A Framework for Biometric and Interaction Performance Assessment of Automated Border Control Processes

Automated Border Control (ABC) in airports and land crossings utilize automated technology to verify passenger identity claims. Accuracy, interaction stability, user error, and the need for a harmonized approach to implementation are required. Two models proposed in this paper establish a global path through ABC processes. The first, the generic model, maps separately the enrolment and verification phases of an ABC scenario. This allows a standardization of the process and an exploration of variances and similarities between configurations across implementations. The second, the identity claim process, decomposes the verification phase of the generic model to an enhanced resolution of ABC implementations. Harnessing a human-biometric sensor interaction framework allows the identification and quantification of errors within the system's use, attributing these errors to either system performance or human interaction. Data from a live operational scenario are used to analyze behaviors, which aid in establishing what effect these have on system performance. Utilizing the proposed method will aid already established methods in improving the performance assessment of a system. Through analyzing interactions and possible behavioral scenarios from the live trial, it was observed that 30.96% of interactions included some major user error. Future development using our proposed framework will see technological advances for biometric systems that are able to categorize interaction errors and feedback appropriately

IGF-I activates caspases 3/7, 8 and 9 but does not induce cell death in colorectal cancer cells

Background: Colorectal cancer is the third most common cancer in the western world. Chemotherapy is often ineffective to treat the advanced colorectal cancers due to the chemoresistance. A major contributor to chemo-resistance is tumour-derived inhibition or avoidance of apoptosis. Insulin-like growth factor I (IGF-I) has been known to play a prominent role in colorectal cancer development and progression. The role of IGF-I in cancer cell apoptosis is not completely understood.Methods: Using three colorectal cancer cell lines and one muscle cell line, associations between IGF-I and activities of caspase 3/7, 8 and 9 have been examined; the role of insulin-like growth factor I receptor (IGF-IR) in the caspase activation has been investigated.Results: The results show that exogenous IGF-I significantly increases activity of caspases 3/7, 8 and 9 in all cell lines used; blocking IGF-I receptor reduce IGF-I-induced caspase activation. Further studies demonstrate that IGF-I induced caspase activation does not result in cell death. This is the first report to show that while IGF-I activates caspases 3/7, 8 and 9 it does not cause colorectal cancer cell death.Conclusion: The study suggests that caspase activation is not synonymous with apoptosis and that activation of caspases may not necessarily induce cell death

The mechanisms of immunopathology underlying B cell depletion therapy-mediated remission and relapse in patients with MuSK MG: Immune mechanisms of MuSK MG

The application of reverse translational medicine allows for the understanding of immune pathogenesis via therapeutic intervention. We applied this approach to the MuSK subtype of myasthenia gravis. Treatment with the CD20-specific B cell depletion therapy (BCDT) demonstrated that MuSK MG patients respond remarkably well; the majority invariably reach remission accompanied by a remarkable drop in autoantibody levels. Circulating antibodies are primarily produced by bone marrow resident plasma cells, which do not express CD20. So, how does BCDT diminish MuSK autoantibodies and induce rapid remission? We developed a mechanistic model, which hypothesized that plasmablasts, which are short-lived antibody secreting B cell populations, produce MuSK-specific autoantibodies. Anti-CD20-mediated BCDT is expected to deplete CD20-expressing plasmablasts or CD20 expressing memory cells that supply the plasmablast population. To test this hypothesis, we performed a series of investigations, which were reported over the last seven years and are summarized in this review. First, we isolated plasmablasts from patients and generated human recombinant monoclonal autoantibodies (mAb) which bound MuSK and had pathogenic capacity, demonstrating that MuSK autoantibodies can be produced by this specific cell population. The characterization of the mAbs showed that MuSK autoantibodies can include unique properties including unusually high antigen binding affinity, and an elevated frequency of N-linked glycosylation in their binding domains. Further characterization suggested that MuSK autoantibody-producing cells may form in the early stages of B cell development due to defective tolerance mechanisms. Finally, we sought to determine how these pathogenic B cell clones behave over time. High throughput B cell receptor sequencing was applied to investigate longitudinally collected samples from patients treated with anti-CD20-mediated BCDT. MuSK-specific clonal variants were detected at multiple timepoints spanning more than five years and reemerged after BCDT-induced remission, predating disease relapse by several months. These collective investigations provide a more detailed mechanistic understanding that MuSK MG, the key features of which include production of autoantibodies by circulating plasmablasts that can be targeted by CD20-specific BCDT, and that pathogenic clones can survive BCDT and reemerge prior to manifestation of clinical relapse

