Wang J.,Nanjing Medical University |
Tang B.,Vazyme Biotechnology Company |
Liu X.,Nanjing Medical University |
Wu X.,Bendical Center |
And 3 more authors.
Atherosclerosis | Year: 2015
Background: Monomeric CRP (mCRP) plays an important role in the process of atherosclerotic plaque rupture. Recently, it has been reported that mCRP was associated with acute myocardial infarction (AMI). Objectives: The aim of this study was to examine whether mCRP is increased in AMI patients and to investigate the possibility of using circulating mCRP as a biomarker for AMI diagnosis and severity assessment of disease. Methods: A mCRP monoclonal antibody was generated and verified for its specificity. Immunofluorescence was used to assess the localization of mCRP in the infarcted myocardium. Furthermore, 101 AMI, 38 unstable angina pectoris (UAP) and 41 stable angina pectoris (SAP) patients were enrolled, and 43 healthy volunteer were recruited as controls in the study. Venous blood samples were collected to measure the circulating mCRP, cardiac Troponin T and hs-CRP levels. Results: Significantly increased mCRP levels were observed in the infarcted myocardium of model mice. In addition, significantly increased plasma mCRP levels were also detected in AMI patients (20.96±1.64ng/ml) compared to those with UAP, SAP or in control patients (all 0ng/ml, p<0.001). ROC analysis revealed that circulating mCRP had considerable diagnostic accuracy for AMI with an AUC of 0.928 (95% confidence interval 0.887-0.969). Furthermore, nine patients (9/101, 8.91%) in AMI group died before the 30-day follow-up, and their plasma mCRP concentration was significantly higher than those in surviving patients (36.70±10.26 vs. 19.41±1.43ng/ml, P=0.002). Conclusions: These results indicate that mCRP is increased in AMI and that circulating mCRP might be a potential biomarker for diagnosis and severity assessment of disease in AMI. © 2015. Source
Chung W.-M.,China Medical University at Taichung |
Chang W.-C.,China Medical University at Taichung |
Chen L.,China Medical University at Taichung |
Chen L.,Bendical Center |
And 4 more authors.
Stem Cell Research and Therapy | Year: 2013
Introduction. Resistance of cancer stem/progenitor cells (CSPCs) to chemotherapy can lead to cancer relapse. Ovarian teratocarcinoma (OVTC) arises from germ cells and comprises pluripotent cells that can be used to study cancer cell stemness. In this study, we evaluated whether microRNA-21 (miR-21) promotes ovarian teratocarcinoma by maintaining cancer stem/progenitor populations. Methods. The lentiviral delivery system was used to upregulate or to suppress the expression of miR-21 in the human ovarian teratocarcinoma cell line PA1 and cell growth assays were used to monitor the expression of miR-21 at different time points. Antibodies directed toward CD133, a stem cell marker, were used to identify CSPCs in the PA1 cell population, and the level of miR-21 expression was determined in enriched CSPCs. Stem cell functional assays (sphere assay and assays for CD133 expression) were used to assess the effects of miR-21 on progression of the CD133+ population. Results: Knockdown of miR-21 in PA1 cells attenuated growth of PA1 cells whereas overexpression of miR-21 promoted cell growth. Moreover, knockdown of miR-21 resulted in a marked reduction in the CD133+ population and sphere formation of CSPCs. In contrast, overexpression of miR-21 resulted in a marked increase in the population of CD133+ cells as well as sphere formation of CSPCs. Conclusions: MicroRNA-21 plays a significant role in cancer growth by regulating stemness in cancer cells. © 2013 Chung et al.; licensee BioMed Central Ltd. Source
Prognostic implications of epidermal growth factor receptor and KRAS gene mutations and epidermal growth factor receptor gene copy numbers in patients with surgically resectable non-small cell lung cancer in Taiwan
Liu H.-P.,Chang Gung University |
Liu H.-P.,Bendical Center |
Isaac Wu H.-D.,National Chung Hsing University |
Chang J.W.-C.,Chang Gung University |
And 7 more authors.
