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Wan M.-J.,China Three Gorges University | Huo M.,Yichang Central Peoples Hospital
International Journal of Ophthalmology | Year: 2010

• AIM: To observe the clinical effect and feasibility of biological amniotic membrane transplantation combined with remedial contact lens in corneal ulcer. • METHODS: Thirty-five eyes of 33 patients with corneal ulcer were cut the ulcer lesions firstly, then the biological amniotic membrane was applied to the ulcer area. The amniotic membrane was interruptedly sutured to the healthy cornea. On the second day of post-operation the patients wore remedial contact lens, and therapeutic eyedrops were used. • RESULTS: The anterior chamber of all the patients recovered in 1-2 days, and the local irritation improved obviously. The mean healing time was 30-45 days. 5 cases occurred corneal neovascularization and cicatrization. The anterior chamber in 2 patients disappeared repeatedly and penetrated corneal transplantation was performed finally. The visual acuity of all patients improved after treatment. • CONCLUSION: Biological amniotic membrane transplantation combined with remedial contact lens are effective for corneal ulcer, and creat favourable local condition for later corneal transplantation. Source

Wen C.,China Three Gorges University | Tao G.,General Surgery of Huaian No. 1 Peoples Hospital | Xu X.,Yichang Central Peoples Hospital | Feng X.,Yichang Central Peoples Hospital | Luo R.,Guangzhou University
Spectrochimica Acta - Part A: Molecular and Biomolecular Spectroscopy | Year: 2011

In this paper, we report the synthesis, crystal structure, photophysical properties, and electronic nature of a phosphorescent Cu(I) complex of [Cu(Phen-Np)(POP)]BF 4, where Phen-Np and POP stand for 2-(naphthalen-1-yl)-1H-imidazo[4,5-f][1,10]phenanthroline and bis(2-(diphenylphosphanyl)phenyl) ether, respectively. [Cu(Phen-Np)(POP)]BF 4 renders a yellow phosphorescence peaking at 545 nm, with a long excited state lifetime of 4.69 μs. Density functional calculation reveals that the emission comes from a triplet metal-to-ligand-charge-transfer excited state. We electrospun composite nanofibers of [Cu(Phen-Np)(POP)]BF 4 and polystyrene (PS), hoping to explore the possibility of using the composite nanofibers as an oxygen sensing material. The finally obtained samples with average diameter of ∼300 nm exhibit a maximum sensitivity of 7.2 towards molecular oxygen with short response time of 7 s due to the large surface-area-to-volume ratio of nanofibrous membranes. No photobleaching is detected in these samples. © 2011 Elsevier B.V. All rights reserved. Source

Yang J.,China Three Gorges University | Chen L.,Yichang Central Peoples Hospital | Ding J.,China Three Gorges University | Rong H.,Shenzhen Mental Health Center | And 2 more authors.
Molecular Biology Reports | Year: 2012

High mobility group box-1 (HMGB1), a potent mediator of inflammation, is known to regulate cellular events through binding to the multiple cell-surface receptors, including RAGE and TLRs. However, the role of TLR4 and details of HMGB1 signaling in vascular smooth muscle cells (VSMCs) migration has not been reported so far. The present study was designed to investigate the hypothesis that HMGB1-induced VSMCs migration is mediated via activation of phosphoinositide 3-kinase/Akt (PI3K/Akt) signalling pathway through TLR4. VSMCs from rat thoracic aorta were studied. HMGB1 (0.1-1000 ng/ml) stimulated VSMCs migration in a dose-dependent manner, with the highest value (about 3.5-fold increase). Incubation of VSMCs with 100 ng/ml caused a rapid increase in PI3K activity and Akt phosphorylation. Migration of VSMCs toward HMGB1 was significantly inhibited by silencing of TLR4 (P\0.05). We also found pretreated cells with TLR4 siRNA or the PI3 K inhibitor LY294002 could markedly block PI3K/Akt pathway activation and VSMCs migration mediated by HMGB1 (P both\0.05). In conclusion, HMGB1 induces migration of VSMCs through a TLR4-dependent PI3 K/Akt signaling pathway, which suggests a possible molecular mechanism for HMGB1 may contribute to neointima formation in restenosis after vascular damage.© Springer Science+Business Media B.V. 2011. Source

