Compressed sensing with near-field THz radiation

We demonstrate a form of near-field terahertz (THz) imaging that is compatible with compressed sensing algorithms. By spatially photomodulating THz pulses using a set of shaped binary optical patterns and employing a 6-μm-thick silicon wafer, we are able to reconstruct THz images of an object placed on the exit interface of the wafer. A single-element detector is used to measure the electric field amplitude of transmitted THz radiation for each projected pattern, with the ultra-thin wafer allowing us to access the THz evanescent near fields to achieve a spatial resolution of ∼9  μm∼9  μm

Non-invasive, near-field terahertz imaging of hidden objects using a single pixel detector

Terahertz (THz) imaging has the ability to see through otherwise opaque materials. However, due to the long wavelengths of THz radiation ({\lambda}=300{\mu}m at 1THz), far-field THz imaging techniques are heavily outperformed by optical imaging in regards to the obtained resolution. In this work we demonstrate near-field THz imaging with a single-pixel detector. We project a time-varying optical mask onto a silicon wafer which is used to spatially modulate a pulse of THz radiation. The far-field transmission corresponding to each mask is recorded by a single element detector and this data is used to reconstruct the image of an object placed on the far side of the silicon wafer. We demonstrate a proof of principal application where we image a printed circuit board on the underside of a 115{\mu}m thick silicon wafer with ~100{\mu}m ({\lambda}/4) resolution. With subwavelength resolution and the inherent sensitivity to local conductivity provided by the THz probe frequencies, we show that it is possible to detect fissures in the circuitry wiring of a few microns in size. Imaging systems of this type could have other uses where non-invasive measurement or imaging of concealed structures with high resolution is necessary, such as in semiconductor manufacturing or in bio-imaging

A forensic acquisition and analysis system for IaaS

Cloud computing is a promising next-generation computing paradigm that offers significant economic benefits to both commercial and public entities. Furthermore, cloud computing provides accessibility, simplicity, and portability for its customers. Due to the unique combination of characteristics that cloud computing introduces (including on-demand self-service, broad network access, resource pooling, rapid elasticity, and measured service), digital investigations face various technical, legal, and organizational challenges to keep up with current developments in the field of cloud computing. There are a wide variety of issues that need to be resolved in order to perform a proper digital investigation in the cloud environment. This paper examines the challenges in cloud forensics that are identified in the current research literature, alongside exploring the existing proposals and technical solutions addressed in the respective research. The open problems that need further effort are highlighted. As a result of the analysis of literature, it is found that it would be difficult, if not impossible, to perform an investigation and discovery in the cloud environment without relying on cloud service providers (CSPs). Therefore, dependence on the CSPs is ranked as the greatest challenge when investigators need to acquire evidence in a timely yet forensically sound manner from cloud systems. Thus, a fully independent model requires no intervention or cooperation from the cloud provider is proposed. This model provides a different approach to a forensic acquisition and analysis system (FAAS) in an Infrastructure as a Service model. FAAS seeks to provide a richer and more complete set of admissible evidences than what current CSPs provide, with no requirement for CSP involvement or modification to the CSP’s underlying architecture

Fog computing security: a review of current applications and security solutions

Fog computing is a new paradigm that extends the Cloud platform model by providing computing resources on the edges of a network. It can be described as a cloud-like platform having similar data, computation, storage and application services, but is fundamentally different in that it is decentralized. In addition, Fog systems are capable of processing large amounts of data locally, operate on-premise, are fully portable, and can be installed on heterogeneous hardware. These features make the Fog platform highly suitable for time and location-sensitive applications. For example, Internet of Things (IoT) devices are required to quickly process a large amount of data. This wide range of functionality driven applications intensifies many security issues regarding data, virtualization, segregation, network, malware and monitoring. This paper surveys existing literature on Fog computing applications to identify common security gaps. Similar technologies like Edge computing, Cloudlets and Micro-data centres have also been included to provide a holistic review process. The majority of Fog applications are motivated by the desire for functionality and end-user requirements, while the security aspects are often ignored or considered as an afterthought. This paper also determines the impact of those security issues and possible solutions, providing future security-relevant directions to those responsible for designing, developing, and maintaining Fog systems

