Wireless Distance-Verifying Security System for ID Card/Document Enrollment Stations

Modern ID Cards and passports have evolved into sophisticated, complex positive-ID instruments that embody a wide variety of anti-cloning and anti-forgery techniques, such as: digitized biometrics, micro-printing, encryption, RFID, embedded processing, holo-graphic overlays, and UV/IR-visible features, among others. This poster describes a practical system for protecting against theft of the enrollment stations that produce these ID instruments, by providing a "lock" to a specific location. If a protected enrollment system is moved from that location, it will fail to function. This non-GPS location-locking technique is strongly protected against sniffing and spoofing, is immune to relay attacks, and cannot be copied - not even by its manufacturer

High-Security, Clone-proof RFID with Secure Distance Bounding

Wireless near-field (NFC) and short-range RFID “security” devices are ubiquitous, commonly found in vehicle security (keyless-entry, remote-start), access control (employee key cards), travel cards, point-of-sale (PoS) transactions via NFC-enabled mobile phone or credit card, among others. Whenever assets of high-value are at stake, adversaries will stop at nothing to gain access to those assets, so it should be assumed that security systems will be subjected to many forms of attack. There have already been several highly publicized successful breaches of keyless entry systems, including relay and key-cloning attacks. This poster describes a a highly-secure, distance-bounding, clone-proof RFID mechanism for protecting high-value assets. The system employs a unique combination of technologies to make it highly-resistant to relay attacks, probing, modeling, cloning and snooping

Context-Free Decoding of High-Density 2D Bit Fields with Alias Disambiguation

PROBLEM: Conventional decoding techniques tend to operate exclusively in the space domain and often rely on code-specific “finder features,” ECC, high-resolution imaging, image resampling (a “lossy” process), encoded data “clues” and low code density relative to image resolution (see EASY examples below). This limits the amount of information that can be reliably encoded into a given area. RESEARCH OBJECTIVES: Recover randomly-oriented 2D bit fields without resampling, without reliance on finder features, and without dependency on encoding or data content. Decode at image densities that produce aliasing of primary grid frequencies – alias disambiguation (see HARD example below). Provide linear code density improvement of 1.5:1 to 2:1 over conventional techniques, resulting in an increase in data density per unit area of 2.25:1 to 4:1

The Sex Ratio and the Out-of-Wedlock Birth Rate in the United States during World War II

This paper provides a theoretical economic framework to study the effects of changes in the sex ratio on the out-of-wedlock birth rate in the United States. We model the demanders and suppliers of sexual relations as potential mates and the relative “price” of human sexual relations as the promises implicit within a traditional marriage (marriage, fidelity, wealth transfers, child support, etc.). We examine an instrument for the implicit “price” of sexual relations, namely the out-of-wedlock birth rate. We show that the reduction in the number of available sex partners for women during World War II decreased the “price”—in terms of marriage—that remaining men had to pay for sex. One result of this lower “price” is an increase in the number of children born out-of-wedlock during the war. According to our regression results, a reduction in the sex ratio of 10 males per 100 females in the U.S. population during World War II increased the out-of wedlock birth rate by six to ten percent

Neurodegeneration and Epilepsy in a Zebrafish Model of CLN3 Disease (Batten Disease)

The neuronal ceroid lipofuscinoses are a group of lysosomal storage disorders that comprise the most common, genetically heterogeneous, fatal neurodegenerative disorders of children. They are characterised by childhood onset, visual failure, epileptic seizures, psychomotor retardation and dementia. CLN3 disease, also known as Batten disease, is caused by autosomal recessive mutations in the CLN3 gene, 80–85% of which are a ~1 kb deletion. Currently no treatments exist, and after much suffering, the disease inevitably results in premature death. The aim of this study was to generate a zebrafish model of CLN3 disease using antisense morpholino injection, and characterise the pathological and functional consequences of Cln3 deficiency, thereby providing a tool for future drug discovery. The model was shown to faithfully recapitulate the pathological signs of CLN3 disease, including reduced survival, neuronal loss, retinopathy, axonopathy, loss of motor function, lysosomal storage of subunit c of mitochondrial ATP synthase, and epileptic seizures, albeit with an earlier onset and faster progression than the human disease. Our study provides proof of principle that the advantages of the zebrafish over other model systems can be utilised to further our understanding of the pathogenesis of CLN3 disease and accelerate drug discovery

Genetic Deletion of a Single Immunodominant T-cell Response Confers Susceptibility to Virus-induced Demyelination

