Copy-move forgery is a specific type of image tampering, where a part of the image is copied and pasted on another part of the same image. In this paper, we propose a new approach for detecting copy-move forgery in digital images, which is considerably more robust to lossy compression, scaling and rotation type of manipulations. Also, to improve the computational complexity in detecting the duplicated image regions, we propose to use the notion of counting bloom filters as an alternative to lexicographic sorting, which is a common component of most of the proposed copy-move forgery detection schemes. Our experimental results show that the proposed features can detect duplicated region in the images very accurately, even when the copied region was undergone severe image manipulations. In addition, it is observed that use of counting bloom filters offers a considerable improvement in time efficiency at the expense of a slight reduction in the robustness.

In this work, we focus our interest on blind source camera identification problem by extending our results in the direction of [1]. The interpolation in the color surface of an image due to the use of a color filter array (CFA) forms the basis of the paper. We propose to identify the source camera of an image based on traces of the proprietary interpolation algorithm deployed by a digital camera. For this purpose, a set of image characteristics are defined and then used in conjunction with a support vector machine based multi-class classifier to determine the originating digital camera. We also provide initial results on identifying source among two and three digital cameras.

Genome-wide association studies of late-onset Alzheimer’s disease risk have previously identified genes primarily expressed in microglia that form a transcriptional network. Using transgenic mouse models of amyloid deposition, we previously showed that many of the mouse orthologues of these risk genes are co-expressed and associated with amyloid pathology. In this new study, we generate an improved RNA-seq-derived network that is expressed in amyloid-responsive mouse microglia and we statistically compare this with gene-level variation in previous human Alzheimer’s disease genome-wide association studies to predict at least four new risk genes for the disease (OAS1, LAPTM5, ITGAM/CD11b and LILRB4). Of the mouse orthologues of these genes Oas1a is likely to respond directly to amyloid at the transcriptional level, similarly to established risk gene Trem2, because the increase in Oas1a and Trem2 transcripts in response to amyloid deposition in transgenic mice is significantly higher than both the increase of the average microglial transcript and the increase in microglial number. In contrast, the mouse orthologues of LAPTM5, ITGAM/CD11b and LILRB4 (Laptm5, Itgam/CD11b and Lilra5) show increased transcripts in the presence of amyloid plaques similar in magnitude to the increase of the average microglial transcript and the increase in microglia number, except that Laptm5 and Lilra5 transcripts increase significantly quicker than the average microglial transcript as the plaque load becomes dense. This work suggests that genetic variability in the microglial response to amyloid deposition is a major determinant for Alzheimer’s disease risk, and identification of these genes may help to predict the risk of developing Alzheimer’s disease. These findings also provide further insights into the mechanisms underlying Alzheimer’s disease for potential drug discovery.

Understanding the earliest changes in Alzheimer’s disease may help in the prevention of cognitive impairment. In a transgenic mouse model, Cummings et al. show that synaptic changes occur shortly after soluble amyloid-β levels become measurable, and before the rapid increases in total Aβ and Aβ42:Aβ40 that lead to detectable plaque deposition.