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  ✔本篇論文使用華聯產品:Human OneArray  
 Evidence-based Complementary And Alternative Medicine. 2013 Nov 18.
 Gene Expression Profiles Underlying Selective T Cell-mediated Immunity Activity of a Chinese Medicine Granule on Mice Infected with Influenza Virus H1N1 
 Lu Na-na, Liu Qi, Ge Shi-jie, Wu Jun, Qiu Ze-ji, Zhang Hong-chun, Zhao En-xiang, Zhang Yi, Yu Zhuo-nan, Gu Li-gang
  Abstract
Background.Efficacy of a Chinese medicine granule, Shu-Feng-Xuan-Fei (SFXF) has been demonstrated in reducing the duration of fever among patients with influenza. SFXF has also been found efficacious in reducing lung index and pathological lesion and regulating natural killer (NK) cell mediated cytotoxicity in pneumonia mice infected with influenza virus. Yet the effects of SFXF on viral infection in T cell-mediated immunity at the gene transcriptional level have never been reported.Objective.To elucidatethe effectsof SFXF on the major pathways and genes involved in T-cell mediated immunity in the lung of mice subjected toinfluenza virus H1N1 infection. Methods.Seventy-two ICR mice were randomly divided into six groups (n=12): normal control group (N), virus control group (M), Oseltamivirgroup, low-dose SFXF(SL), medium-dose SFXF(SM) and high-dose SFXF(SH). Mice were anesthetized with 2, 2, 2-tribromoethanol in tert-amyl alcohol and inoculated (i.n.) with 4LD50 of virus except normal control group. Oseltamivir groupreceived 11.375 mg•kg-1•d-1Oseltamivir Phosphate. SFXF 3.76, 1.88 and 0.94 g•kg-1•d-1were administrated to mice in all SFXF groups by gastric perfusion. Each group was in equal dose of 0.2ml daily for 4 consecutive days. Mice were sacrificed and then total RNA were extracted in lung tissue. Some genes involved in T cell-mediated immunity were selected by DNA microarray. These candidate genes were verified by Real-Time PCR and western immunoblotting. Results. Compared with virus control group, in Toll-like receptor signaling pathway, 12 virus-altered genes were significantly reduced following the medium-dose SFXF treatment. Eighteen antigen processing presentation-associated genes were up-regulated by medium-dose SFXF, among which 13 genes and 5 genes belong to MHC-I and MHC-II family respectively. In the process of T cell receptor signaling pathway, 19 genes were down-regulated by the medium-dose SFXF treatment. Exploration into effector T cells activation and cytokines, all of altered genes in virus control group were reversed by the medium-dose SFXF. Real-time PCR and western immunoblotting showed the regulation of the medium-dose SFXF in IL-4, IFN-, TNF-, IL-1, TLR7, MyD88, p38 and JNKwas superior to Oseltamivir and high-dose SFXF group. As expected, real-time PCR and western immunoblotting data were consistent with the results of microarray assay. Conclusion. Viral replication was found to have been prevented and the viral infection was eliminated with exposure to SFXF granules. The mechanism could be through the reduction of influenzainfected cells and activationof T cells. This immunomodulation effects could be realized by regulating gene expressions of T cells activation. Thus, SFXF could help to restore a balance of the host immune system, which may be critical for viral clearance in early phase of influenza virus infection.
   

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 Human Immunology. doi:10.1016/j.humimm.2015.09.033. Epub 2015 Sep 30..
 Functional relevance for type 1 diabetes mellitus-associated genetic variants by using integrative analyses
 
 
 
  Abstract
Type 1 diabetes mellitus (type 1 DM) is an autoimmune disease. Although genome-wide association studies (GWAS) and meta-analyses have successfully identified numerous type 1 DM-associated susceptibility loci, the underlying mechanisms for these susceptibility loci are currently largely unclear.
   

  ✔本篇論文使用華聯產品:Mouse OneArray  
 Scientific Reports. 2015, ;5:12061. doi: 10.1038/srep12061.
 Nogo-B protects mice against lipopolysaccharide-induced acute lung injury
 
 
 Wujian Xu, Ying Zhu, Yunye Ning, Yuchao Dong, Haidong Huang, Wei Zhang, Qinying Sun, Qiang Li
  Abstract
Nogo-B, a member of the reticulon 4 protein family, plays a critical role in tissue repair and acute inflammation. Its role in acute lung injury (ALI) remains unclear. Here, we assessed the function of Nogo-B during tissue injury in a lipopolysaccharide (LPS)-induced ALI mouse model. We found that pulmonary Nogo-B was significantly repressed after LPS instillation in C57BL/6 mice. Over-expression of pulmonary Nogo-B using an adenovirus vector carrying the Nogo-B-RFP-3flag gene (Ad-Nogo-B) significantly prolonged the survival of mice challenged with a lethal dose of LPS. The Ad-Nogo-B-treated mice also had less severe lung injury, less alveolar protein exudation, and a higher number of macrophages but less neutrophil infiltration compared with Ad-RFP-treated mice. Interestingly, microarray analysis showed that the Ad-Nogo-B-treated mice had different gene expression profiles compared with the controls and the prominent expression of genes related to wound healing and the humoral immune response after LPS induction. Of the 49 differently expressed genes, we found that the expression of PTX3 was significantly up-regulated following Nogo-B over-expression as observed in lung tissues and RAW264.7 cells. In conclusion, Nogo-B plays a protective role against LPS-induced ALI, and this effect might be exerted through the modulation of alveolar macrophage recruitment and PTX3 production.
   

