CRAI Biblioteca del Campus de Mundet. Memòria d'activitats 2016

Memòria que recull les activitats realitzades al CRAI Biblioteca del Campus de Mundet durant l'any 2016

Postoperative complications comparing Ex-PRESS to trabeculectomy.

<p>M-H = Mantel-Haenszel; CI = confidence interval; Ex-PRESS = Ex-PRESS implantation.</p

Postoperative interventions comparing Ex-PRESS to trabeculectomy.

<p>M-H = Mantel-Haenszel; CI = confidence interval; Ex-PRESS = Ex-PRESS implantation.</p

Characteristics and quality scores of included studies.

*<p>Ex-PRESS implantation group/Trabeculectomy group;</p>**<p>Without mean age records; RCCT = randomized controlled clinical trial.</p

Flow diagram of studies included in this meta-analysis. RCCT = randomized controlled clinical trial.

<p>Flow diagram of studies included in this meta-analysis. RCCT = randomized controlled clinical trial.</p

Complete success at one year after surgery comparing Ex-PRESS to trabeculectomy.

<p>M-H = Mantel-Haenszel; CI = confidence interval; Ex-PRESS = Ex-PRESS implantation.</p

Data_Sheet_1_Hydrogen peroxide-induced oxidative damage and protective role of peroxiredoxin 6 protein via EGFR/ERK signaling pathway in RPE cells.PDF

IntroductionDamage to retinal pigment epithelium (RPE) cells caused by oxidative stress is closely related to the pathogenesis of several blinding retinal diseases, such as age-related macular degeneration (AMD), retinitis pigmentosa, and other inherited retinal degenerative conditions. However, the mechanisms of this process are poorly understood. Hence, the goal of this study was to investigate hydrogen peroxide (H2O2)-induced oxidative damage and protective role of peroxiredoxin 6 (PRDX6) protein via EGFR/ERK signaling pathway in RPE cells.MethodsCells from a human RPE cell line (ARPE-19 cells) were treated with H2O2, and then cell viability was assessed using the methyl thiazolyl tetrazolium assay. Cell death and reactive oxygen species (ROS) were detected by flow cytometry. The levels of PRDX6, epidermal growth factor receptor (EGFR), P38 mitogen-activated protein kinase (P38MAPK), c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) were detected by Western blot assay. PRDX6 and EGFR were also detected via immunofluorescence staining.ResultsOur results show that H2O2 inhibited cell viability, induced cell death, and increased ROS levels in ARPE-19 cells. It was also found that H2O2 decreased the levels of PRDX6, EGFR, and phosphorylated ERK but increased the levels of phosphorylated P38MAPK and JNK. PRDX6 overexpression was found to attenuate H2O2-induced inhibition of cell viability and increased cell death and ROS production in ARPE-19 cells. PRDX6 overexpression also increased the expression of EGFR and alleviated the H2O2-induced decrease in EGFR and phosphorylated ERK. Moreover, inhibition of epidermal growth factor-induced EGFR and ERK signaling in oxidative stress was partially blocked by PRDX6 overexpression.DiscussionOur findings indicate that PRDX6 overexpression protects RPE cells from oxidative stress damage caused by decreasing ROS production and partially blocking the inhibition of the EGFR/ERK signaling pathway induced by oxidative stress. Therefore, PRDX6 shows promise as a therapeutic target for the prevention of RPE cell damage caused by oxidative stress associated with retinal diseases.</p

Subfoveal Choroidal Thickness in Central Serous Chorioretinopathy: A Meta-Analysis

<div><p>Purpose</p><p>To evaluate the relationship between subfoveal choroidal thickness (SFCT) and eyes with central serous chorioretinopathy (CSC) versus fellow or control eyes.</p><p>Methods</p><p>We performed a meta-analysis using databases including PubMed, Embase and ISI Web of Science to find relevant studies. Weighted mean difference (WMD) was calculated for the SFCT in CSC eyes, the unaffected fellow eyes and normal controls.</p><p>Results</p><p>Twelve studies were selected for this meta-analysis, including 1108 eyes (397 CSC eyes, 228 unaffected fellow eyes and 483 eyes of normal controls). The meta-analysis clearly demonstrated that the subfoveal choiroid of eyes with a clinical presentation of CSC was thickened compared to unaffected fellow eyes (WMD = 52.81, 95% confidence interval (CI), 39.13–66.49, P<0.00001) and was thickened compared to control eyes (WMD = 145.03, 95%CI, 121.33–168.73, P<0.00001). The mean SFCT measurement of the unaffected fellow eyes showed also significantly increased choroidal thickness compared to that of normal control eyes (WMD = 77.20, 95% CI, 44.98–109.42, P<0.00001). Similar results were obtained in a sub-analysis based on the same instrument.</p><p>Conclusion</p><p>It is demonstrated that SFCT is significantly increased in eyes with clinical manifestation of CSC, and in the clinically non-manifested fellow eyes. These results support the hypothesis that CSC is a bilateral disorder with an initial unilateral clinical presentation.</p></div

Mean values and standard deviations of subfoveal choroidal thickness in all studies included in the current meta-analysis.

<p>Mean values and standard deviations of subfoveal choroidal thickness in all studies included in the current meta-analysis.</p

Data_Sheet_3_Hydrogen peroxide-induced oxidative damage and protective role of peroxiredoxin 6 protein via EGFR/ERK signaling pathway in RPE cells.PDF

IntroductionDamage to retinal pigment epithelium (RPE) cells caused by oxidative stress is closely related to the pathogenesis of several blinding retinal diseases, such as age-related macular degeneration (AMD), retinitis pigmentosa, and other inherited retinal degenerative conditions. However, the mechanisms of this process are poorly understood. Hence, the goal of this study was to investigate hydrogen peroxide (H2O2)-induced oxidative damage and protective role of peroxiredoxin 6 (PRDX6) protein via EGFR/ERK signaling pathway in RPE cells.MethodsCells from a human RPE cell line (ARPE-19 cells) were treated with H2O2, and then cell viability was assessed using the methyl thiazolyl tetrazolium assay. Cell death and reactive oxygen species (ROS) were detected by flow cytometry. The levels of PRDX6, epidermal growth factor receptor (EGFR), P38 mitogen-activated protein kinase (P38MAPK), c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) were detected by Western blot assay. PRDX6 and EGFR were also detected via immunofluorescence staining.ResultsOur results show that H2O2 inhibited cell viability, induced cell death, and increased ROS levels in ARPE-19 cells. It was also found that H2O2 decreased the levels of PRDX6, EGFR, and phosphorylated ERK but increased the levels of phosphorylated P38MAPK and JNK. PRDX6 overexpression was found to attenuate H2O2-induced inhibition of cell viability and increased cell death and ROS production in ARPE-19 cells. PRDX6 overexpression also increased the expression of EGFR and alleviated the H2O2-induced decrease in EGFR and phosphorylated ERK. Moreover, inhibition of epidermal growth factor-induced EGFR and ERK signaling in oxidative stress was partially blocked by PRDX6 overexpression.DiscussionOur findings indicate that PRDX6 overexpression protects RPE cells from oxidative stress damage caused by decreasing ROS production and partially blocking the inhibition of the EGFR/ERK signaling pathway induced by oxidative stress. Therefore, PRDX6 shows promise as a therapeutic target for the prevention of RPE cell damage caused by oxidative stress associated with retinal diseases.</p