Macular ganglion cell layer thickness after macula-off rhegmatogenous retinal detachment repair: scleral buckling versus pars plana vitrectomy

(1) Background: We evaluated macular ganglion cell layer-inner plexiform layer (GCL-IPL) thickness in patients with primary macula-off rhegmatogenous retinal detachment (RRD) treated with scleral buckling (SB) or pars plana vitrectomy (PPV) using spectral domain optical coherence tomography (SD-OCT). (2) Methods: In this retrospective, observational study, we reviewed the medical records of patients undergoing SB or PPV surgery for macula-off RRD. SD-OCT was performed at three and 12 months after surgery. The central and parafoveal GCL-IPL thicknesses in treated eyes were compared with those of healthy fellow eyes. OCT measurements between the SB and PPV group were also compared using the analysis of covariance. (3) Results: Seventy-one eyes of 71 patients with a mean age of 61.2 ± 11.7 years were included. The parafoveal GCL-IPL thickness of the PPV group was significantly reduced, with respect to fellow eyes, at three and 12 months (p < 0.01). After adjusting for age, axial length, spherical equivalent, RD extent, preoperative intraretinal cysts, duration of symptoms and postoperative IOP, the parafoveal GCL-IPL thickness in the PPV group was significantly reduced with respect to the SB group, both at three and 12 months (F = 11.45, p = 0.001 and F = 12.37, p = 0.001, respectively). (4) Conclusions: In conclusion, the GCL-IPL is reduced in thickness in eyes with macula-off RRD treated with vitrectomy and is significantly thinner compared to eyes undergoing scleral buckling surgery

: RIP140 in colon cancer

International audienceDeregulation of the Wnt/APC/β-catenin signaling pathway is an important consequence of tumor suppressor APC dysfunction. Genetic and molecular data have established that disruption of this pathway contributes to the development of colorectal cancer. Here, we demonstrate that the transcriptional coregulator RIP140 regulates intestinal homeostasis and tumorigenesis. Using Rip140-null mice and mice overexpressing human RIP140, we found that RIP140 inhibited intestinal epithelial cell proliferation and apoptosis. Interestingly, following whole-body irradiation, mice lacking RIP140 exhibited improved regenerative capacity in the intestine, while mice overexpressing RIP140 displayed reduced recovery. Enhanced RIP140 expression strongly repressed human colon cancer cell proliferation in vitro and after grafting onto nude mice. Moreover, in murine tissues and human cancer cells, RIP140 stimulated APC transcription and inhibited β-catenin activation and target gene expression. Finally, RIP140 mRNA and RIP140 protein levels were decreased in human colon cancers compared with those in normal mucosal tissue, and low levels of RIP140 expression in adenocarcinomas from patients correlated with poor prognosis. Together, these results support a tumor suppressor role for RIP140 in colon cancer

Author Correction: EMPReSS: standardized phenotype screens for functional annotation of the mouse genome

International audienceCorrection to: Nature Genetics, published online 1 November 2005.In the version of this article initially published, members of the Eumorphia Consortium appeared in the Supplementary Information but were not included in the main article. The full list of members appears below