The 148 Central Hospital of PLA

Zibo, China

The 148 Central Hospital of PLA

Zibo, China
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Hui Z.,The 148 Central Hospital of PLA | Wei Z.,Zhengzhou University | Linlin H.,Zhengzhou University | Yutong W.,Henan University | And 10 more authors.
Oncotarget | Year: 2017

Aims: To investigate the impact of sortilin-related receptor 1 gene 1 (SORL1) and peroxisome proliferator activated receptor gamma (PPAR G) gene single nucleotide polymorphisms (SNPs), gene- gene and gene- environment interactions and haplotype on late-onset Alzheimer's disease (LOAD) risk. Methods: Hardy-Weinberg equilibrium (HWE), haplotype analysis and pairwise linkage disequilibrium (LD) analysis were investigated by using SNPStats (available online at http://bioinfo.iconcologia.net/SNPstats). Logistic regression was performed to investigate association between SNPs and LOAD. Generalized multifactor dimensionality reduction (GMDR) was used to investigate the interaction among genegene and gene- environment interaction. Results: Logistic regression analysis showed that LOAD risk was significantly higher in carriers of the A allele of rs1784933 polymorphism than those with GG (GA+ AA versus GG), adjusted OR (95%CI) = 1.63(1.27-1.98), and higher in carriers of G allele of the rs1805192 polymorphism than those with CC (CG+ GG versus CC), adjusted OR (95%CI) = 1.70 (1.25-2.27). GMDR analysis suggested a significant two-locus model (p = 0.0010) involving rs1784933 and rs1805192, and a significant two-locus model (p = 0.0100) involving rs1784933 and alcohol drinking. Haplotype containing the rs1784933- A and rs689021- C alleles were associated with a statistically increased LOAD risk (OR = 1.86, 95%CI = 1.37- 2.52, p < 0.001). Conclusions: We conclude that rs1784933 and rs1805192 minor alleles, genegene interaction between rs1784933 and rs1805192, gene- environment interaction between rs1784933 and alcohol drinking, and haplotype containing the rs1784933- A and rs689021- C alleles are all associated with increased LOAD risk. © Hui et al.


Ji H.,Zhejiang University | Wang Y.,The 148 Central Hospital of PLA | Liu G.,Zhejiang University | Xu X.,Zhejiang University | And 17 more authors.
Neuroscience Letters | Year: 2015

As a member of the opioid family, κ-opioid receptors play important role in cognitive and learning functions. The purpose of this study was to evaluate the association of OPRK1 promoter methylation with Alzheimer's disease (AD). OPRK1 DNA methylation levels of 48 cases and 58 well matched controls were measured using the bisulphite pyrosequencing technology. Our results showed that there was a significant correlation between three CpG sites on the OPRK1 promoter region (r>= 0.715, p< 0.001). Thus, the mean methylation value of the three CpG sites was used for the case-control comparison. And our results showed there was a significantly higher OPRK1 promoter methylation in AD cases than in controls (p= 0.006, adjusted p= 0.012). Subsequent luciferase reporter assay showed the CpGs containing fragment of OPRK1 promoter significantly increased the expression of reporter gene (Fold = 2.248, p= 0.0235). In summary, our results suggested that OPRK1 promoter hypermethylation might increase the risk of AD through its regulation on the gene expression of OPRK1. © 2015 Elsevier Ireland Ltd.


PubMed | Ningbo Kangning Hospital, Ningbo No 1 Hospital, the 148 Central Hospital of PLA, Xinjiang Medical University and Zhejiang University
Type: | Journal: Neuroscience letters | Year: 2015

As a member of the opioid family, -opioid receptors play important role in cognitive and learning functions. The purpose of this study was to evaluate the association of OPRK1 promoter methylation with Alzheimers disease (AD). OPRK1 DNA methylation levels of 48 cases and 58 well matched controls were measured using the bisulphite pyrosequencing technology. Our results showed that there was a significant correlation between three CpG sites on the OPRK1 promoter region (r>=0.715, p<0.001). Thus, the mean methylation value of the three CpG sites was used for the case-control comparison. And our results showed there was a significantly higher OPRK1 promoter methylation in AD cases than in controls (p=0.006, adjusted p=0.012). Subsequent luciferase reporter assay showed the CpGs containing fragment of OPRK1 promoter significantly increased the expression of reporter gene (Fold=2.248, p=0.0235). In summary, our results suggested that OPRK1 promoter hypermethylation might increase the risk of AD through its regulation on the gene expression of OPRK1.


