Changzhi, China
Changzhi, China

Changzhi Medical College is a university in Shanxi, People's Republic of China under the authority of the provincial government. Wikipedia.

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Chang N.,Peking University | Yi J.,Peking University | Guo G.,Changzhi Medical College | Liu X.,Peking University | And 6 more authors.
Molecular and Cellular Biology | Year: 2010

In this study, we show that HuR destabilizes p16INK4 mRNA. Although the knockdown of HuR or AUF1 increased p16 expression, concomitant AUF1 and HuR knockdown had a much weaker effect. The knockdown of Ago2, a component of the RNA-induced silencing complex (RISC), stabilized p16 mRNA. The knockdown of HuR diminished the association of the p16 3′ untranslated region (3′UTR) with AUF1 and vice versa. While the knockdown of HuR or AUF1 reduced the association of Ago2 with the p16 3′UTR, Ago2 knockdown had no influence on HuR or AUF1 binding to the p16 3′UTR. The use of EGFP-p16 chimeric reporter transcripts revealed that p16 mRNA decay depended on a stem-loop structure present in the p16 3′UTR, as HuR and AUF1 destabilized EGFP-derived chimeric transcripts bearing wild-type sequences but not transcripts with mutations in the stem-loop structure. In senescent and HuR-silenced IDH4 human diploid fibroblasts, the EGFPp16 3′UTR transcript was more stable. Our results suggest that HuR destabilizes p16 mRNA by recruiting the RISC, an effect that depends on the secondary structure of the p16 3′UTR and requires AUF1 as a cofactor. Copyright © 2010, American Society for Microbiology. All Rights Reserved.

Ding D.-P.,Southern Medical University | Ma W.-L.,Southern Medical University | He X.-F.,Changzhi Medical College | Zhang Y.,Jinan University
Molecular Biology Reports | Year: 2012

Abstract The published data on the association between xeroderma pigmentosum group D (XPD) Lys751Gln polymorphism and esophageal cancer (EC) remained controversial. The present meta-analysis of literatures was performed to derive a more precise estimation of the relationship. A comprehensive literature search was conducted to identify all case-control studies of Lys751Gln polymorphism and risk for two main types of EC: esophageal adenocarcinoma (EADC) and esophageal squamous cell carcinoma (ESCC). A total of 12 studies were identified to the meta-analysis, including 2,575 cases (1,294 ESCC and 1,281 EADC) and 4,951 controls (1,891 ESCC and 3,060 EADC). Random-effects or fix-effects model was used according to between-study heterogeneity. The odds ratio (OR) for the variant homozygous genotype Gln/ Gln of the Lys751Gln polymorphism, compared with the wild type homozygote Lys/Lys, was 1.26, with 95% confidence interval (95% CI) 1.02-1.56, for EADC risk without between-study heterogeneity. When stratified by ethnicity, statistically significantly elevated risk was found among Chinese (Gln/Gln vs. Lys/Lys: OR 2.45, 95% CI = 1.10-5.44). However, no significant associations were found between XPD Lys751Gln polymorphism and EC risk when all studies pooled into the meta-analysis (Lys/Gln vs. Lys/Lys: OR 1.07, 95% CI = 0.88-1.28; Gln/ Gln Lys/Lys: OR 1.25, 95% CI = 0.92-1.71; dominant model: OR 1.09, 95% CI = 0.90-1.33). In conclusion, this meta-analysis suggests that the Lys751Gln genetic polymorphism may be a potential biomarker of EC susceptibility in Chinese populations. And a study with the larger sample size is needed to further evaluate gene- environment interaction on XPD Lys751Gln polymorphism and EC risk. © Springer Science+Business Media B.V. 2011.

