No451 Hospital Of Pla

Fengcheng, China

No451 Hospital Of Pla

Fengcheng, China
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Du Z.-J.,PLA Fourth Military Medical University | Li P.,No451 Hospital Of Pla | Wang L.,Xian Medical University
International Journal of Ophthalmology | Year: 2017

Age-related macular degeneration (AMD) is the leading cause of vision loss in the elderly throughout the world. Treatment of AMD utilizing retinal pigment epithelium (RPE) transplantation represents a promising therapy. However, simplex RPE transplantation can only replace the diseased RPE cells, but has no abilities to stop the development of AMD. It has been indicated that oxidization triggers the development of AMD by inducing the dysfunction and degeneration of RPE cells, which results in the upregulation of local monocyte chemotactic protein-1 (MCP-1) expression. MCP-1 induces macrophage recruiment which triggers local inflammation. As a result, the expression of vascular endothelial growth factor (VEGF) is upregulated by MCP-1 mediated inflammation and results in the formation of choroidal neovascularization (CNV). We accordingly propose a targeted therapy of AMD by subretinal transplanting the compound of RPE cell, MCP-1 antibody, and VEGF antibody and using a magnetic system to guide RPE cell compounds conjugated with superparamagnetic iron oxide nanoparticles (SPIONs). Furthermore, SPION-labelled RPE cells can be tracked and detected in vivo by non-invasive magnetic resonance imaging (MRI). This novel RPE cell transplantation methodology seems very promising to provide a new therapeutic approach for the treatment of AMD. © 2017, International Journal of Ophthalmology (c/o Editorial Office). All rights reserved.

PubMed | No451 Hospital Of Pla, Xian Medical College, Chinese Medicine Research Institute and PLA Fourth Military Medical University
Type: Journal Article | Journal: Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie | Year: 2016

Age-related macular degeneration (AMD) is a major cause of progressive and degenerative visual impairment. Although the exact pathogenic mechanism of AMD is still unknown, clinical observations such as the high accumulation of oxidative products and macrophages in retina suggest the importance of oxidative stress and inflammation in AMD.Mouse photoreceptor-derived 661W cells and human ARPE-19 cells were treated with oxidized phospholipids (Ox-PC) or HOxidative damage by both HThe results indicated that oxidative damage increases intracellular Ox-PC and the secretion of MCP-1 in retina cells. The increased MCP-1 induced by oxidative damage attracts macrophages to retinas, and macrophages release pro-inflammatory factor and promote the process of AMD.

Li H.,No451 Hospital Of Pla | Zhong X.,No451 Hospital Of Pla | Li C.,No451 Hospital Of Pla | Peng L.,No451 Hospital Of Pla | And 3 more authors.
Archives of Biological Sciences | Year: 2014

Coronary artery disease (CAD) is the leading cause of death worldwide. Microarray analysis is a practical approach to study gene transcription changes that may reflect signatures that underlie the pathogenesis of CAD. Using gene expression profile data from the Gene Expression Omnibus database, we identified differentially expressed genes that can contribute to the pathology of CAD. Further pathway and network analyses were also implemented to identify pathways and hub genes related to the disease. We observed 466 downregulated and 560 upregulated genes. The ribosome pathway was the most significantly over-represented pathway with differentially expressed genes. Over 35% of the genes in this pathway were downregulated. Hub genes in the network, such as IL7R, FYN, CALM1 ESR1 and PLCG1, may play crucial roles in the pathogenesis of CAD. Our results facilitate the identification of molecular mechanisms that underlie CAD.

Tuo B.-X.,No451 Hospital Of Pla | Li H.,No451 Hospital Of Pla | Li C.-M.,No451 Hospital Of Pla | Yang Y.-Y.,No451 Hospital Of Pla
Chinese Journal of Evidence-Based Medicine | Year: 2014

Objective To systematically review the risk factors in elderly patients with primary hypertension with morning blood pressure surge in China, so asto provide references for clinical treatment and prevention of complications. Methods Such databases as PubMed, EMbase, The Cochrane Library (Issue 11, 2013), CNKI, VIP and WanFang Data were electronically searched for the case-control studies about morning blood pressure surge (MBPS) among elderly patients with primary hypertension in China from January 2006 to June 2014 were collected. Literature was screened according to inclusion and exclusion criteria, data were extracted and the methodological quality of the included studies was assessed, and then meta-analysis was conducted using RevMan 5.2 software. Results A total of 16 studies involving 2 007 cases were finally included, of which 956 cases were detected with MBPS. The results of meta-analysis showed that significant differences were found in glucose levels (MD=0.42, 95%CI 0.04 to 0.81, P=0.03), urinary microalbumin levels (MD=23.85, 95%CI 6.64 to 41.07, P=0.007), incidences of cerebrovascular events (OR=1.96, 95%CI 1.25 to 3.08, P=0.004), carotid atherosclerosis (OR=5.13, 95%CI 1.70 to 15.45, P=0.004) and left ventricular hypertrophy (OR=2.49, 95%CI 1.70 to 3.64, P<0.000 01), left ventricular mass (MD=12.89, 95%CI 3.94 to 21.84, P=0.005), and carotid artery intima-media thickness (MD=0.08, 95%CI 0.02 to 0.14, P=0.009); while no significant difference was found in gender (OR=1.12, 95%CI 0.84 to 1.49, P=0.44), total cholesterol levels (MD=0.01, 95%CI –0.11 to 0.12, P=0.92), and creatinine levels (MD=1.77, 95%CI –1.16 to 4.70, P=0.24) between patients with or without MBPS. Conclusion Current evidence shows that glucose levels, early kidney damage, emergent cerebrovascular events and the reconstruction of the artery and the left ventricle are risk factors of abnormal MBPS in China. However, the above conclusion needs to be verified by further conducting high quality prospective studies. © 2014 Editorial Board of Chin J Evid-based Med.

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