The effects of noise from combined traffic sources on annoyance: the case of interactions between rail and road noise (invited paper)

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Cardiovascular effects of environmental noise: research in Austria

Cardiovascular effects of noise rank second in terms of disability-adjusted life year (DALYs) after annoyance. Although research during the past decade has consolidated the available data base, the most recent meta-analysis still shows wide confidence intervals - indicating imprecise information for public health risk assessment. The alpine area of Tyrol in the Austrian part of the Alps has experienced a massive increase in car and heavy goods traffic (road and rail) during the last 35 years. Over the past 25 years small-, middle-, and large-sized epidemiological health surveys have been conducted - mostly within the framework of environmental health impact assessments. By design, these studies have emphasized a contextually driven environmental stress perspective, where the adverse health effects on account of noise are studied in a broader framework of environmental health, susceptibility, and coping. Furthermore, innovative exposure assessment strategies have been implemented. This article reviews the existing knowledge from these studies over time, and presents the exposure-response curves, with and without interaction assessment, based on standardized re-analyses and discusses it in the light of past and current cardiovascular noise effects research. The findings support relevant moderation by age, gender, and family history in nearly all studies and suggest a strong need for consideration of non-linearity in the exposure-response analyses. On the other hand, air pollution has not played a relevant role as a moderator in the noise-hypertension or the noise-angina pectoris relationship. Finally, different noise modeling procedures can introduce variations in the exposure response curves, with substantive consequences for public health risk assessment of noise exposure

Sound propagation in a valley-slope configuration: measurements and simulations (invited paper)

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Mass Spectrometry Analysis of Hepcidin Peptides in Experimental Mouse Models

The mouse is a valuable model for unravelling the role of hepcidin in iron homeostasis, however, such studies still report hepcidin mRNA levels as a surrogate marker for bioactive hepcidin in its pivotal function to block ferroportin-mediated iron transport. Here, we aimed to assess bioactive mouse Hepcidin-1 (Hep-1) and its paralogue Hepcidin-2 (Hep-2) at the peptide level. To this purpose, fourier transform ion cyclotron resonance (FTICR) and tandem-MS was used for hepcidin identification, after which a time-of-flight (TOF) MS-based methodology was exploited to routinely determine Hep-1 and -2 levels in mouse serum and urine. This method was biologically validated by hepcidin assessment in: i) 3 mouse strains (C57Bl/6; DBA/2 and BABL/c) upon stimulation with intravenous iron and LPS, ii) homozygous Hfe knock out, homozygous transferrin receptor 2 (Y245X) mutated mice and double affected mice, and iii) mice treated with a sublethal hepatotoxic dose of paracetamol. The results showed that detection of Hep-1 was restricted to serum, whereas Hep-2 and its presumed isoforms were predominantly present in urine. Elevations in serum Hep-1 and urine Hep-2 upon intravenous iron or LPS were only moderate and varied considerably between mouse strains. Serum Hep-1 was decreased in all three hemochromatosis models, being lowest in the double affected mice. Serum Hep-1 levels correlated with liver hepcidin-1 gene expression, while acute liver damage by paracetamol depleted Hep-1 from serum. Furthermore, serum Hep-1 appeared to be an excellent indicator of splenic iron accumulation. In conclusion, Hep-1 and Hep-2 peptide responses in experimental mouse agree with the known biology of hepcidin mRNA regulators, and their measurement can now be implemented in experimental mouse models to provide novel insights in post-transcriptional regulation, hepcidin function, and kinetics