TOPOGRAPHIC CHANGES IN CHOROIDAL THICKNESS IN AGE-RELATED MACULAR DEGENERATION DURING THE DEVELOPMENT OF ACTIVE CHOROIDAL NEOVASCULARIZATION.

PURPOSE: To evaluate topographic changes in choroidal thickness during development of choroidal neovascularization (CNV) in treatment-naive age-related macular degeneration (AMD) and to test the value of such changes as a predictive tool of CNV development. METHODS: This retrospective cohort included 86 eyes that developed CNV from intermediate AMD, 43 eyes with intermediate AMD, and 36 eyes without AMD. Patients with intermediate AMD underwent spectral domain optical coherence tomography using enhanced depth imaging mode every 6 months until CNV was detected. Choroidal neovascularization was localized to one of the subfields of Early Treatment of Diabetic Retinopathy Study grid on fluorescein angiography. Average choroidal thickness of each subfield was calculated. RESULTS: Choroidal thickness of the subfield where CNV developed at first clinical detection significantly increased compared with that 6 months before (P = 0.000 for central, P = 0.001 for superior parafoveal, P = 0.002 for temporal parafoveal, P = 0.002 for inferior parafoveal, and P = 0.001 for nasal parafoveal subfield). In eight patients who visited unexpectedly 3 months before CNV development in central subfield, choroidal thickness of central subfield increased significantly compared with that 6 months before CNV development (P = 0.001). CONCLUSION: Choroidal neovascularization development accompanied choroidal thickening of the corresponding subfield. Regular measurement of choroidal thickness may assist in prediction of CNV.

Intravitreal Bevacizumab for Inflammatory Neovascularization of the Lens after Traumatic Open Globe Injury.

To describe a case of inflammatory neovascularization of the lens after open globe injury.Case report.A 57-year-old man presented with severe inflammation, posterior synechiae with traumatic cataract, and thick neovascularization of the intralenticular and anterior lens capsule after open globe injury in the left eye. We administered an intravitreal bevacizumab injection and performed cataract surgery with synechiolysis 1 month later.Inflammation after open globe injury may present as intralenticular neovascularization. Before cataract surgery for traumatic cataract with intralenticular neovascularization, the use of intravitreal bevacizumab injection was ineffective.

Silencing of mitochondrial NADP+-dependent isocitrate dehydrogenase gene enhances selenite-induced apoptosis.

Selenium has been shown to play a chemopreventive role in human cancer, presumably by inducing tumour cell apoptosis. Selenite is thought to induce oxidative stress by the generation of the superoxide anion and catalysing the oxidation of thiol groups. It has previously been reported that control of the mitochondrial redox balance is a primary function of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) by supplying NADPH for antioxidant systems. When investigating whether IDPm would be a vulnerable target of selenite, the loss of enzyme activity was observed. Transfection of HeLa cells with an IDPm small interfering RNA (siRNA) markedly decreased activity of IDPm and enhanced cells' susceptibility of selenite-induced apoptosis, as indicated by morphological evidence of apoptosis, DNA fragmentation and the modulation of mitochondrial function and apoptotic marker proteins. These results suggest that IDPm siRNA sensitizes HeLa cells to selenite-induced apoptotic cell death, presumably through the perturbation of the cellular redox status.