Ubic: Bridging the gap between digital cryptography and the physical world

Advances in computing technology increasingly blur the boundary between the digital domain and the physical world. Although the research community has developed a large number of cryptographic primitives and has demonstrated their usability in all-digital communication, many of them have not yet made their way into the real world due to usability aspects. We aim to make another step towards a tighter integration of digital cryptography into real world interactions. We describe Ubic, a framework that allows users to bridge the gap between digital cryptography and the physical world. Ubic relies on head-mounted displays, like Google Glass, resource-friendly computer vision techniques as well as mathematically sound cryptographic primitives to provide users with better security and privacy guarantees. The framework covers key cryptographic primitives, such as secure identification, document verification using a novel secure physical document format, as well as content hiding. To make a contribution of practical value, we focused on making Ubic as simple, easily deployable, and user friendly as possible.Comment: In ESORICS 2014, volume 8712 of Lecture Notes in Computer Science, pp. 56-75, Wroclaw, Poland, September 7-11, 2014. Springer, Berlin, German

Idd9.2 and Idd9.3 Protective Alleles Function in CD4+ T-Cells and Nonlymphoid Cells to Prevent Expansion of Pathogenic Islet-Specific CD8+ T-Cells

OBJECTIVE - Multiple type 1 diabetes susceptibility genes have now been identified in both humans and mice, yet mechanistic understanding of how they impact disease pathogenesis is still minimal. We have sought to dissect the cellular basis for how the highly protective mouse Idd9 region limits the expansion of autoreactive CD8 T-cells, a key cell type in destruction of the islets. RESEARCH DESIGN AND METHODS - We assess the endogenous CD8 T-cell repertoire for reactivity to the islet antigen glucose-6-phosphatase-related protein (IGRP). Through the use of adoptively transferred T-cells, bone marrow chimeras, and reconstituted severe combined immunodeficient mice, we identify the protective cell types involved. RESULTS - IGRP-specific CD8 T-cells are present at low frequency in the insulitic lesions of Idd9 mice and could not be recalled in the periphery by viral expansion. We show that Idd9 genes act extrinsically to the CD8 T-cell to prevent the massive expansion of pathogenic effectors near the time of disease onset that occurs in NOD mice. The subregions Idd9.2 and Idd9.3 mediated this effect. Interestingly, the Idd9.1 region, which provides significant protection from disease, did not prevent the expansion of autoreactive CD8 T-cells. Expression of Idd9 genes was required by both CD4 T-cells and a nonlymphoid cell to induce optimal tolerance. CONCLUSIONS - Idd9 protective alleles are associated with reduced expansion of IGRP-specific CD8 T-cells. Intrinsic expression of protective Idd9 alleles in CD4 T-cells and nonlymphoid cells is required to achieve an optimal level of tolerance. Protective alleles in the Idd9.2 congenic subregion are required for the maximal reduction of islet-specific CD8 T-cells

Computation of the weight distribution of CRC codes

In this article, we illustrate an algorithm for the computation of the weight distribution of CRC codes. The recursive structure of CRC codes will give us an iterative way to compute the weight distribution of their dual codes starting from some “representative” words. Thanks to MacWilliams’ Theorem, the computation of the weight distribution of the dual codes can be easily brought back to that of CRC codes