PubMed | Ningbo Kangning Hospital, Ningbo No 1 Hospital, The 148 Central Hospital of PLA, Ningbo University and 2 more.
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016

Aberrant promoter methylation of multiple genes is associated with various diseases, including Alzheimers disease (AD). The goal of the present study was to determine whether dopamine receptor D4 (DRD4) promoter methylation is associated with AD. In the current study, the methylation levels of the DRD4 promoter were measured in 46 AD patients and 61 controls using bisulfite pyrosequencing technology. The results of the present study demonstrated that DRD4 promoter methylation was significantly higher in AD patients than in controls. A further breakdown analysis by gender revealed that there was a significant association of DRD4 promoter methylation with AD in males (23patients and 45 controls). In conclusion, the results of the present study demonstrated that elevated DRD4 promoter methylation was associated with AD risk in males.


PubMed | Ningbo Kangning Hospital, Ningbo No 1 Hospital, the 148 Central Hospital of PLA, Xinjiang Medical University and Zhejiang University
Type: Journal Article | Journal: PloS one | Year: 2014

Brain derived neurotrophic factor (BDNF) has been known to play an important role in various mental disorders or diseases such as Alzheimers disease (AD). The aim of our study was to assess whether BDNF promoter methylation in peripheral blood was able to predict the risk of AD. A total of 44 AD patients and 62 age- and gender-matched controls were recruited in the current case-control study. Using the bisulphite pyrosequencing technology, we evaluated four CpG sites in the promoter of the BDNF. Our results showed that BDNF methylation was significantly higher in AD cases than in the controls (CpG1: p=10.021; CpG2: p=0.002; CpG3: p=0.007; CpG4: p=0.005; average methylation: p=0.004). In addition, BDNF promoter methylation was shown to be significantly correlated with the levels of alkaline phosphatase (ALP), glucose, Lp(a), ApoE and ApoA in males (ALP: r=-0.308, p=0.042; glucose: r=-0.383, p=0.010; Lp(a): r=0.333, p=0.027; ApoE: r=-0.345, p=0.032;), ApoA levels in females (r=0.362, p=0.033), and C Reactive Protein (CRP) levels in both genders (males: r=-0.373, p=0.016; females: r=-0.399, p=0.021). Our work suggested that peripheral BDNF promoter methylation might be a diagnostic marker of AD risk, although its underlying function remains to be elaborated in the future.


PubMed | Nantong University, University of Chicago, the First Peoples Hospital of Kunshan City, Jiangsu University and 4 more.
Type: Journal Article | Journal: International journal of oncology | Year: 2016

Aurora kinase A (AURKA) is an oncogenic serine/threonine kinase, it plays important roles in tumorigenesis and chemoresistance. In this study, we investigated the expression of AURKA in lung adenocarcinoma tissues, the role of small interference RNA targeting AURKA on growth, cell cycle, and apoptosis of lung adenocarcinoma cell lines invitro. The AURKA is highly expressed in lung adenocarcinoma tissues and human lung adenocarcinoma cell lines. Lentivirus-mediated short hairpin RNA (shRNA) was used to knock down AURKA expression in human lung adenocarcinoma cell lines H1299 and A549. The results indicated that depletion of AURKA could inhibit cell growth, cause cell cycle arrest and apoptosis. The potential mechanisms of AURKA inhibition induced cell cycle arrest and apoptosis are associated with downregulated RAF-1, CCND2, CCND3, CDK4, PAK4, EGFR and upregulated WEE1 expression. Furthermore, AURKA knockdown cooperated with vincristine (VCR) to repress A549 cell proliferation. Therefore, AURKA plays important roles in the proliferation of human lung adenocarcinoma cells, which suggests that AURKA could be a promising tool for lung adenocarcinoma therapy.


