Predicting the causal agent in verbally described social interactions

Implicit causality in interpersonal verbs (i.e., causal assumptions about the initiator of a social interaction) has been extensively investigated, especially in English and German language (cf. Rudolph & Försterling, 1997). The present study is the first to investigate verb causality in Danish language using a student sample (N = 96) while simultaneously examining consensus (i.e., to what extent others besides the grammatical subject treat the object like this) and distinctiveness (i.e., to what extent solely the object person is treated by the subject like this) as predictors of causal attribution to subject or object. A strong verb causality effect in Danish language emerged. Consensus proved to be a better predictor than distinctiveness for causal attribution

Cure of chronic viral infection and virus-induced type 1 diabetes by neutralizing antibodies

The use of neutralizing antibodies is one of the most successful methods to interfere with receptor–ligand interactions in vivo. In particular blockade of soluble inflammatory mediators or their corresponding cellular receptors was proven an effective way to regulate inflammation and/or prevent its negative consequences. However, one problem that comes along with an effective neutralization of inflammatory mediators is the general systemic immunomodulatory effect. It is, therefore, important to design a treatment regimen in a way to strike at the right place and at the right time in order to achieve maximal effects with minimal duration of immunosuppression or hyperactivation. In this review, we reflect on two examples of how short time administration of such neutralizing antibodies can block two distinct inflammatory consequences of viral infection. First, we review recent findings that blockade of IL-10/IL-10R interaction can resolve chronic viral infection and second, we reflect on how neutralization of the chemokine CXCL10 can abrogate virus-induced type 1 diabetes

Impact of videoconferencing on the demand for air travel

Thesis (M.S.)--Massachusetts Institute of Technology, Dept. of Aeronautics and Astronautics, 1995.Includes bibliographical references (leaves 260-266).by Matthias Mette.M.S

Streptococcus pneumoniae induces expression of the antibacterial CXC chemokine MIG/CXCL9 via MyD88-dependent signaling in a murine model of airway infection.

MIG/CXCL9 belongs to the CXC family of chemokines and participates in the regulation of leukocyte-trafficking and angiogenesis. Certain chemokines, including human MIG/CXCL9, exert strong antibacterial activity in vitro, although the importance of this property in vivo is unknown. In the present study, we investigated the expression and a possible role for MIG/CXCL9 in host defense during mucosal airway infection caused by Streptococcus pneumoniae in vivo. We found that intranasal challenge of C57BL/6 wild-type mice with pneumococci elicited production of high levels of MIG/CXCL9 in the lungs via the MyD88-dependent signaling pathway. Whereas both human and murine MIG/CXCL9 showed efficient killing of S. pneumoniae in vitro, MIG/CXCL9 knock-out mice were not more susceptible to pneumococcal infection. Our data demonstrate that, in vivo this chemokine probably has a redundant role, acting together with other antibacterial peptides and chemokines, in innate and adaptive host defense mechanisms against pneumococcal infections

The "exposome" concept - how environmental risk factors influence cardiovascular health

There is general consensus that environmental pollution and non-chemical stressors contribute to the in- cidence and prevalence of chronic noncommunicable disease (e.g. cardiovascular, metabolic and mental). Clinical and epidemiological studies support that air pollution and traffic noise are associated with a higher risk for cardiovascular disease and significantly contribute to overall mortality. In this respect, the "exposome" provides a comprehensive description of lifelong exposure history. A recent publication using an updated global exposure-mortality model found that the global all-cause mortality rate attributable to ambient air pollution by PM2.5 and O-3 was 8.79 (95% CI 7.11-10.41) million in 2015 - much higher than previously calculated. For Europe this corresponds to 790,000 premature deaths due to ambient air pollution. Various large scale studies and expert commissions have identified air pollution as the leading health risk factor in the physical environment, followed by water and soil pollution with heavy metals, pesticides, other chemicals and occupational exposures, however neglecting the non-chemical environmental health risk factors: mental stress, light exposure, climatic changes and traffic noise. Especially for traffic noise-related health effects there are numerous clinical and epidemiological studies reporting significant impact on cardiovascular disease. We here provide an in-depth review on the health effects of the external exposome, with emphasis on air pollution and traffic noise and to a lesser degree mental stress and other environmental pollutants. In addition, we summarize our previously published experimental research investigating effects of aircraft noise exposure in mice and provide mechanistic insights on how noise contributes to noncommunicable disease

Long-term residential exposure to PM2.5, PM10, black carbon, NO2, and ozone and mortality in a Danish cohort

Air pollutants such as NO2 and PM2.5 have consistently been linked to mortality, but only few previous studies have addressed associations with long-term exposure to black carbon (BC) and ozone (O3). We investigated the association between PM2.5, PM10, BC, NO2, and O3 and mortality in a Danish cohort of 49,564 individuals who were followed up from enrollment in 1993–1997 through 2015. Residential address history from 1979 onwards was combined with air pollution exposure obtained by the state-of-the-art, validated, THOR/AirGIS air pollution modelling system, and information on residential traffic noise exposure, lifestyle and socio-demography. We observed higher risks of all-cause as well as cardiovascular disease (CVD) mortality with higher long-term exposure to PM2.5, PM10, BC, and NO2. For PM2.5 and CVD mortality, a hazard ratio (HR) of 1.29 (95% CI: 1.13–1.47) per 5 μg/m3 was observed, and correspondingly HRs of 1.16 (95% CI: 1.05–1.27) and 1.11 (95% CI: 1.04–1.17) were observed for BC (per 1 μg/m3) and NO2 (per 10 μg/m3), respectively. Adjustment for noise gave slightly lower estimates for the air pollutants and CVD mortality. Inverse relationships were observed for O3. None of the investigated air pollutants were related to risk of respiratory mortality. Stratified analyses suggested that the elevated risks of CVD and all-cause mortality in relation to long-term PM, NO2 and BC exposure were restricted to males. This study supports a role of PM, BC, and NO2 in all-cause and CVD mortality independent of road traffic noise exposure