An important question in neuropathology involves determining the antigens that are targeted during demyelinating disease. Viral infection of the central nervous system (CNS) leads to T-cell responses that can be protective as well as pathogenic. In the Theiler’s murine encephalomyelitis virus (TMEV) model of demyelination it is known that the immune response to the viral capsid protein 2 (VP2) is critical for disease pathogenesis. This study shows that expressing the whole viral capsid VP2 or the minimal CD8-specific peptide VP2(121-130) as “self” leads to a loss of VP2-specific immune responses. Loss of responsiveness is caused by T cell-specific tolerance, as VP2-specific antibodies are generated in response to infection. More importantly, these mice lose the CD8 T-cell response to the immunodominant peptide VP2(121-130), which is critical for the development of demyelinating disease. The transgenic mice fail to clear the infection and develop chronic demyelinating disease in the spinal cord white matter. These findings demonstrate that T-cell responses can be removed by transgenic expression and that lack of responsiveness alters viral clearance and CNS pathology. This model will be important for understanding the mechanisms involved in antigen-specific T-cell deletion and the contribution of this response to CNS pathology

The small molecule specific EphB4 kinase inhibitor NVP-BHG712 inhibits VEGF driven angiogenesis

EphB4 and its cognitive ligand ephrinB2 play an important role in embryonic vessel development and vascular remodeling. In addition, several reports suggest that this receptor ligand pair is also involved in pathologic vessel formation in adults including tumor angiogenesis. Eph/ephrin signaling is a complex phenomena characterized by receptor forward signaling through the tyrosine kinase of the receptor and ephrin reverse signaling through various protein–protein interaction domains and phosphorylation motifs of the ephrin ligands. Therefore, interfering with EphR/ephrin signaling by the means of targeted gene ablation, soluble receptors, dominant negative mutants or antisense molecules often does not allow to discriminate between inhibition of Eph/ephrin forward and reverse signaling. We developed a specific small molecular weight kinase inhibitor of the EphB4 kinase, NVP-BHG712, which inhibits EphB4 kinase activity in the low nanomolar range in cellular assays showed high selectivity for targeting the EphB4 kinase when profiled against other kinases in biochemical as well as in cell based assays. Furthermore, NVP-BHG712 shows excellent pharmacokinetic properties and potently inhibits EphB4 autophosphorylation in tissues after oral administration. In vivo, NVP-BHG712 inhibits VEGF driven vessel formation, while it has only little effects on VEGF receptor (VEGFR) activity in vitro or in cellular assays. The data shown here suggest a close cross talk between the VEGFR and EphR signaling during vessel formation. In addition to its established function in vascular remodeling and endothelial arterio-venous differentiation, EphB4 forward signaling appears to be an important mediator of VEGF induced angiogenesis since inhibition of EphB4 forward signaling is sufficient to inhibit VEGF induced angiogenesis

Corporate boards and performance pricing in private debt contracts

This paper investigates the effects of corporate governance on the use of performance pricing in debt contracts on a sample of newly syndicated loans in the U.S. private debt market. While cross-sectional results provide no evidence for the predicted relation between corporate governance quality and the likelihood of using performance pricing in debt contracts, there is evidence for the predicted positive relation between corporate governance quality and the use of interest-increasing performance pricing provisions. Evidence also provides support for the predicted negative relation between corporate governance quality and the use of financial ratio as the measure of performance underlying the provisions. Overall, empirical evidence supports the hypothesis that debt-holders perceive aspects of corporate governance to be beneficial and factor them in their contracting decisions

Increased autophagy in EphrinB2-deficient osteocytes is associated with elevated secondary mineralization and brittle bone

Mineralized bone forms when collagen-containing osteoid accrues mineral crystals. This is initiated rapidly (primary mineralization), and continues slowly (secondary mineralization) until bone is remodeled. The interconnected osteocyte network within the bone matrix differentiates from bone-forming osteoblasts; although osteoblast differentiation requires EphrinB2, osteocytes retain its expression. Here we report brittle bones in mice with osteocyte-targeted EphrinB2 deletion. This is not caused by low bone mass, but by defective bone material. While osteoid mineralization is initiated at normal rate, mineral accrual is accelerated, indicating that EphrinB2 in osteocytes limits mineral accumulation. No known regulators of mineralization are modified in the brittle cortical bone but a cluster of autophagy-associated genes are dysregulated. EphrinB2-deficient osteocytes displayed more autophagosomes in vivo and in vitro, and EphrinB2-Fc treatment suppresses autophagy in a RhoA-ROCK dependent manner. We conclude that secondary mineralization involves EphrinB2-RhoA-limited autophagy in osteocytes, and disruption leads to a bone fragility independent of bone mass