI=1.40-2.38, P<0.001). The frequencies of 143Val allele gene in the glioma patients was 0.11, which was no evidence of an association in controls 0.10(χ2=0.242, P=0.623). Compared with individuals with the Ile/Ile genetype, individuals with the Ile/Val or Val/Val or Ile/Val + Val/Val and allele Val individual did not increase the glioma risk(P>0.05). CONCLUSIONS: The XRCC1 Arg399Gln and MGMT Leu84Phe polymorphism can add the risk to the occurrence of glioma in a Han population in northeastern China, which can elevate the occurrence of glioma. No significant correlation is found between MGMT gene polymorphism of Ile143Val and glioma.

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