474 Hospital of PLA
474 Hospital of PLA
Li Z.,PLA Fourth Military Medical University |
Liu Y.,PLA Fourth Military Medical University |
Dong H.,474 Hospital of PLA |
Li M.,PLA Fourth Military Medical University |
And 4 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2017
Objective: The genetic mutation of FGFR2S252W in Apert syndrome leads to the incidence of pre-differentiation of osteoblasts. Methods: FGFR2S252W as a gain of function mutation was found in some endothelial cell-derived cancerous tissues. We found over-expression of FGFR2IIIcS252W in osteosarcoma U2OS cells could induce the cell apoptosis. Therefore, we explored the mechanism underlying whether FGFR2IIIcS252W could inhibit the proliferation of U2OS cells. Results: Compared with vector controls, FGFR2IIIcS252W and FGFR2IIIcWT groups, FGFR2IIIcS252W not only deformed cellular morphology, but also activated the ERK1/2 and JNK signaling pathways. In spite of the growth inhibition probably associated with caspase signaling pathway, we found Egr-1, a transcription factor, was significantly up-regulated accompanied with FGFR2IIIcS252W over-expression. The promoter activation assay revealed that FGFR2IIIcS252W increased Egr-1 promoter activity in a dose-dependent manner. Subsequent results demonstrated that transient over-expression of Egr-1 in U2OS cells could also induce cell apoptosis. Conclusion: Taken together, our results suggested that FGFR2IIIcS252W could inhibit U2OS cell proliferation with the activated ERK and JNK signaling pathways accompanied with up-regulated expression levels of Egr-1, which plays a pivotal role in the growth inhibition by FGFR2IIIcS252W overexpression in osteosarcoma U2OS cells.
Bao D.,General Hospital of Shenyang Military Command |
Xu K.,General Hospital of Shenyang Military Command |
Qiu J.,General Hospital of Guangzhou Military Command |
Ding S.-F.,General Hospital of Guangzhou Military Command |
And 15 more authors.
Medical Journal of Chinese People's Liberation Army | Year: 2016
Objective To investigate the effect of gender on in-hospital mortality in patients with acute ST-elevated myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). Methods To retrospectively analyze the data collected from the Management System of Cardiovascular Interventional Treatment in Military Hospitals. A total of 8878 consecutive patients with acute STEMI undergoing PPCI were enrolled, including 7137 males and 1741 females. Data were grouped by gender to evaluate the impact of gender difference on the in-hospital mortality, and the impact was further evaluated by a propensity score analysis to adjust the differences of patients' ages in baseline characteristics between females and males. Results Compared with that in male patients, female patients were older (P<0.05), more likely to have hypertension, diabetes, cerebrovascular disease and cardiac dysfunction (P<0.05), but less likely to have history of PCI (P<0.05). The proportions of suffering from triple vessel disease and postoperative hemorrhage were higher in females than in males (P<0.05). Both symptomonset-to-balloon time and door-to-balloon time were longer in female patients than in male patients (P<0.05). Female patients also presented higher in-hospital mortality (4.4% vs 2.4%, P<0.001). The impact of gender on in-hospital mortality disappeared by a propensity score matching adjusting the differences in baseline characteristics between females and males (Female vs Male: 4.4% vs 4.0%, P=0.610). Multi-logistic regression showed that female was not an independent predictor for in-hospital mortality, while age, cardiac dysfunction, slow blood flow and postoperative hemorrhage were the independent predictors for in-hospital mortality. Conclusion Female itself is not an independent predictor for in-hospital mortality in patients with acute STEMI undergoing PPCI. © 2016, People’s Military Medical Press. All rights reserved.
Lv B.,474 Hospital of PLA |
Wang R.,474 Hospital of PLA |
Gao X.,474 Hospital of PLA |
Dong X.,474 Hospital of PLA |
Ji X.,474 Hospital of PLA
International Journal of Clinical and Experimental Pathology | Year: 2014
Aim: To investigate the effect of vascular endothelial growth factor (VEGF) on the expression of pigment epithelium-derived factor (PEDF) in retina and the protective effect of VEGF on retinal ganglion cells (RGCs) of rats with chronic elevated intraocular pressure (EIOP) and it's potential mechanism. Methods: 30 females Sprague-Dawley rats were randomly divided into three groups: EIOP + VEGF group (A), EIOP + vehicle group (B) and sham operated + VEGF group (C). The EIOP was introduced by obstructing episcleral veins in Group A and Group B. In the Group C, only the bulber conjunctiva was opened without obstructing episcleral veins. Immediately after surgery, rats in the Group A and Group C were intravitreously injected with 2 μL of VEGF. In the Group B, rats were intravitreously treated with 2 μL of normal saline. At 3 and 14 days after injection, animals were sacrificed and the eyes were collected for preparation of frozen sections. Results: After surgery, the IOP increased significantly in the Group A and Group B. There was no significant difference in the IOP at day 3 and day 14 after operation. The PEDF expression in the Group A and Group B was higher than that in the Group C. TUNEL staining showed the apoptotic RGCs markedly reduced after VEGF treatment when compared with rats without treatment. Conclusion: Intravitreal treatment with VEGF may reduce the apoptosis of RGCs in rats with chronic intraocular hypertension.