Public perception of drones… or should that be remotely piloted aircraft systems?

The media coverage of remotely piloted aircraft systems (RPAS) has highlighted some issues, particularly in terms of security and privacy concerns. As such, it is essential to understand the public\u27s perception towards these systems. The purpose of this study was to assess the public\u27s perception towards 1) The terminology used to define RPAS, which varies across the industry; 2) The applications, current and future, of RPAS; 3) The future of passenger transport involving RPAS, and 4) RPAS in general. It was found that there was little difference between the terms used to describe RPAS; however, there was a significant difference at the 90% confidence level for remotely piloted aircraft systems over drones . In terms of RPAS applications, community based applications had a positive perception, while personal applications were neutral. The implementation of RPAS into passenger transport aircraft was strongly negative. Finally, there was an overall positive perception towards RPAS

The two tryptophans of β2-microglobulin have distinct roles in function and folding and might represent two independent responses to evolutionary pressure

We have recently discovered that the two tryptophans of human β2-microglobulin have distinctive roles within the structure and function of the protein. Deeply buried in the core, Trp95 is essential for folding stability, whereas Trp60, which is solvent-exposed, plays a crucial role in promoting the binding of β2-microglobulin to the heavy chain of the class I major histocompatibility complex (MHCI). We have previously shown that the thermodynamic disadvantage of having Trp60 exposed on the surface is counter-balanced by the perfect fit between it and a cavity within the MHCI heavy chain that contributes significantly to the functional stabilization of the MHCI. Therefore, based on the peculiar differences of the two tryptophans, we have analysed the evolution of β2-microglobulin with respect to these residues

Structure of a Classical MHC Class I Molecule That Binds “Non-Classical” Ligands

The chicken MHC YF1*7.1 X-ray structures reveal that this protein binds lipids and thus represents a "hybrid" class I complex with features of classical as well as non-classical MHC molecules

Cross-talk between cd1d-restricted nkt cells and γδ cells in t regulatory cell response

CD1d is a non-classical major histocompatibility class 1-like molecule which primarily presents either microbial or endogenous glycolipid antigens to T cells involved in innate immunity. Natural killer T (NKT) cells and a subpopulation of γδ T cells expressing the Vγ4 T cell receptor (TCR) recognize CD1d. NKT and Vγ4 T cells function in the innate immune response via rapid activation subsequent to infection and secrete large quantities of cytokines that both help control infection and modulate the developing adaptive immune response. T regulatory cells represent one cell population impacted by both NKT and Vγ4 T cells. This review discusses the evidence that NKT cells promote T regulatory cell activation both through direct interaction of NKT cell and dendritic cells and through NKT cell secretion of large amounts of TGFβ, IL-10 and IL-2. Recent studies have shown that CD1d-restricted Vγ4 T cells, in contrast to NKT cells, selectively kill T regulatory cells through a caspase-dependent mechanism. Vγ4 T cell elimination of the T regulatory cell population allows activation of autoimmune CD8+ effector cells leading to severe cardiac injury in a coxsackievirus B3 (CVB3) myocarditis model in mice. CD1d-restricted immunity can therefore lead to either immunosuppression or autoimmunity depending upon the type of innate effector dominating during the infection

Structural studies of molecular recognition events at the cell surface

EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Human urotensin-II receptor desensitisation

Human Urotensin-II (U-II) is a cyclic undecapeptide that binds to the U-II receptor UT. The desensitisation mechanisms of the UT receptor (G_{q/11} coupled GPCR) are not well defined and hampered by (1) lack of native (in-vitro) models; (2) paucity of ligands, especially non-peptides and (3) irreversible binding of U-II. There are some limited studies using rat aorta, where a U-II induced primary contractile response was reduced upon a secondary re-challenge after 5-hours. Studies were undertaken to characterise cell lines expressing native (SJCRH30) and recombinant human hUT (HEK293 and CHO) for their suitability in binding and functional assays (PI and Ca^2+). SAR studies were carried out to characterise novel analogues modified at Tyr^9 of the U-II(4-11) template. This led to the identification of [3,5-diiodoTyr^9]U-II(4-11) a partial agonist in aorta and Ca^2+ assays at rat UT. Full agonism was demonstrated at hUT in PI and Ca^2+ assays. Efforts were made to delineate functional and genomic desensitisation of hUT. There was no functional desensitisation in SJCRH30. In HEK293hUT functional heterologous desensitisation of hUT was observed, this was not so in CHOhUT; instead P_2YR was functionally attenuated. In SJCRH30 6-hr U-II treatments led to UT mRNA reduction. Genomic desensitisation was also studied in Peripheral blood mononuclear cells (PBMCs). U-II treatments alone did not affect UT mRNA. Lipolysaccharide treatment of PBMCs led to UT mRNA upregulation which was desensitised with U-II treatments. In recombinant systems UT mRNA was upregulated at 6-hr U-II treatments. In conclusion modification of the U-II(4-11) template at Tyr^9 is useful for reducing efficacy. There is a difference in desensitisation profiles of native and recombinant hUT, where native receptors are not prone to functional desensitisation while receptor mRNA is reduced. In recombinant systems, hUT undergoes desensitisation (HEK293hUT only) while receptor mRNA is increased in both systems