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  ✔本篇論文使用華聯產品:Human OneArray  
 Bmc Cancer. DOI 10.1186/s12885-015-1671-5.
 Upregulation of MicroRNA-19b predicts good prognosis in patients with hepatocellular carcinoma presenting with vascular invasion or multifocal disease
 
 
 
  Abstract
Background After surgical resection of hepatocellular carcinoma (HCC), recurrence is common, especially in patients presenting with vascular invasion or multifocal disease after curative surgery. Consequently, we examined the expression pattern and prognostic value of miR-19b in samples from these patients. Methods We performed a miRNA microarray to detect differential expression of microRNAs (miRNAs) in 5 paired samples of HCC and non-tumoral adjacent liver tissue and a quantitative real-time polymerase chain reaction (PCR) analysis to validate the results in 81 paired samples of HCC and adjacent non-tumoral liver tissues. We examined the associations of miR-19b expression with clinicopathological parameters and survival. MiR-19b was knocked down in Hep3B and an mRNA microarray was performed to detect the affected genes. Results In both the miRNA microarray and real-time PCR, miR-19b was significantly overexpressed in the HCC tumor compared with adjacent non-tumor liver tissues (P < 0.001). The expression of miR-19b was significantly higher in patients who were disease-free 2 years after surgery (P < 0.001). High miR-19b expression levels were associated with higher α-fetoprotein levels (P = 0.017). In the log-rank test, high miR-19b was associated with better disease-free survival (median survival 37.107 vs. 11.357; P = 0.022). In Cox multivariate analysis, high miR-19b predicted better disease-free survival and overall survival (hazards ratio [HR] = 0.453, 95 % confidence interval [CI] = 0.245–0.845, P = 0.013; HR = 0.318, CI = 0.120–0.846, P = 0.022, respectively). N-myc downstream regulated 1 (NDRG1) was downregulated, while epithelial cell adhesion molecule (EPCAM), hypoxia-inducible factor 1-alpha (HIF1A), high-mobility group protein B2 (HMGB2), and mitogen activated protein kinase 14 (MAPK14) were upregulated when miR-19b was knocked down in Hep3B. Conclusions The overexpression of miR-19b was significantly correlated with better disease-free and overall survival in patients with HCC presenting with vascular invasion or multifocal disease after curative surgery. MiR-19b may influence the expression of NDRG1, EPCAM, HMGB2, HIF1A, and MAPK14.
   

  ✔本篇論文使用華聯產品:Human OneArray  
 Amino Acids. doi: 10.1007/s00726-015-1956-7. Epub 2015 Mar 24..
 Homocysteine thiolactone and N-homocysteinylated protein induce pro-atherogenic changes in gene expression in human vascular endothelial cells
 
 
 
  Abstract
Genetic or nutritional deficiencies in homocysteine (Hcy) metabolism lead to hyperhomocysteinemia (HHcy) and cause endothelial dysfunction, a hallmark of atherosclerosis. In addition to Hcy, related metabolites accumulate in HHcy but their role in endothelial dysfunction is unknown. Here, we examine how Hcy-thiolactone, N-Hcy-protein, and Hcy affect gene expression and molecular pathways in human umbilical vein endothelial cells. We used microarray technology, real-time quantitative polymerase chain reaction, and bioinformatic analysis with PANTHER, DAVID, and Ingenuity Pathway Analysis (IPA) resources. We identified 47, 113, and 30 mRNAs regulated by N-Hcy-protein, Hcy-thiolactone, and Hcy, respectively, and found that each metabolite induced a unique pattern of gene expression. Top molecular pathways affected by Hcy-thiolactone were chromatin organization, one-carbon metabolism, and lipid-related processes [−log(P value) = 20–31]. Top pathways affected by N-Hcy-protein and Hcy were blood coagulation, sulfur amino acid metabolism, and lipid metabolism [−log(P value)] = 4–11; also affected by Hcy-thiolactone, [−log(P value) = 8–14]. Top disease related to Hcy-thiolactone, N-Hcy-protein, and Hcy was ‘atherosclerosis, coronary heart disease’ [−log(P value) = 9–16]. Top-scored biological networks affected by Hcy-thiolactone (score = 34–40) were cardiovascular disease and function; those affected by N-Hcy-protein (score = 24–35) were ‘small molecule biochemistry, neurological disease,’ and ‘cardiovascular system development and function’; and those affected by Hcy (score = 25–37) were ‘amino acid metabolism, lipid metabolism,’ ‘cellular movement, and cardiovascular and nervous system development and function.’ These results indicate that each Hcy metabolite uniquely modulates gene expression in pathways important for vascular homeostasis and identify new genes and pathways that are linked to HHcy-induced endothelial dysfunction and vascular disease.