Dynamic weighting of feature dimensions in visual search: behavioral and psychophysiological evidence

Dimension-based accounts of visual search and selection have significantly contributed to the understanding of the cognitive mechanisms of attention. Extensions of the original approach assuming the existence of dimension-based feature contrast saliency signals that govern the allocation of focal attention have recently been employed to explain the spatial and temporal dynamics of the relative strengths of saliency representations. Here we review behavioral and neurophysiological findings providing evidence for the dynamic trial-by-trial weighting of feature dimensions in a variety of visual search tasks. The examination of the effects of feature and dimension-based inter-trial transitions in feature detection tasks shows that search performance is affected by the change of target-defining dimensions, but not features. The use of the redundant-signals paradigm shows that feature contrast saliency signals are integrated at a pre-selective processing stage. The comparison of feature detection and compound search tasks suggests that the relative significance of dimension-dependent and dimension-independent saliency representations is task-contingent. Empirical findings that explain reduced dimension-based effects in compound search tasks are discussed. Psychophysiological evidence is presented that confirms the assumption that the locus of the effects of feature dimension changes is perceptual pre-selective rather than post-selective response-based. Behavioral and psychophysiological results are considered within in the framework of the dimension weighting account of selective visual attention

Completing the triad: Synthesis and full characterization of homoleptic and heteroleptic carbonyl and nitrosyl complexes of the group VI metals

Oxidation of M(CO)$_{6}$ (M = Cr, Mo, W) with the synergistic oxidative system Ag[WCA]/0.5 I$_{2}$ yields the fully characterized metalloradical salts [M(CO)$_{6}$]+˙[WCA]− (weakly coordinating anion WCA = [F-{Al(OR$^{F}$)$_{3}$}$_{2}$]$^{-}$, R$^{F}$ = C(CF$_{3}$)$_{3}$). The new metalloradical cations with M = Mo and W showcase a similar structural fluxionality as the previously reported [Cr(CO)$_{6}$]$^{+}$˙. Their reactivity increases from M = Cr < Mo < W and their syntheses allow for in-depth insights into the properties of the group 6 carbonyl triad. Furthermore, the reaction of NO$^{+}$[WCA]$^{-}$ with neutral carbonyl complexes M(CO)$_{6}$ gives access to the heteroleptic carbonyl/nitrosyl cations [M(CO)$_{5}$(NO)]$^{+}$ as salts of the WCA [Al(ORF)$_{4}$]$^{-}$, the first complete transition metal triad of their kind

α-Herpesvirus glycoprotein D interaction with sensory neurons triggers formation of varicosities that serve as virus exit sites

α-Herpesviruses constitute closely related neurotropic viruses, including herpes simplex virus in man and pseudorabies virus (PRV) in pigs. Peripheral sensory neurons, such as trigeminal ganglion (TG) neurons, are predominant target cells for virus spread and lifelong latent infections. We report that in vitro infection of swine TG neurons with the homologous swine α-herpesvirus PRV results in the appearance of numerous synaptophysin-positive synaptic boutons (varicosities) along the axons. Nonneuronal cells that were juxtaposed to these varicosities became preferentially infected with PRV, suggesting that varicosities serve as axonal exit sites for the virus. Viral envelope glycoprotein D (gD) was found to be necessary and sufficient for the induction of varicosities. Inhibition of Cdc42 Rho GTPase and p38 mitogen-activated protein kinase signaling pathways strongly suppressed gD-induced varicosity formation. These data represent a novel aspect of the cell biology of α-herpesvirus infections of sensory neurons, demonstrating that virus attachment/entry is associated with signaling events and neuronal changes that may prepare efficient egress of progeny virus

Micropower front-end interface for differential-capacitive sensor systems

Accepted versio

Cytolethal Distending Toxin-Induced Cell Cycle Arrest of Lymphocytes is Dependent Upon Recognition and Binding to Cholesterol

Induction of cell cycle arrest in lymphocytes after exposure to the Aggregatibacter actinomycetemcomitans cytolethal distending toxin (Cdt) is dependent upon the integrity of lipid membrane microdomains. In this study we further demonstrate that the association of Cdt with lymphocyte plasma membranes is dependent upon binding to cholesterol. Depletion of cholesterol resulted in reduced toxin binding, whereas repletion of cholesterol-depleted cells restored binding. We employed fluorescence resonance energy transfer and surface plasmon resonance to demonstrate that toxin association with model membranes is dependent upon the concentration of cholesterol; moreover, these interactions were cholesterol-specific as the toxin failed to interact with model membranes containing stigmasterol, ergosterol, or lanosterol. Further analysis of the toxin indicated that the CdtC subunit contains a cholesterol recognition/interaction amino acid consensus (CRAC) region. Mutation of the CRAC site resulted in decreased binding of the holotoxin to cholesterol-containing model membranes as well as to the surface of Jurkat cells. The mutant toxin also exhibited reduced capacity for intracellular transfer of the active toxin subunit, CdtB, as well as reduced toxicity. Collectively, these observations indicate that membrane cholesterol serves as an essential ligand for Cdt and that this association can be blocked by either depleting membranes of cholesterol or mutation of the CRAC site. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc

Utilizing linked open data for web service selection and composition to support e-commerce transactions

© Springer International Publishing Switzerland 2016. Web Services (WS) have emerged during the past decades as a means for loosely coupled distributed systems to interact and communicate. Nevertheless, the abundance of services that can be retrieved online, often providing similar functionalities, can raise questions regarding the selection of the optimal service to be included in a value added composition. We propose a framework for the selection and composition of WS utilizing Linked open Data (LoD). The proposed method is based on RDF triples describing the functional and non-functional characteristics of WS. We aim at the optimal composition of services as a result of specific SPARQL queries and personalized weights for QoS criteria. Finally we utilize an approach based on the particle swarm optimization (PSO) method for the ranking of returned services

ENABLING COLLABORATIVE E-HEALTH THROUGH TRIPLESPACE COMPUTING

Abstract The design and promotion of electronic patient summaries as an instrument to facilitate the pervasive delivery of healthcare is emerging as a key technology in eHealth solutions. From the technical point of view this requires powerful middleware systems supporting interoperability, multi-lingualism, security and patient privacy. In this paper we present a semantic coordination model and describe how it can be used to support pervasive access to electronic patient summaries

Structure of Herpes Simplex Virus Glycoprotein D Bound to the Human Receptor Nectin-1

Binding of herpes simplex virus (HSV) glycoprotein D (gD) to a cell surface receptor is required to trigger membrane fusion during entry into host cells. Nectin-1 is a cell adhesion molecule and the main HSV receptor in neurons and epithelial cells. We report the structure of gD bound to nectin-1 determined by x-ray crystallography to 4.0 Å resolution. The structure reveals that the nectin-1 binding site on gD differs from the binding site of the HVEM receptor. A surface on the first Ig-domain of nectin-1, which mediates homophilic interactions of Ig-like cell adhesion molecules, buries an area composed by residues from both the gD N- and C-terminal extensions. Phenylalanine 129, at the tip of the loop connecting β-strands F and G of nectin-1, protrudes into a groove on gD, which is otherwise occupied by C-terminal residues in the unliganded gD and by N-terminal residues in the gD/HVEM complex. Notably, mutation of Phe129 to alanine prevents nectin-1 binding to gD and HSV entry. Together these data are consistent with previous studies showing that gD disrupts the normal nectin-1 homophilic interactions. Furthermore, the structure of the complex supports a model in which gD-receptor binding triggers HSV entry through receptor-mediated displacement of the gD C-terminal region

Modeling violations of the race model inequality in bimodal paradigms: co-activation from decision and non-decision components

The redundant-signals paradigm (RSP) is designed to investigate response behavior in perceptual tasks in which response-relevant targets are defined by either one or two features, or modalities. The common finding is that responses are speeded for redundantly compared to singly defined targets. This redundant-signals effect (RSE) can be accounted for by race models if the response times do not violate the race model inequality (RMI). When there are violations of the RMI, race models are effectively excluded as a viable account of the RSE. The common alternative is provided by co-activation accounts, which assume that redundant target signals are integrated at some processing stage. However, “co-activation” has mostly been only indirectly inferred and the accounts have only rarely been explicitly modeled; if they were modeled, the RSE has typically been assumed to have a decisional locus. Yet, there are also indications in the literature that the RSE might originate, at least in part, at a non-decisional or motor stage. In the present study, using a distribution analysis of sequential-sampling models (ex-Wald and Ratcliff Diffusion model), the locus of the RSE was investigated for two bimodal (audio-visual) detection tasks that strongly violated the RMI, indicative of substantial co-activation. Three model variants assuming different loci of the RSE were fitted to the quantile reaction time proportions: a decision, a non-decision, and a combined variant both to vincentized group as well as individual data. The results suggest that for the two bimodal detection tasks, co-activation has a shared decisional and non-decisional locus. These findings point to the possibility that the mechanisms underlying the RSE depend on the specifics (task, stimulus, conditions, etc.) of the experimental paradigm