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Photo deblurring has been a major research topic in the past few years. So far, existing methods have focused on removing the blur due to camera shake and object motion. In this paper, we show that the optical system of the camera also generates significant blur, even with professional lenses. We introduce a method to estimate the blur kernel densely over the image and across multiple aperture and zoom settings. Our measures show that the blur kernel can have a non-negligible spread, even with top-of-the-line equipment, and that it varies nontrivially over this domain. In particular, the spatial variations are not radially symmetric and not even left-right symmetric. We develop and compare two models of the optical blur, each of them having its own advantages. We show that our models predict accurate blur kernels that can be used to restore photos. We demonstrate that we can produce images that are more uniformly sharp unlike those produced with spatially-invariant deblurring techniques.

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PURPOSE To investigate the presence of TBK1 copy number variations in a large, well-characterized Australian cohort of patients with glaucoma comprising both normal-tension glaucoma and high-tension glaucoma cases. DESIGN A retrospective cohort study. METHODS DNA samples from patients with normal-tension glaucoma and high-tension glaucoma and unaffected controls were screened for TBK1 copy number variations using real-time quantitative polymerase chain reaction. Samples with additional copies of the TBK1 gene were further tested using custom comparative genomic hybridization arrays. RESULTS Four out of 334 normal-tension glaucoma cases (1.2%) were found to carry TBK1 copy number variations using quantitative polymerase chain reaction. One extra dose of the TBK1 gene (duplication) was detected in 3 normal-tension glaucoma patients, while 2 extra doses of the gene (triplication) were detected in a fourth normal-tension glaucoma patient. The results were further confirmed by custom comparative genomic hybridization arrays. Further, the TBK1 copy number variation segregated with normal-tension glaucoma in the family members of the probands, showing an autosomal dominant pattern of inheritance. No TBK1 copy number variations were detected in 1045 Australian patients with high-tension glaucoma or in 254 unaffected controls. CONCLUSION We report the presence of TBK1 copy number variations in our Australian normal-tension glaucoma cohort, including the first example of more than 1 extra copy of this gene in glaucoma patients (gene triplication). These results confirm TBK1 to be an important cause of normal-tension glaucoma, but do not suggest common involvement in high-tension glaucoma.

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