Yang J.,China Three Gorges University | Jin L.-Y.,China Three Gorges University | Ding J.-W.,Yichang Central Peoples Hospital | Zhou Y.-Q.,China Three Gorges University | And 2 more authors.
Archives of Medical Research | Year: 2010

Background and Aims: TLR4 has been shown to mediate inflammation in animal models of myocardial ischemia/reperfusion injury (MI/RI). Here we hypothesized that TLR4 on peripheral blood mononuclear cells (PBMCs) may be involved in the inflammatory response in this type of clinical event. Methods: Seventy two patients with acute myocardial infarction (AMI) who underwent thrombolysis were assigned into reperfusion group (n = 43) and non-reperfusion group (n = 29) according to recanalization of infarct-related artery (IRA) and 40 healthy volunteers were enrolled in this experiment. Eight mL of venous blood was taken from all patients 0 h before and 2, 6, 12, and 24 h after thrombolysis. Flow cytometry (FCM) was used to detect TLR4 protein expression and real-time quantitative RT-PCR was performed to determine TLR4 mRNA and myeloid differentiation protein-88 (Myd88) mRNA expression. The concentration of tumor necrosis factor-α (TNF-α) in plasma was evaluated using enzyme-linked immunosorbent assay (ELISA). Results: Compared with controls, all detected indicators in AMI patients were upregulated before thrombolysis (p <0.01). After thrombolysis, they were further increased. In reperfusion group, all attained their peaks in earlier hours and the peak values were lower compared with non-reperfusion group. In both cases, either reperfusion or non-perfusion, TLR4 mRNA expression was positively correlated with the levels of Myd88 mRNA (r = 0.886 and 0.694, p <0.01), respectively. Conclusions: TLR4 expression on PBMCs was markedly elevated in AMI patients either reperfused or non-reperfused. Inflammatory reaction by activated TLR4 in MI/RI in patients may be through TLR4-Myd88-dependent signal pathway. © 2010 IMSS. Source

Yang J.,China Three Gorges University | Zhang X.-D.,China Three Gorges University | Ding J.-W.,Yichang Central Peoples Hospital | Liu Z.-Q.,China Three Gorges University | And 2 more authors.
Molecular Biology Reports | Year: 2011

To determine whether the cardioprotection effect of fluvastatin mediates by toll-like receptor 4 (TLR4) signaling pathway, fifty Sprague-Dawley rats were randomly divided into five groups: sham operation group, ischemia/reperfusion (I/R) group, fluvastatin groups (highdosage, medium-dosage, low-dosage, n = 10 in each group). Except sham operation group, the rest four groups of rats were artificially afflicted with coronary occlusion for 30 min, then reperfusion 2 h. Light microscope and transmission electronic microscope were used to observe structural changes of myocardium. RT-PCR was used to measure TLR4 mRNA expression level, TLR4 protein expression was detected by immunohistochemistry. Western blot was used to measure myocardial NF-κB protein level; ELISA was used to measure the level of TNF-α in myocardium. The results demonstrated that fluvastatin treatment markedly decreased ischemic injury caused by ischemia/reperfusion, and inhibited the expression levels of TLR4, TNF-α and NF-κB, all of which up-regulated by ischemia/reperfusion. Taken together, our results suggest that proper dosage of fluvastatin may have protective effect on the ischemic injury mediated by ischemia/reperfusion in the hearts, which might be associated with inhibition of TLR4 signaling pathway and inflammatory response during ischemia/reperfusion. Source

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