An Evaluation of Popular Copy-Move Forgery Detection Approaches

A copy-move forgery is created by copying and pasting content within the same image, and potentially post-processing it. In recent years, the detection of copy-move forgeries has become one of the most actively researched topics in blind image forensics. A considerable number of different algorithms have been proposed focusing on different types of postprocessed copies. In this paper, we aim to answer which copy-move forgery detection algorithms and processing steps (e.g., matching, filtering, outlier detection, affine transformation estimation) perform best in various postprocessing scenarios. The focus of our analysis is to evaluate the performance of previously proposed feature sets. We achieve this by casting existing algorithms in a common pipeline. In this paper, we examined the 15 most prominent feature sets. We analyzed the detection performance on a per-image basis and on a per-pixel basis. We created a challenging real-world copy-move dataset, and a software framework for systematic image manipulation. Experiments show, that the keypoint-based features SIFT and SURF, as well as the block-based DCT, DWT, KPCA, PCA and Zernike features perform very well. These feature sets exhibit the best robustness against various noise sources and downsampling, while reliably identifying the copied regions.Comment: Main paper: 14 pages, supplemental material: 12 pages, main paper appeared in IEEE Transaction on Information Forensics and Securit

Haploinsufficiency of ARID1B, a member of the SWI/SNF-a chromatin-remodeling complex, is a frequent cause of intellectual disability

Intellectual disability (ID) is a clinically and genetically heterogeneous common condition that remains etiologically unresolved in the majority of cases. Although several hundred diseased genes have been identified in X-linked, autosomal-recessive, or syndromic types of ID, the establishment of an etiological basis remains a difficult task in unspecific, sporadic cases. Just recently, de novo mutations in SYNGAP1, STXBP1, MEF2C, and GRIN2B were reported as relatively common causes of ID in such individuals. On the basis of a patient with severe ID and a 2.5 Mb microdeletion including ARID1B in chromosomal region 6q25, we performed mutational analysis in 887 unselected patients with unexplained ID. In this cohort, we found eight (0.9%) additional de novo nonsense or frameshift mutations predicted to cause haploinsufficiency. Our findings indicate that haploinsufficiency of ARID1B, a member of the SWI/SNF-A chromatin-remodeling complex, is a common cause of ID, and they add to the growing evidence that chromatin-remodeling defects are an important contributor to neurodevelopmental disorders