Receiver-Autonomous Spoofing Detection: Experimental Results of a Multi-antenna Receiver Defense Against a Portable Civil GPS Spoofer

In this work we demonstrate the use of a dual antenna receiver that employs a receiver-autonomous angle-ofarrival spoofing countermeasure. This defense is conjectured to be effective against all but the most sophisticated spoofing attempts. The technique is based on observation of L1 carrier differences between multiple antennas referenced to a common oscillator. We first employ a moderately sophisticated spoofer to "fool" a single-antenna civil receiver. We then deploy the same attack after augmenting the receiver with an additional antenna and with receiver-autonomous spoofdetection software. The work discusses the experimental results together with various issues related to sensitivity, probability of false alarm, impact of carrier multipath, line-bias-calibration, and physical setup and security. We suggest that this work is important to the community as it provides experimental validation of a low-cost technique for receiver-autonomous spoofing detection. Furthermore, the technique, when combined with physical security of the antenna installation, provides a strong defense against even a sophisticated attack. The receiver employed is an L1-only civil GPS receiver with multiple antenna capability. The GPS chipset employed is the venerable GP2015/GP2021 that has been freely available for over a decade. As such, this receiver is representative of many civil receivers in use today for a variety of applications. Multiple antennas are enabled either through multiple independent RF front ends and correlators or via antenna multiplexing into a single RF front end and correlator bank.Aerospace Engineering and Engineering Mechanic

Continuity of Optimal Control Costs and its application to Weak KAM Theory

We prove continuity of certain cost functions arising from optimal control of affine control systems. We give sharp sufficient conditions for this continuity. As an application, we prove a version of weak KAM theorem and consider the Aubry-Mather problems corresponding to these systems.Comment: 23 pages, 1 figures, added explanations in the proofs of the main theorem and the exampl

Immunopathology of CD4+ T Cell-Mediated Autoimmune Responses to Central Nervous System Antigens: Role of IL-16

Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating and degenerative disease of the central nervous system (CNS). While etiology of the disease remains unknown, genetic susceptibility and autoimmune mechanisms in the initiation and progression of the disease have been strongly suggested. Experimental autoimmune encephalomyelitis (EAE) is commonly used to study immune regulation of MS. Infiltration by CD4+ T cells, through blood-brain barrier (BBB), precedes the onset and relapses of MS. CNS migration and homing patterns of T cells are tightly synchronized by astrocyte and microglia derived cytokines and chemokines. Autoimmune, CNS antigenreactive, infiltrating T cells produce and locally release cytokines including but not limited to IFNγ, IL-2, IL-6, IL-16, IL-17, TNFα, and chemokines including CCL2, CCL5 and CXCL10. Chemokine mediated chemotaxis is exclusive for activated cell state and most chemokines do not discriminate between distinct cell types. Conversely, a cytokine IL-16 is a CD4-specific cytokine-ligand and exclusively induces chemotaxis of CD4+T cells, by binding and signaling through CD4, regardless of T cell activation state. In this article we focus on CD4+ T cell-mediated autoimmune responses to CNS antigens because of their importance for immunopathology of MS and EAE. We focus on autoimmune responses to myelin oligodendrocyte glycoprotein (MOG) because of its relevance for immunopathology of MS. We emphasize a role of IL-16 in regulation of CD4+T cell mediated autoimmune responses to MOG in EAE and MS. While a role of IL-16 in regulation of other CD4+T cell mediated autoimmune diseases has been established, its role in regulation of MS remains to be determined. Emerging data from our laboratories have indicated that IL-16-mediated CD4+ T cell chemoattraction has a significant role in regulation of CD4+ T cell-mediated autoimmune responses to CNS antigens. We propose an important function of this cytokine in regulation of relapsing-remitting EAE