A Decline in CCL3-5 Chemokine Gene Expression during Primary Simian-Human Immunodeficiency Virus Infection

BACKGROUND: The CC-chemokines CCL3, CCL4 and CCL5 have been found to block the entry of CCR5-tropic HIV into host cells and to suppress the viral replication in vitro, but the in vivo role of endogenous CC-chemokines in HIV-1 infection is still incompletely understood. METHODOLOGY/PRINCIPLE FINDINGS: In this study, the primate host CCL3, CCL4 and CCL5 gene expression was evaluated in response to simian-human immunodeficiency virus (SHIV) infection in rhesus macaque model. Five rhesus macaques were inoculated with CCR5-tropic SHIV(SF162P4). The mRNA levels of CCL3, CCL4 and CCL5 were measured by real-time PCR at post inoculation day (PID) 0, 7, 14, 21, 35, 56 and 180 in peripheral blood. In addition, a selected subset of samples from CXCR4-tropic SHIV(Ku1)-infected macaques was included with objective to compare the differences in CC-chemokine down-regulation caused by the two SHIVs. Gut-associated lymphoid tissues (GALT) collected from SHIV(SF162P4)-infected animals were also tested by flow cytometry and confocal microscopy to corroborate the gene expression results. Predictably, higher viral loads and CD4+ T cell losses were observed at PID 14 in macaques infected with SHIV(Ku1) than with SHIV(SF162P4). A decline in CC-chemokine gene expression was also found during primary (PID 7-21), but not chronic (PID 180) stage of infection. CONCLUSIONS: It was determined that A) SHIV(SF162P4) down-regulated the CC-chemokine gene expression during acute stage of infection to a greater extent (p<0.05) than SHIV(Ku1), and B) such down-regulation was not paralleled with the CD4+ T cell depletion. Evaluation of CC-chemokine enhancing immunomodulators such as synthetic CpG-oligonucleotides could be explored in future HIV vaccine studies

Role of Abl Kinase and the Wave2 Signaling Complex in HIV-1 Entry at a Post-Hemifusion Step

Entry of human immunodeficiency virus type 1 (HIV-1) commences with binding of the envelope glycoprotein (Env) to the receptor CD4, and one of two coreceptors, CXCR4 or CCR5. Env-mediated signaling through coreceptor results in Gαq-mediated Rac activation and actin cytoskeleton rearrangements necessary for fusion. Guanine nucleotide exchange factors (GEFs) activate Rac and regulate its downstream protein effectors. In this study we show that Env-induced Rac activation is mediated by the Rac GEF Tiam-1, which associates with the adaptor protein IRSp53 to link Rac to the Wave2 complex. Rac and the tyrosine kinase Abl then activate the Wave2 complex and promote Arp2/3-dependent actin polymerization. Env-mediated cell-cell fusion, virus-cell fusion and HIV-1 infection are dependent on Tiam-1, Abl, IRSp53, Wave2, and Arp3 as shown by attenuation of fusion and infection in cells expressing siRNA targeted to these signaling components. HIV-1 Env-dependent cell-cell fusion, virus-cell fusion and infection were also inhibited by Abl kinase inhibitors, imatinib, nilotinib, and dasatinib. Treatment of cells with Abl kinase inhibitors did not affect cell viability or surface expression of CD4 and CCR5. Similar results with inhibitors and siRNAs were obtained when Env-dependent cell-cell fusion, virus-cell fusion or infection was measured, and when cell lines or primary cells were the target. Using membrane curving agents and fluorescence microscopy, we showed that inhibition of Abl kinase activity arrests fusion at the hemifusion (lipid mixing) step, suggesting a role for Abl-mediated actin remodeling in pore formation and expansion. These results suggest a potential utility of Abl kinase inhibitors to treat HIV-1 infected patients

The Membrane Fusion Step of Vaccinia Virus Entry Is Cooperatively Mediated by Multiple Viral Proteins and Host Cell Components