Objective: To analyze the MRI data of misdiagnosed and missed diagnosed of breast lesions and their histopathological features. Methods: Data from 241 breast lesions within 121 patients were recruited in this study. The data included MRI images, ultrasounds and X-ray images were retrospectively interpreted by two radiologist and each lesion was assessed according to the BI-RADS classification. The pathologic features of miss or error diagnosed lesions on MRI were analyzed. Results: In 241 breast lesions (malignance 120, benign 121), 4 lesions were miss diagnosed on MRI. They were 2 intraductal papillomatosis and 2 fibroadenoma. All was benign. Twenty three lesions were misdiagnosed on MRI. Sixteen were overestimation, including 3 chronic inflammations, 3 sclerosing adenosis, 2 fibroadenoma, 4 fibrocystic changes with or without atypical ductal hyperplasia (ADH), 2 intraductal papilloma, 1 infiltration of pectoralis major muscle and 1 axillary lymphnode metastasis. Meanwhile, there were 7 lesions were underestimation. These lesions included 2 invasive ductal carcinomas, 1 mucinous adenocarcinoma, 2 DCIS and 1 blunt duct adenosis with ADH and focal cancerous, 1 inflammatory breast cancer underwent chemotherapy. The sensitivity and specificity and accuracy of breast MRI were 95.83% (115/120), 72.73% (88/121), 84.23% (203/241), respectively. MRI findings had no difference with respect to mammogram or ultrasound was 75.10% (181/241). Conclusion: MRI misdiagnosis and missed often occurs in smaller breast lesions, morphologic and hemodynamic malignant manifestation atypical, especially intraductal lesions. MRI diagnosis should be combined with physical examination, X-ray mammogram and ultrasound to improve diagnostic accuracy and reduce missed diagnosis.

Zhang X.Y.,Changzhi Medical College
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2011

To explore the correlativity between HLA-DQ allele and primary Sjogren's syndrome(pSS) of the Han nationality in Shanxi province and to understand the pathogenesis of pSS at the gene level. Polymerase chain reaction sequence specific primers (PCR-SSP) technique was used to determine the alleles of HLA-DQA1 and HLA-DQB1 of pSS patients and healthy populations, and the difference in their HLA-DQA1 and HLA-DQB1 allelic frequencies were analyzed by using chi-square test and Fisher's exact test. (1) The gene frequency of HLA-DQA1*0501 in pSS patients was significantly higher than that in healthy controls(22.0% vs 12.0%, x(2);=7.087, P<0.05, RR=2.068). (2)The gene frequency of HLA-DQA1*0301/2 in pSS patients was significantly lower than that in controls(13.0% vs 24.5%, x(2);=8.681, P<0.05, RR=0.460). (3) The gene frequency of HLA-DQB1*0201 in pSS patients was significantly higher than that in controls(28.5% vs 18.5%, x(2);=5.563, P<0.05, RR=1.756). In Han nationality of Shanxi province, HLA-DQA1*0501 and HLA-DQB1*0201 alleles probably are susceptible genes of pSS, while HLA-DQA1*0301/2 allele probably is a protective gene of pSS.

Ren J.,Changzhi Medical College
Wei sheng wu xue bao = Acta microbiologica Sinica | Year: 2012

Phosphate-solubilizing bacteria (PSB) were isolated, screened and identified from the rhizosphere of Taxus chinensis var. mairei, and growth-promoting effects on T. chinensis var. mairei by high effective PSB were determined. By using selective culture media, PSB were isolated from rhizospheric soil, the high effective PSB was further screened using NBRI-BPB medium, and the molybdenum-antimony anti-spectrophotometric method was applied to determine the phosphate-dissolving ability of the high effective PSB after four days fermentation in NBRIP medium. Bacteria were identified by the Biolog system combined with 16S rDNA gene sequence analysis and morphological, physiological and biochemical characteristics. The inoculation test in potted seedlings was carried out under the greenhouse. Four strains of high effective PSB were screened and identified as Pseudomonas fluorescens, Bacillus cereus, Sinorhizobium meliloti and Bacillus licheniformis, respectively. These strains had significant effects on improving the growth of the seedlings of T. chinensis var. mairei.

Xu L.,Central South University | Jiang Y.,Central South University | Zheng J.,Central South University | Zheng J.,Changzhi Medical College | And 4 more authors.
Human Pathology | Year: 2013

