Nong L.M.,Nanjing Medical University |
Ren K.W.,Southeast University Medical School |
Mi Y.Y.,Nantong University |
Xu N.W.,Nanjing Medical University |
Zhou D.,Nanjing Medical University
Scandinavian Journal of Rheumatology | Year: 2013
Objectives: Published studies have shown conflicting results concerning the association between the -169T/C promoter polymorphism in the Fc receptor-like 3 (FCRL3) gene and rheumatoid arthritis (RA). In this study we conducted an up-to-date meta-analysis to examine the relationship. Method: We searched the PubMed database for all papers published up to 20 April 2012. Overall, 18 case-control studies with 12 620 cases and 12 613 controls were retrieved based on the search criteria for RA susceptibility related to the FCRL3 -169T/C polymorphism. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of this association. Publication bias was assessed using the Egger test. Results: We found that the FCRL3 -169T/C polymorphism increased the risk for RA overall in genetic models (allelic contrast: OR 1.09, 95% CI 1.03-1.14, p = 0.001; homozygote comparison: OR 1.20, 95% CI 1.08-1.34, p = 0.001; dominant genetic model: OR 1.03, 95% CI 1.01-1.05, p = 0.001). Stratified analysis by race also showed a significant positive association with Asians and Caucasians. Subgroup analysis of rheumatoid factor (RF) revealed a slightly positive relationship between the FCRL3 -169T/C polymorphism and RF-positive RA risk. No obvious evidence of publication bias was detected in the overall analysis. Conclusion: Our study indicates that the FCRL3 -169T/C polymorphism is significantly associated with increased RA risk. © 2013 Taylor & Francis on license from Scandinavian Rheumatology Research Foundation.
Liu D.-H.,Southeast University Medical School |
Liu D.-B.,Southeast University Medical School |
Zhang J.-Y.,Southeast University Medical School
Journal of Clinical Neurology (China) | Year: 2012
Objective: To investigate the changes of brain default-mode network (DMN) connectivity in patients with transient ischemic attack (TIA). Methods: Sixteen interictal TIA patients and 16 normal controls were underwent with functional MR scan. The regions of interest (ROI) were set on the cingulate/precuneus and ventral anterior cingulate/medial prefrontal, and the average time signal in which were extraction. The connectivity of brain regions connected with ROI was analyzed. Results: Compared with the normal control group, the functional connectivity in TIA group was reduced on left anterior cingulate gyrus and hippocampus, right anterior frontal gyrus, insular lobe, precuneus and inferior parietal lobule; and which enhanced on right cerebellum, thalamus and caudate nucleus. Conclusions The brain DMN is abnormal in TIA patients. The connectivity of part brain region reduced. The connectivity increased on thalamus and cerebellum may be the compensation of brain function or protective response.
Gao G.,Nanjing Medical University |
Shen N.,Southeast University Medical School |
Jiang X.,Southeast University Medical School |
Sun H.,Southeast University Medical School |
And 4 more authors.
Biochemical and Biophysical Research Communications | Year: 2016
The mitogenic effects of periodic mechanical stress on nucleus pulpous cells have been studied extensively but the mechanisms whereby nucleus pulpous cells sense and respond to mechanical stimulation remain a matter of debate. We explored this question by performing cell culture experiments in our self-developed periodic stress field and perfusion culture system. Under periodic mechanical stress, rat nucleus pulpous cell proliferation was significantly increased (p < 0.05 for each) and was associated with increases in the phosphorylation and activation of EGFR, Rac1, and ERK1/2 (p < 0.05 for each). Pretreatment with the ERK1/2 selective inhibitor PD98059 reduced periodic mechanical stress-induced nucleus pulpous cell proliferation (p < 0.05 for each), while the activation levels of EGFR and Rac1 were not inhibited. Proliferation and phosphorylation of ERK1/2 were inhibited after pretreatment with the Rac1 inhibitor NSC23766 in nucleus pulpous cells in response to periodic mechanical stress (p < 0.05 for each), while the phosphorylation site of EGFR was not affected. Inhibition of EGFR activity with AG1478 abrogated nucleus pulpous cell proliferation (p < 0.05 for each) and attenuated Rac1 and ERK1/2 activation in nucleus pulpous cells subjected to periodic mechanical stress (p < 0.05 for each). These findings suggest that periodic mechanical stress promotes nucleus pulpous cell proliferation in part through the EGFR-Rac1-ERK1/2 signaling pathway, which links these three important signaling molecules into a mitogenic cascade. © 2015 Elsevier Inc. All rights reserved.