E-Voting in an ubicomp world: trust, privacy, and social implications

The advances made in technology have unchained the user from the desktop into interactions where access is anywhere, anytime. In addition, the introduction of ubiquitous computing (ubicomp) will see further changes in how we interact with technology and also socially. Ubicomp evokes a near future in which humans will be surrounded by “always-on,” unobtrusive, interconnected intelligent objects where information is exchanged seamlessly. This seamless exchange of information has vast social implications, in particular the protection and management of personal information. This research project investigates the concepts of trust and privacy issues specifically related to the exchange of e-voting information when using a ubicomp type system

Variabilidade na coordenação motora: uma abordagem centrada no delineamento gemelar

O propósito deste estudo foi estimar a contribuição dos fatores genéticos e ambientais na variabilidade do desempenho interindividual na coordenação motora. A amostra foi constituída por 64 pares de gêmeos portugueses, com idades entre cinco e 14 anos. Avaliou-se o desempenho da coordenação através das quatro provas da bateria KTK: equilíbrio à retaguarda (ER); saltos monopedais (SM); transposição lateral (TL); saltos laterais (SL). Calculou-se o coeficiente de correlação intraclasse (t), sendo estimada a contribuição dos fatores genéticos (a²), ambientais comuns (c²) e únicos (e²). Os resultados mostram valores de t mais elevados entre gêmeos monozigóticos, sugerindo presença de fatores genéticos. Entretanto, estimativas de a² foram baixas, variando entre 15% (TL) e 41% (SM), enquanto para c² situaram-se entre 46% (SL) e 58% (TL), e para e² entre 11% (SM) e 28% (TL). Conclui-se que fatores ambientais são responsáveis pela maior parcela de influência na variabilidade do desempenho na coordenação motora.El objetivo del presente estudio fue estimar la contribución de los factores genéticos y ambientales en la vEl objetivo del presente estudio fue estimar la contribución de los factores genéticos y ambientales en la variabilidad del desempeño interindividual en la coordinación motora. La muestra fue constituida por 64 pares de gemelos portugueses, con edades entre 5 y 14 años. Se evaluó el desempeño de la coordinación a través de las cuatro pruebas de la batería KTK: equilibrio a la retaguardia (ER); saltos monopedales (SM); transposición lateral (TL); saltos laterales (SL). Se calculó el coeficiente intraclase (t), siendo estimada la contribución de los factores genéticos (a²), ambientales comunes (c²) y únicos (e²). Los resultados muestran valores t mas elevados entre gemelos monocigóticos, sugiriendo la presencia de factores genéticos. Por otro lado, estimaciones de a² fueron bajas, variando entre 15% (TL) y 41% (SM), mientras para c² se sitúan entre 46% (SL) y 58% (TL), y para e² entre 11% (SM) y 28% (TL). Se concluye que factores ambientales son responsables por la mayor porción de influencia de la variabilidad del desempeño en la coordinación motora.The purpose of this study was to estimate the contribution of environmental and genetic factors on the variability of interindividual performance in motor coordination. Sample comprised 64 twin pairs, aged 5 to 14 years old, from Portugal. Motor coordination was evaluated by KTK battery: backward balance (ER); hopping on one leg (SM); shifting platforms (TL); jumping sideways (SL). Intraclass correlation coefficient (t) was calculated. Contributions of genetic (a²), shared (c²) and unique environmental (e²) factors were estimated. Our results showed t values higher in monozygotic twins, suggesting the presence of genetic factors. Nevertheless, a² estimates were low, ranging from 15% (TL) to 41% (SM), while to common environment (c²) ranged from 46% (SL) to 58% (TL), and unique effects ranged from 11% (SM) to 28% (TL). These results suggest that environmental factors are responsible for the greatest part of influence on variability of interindividual performance in motor coordination tests

A Geodetic Approach to Gravity Reduction for Geophysics

The currently adopted approach to reduce observed gravity data for geophysical purposes includes several approximations. These were originally used to reduce computational effort, but have remained standard practice even though the required computing power is now readily available. In contrast, more precise gravity reductions are routinely employed in physical geodesy. The difference between simple Bouguer gravity anomalies derived using the geophysical and geodetic approaches can reach several tens of μms-2. The geodetic reductions include a more accurate calculation of normal gravity as a function of latitude, and a free air correction that accounts for the non-sphericity of the figure of the Earth. Also important, especially given the advent of Global Positioning System coordination of gravity surveys, is the need to ensure that the correct vertical and horizontal coordinate systems are used for the gravity reduction procedure. Errors associated with the use of non-geocentric horizontal coordinates and ellipsoidal heights are significant when compared with the accuracy of an individual gravity measurement. A generalised gravity reduction program and a coordinate transformation program are presented which can be employed to reduce geophysical data in a geodetic manner

Complement factor H protects mice from ischemic acute kidney injury but is not critical for controlling complement activation by glomerular IgM

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Factor H related proteins modulate complement activation on kidney cells

Complement activation at a particular location is determined by the balance of activating and inhibitory proteins. Factor H is a key regulator of the alternative pathway of complement, and genetic or acquired impairments in Factor H are associated with glomerular injury. The human Factor H-related proteins (FHRs) comprise a family of five proteins that are structurally related to Factor H. Variations in the genes or expression levels of the FHRs are also associated with glomerular disease, although the mechanisms of glomerular protection/injury are incompletely understood. To explore the role of the FHRs on complement regulation/ dysregulation in the kidney, we expressed and purified recombinant murine FHRs (FHRs A, B, C and E). These four distinct FHRs contain binding regions with high amino acid sequence homology to binding regions within Factor H, but we observed different interactions of the FHRs with Factor H binding ligands, including heparin and C3d. There was differential binding of the FHRs to the resident kidney cell types (mesangial, glomerular endothelial, podocytes, and tubular epithelial). All four FHRs caused complement dysregulation on kidney cell surfaces in vitro, although the magnitude of the effect differed among the FHRs and also varied among the different kidney cells. However, only FHR E caused glomerular complement dysregulation when injected in vivo but did not exacerbate injury when injected into mice with ischemic acute kidney injury, an alternative pathway-mediated model. Thus, our experiments demonstrate that the FHRs have unique, and likely context-dependent, effects on the different cell types within the kidney.Nephrolog

Factor H related proteins modulate complement activation on kidney cells

Complement activation at a particular location is determined by the balance of activating and inhibitory proteins. Factor H is a key regulator of the alternative pathway of complement, and genetic or acquired impairments in Factor H are associated with glomerular injury. The human Factor H-related proteins (FHRs) comprise a family of five proteins that are structurally related to Factor H. Variations in the genes or expression levels of the FHRs are also associated with glomerular disease, although the mechanisms of glomerular protection/injury are incompletely understood. To explore the role of the FHRs on complement regulation/ dysregulation in the kidney, we expressed and purified recombinant murine FHRs (FHRs A, B, C and E). These four distinct FHRs contain binding regions with high amino acid sequence homology to binding regions within Factor H, but we observed different interactions of the FHRs with Factor H binding ligands, including heparin and C3d. There was differential binding of the FHRs to the resident kidney cell types (mesangial, glomerular endothelial, podocytes, and tubular epithelial). All four FHRs caused complement dysregulation on kidney cell surfaces in vitro, although the magnitude of the effect differed among the FHRs and also varied among the different kidney cells. However, only FHR E caused glomerular complement dysregulation when injected in vivo but did not exacerbate injury when injected into mice with ischemic acute kidney injury, an alternative pathway-mediated model. Thus, our experiments demonstrate that the FHRs have unique, and likely context-dependent, effects on the different cell types within the kidney