Liao Q.,Zhejiang University | Wang Y.,The 148 Central Hospital of PLA | Cheng J.,Ningbo Kangning Hospital | Dai D.,Zhejiang University | And 4 more authors.
European Journal of Medical Genetics | Year: 2015

Schizophrenia (SCZ) is a complex mental disorder contributed by both genetic and epigenetic factors. Long noncoding RNAs (lncRNAs) was recently found playing an important regulatory role in mental disorders. However, little was known about the DNA methylation of lncRNAs, although numerous SCZ studies have been performed on genetic polymorphisms or epigenetic marks in protein coding genes. We presented a comprehensive genome wide DNA methylation study of both protein coding genes and lncRNAs in female patients with paranoid and undifferentiated SCZ. Using the methyl-CpG binding domain (MBD) protein-enriched genome sequencing (MBD-seq), 8,163 and 764 peaks were identified in paranoid and undifferentiated SCZ, respectively (. p<1×10-5). Gene ontology analysis showed that the hypermethylated regions were enriched in the genes related to neuron system and brain for both paranoid and undifferentiated SCZ (. p<0.05). Among these peaks, 121 peaks were located in gene promoter regions that might affect gene expression and influence the SCZ related pathways. Interestingly, DNA methylation of 136 and 23 known lncRNAs in Refseq database were identified in paranoid and undifferentiated SCZ, respectively. In addition, ~20% of intergenic peaks annotated based on Refseq genes were overlapped with lncRNAs in UCSC and gencode databases. In order to show the results well for most biological researchers, we created an online database to display and visualize the information of DNA methyation peaks in both types of SCZ (. http://www.bioinfo.org/scz/scz.htm). Our results showed that the aberrant DNA methylation of lncRNAs might be another important epigenetic factor for SCZ. © 2014.


Wang Y.,The 148 Central Hospital of PLA | Li J.,The 148 Central Hospital of PLA | Zhang Y.,The 148 Central Hospital of PLA | Yin H.,The 148 Central Hospital of PLA | Han B.,The 148 Central Hospital of PLA
Cancer Letters | Year: 2015

The transcripts of the gene Colorectal Neoplasia Differentially Expressed (CRNDE) are recognized as long-noncoding RNAs (lncRNAs), which are expressed in specific regions within the human brain, and are the most upregulated lncRNA in gliomas. However, the underlying regulation and function of CRNDE in gliomas are largely unknown. In this study, the upregulation of CRNDE was confirmed in both primary specimens from glioma patients and in vitro with cell lines. Overexpression of specific CRNDE transcript promotes cell growth and migration in vitro while knockdown of CRNDE expression manifests a repressive function during these cellular processes. The growth promoting effect of CRNDE was also demonstrated in a xenograft mouse model. Mechanistic studies further revealed that histone acetylation in the promoter region might account for the upregulation of CRNDE, and the level of CRNDE expression could be modulated by mammalian Target of Rapamycin (mTOR) signaling in glioma. Thus, our results shed a light on utilizing CRNDE as a potential novel therapeutic target for the treatment of glioma. © 2015.


PubMed | The 148 Central Hospital of PLA
Type: Journal Article | Journal: Cancer letters | Year: 2015

The transcripts of the gene Colorectal Neoplasia Differentially Expressed (CRNDE) are recognized as long-noncoding RNAs (lncRNAs), which are expressed in specific regions within the human brain, and are the most upregulated lncRNA in gliomas. However, the underlying regulation and function of CRNDE in gliomas are largely unknown. In this study, the upregulation of CRNDE was confirmed in both primary specimens from glioma patients and in vitro with cell lines. Overexpression of specific CRNDE transcript promotes cell growth and migration in vitro while knockdown of CRNDE expression manifests a repressive function during these cellular processes. The growth promoting effect of CRNDE was also demonstrated in a xenograft mouse model. Mechanistic studies further revealed that histone acetylation in the promoter region might account for the upregulation of CRNDE, and the level of CRNDE expression could be modulated by mammalian Target of Rapamycin (mTOR) signaling in glioma. Thus, our results shed a light on utilizing CRNDE as a potential novel therapeutic target for the treatment of glioma.

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