Journal of Thoracic Oncology | Year: 2010
Introdution: The prognostic role of epidermal growth factor receptor (EGFR) mutations in patients with surgically resectable non-small cell lung cancer (NSCLC) without EGFR tyrosine kinase inhibitor treatment has not been well established, because the reports are still few. MATERIALS AND Methods:We analyzed the survival data of 164 patients with surgically resectable (stages I to IIIA) NSCLC of two year groups (1996-1998 and 2002-2004), and compared with EGFR mutations, KRAS mutations, and EGFR gene copy numbers. Results: Comparing the survival of wild-type patients and patients having L858R mutations or exon 19 deletion, the median survival was much longer for patient with EGFR mutations (54.7 months) than wild type (34.9 months). The difference was not statistically significant by univariate analysis (p = 0.1981) but had borderline significance by multivariate analyses (p = 0.0506). In addition, the 3-year survival rates of patients with EGFR mutations were also significantly higher than wild type (p = 0.0232). After exclusion of 18 patients treated by EGFR-tyrosine kinase inhibitor for tumor recurrence, the trends were still the same. Patients with KRAS mutations had shorter median survival (21 months) than wild type (44.4 months). Patients with EGFR polysomy (≥copies) also had longer median survival (56.2 months) than wild type (53.4 months). But the survival differences of these two genetic markers were all not significant statistically. Conclusion: It is intriguing that patients with NSCLC with EGFR mutations had better survival than wild type. Such a tumor biology may confound the survival data in a study without the stratification by EGFR mutation. © 2010 by the International Association for the Study of Lung Cancer. Source
Wang M.,Nanjing University |
Liu Z.,Southern Medical University |
Liu C.,Southern Medical University |
Wu T.,Nanjing University |
And 4 more authors.
BMC Infectious Diseases | Year: 2016
Background: Invasive aspergillosis is a life-threatening disease, and its incidence has increased in the recent past. Dectin-1 recognizes β-glucans and mediates innate immune responses to Aspergillus fumigatus. Transcription factor PU.1 has been the focus of recent research due to its role in inflammation and infection. However, its role in Dectin-1 regulation during A. fumigatus infection remains to be elucidated. Methods: THP-1 cells were stimulated with A. fumigatus conidia. We then used real-time RT-PCR, Western blot, and immunofluorescence assays to analyze the mRNA and protein levels and cellular distribution, respectively, of Dectin-1 and PU.1 in stimulated THP-1 cells. Additionally, we used the luciferase reporter assays, chromatin immunoprecipitation (ChIP) assays, electrophoretic mobility shift assays (EMSA), and RNA interference experiments to investigate the role of PU.1 in Dectin-1 regulation. Results: Our results revealed that Dectin-1 mRNA and protein levels as well as the PU.1 protein level were increased in THP-1 cells stimulated with A. fumigatus conidia, while the mRNA expression level did not significantly change between the stimulated and control groups. We also observed that PU.1 translocated into the nucleus in stimulated THP-1 cells. The results of the luciferase reporter assay showed that PU.1 promoted human Dectin-1 (hDectin-1) gene activity. ChIP and EMSA indicated that PU.1 could bind with hDectin-1 gene promoter at three potential transcription factor-binding sites (TFBSs). In addition, knockdown of PU.1 significantly decreased Dectin-1 expression. Conclusions: This study demonstrated the novel role of PU.1 in the immune response to A. fumigatus through upregulation of Dectin-1 expression and its translocation to the nucleus in A. fumigatus-stimulated THP-1 cells. © 2016 The Author(s). Source
Du X.,Nanjing Medical University |
Zhang R.,Nanjing Medical University |
Xue Y.,Nanjing Medical University |
Li D.,Bendical Center |
And 5 more authors.
International Journal of Biological Markers | Year: 2012
Aims: Recently, more and more attention has been drawn on the long-term effects of insulin glargine. Here we strived to estimate the association of cancer occurrence with the use of insulin glargine. Methods: We searched all the publications regarding the association between cancer occurrence and the use of insulin glargine using the US National Library of Medicine's PubMed database. Data were independently extracted and analyzed using random or fixed effects meta-analysis depending upon the degree of heterogeneity. Results: Seven cohort studies were included in the meta-analysis. Cancer occurrence had no significant difference in glargine-treated patients compared to patients treated with other insulins (RR=0.86, 95% CI=0.69-1.07, p=0.17, Pheterogeneity< 0.00001). In our subgroup analysis, glargine, compared to other insulins, did not increase the risk of breast cancer (RR=1.14, 95% CI=0.65-2.02, p=0.65, Pheterogeneity=0.002), prostate cancer (RR=1.00, 95% CI=0.79-1.26, p=0.99, Pheterogeneity= 0.78), pancreatic cancer (RR=0.57, 95% CI=0.14-2.35, p=0.44, Pheterogeneity=0.0002) and gastrointestinal cancer (RR=0.80, 95% CI=0.62-1.02, p=0.07, Pheterogeneity=0.86). Conclusions: This meta-analysis of open-label studies does not support an increased cancer risk in patients treated with insulin glargine. The result provides confidence for the development of insulin glargine, but needs confirmation by further clinical studies. © 2012 Wichtig Editore. Source