Effects of ecstasy/polydrug use on memory for associative information

Rationale Associative learning underpins behaviours that are fundamental to the everyday functioning of the individual. Evidence pointing to learning deficits in recreational drug users merits further examination. Objectives A word pair learning task was administered to examine associative learning processes in ecstasy/polydrug users. Methods After assignment to either single or divided attention conditions, 44 ecstasy/polydrug users and 48 non-users were presented with 80 word pairs at encoding. Following this, four types of stimuli were presented at the recognition phase: the words as originally paired (old pairs), previously presented words in different pairings (conjunction pairs), old words paired with new words, and pairs of new words (not presented previously). The task was to identify which of the stimuli were intact old pairs. Results Ecstasy/ploydrug users produced significantly more false-positive responses overall compared to non-users. Increased long-term frequency of ecstasy use was positively associated with the propensity to produce false-positive responses. It was also associated with a more liberal signal detection theory decision criterion value. Measures of long term and recent cannabis use were also associated with these same word pair learning outcome measures. Conjunction word pairs, irrespective of drug use, generated the highest level of false-positive responses and significantly more false-positive responses were made in the divided attention condition compared to the single attention condition. Conclusions Overall, the results suggest that long-term ecstasy exposure may induce a deficit in associative learning and this may be in part a consequence of users adopting a more liberal decision criterion value

Bishop and Laplacian Comparison Theorems on Three Dimensional Contact Subriemannian Manifolds with Symmetry

We prove a Bishop volume comparison theorem and a Laplacian comparison theorem for three dimensional contact subriemannian manifolds with symmetry

Mass equidistribution of Hilbert modular eigenforms

Let F be a totally real number field, and let f traverse a sequence of non-dihedral holomorphic eigencuspforms on GL(2)/F of weight (k_1,...,k_n), trivial central character and full level. We show that the mass of f equidistributes on the Hilbert modular variety as max(k_1,...,k_n) tends to infinity. Our result answers affirmatively a natural analogue of a conjecture of Rudnick and Sarnak (1994). Our proof generalizes the argument of Holowinsky-Soundararajan (2008) who established the case F = Q. The essential difficulty in doing so is to adapt Holowinsky's bounds for the Weyl periods of the equidistribution problem in terms of manageable shifted convolution sums of Fourier coefficients to the case of a number field with nontrivial unit group.Comment: 40 pages; typos corrected, nearly accepted for

Endothelin receptor B antagonists decrease glioma cell viability independently of their cognate receptor

Background: Endothelin receptor antagonists inhibit the progression of many cancers, but research into their influence on glioma has been limited. Methods: We treated glioma cell lines, LN-229 and SW1088, and melanoma cell lines, A375 and WM35, with two endothelin receptor type B (ETRB)-specific antagonists, A-192621 and BQ788, and quantified viable cells by the capacity of their intracellular esterases to convert non-fluorescent calcein AM into green-fluorescent calcein. We assessed cell proliferation by labeling cells with carboxyfluorescein diacetate succinimidyl ester and quantifying the fluorescence by FACS analysis. We also examined the cell cycle status using BrdU/propidium iodide double staining and FACS analysis. We evaluated changes in gene expression by microarray analysis following treatment with A-192621 in glioma cells. We examined the role of ETRB by reducing its expression level using small interfering RNA (siRNA). Results: We report that two ETRB-specific antagonists, A-192621 and BQ788, reduce the number of viable cells in two glioma cell lines in a dose- and time-dependent manner. We describe similar results for two melanoma cell lines. The more potent of the two antagonists, A-192621, decreases the mean number of cell divisions at least in part by inducing a G2/M arrest and apoptosis. Microarray analysis of the effects of A-192621 treatment reveals up-regulation of several DNA damage-inducible genes. These results were confirmed by real-time RT-PCR. Importantly, reducing expression of ETRB with siRNAs does not abrogate the effects of either A-192621 or BQ788 in glioma or melanoma cells. Furthermore, BQ123, an endothelin receptor type A (ETRA)-specific antagonist, has no effect on cell viability in any of these cell lines, indicating that the ETRB-independent effects on cell viability exhibited by A-192621 and BQ788 are not a result of ETRA inhibition. Conclusion: While ETRB antagonists reduce the viability of glioma cells in vitro, it appears unlikely that this effect is mediated by ETRB inhibition or cross-reaction with ETRA. Instead, we present evidence that A-192621 affects glioma and melanoma viability by activating stress/DNA damage response pathways, which leads to cell cycle arrest and apoptosis. This is the first evidence linking ETRB antagonist treatment to enhanced expression of DNA damage-inducible genes

Characterization and Comparison of 2 Distinct Epidemic Community-Associated Methicillin-Resistant Staphylococcus aureus Clones of ST59 Lineage.