For many viruses, one or two proteins allow cell attachment and entry, which occurs through the plasma membrane or following endocytosis at low pH. In contrast, vaccinia virus (VACV) enters cells by both neutral and low pH routes; four proteins mediate cell attachment and twelve that are associated in a membrane complex and conserved in all poxviruses are dedicated to entry. The aim of the present study was to determine the roles of cellular and viral proteins in initial stages of entry, specifically fusion of the membranes of the mature virion and cell. For analysis of the role of cellular components, we used well characterized inhibitors and measured binding of a recombinant VACV virion containing Gaussia luciferase fused to a core protein; viral and cellular membrane lipid mixing with a self-quenching fluorescent probe in the virion membrane; and core entry with a recombinant VACV expressing firefly luciferase and electron microscopy. We determined that inhibitors of tyrosine protein kinases, dynamin GTPase and actin dynamics had little effect on binding of virions to cells but impaired membrane fusion, whereas partial cholesterol depletion and inhibitors of endosomal acidification and membrane blebbing had a severe effect at the later stage of core entry. To determine the role of viral proteins, virions lacking individual membrane components were purified from cells infected with members of a panel of ten conditional-lethal inducible mutants. Each of the entry protein-deficient virions had severely reduced infectivity and except for A28, L1 and L5 greatly impaired membrane fusion. In addition, a potent neutralizing L1 monoclonal antibody blocked entry at a post-membrane lipid-mixing step. Taken together, these results suggested a 2-step entry model and implicated an unprecedented number of viral proteins and cellular components involved in signaling and actin rearrangement for initiation of virus-cell membrane fusion during poxvirus entry

Macrophage signaling in HIV-1 infection

The human immunodeficiency virus-1 (HIV-1) is a member of the lentivirus genus. The virus does not rely exclusively on the host cell machinery, but also on viral proteins that act as molecular switches during the viral life cycle which play significant functions in viral pathogenesis, notably by modulating cell signaling. The role of HIV-1 proteins (Nef, Tat, Vpr, and gp120) in modulating macrophage signaling has been recently unveiled. Accessory, regulatory, and structural HIV-1 proteins interact with signaling pathways in infected macrophages. In addition, exogenous Nef, Tat, Vpr, and gp120 proteins have been detected in the serum of HIV-1 infected patients. Possibly, these proteins are released by infected/apoptotic cells. Exogenous accessory regulatory HIV-1 proteins are able to enter macrophages and modulate cellular machineries including those that affect viral transcription. Furthermore HIV-1 proteins, e.g., gp120, may exert their effects by interacting with cell surface membrane receptors, especially chemokine co-receptors. By activating the signaling pathways such as NF-kappaB, MAP kinase (MAPK) and JAK/STAT, HIV-1 proteins promote viral replication by stimulating transcription from the long terminal repeat (LTR) in infected macrophages; they are also involved in macrophage-mediated bystander T cell apoptosis. The role of HIV-1 proteins in the modulation of macrophage signaling will be discussed in regard to the formation of viral reservoirs and macrophage-mediated T cell apoptosis during HIV-1 infection

The macrophage in HIV-1 infection: From activation to deactivation?

Macrophages play a crucial role in innate and adaptative immunity in response to microorganisms and are an important cellular target during HIV-1 infection. Recently, the heterogeneity of the macrophage population has been highlighted. Classically activated or type 1 macrophages (M1) induced in particular by IFN-γ display a pro-inflammatory profile. The alternatively activated or type 2 macrophages (M2) induced by Th-2 cytokines, such as IL-4 and IL-13 express anti-inflammatory and tissue repair properties. Finally IL-10 has been described as the prototypic cytokine involved in the deactivation of macrophages (dM). Since the capacity of macrophages to support productive HIV-1 infection is known to be modulated by cytokines, this review shows how modulation of macrophage activation by cytokines impacts the capacity to support productive HIV-1 infection. Based on the activation status of macrophages we propose a model starting with M1 classically activated macrophages with accelerated formation of viral reservoirs in a context of Th1 and proinflammatory cytokines. Then IL-4/IL-13 alternatively activated M2 macrophages will enter into the game that will stop the expansion of the HIV-1 reservoir. Finally IL-10 deactivation of macrophages will lead to immune failure observed at the very late stages of the HIV-1 disease