Human urotensin-II receptor desensitisation

Human Urotensin-II (U-II) is a cyclic undecapeptide that binds to the U-II receptor UT. The desensitisation mechanisms of the UT receptor (G_{q/11} coupled GPCR) are not well defined and hampered by (1) lack of native (in-vitro) models; (2) paucity of ligands, especially non-peptides and (3) irreversible binding of U-II. There are some limited studies using rat aorta, where a U-II induced primary contractile response was reduced upon a secondary re-challenge after 5-hours. Studies were undertaken to characterise cell lines expressing native (SJCRH30) and recombinant human hUT (HEK293 and CHO) for their suitability in binding and functional assays (PI and Ca^2+). SAR studies were carried out to characterise novel analogues modified at Tyr^9 of the U-II(4-11) template. This led to the identification of [3,5-diiodoTyr^9]U-II(4-11) a partial agonist in aorta and Ca^2+ assays at rat UT. Full agonism was demonstrated at hUT in PI and Ca^2+ assays. Efforts were made to delineate functional and genomic desensitisation of hUT. There was no functional desensitisation in SJCRH30. In HEK293hUT functional heterologous desensitisation of hUT was observed, this was not so in CHOhUT; instead P_2YR was functionally attenuated. In SJCRH30 6-hr U-II treatments led to UT mRNA reduction. Genomic desensitisation was also studied in Peripheral blood mononuclear cells (PBMCs). U-II treatments alone did not affect UT mRNA. Lipolysaccharide treatment of PBMCs led to UT mRNA upregulation which was desensitised with U-II treatments. In recombinant systems UT mRNA was upregulated at 6-hr U-II treatments. In conclusion modification of the U-II(4-11) template at Tyr^9 is useful for reducing efficacy. There is a difference in desensitisation profiles of native and recombinant hUT, where native receptors are not prone to functional desensitisation while receptor mRNA is reduced. In recombinant systems, hUT undergoes desensitisation (HEK293hUT only) while receptor mRNA is increased in both systems.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Feature article: Certification challenges for next-generation avionics and air traffic management systems

Air traffic is doubling every 15 years, and aviation systems must modernize to address sustainability challenges. The need to balance capacity, efficiency, safety, and environmental requirements is reflected by the several air traffic management (ATM) and avionics modernization initiatives under way. The major collaborative research programs today are the European Union's Single European Sky ATM Research (SESAR) project and the United States' Next-Generation Air Transportation System (NextGen) led by the Federal Aviation Administration (FAA). Other modernization initiatives include the Collaborative Action for Renovation of Air Traffic Systems in Japan, SIRIUS in Brazil, OneSky in Australia, and similar programs in Canada, China, India, and Russia [1]. The International Civil Aviation Organization (ICAO) has authorized a globally coordinated plan, published as the Global Air Navigation Plan (GANP) [1], to guide the harmonized implementation of communication, navigation, surveillance, and avionics (CNS+A) enhancements across regions and states. In the CNS+A context, aircraft safety is a shared responsibility between airborne and ground-based resources [1]. Hence, this is a safety challenge requiring changes to the current regulatory framework to properly capture the nature of this shared responsibility and the concept of integrated CNS+A systems. Certification of aircraft and ground equipment (hardware and software) and organizational approvals are essential elements to ensure continued and enhanced safety