Nasopharyngeal carcinoma has a high incidence in southern China. The Wnt/β-catenin signaling pathway plays a major role in cancer development and progression. Our current study aims to determine the clinical significance of the Wnt/β-catenin pathway components such as β-catenin, cyclooxygenase 2, cyclin D1, c-Myc, and E-cadherin in 148 nasopharyngeal carcinomas by immunohistochemistry. We found that nasopharyngeal carcinoma stage T3+T4 had significantly higher expression of β-catenin, cyclooxygenase 2, cyclin D1, and c-Myc and lower expression of E-cadherin than nasopharyngeal carcinoma stage T1+T2 (P <.001, P <.05, respectively).There was significantly higher expression of β-catenin (P =.001) and cyclooxygenase 2 (P =.003) and lower expression of E-cadherin (P =.001) in nasopharyngeal carcinoma with lymph node metastasis than in nasopharyngeal carcinoma without lymph node metastasis. The expression of β-catenin in nasopharyngeal carcinoma was positively correlated with cyclooxygenase 2 (r = 0.458, P <.0001), cyclin D1 (r = 0.700, P <.0001), and c-Myc expression (r = 0.144, P =.006) but negatively correlated with E-cadherin expression (r = -0.601, P <.0001), respectively. The univariate analysis confirmed that overexpression of β-catenin and cyclooxygenase 2 and decreased expression of E-cadherin were significantly correlated with disease-free survival (P <.01, P <.05, respectively). Overexpression of β-catenin and cyclooxygenase 2 and reduced expression of E-cadherin significantly correlated with a poor prognosis (P =.005, P =.044, P =.019, respectively) by Kaplan-Meier survival curves and the log-rank test. Multivariate analysis indicated that high expression of β-catenin and decreased expression of E-cadherin were independent prognostic factors (P =.002, P =.011, respectively) regardless of TNM stage and lymph node status. In conclusion, the aberrant high expression of β-catenin and decreased expression of E-cadherin is associated with poor prognosis in nasopharyngeal carcinoma. © 2013 Elsevier Inc.

Sun C.-Y.,Changzhi Medical College | Che Y.-J.,Changzhi Medical College | Lu S.-J.,Central South University
Biotechnology Letters | Year: 2014

The healing of contaminated/infected bone defects is a significant clinical challenge. Here, a novel collagen scaffold composite encapsulating silver nanoparticles (AgNP) and bone morphogenetic protein 2 (BMP-2) was prepared to enhance the healing of infected bone defects. Collagen scaffolds conjugated with AgNP possessed strong antibacterial properties that were dependent on the release rate of Ag+. After introducing BMP-2, the BMP-2/AgNP/collagen scaffold composites did not adversely affect the adherence or proliferation of bone marrow-derived mesenchymal stromal cells (BMSCs). Differentiation of BMSCs toward osteoblasts was induced by the upregulation of RUNX2, osteopontin and osteonectin expression. BMP-2/AgNP/collagen scaffold composites, therefore, possess the antibacterial activity of AgNP and the osteoinductivity of BMP-2, making these composites an ideal pharmaceutical for the regeneration of bone in infected wounds. © 2014, Springer Science+Business Media Dordrecht.

The previous published data on the association between the 8-oxo-guanine glycosylase-1 (OGG1) and apurinic/apyrimidinic-endonuclease-1 (APEX1/APE1) polymorphisms and lung cancer risk remained controversial. Several polymorphisms in the OGG1 and APEX1 gene have been described, including the commonly occurring Ser326Cys in OGG1 and Asp148Glu in APEX1. This meta-analysis of literatures was performed to derive a more precise estimation of the relationship. A total of 37 studies were identified to the meta-analysis, including 9,203 cases and 10,994 controls for OGG1 Ser326Cys (from 25 studies) and 3,491 cases and 4,708 controls for APEX1 Asp148Glu (from 12 studies). When all the eligible studies were pooled into the meta-analysis of OGG1 Ser326Cys polymorphism, significantly increased lung cancer risk was observed in recessive model (OR = 1.17, 95 % CI = 1.03-1.33) and in additive model (OR = 1.21, 95 % CI = 1.03-1.42). In the stratified analysis, significantly increased risk of lung cancer was also observed on the population-based studies (recessive model: OR = 1.26, 95 % CI = 1.08-1.46, additive model: OR = 1.42, 95 % CI = 1.06-1.73) and non-smokers (dominant model: OR = 1.20, 95 % CI = 1.02-1.42, recessive model: OR = 1.20, 95 % CI = 1.02-1.40, additive model: OR = 1.35, 95 % CI = 1.08-1.68). Additionally, when one study was deleted in the sensitive analysis, the results of OGG1 Ser326Cys were changed in Asians (recessive model: OR = 1.16, 95 % CI = 1.06-1.27, additive model: OR = 1.23, 95 % CI = 1.09-1.38). When all the eligible studies were pooled into the meta-analysis of APEX1 Asp148Glu polymorphism, there was no evidence of significant association between lung cancer risk and APEX1 Asp148Glu polymorphism in any genetic model. In the stratified analysis, significantly decreased lung adenocarcinoma risk was observed in recessive model (OR = 0.68, 95 % CI = 0.48-0.97, P (h) = 0.475, I(2) = 0.0 %). Additionally, when one study was deleted in the sensitive analysis, the results of APEX1 Asp148Glu were changed in Asians (recessive model: OR = 1.21, 95 % CI = 1.03-1.43) and smokers (dominant model: OR = 1.62, 95 % CI = 1.08-2.44, additive model: OR = 1.37, 95 % CI = 1.02-1.84). In summary, this meta-analysis indicates that OGG1 Ser326Cys show an increased lung cancer risk in Asians and non-smokers, APEX1 Asp148Glu polymorphism may be associated with decreased lung adenocarcinoma risk, and APEX1 Asp148Glu polymorphism show an increased lung cancer risk in Asians and smokers. However, a study with the larger sample size is needed to further evaluated gene-environment interaction on OGG1 Ser326Cys and APEX1 Asp148Glu polymorphisms and lung cancer risk.