Time series analysis of the skyline and employment changes in the CBD of Melbourne

This paper covers historical and micro level analyses of floor space and employment in the CBD of Melbourne during the last two decades. The time-series patterns and processes of high-rise building provision in the CBD are also focused on. The CBD has experienced very complicated changes over the last two decades. While particular types of urban functions, say finance and insurance offices and many retail activities, have been dispersed to the suburbs, newly emerged activities have replaced the old and traditional ones. Despite the growth of suburban cores (office and retail), the CBD of Melbourne has still kept its strong centrality through a role as the main location of office activity in particular. Historical and micro level viewpoints provide a new understanding of the metropolitan area. The key question must be Why is the role of the CBD of Melbourne still so strong, given substantial dispersal of population and economic activity to suburban locations

NUMOD and NUTSA : software for interactive acquisition and analysis of time domain reflectometry measurements /

Includes bibliographical references (page 29) and index.Mode of access: Internet

Vitamin D Status and Indices of Bone Turnover in Older European Adults

International audienceAn increased rate of bone turnover increases risk of osteoporotic fracture later in life. The concentration of 25-hydroxyvitamin D that contributes to an elevated rate of bone turnover in older adults is unclear. The objective of this study was to investigate the associations between 25-hydroxyvitamin D and biochemical markers of bone turnover in an older, pan-European cohort. 25-hydroxyvitamin D and serum markers of bone-formation (osteocalcin and bone-specific alkaline phosphatase) were assessed by ELISA, while urinary markers of bone-resorption (pyridinoline and deoxypyridinoline) were assessed by HPLC. Six percent, 36%, and 64% of subjects had 25-hydroxyvitamin D concentrations 85.8 [T-3] nmol/L), showed that urinary pyridinoline and deoxypyridinoline were significantly lower in subjects in the 2nd and 3rd compared to the 1st tertile (p < 0.015). Low vitamin D status (<50 nmol/L) was associated with an increased rate of bone turnover in this older pan-European cohort

Precision targeting of autoantigen-specific B cells in muscle-specific tyrosine kinase myasthenia gravis with chimeric autoantibody receptor T cells.

Muscle-specific tyrosine kinase myasthenia gravis (MuSK MG) is an autoimmune disease that causes life-threatening muscle weakness due to anti-MuSK autoantibodies that disrupt neuromuscular junction signaling. To avoid chronic immunosuppression from current therapies, we engineered T cells to express a MuSK chimeric autoantibody receptor with CD137-CD3ζ signaling domains (MuSK-CAART) for precision targeting of B cells expressing anti-MuSK autoantibodies. MuSK-CAART demonstrated similar efficacy as anti-CD19 chimeric antigen receptor T cells for depletion of anti-MuSK B cells and retained cytolytic activity in the presence of soluble anti-MuSK antibodies. In an experimental autoimmune MG mouse model, MuSK-CAART reduced anti-MuSK IgG without decreasing B cells or total IgG levels, reflecting MuSK-specific B cell depletion. Specific off-target interactions of MuSK-CAART were not identified in vivo, in primary human cell screens or by high-throughput human membrane proteome array. These data contributed to an investigational new drug application and phase 1 clinical study design for MuSK-CAART for the treatment of MuSK autoantibody-positive MG