Two Half-Truths Make a Whole? On Bias in Self-Reports and Tracking Data

The pervasive use of mobile information technologies brings new patterns of media usage, but also challenges to the measurement of media exposure. Researchers wishing to, for example, understand the nature of selective exposure on algorithmically driven platforms need to precisely attribute individuals’ exposure to specific content. Prior research has used tracking data to show that survey-based self-reports of media exposure are critically unreliable. So far, however, little effort has been invested into assessing the specific biases of tracking methods themselves. Using data from a multimethod study, we show that tracking data from mobile devices is linked to systematic distortions in self-report biases. Further inherent but unobservable sources of bias, along with potential solutions, are discussed

Indoleamine 2,3-Dioxygenase in Human Hematopoietic Stem Cell Transplantation

In recent years tryptophan metabolism and its rate limiting enzyme indoleamine 2,3-dioxygenase (IDO) have attracted increasing attention for their potential to modulate immune responses including the regulation of transplantation tolerance. The focus of this review is to discuss some features of IDO activity which particularly relate to hematopoietic stem cell transplantation (HSCT). HSCT invariably involves the establishment of some degree of a donor-derived immune system in the recipient. Thus, the outstanding feature of tolerance in HSCT is that in this type of transplantation it is not rejection, which causes the most severe problems to HSCT recipients, but the reverse, graft-versus-host (GvH) directed immune responses. We will discuss the peculiar role of IDO activity and accelerated tryptophan metabolism at the interface between immune activation and immune suppression and delineate from theoretical and experimental evidence the potential significance of IDO in mediating tolerance in HSCT. Finally, we will examine therapeutic options for exploitation of IDO activity in the generation of allo-antigen-specific tolerance, i.e. avoiding allo-reactivity while maintaining immunocompetence, in HSCT

Messung von Personalisierung in computervermittelter Kommunikation

Das Ziel personalisierter Online-Angebote ist, Rezipienten bei der Informationssuche zu unterstützen. Dabei greifen sie zwangsläufig in deren Auswahlentscheidungen ein und müssen deshalb als eigenständiger Einflussfaktor empirisch erschlossen werden. Die dahinterstehenden Algorithmen kommerzieller Anbieter sind für die Forschung größtenteils eine intransparente "Black Box". Automatisierte Online-Experimente stellen eine selten eingesetzte Methode dar, die durch systematische Simulation von Nutzerverhalten die Funktionsweise von Personalisierungsalgorithmen ermitteln kann. Der Beitrag diskutiert zunächst Auswirkungen und Funktionsweise von Personalisierung und stellt daraufhin ein automatisiertes Online-Experiment am Beispiel der Google-Suche dar. Die vorgestellte Methode ermöglicht einen sozialwissenschaftlichen Zugriff auf die Funktionsweise und Inhalte von personalisierten Angeboten und fördert gleichzeitig Validität, Transparenz und Replizierbarkeit von Nutzungsstudien.Personalized web pages are explicitly designed to curate the information available to their users. By definition, they influence users' selectivity and need to be considered as a new factor affecting selection decisions. In most cases, the algorithms that determine recommendations are "black boxes" whose precise functionality remains opaque to researchers. Drawing on a pilot study of Google Search, this chapter argues that the rarely employed automated online experiment represents a promising method for studying "personalization effects". The method presented not only gives researchers access to the effects and contents of personalized web pages, but it also reinforces scientific rigor through higher validity, transparency and replicability of studies on selection behavior

Neutralität, Transparenz und Kompetenz: rechtliche Ansatzpunkte für eine Neuregulierung des Suchmaschinenmarktes

Die Frage nach den gesellschaftlichen Implikationen der Google-Dienste steht schon länger auf der wissenschaftlichen Agenda. Auch die Rechtswissenschaft hat sich dieser Frage in der Vergangenheit bereits angenommen: Ansatz waren dabei häufig Fragen des Datenschutzes und des Rechts der Nutzer auf informationelle Selbstbestimmung. Eine Evaluierung der Relevanz des Suchmaschinendienstes als ein zentrales Funktionselement im Internet für die öffentliche Meinungsbildung steht allerdings noch aus. Dieser Frage versucht sich der Aufsatz unter Rückgriff auf neue Forschungsergebnisse aus der Kommunikationswissenschaft rechtswissenschaftlich zu nähern. Danach ist die Suchmaschine wegen ihrer Relevanz für die Meinungsvielfaltssicherung in eine gesellschaftliche Verantwortung hineingewachsen, deren Erfüllung der Gesetzgeber aufgrund seiner Gewährleistungsverantwortung absichern muss. Hierfür werden erste Regulierungsansätze vorgeschlagen, an denen sich eine Neuregulierung orientieren könnte.Scientific research on the societal implications of Google’s manifold set of services has a long-standing tradition. Legal scholars have so far mainly focused on data protection, privacy and the "right to informational self-determination". Search engines’ role in opinion formation, however, has rarely if ever been the subject of a rigorous analysis. This article draws on recent research from mass communication research in order to provide a first assessment of the necessity and possible approaches to search engine regulation from the perspective of media law and plurality

Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration

Varicella zoster virus (VZV) is a highly prevalent human pathogen that establishes latency in neurons of the peripheral nervous system. Primary infection causes varicella whereas reactivation results in zoster, which is often followed by chronic pain in adults. Following infection of epithelial cells in the respiratory tract, VZV spreads within the host by hijacking leukocytes, including T cells, in the tonsils and other regional lymph nodes, and modifying their activity. In spite of its importance in pathogenesis, the mechanism of dissemination remains poorly understood. Here we addressed the influence of VZV on leukocyte migration and found that the purified recombinant soluble ectodomain of VZV glycoprotein C (rSgC) binds chemokines with high affinity. Functional experiments show that VZV rSgC potentiates chemokine activity, enhancing the migration of monocyte and T cell lines and, most importantly, human tonsillar leukocytes at low chemokine concentrations. Binding and potentiation of chemokine activity occurs through the C-terminal part of gC ectodomain, containing predicted immunoglobulin-like domains. The mechanism of action of VZV rSgC requires interaction with the chemokine and signalling through the chemokine receptor. Finally, we show that VZV viral particles enhance chemokine-dependent T cell migration and that gC is partially required for this activity. We propose that VZV gC activity facilitates the recruitment and subsequent infection of leukocytes and thereby enhances VZV systemic dissemination in humans

Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration

Varicella zoster virus (VZV) is a highly prevalent human pathogen that establishes latency in neurons of the peripheral nervous system. Primary infection causes varicella whereas reactivation results in zoster, which is often followed by chronic pain in adults. Following infection of epithelial cells in the respiratory tract, VZV spreads within the host by hijacking leukocytes, including T cells, in the tonsils and other regional lymph nodes, and modifying their activity. In spite of its importance in pathogenesis, the mechanism of dissemination remains poorly understood. Here we addressed the influence of VZV on leukocyte migration and found that the purified recombinant soluble ectodomain of VZV glycoprotein C (rSgC) binds chemokines with high affinity. Functional experiments show that VZV rSgC potentiates chemokine activity, enhancing the migration of monocyte and T cell lines and, most importantly, human tonsillar leukocytes at low chemokine concentrations. Binding and potentiation of chemokine activity occurs through the C-terminal part of gC ectodomain, containing predicted immunoglobulin-like domains. The mechanism of action of VZV rSgC requires interaction with the chemokine and signalling through the chemokine receptor. Finally, we show that VZV viral particles enhance chemokine-dependent T cell migration and that gC is partially required for this activity. We propose that VZV gC activity facilitates the recruitment and subsequent infection of leukocytes and thereby enhances VZ

Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration.

Varicella zoster virus (VZV) is a highly prevalent human pathogen that establishes latency in neurons of the peripheral nervous system. Primary infection causes varicella whereas reactivation results in zoster, which is often followed by chronic pain in adults. Following infection of epithelial cells in the respiratory tract, VZV spreads within the host by hijacking leukocytes, including T cells, in the tonsils and other regional lymph nodes, and modifying their activity. In spite of its importance in pathogenesis, the mechanism of dissemination remains poorly understood. Here we addressed the influence of VZV on leukocyte migration and found that the purified recombinant soluble ectodomain of VZV glycoprotein C (rSgC) binds chemokines with high affinity. Functional experiments show that VZV rSgC potentiates chemokine activity, enhancing the migration of monocyte and T cell lines and, most importantly, human tonsillar leukocytes at low chemokine concentrations. Binding and potentiation of chemokine activity occurs through the C-terminal part of gC ectodomain, containing predicted immunoglobulin-like domains. The mechanism of action of VZV rSgC requires interaction with the chemokine and signalling through the chemokine receptor. Finally, we show that VZV viral particles enhance chemokine-dependent T cell migration and that gC is partially required for this activity. We propose that VZV gC activity facilitates the recruitment and subsequent infection of leukocytes and thereby enhances VZV systemic dissemination in humans

Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration

Varicella zoster virus (VZV) is a highly prevalent human pathogen that establishes latency in neurons of the peripheral nervous system. Primary infection causes varicella whereas reactivation results in zoster, which is often followed by chronic pain in adults. Following infection of epithelial cells in the respiratory tract, VZV spreads within the host by hijacking leukocytes, including T cells, in the tonsils and other regional lymph nodes, and modifying their activity. In spite of its importance in pathogenesis, the mechanism of dissemination remains poorly understood. Here we addressed the influence of VZV on leukocyte migration and found that the purified recombinant soluble ectodomain of VZV glycoprotein C (rSgC) binds chemokines with high affinity. Functional experiments show that VZV rSgC potentiates chemokine activity, enhancing the migration of monocyte and T cell lines and, most importantly, human tonsillar leukocytes at low chemokine concentrations. Binding and potentiation of chemokine activity occurs through the C-terminal part of gC ectodomain, containing predicted immunoglobulin-like domains. The mechanism of action of VZV rSgC requires interaction with the chemokine and signalling through the chemokine receptor. Finally, we show that VZV viral particles enhance chemokine-dependent T cell migration and that gC is partially required for this activity. We propose that VZV gC activity facilitates the recruitment and subsequent infection of leukocytes and thereby enhances VZV systemic dissemination in humans