Radak Z.,Semmelweis University | Zhao Z.,Semmelweis University | Zhao Z.,Changzhi Medical College | Goto S.,Semmelweis University | And 2 more authors.
Molecular Aspects of Medicine | Year: 2011

Lipids, proteins and DNA in the central nervous system have a high sensitivity to oxidative stress. Reactive oxygen species (ROS)-induced damage increases with aging, especially in the last quarter of the life span. The so called base level of oxidative modification of lipids could be important to cell signaling, and membrane remodeling, but the ROS-mediated post translation modifications of proteins could be important to the homeostasis of protein turnover. Low levels of 8-oxo-7,8-dihydroguanine (8-oxoG) might be necessary for transcription. A high level of accumulation of lipid peroxidation, oxidative protein damage or 8-oxoG, on the other hand, accelerates the progress of aging and neurodegenerative diseases. Therefore, agents that induce the activity of repair enzymes, such as Ca(2 +)-independent phospholipase A(2) (iPLA(2)beta), methionine sulfoxide reductase, and 8-oxoguanine DNA glycosylase, or the activity of enzymes that could prevent the accumulation of oxidized, toxic proteins, such as proteasome, Lon protease, neprilysin or insulin degrading enzyme, may act as potential therapeutic tools to slow the aging process and the progress of neurodegenerative diseases. © 2011 Elsevier Ltd. All rights reserved.

Radak Z.,Semmelweis University | Zhao Z.,Semmelweis University | Zhao Z.,Changzhi Medical College | Koltai E.,Semmelweis University | And 2 more authors.
Antioxidants and Redox Signaling | Year: 2013

The complexity of human DNA has been affected by aerobic metabolism, including endurance exercise and oxygen toxicity. Aerobic endurance exercise could play an important role in the evolution of Homo sapiens, and oxygen was not important just for survival, but it was crucial to redox-mediated adaptation. The metabolic challenge during physical exercise results in an elevated generation of reactive oxygen species (ROS) that are important modulators of muscle contraction, antioxidant protection, and oxidative damage repair, which at moderate levels generate physiological responses. Several factors of mitochondrial biogenesis, such as peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), mitogen-activated protein kinase, and SIRT1, are modulated by exercise-associated changes in the redox milieu. PGC-1α activation could result in decreased oxidative challenge, either by upregulation of antioxidant enzymes and/or by an increased number of mitochondria that allows lower levels of respiratory activity for the same degree of ATP generation. Endogenous thiol antioxidants glutathione and thioredoxin are modulated with high oxygen consumption and ROS generation during physical exercise, controlling cellular function through redox-sensitive signaling and protein-protein interactions. Endurance exercise-related angiogenesis, up to a significant degree, is regulated by ROS-mediated activation of hypoxia-inducible factor 1α. Moreover, the exercise-associated ROS production could be important to DNA methylation and post-translation modifications of histone residues, which create heritable adaptive conditions based on epigenetic features of chromosomes. Accumulating data indicate that exercise with moderate intensity has systemic and complex health-promoting effects, which undoubtedly involve regulation of redox homeostasis and signaling. Antioxid. Redox Signal. 18, 1208-1246. © 2013, Mary Ann Liebert, Inc.

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