Sequence type (ST) 59 is an epidemic lineage of community-associated (CA) methicillin-resistant Staphylococcus aureus (MRSA) isolates. Taiwanese CA-MRSA isolates belong to ST59 and can be grouped into 2 distinct clones, a virulent Taiwan clone and a commensal Asian-Pacific clone. The Taiwan clone carries the Panton-Valentine leukocidin (PVL) genes and the staphylococcal chromosomal cassette mec (SCCmec) VT, and is frequently isolated from patients with severe disease. The Asian-Pacific clone is PVL-negative, carries SCCmec IV, and a frequent colonizer of healthy children. Isolates of both clones were characterized by their ability to adhere to respiratory A549 cells, cytotoxicity to human neutrophils, and nasal colonization of a murine and murine sepsis models. Genome variation was determined by polymerase chain reaction of selected virulence factors and by multi-strain whole genome microarray. Additionally, the expression of selected factors was compared between the 2 clones. The Taiwan clone showed a much higher cytotoxicity to the human neutrophils and caused more severe septic infections with a high mortality rate in the murine model. The clones were indistinguishable in their adhesion to A549 cells and persistence of murine nasal colonization. The microarray data revealed that the Taiwan clone had lost the ø3-prophage that integrates into the β-hemolysin gene and includes staphylokinase- and enterotoxin P-encoding genes, but had retained the genes for human immune evasion, scn and chps. Production of the virulence factors did not differ significantly in the 2 clonal groups, although more α-toxin was expressed in Taiwan clone isolates from pneumonia patients. In conclusion, the Taiwan CA-MRSA clone was distinguished by enhanced virulence in both humans and an animal infection model. The evolutionary acquisition of PVL, the higher expression of α-toxin, and possibly the loss of a large portion of the β-hemolysin-converting prophage likely contribute to its higher pathogenic potential than the Asian-Pacific clone

Functional alpha-1B adrenergic receptors on human epicardial coronary artery endothelial cells

Alpha-1-adrenergic receptors (α1-ARs) regulate coronary arterial blood flow by binding catecholamines, norepinephrine (NE), and epinephrine (EPI), causing vasoconstriction when the endothelium is disrupted. Among the three α1-AR subtypes (α1A, α1B, and α1D), the α1D subtype predominates in human epicardial coronary arteries and is functional in human coronary smooth muscle cells (SMCs). However, the presence or function of α1-ARs on human coronary endothelial cells (ECs) is unknown. Here we tested the hypothesis that human epicardial coronary ECs express functional α1-ARs. Cultured human epicardial coronary artery ECs were studied using quantitative real-time reverse transcription polymerase chain reaction, radioligand binding, immunoblot, and 3H-thymidine incorporation. The α1B-subtype messenger ribonucleic acid (mRNA) was predominant in cultured human epicardial coronary ECs (90–95% of total α1-AR mRNA), and total α1-AR binding density in ECs was twice that in coronary SMCs. Functionally, NE and EPI through the α1B subtype activated extracellular signal-regulated kinase (ERK) in ECs, stimulated phosphorylation of EC endothelial nitric oxide synthase (eNOS), and increased deoxyribonucleic acid (DNA) synthesis. These results are the first to demonstrate α1-ARs on human coronary ECs and indicate that the α1B subtype is predominant. Our findings provide another potential mechanism for adverse cardiac effects of drug antagonists that nonselectively inhibit all three α1-AR subtypes

Toward a theory‐based specification of non‐pharmacological treatments in aging and dementia: Focused reviews and methodological recommendations

Introduction: Non‐pharmacological treatments (NPTs) have the potential to improve meaningful outcomes for older people at risk of, or living with dementia, but research often lacks methodological rigor and continues to produce mixed results. Methods: In the current position paper, experts in NPT research have specified treatment targets, aims, and ingredients using an umbrella framework, the Rehabilitation Treatment Specification System. Results: Experts provided a snapshot and an authoritative summary of the evidence for different NPTs based on the best synthesis efforts, identified main gaps in knowledge and relevant barriers, and provided directions for future research. Experts in trial methodology provide best practice principles and recommendations for those working in this area, underscoring the importance of prespecified protocols. Discussion: We conclude that the evidence strongly supports various NPTs in relation to their primary targets, and discuss opportunities and challenges associated with a unifying theoretical framework to guide future efforts in this area