Defining true propagation patterns of underwater noise produced by stationary vessels

The study of underwater vessel noise over the past sixty years has predominantly focused upon the increase in ambient noise caused by the propulsion mechanisms of large commercial vessels. Studies have identified that the continuous rise of ambient noise levels in open waters is linked to the increase in size and strength of anthropogenic sound sources. Few studies have investigated the noise contribution of smaller vessels or ambient noise levels present in coastal and in-shore waters. This study aimed to identify the level of noise common to non-commercial harbors by studying the noise emissions of a diesel generator on board a 70m long sailing vessel. Propagation patterns revealed an unconventional shape (specific to the precise location of the noise source on board the vessel), unlike those of standard geometric spreading models, as typically assumed when predicting vessel noise emission. Harbor attributes (including water depth, ground sediment and structural material components) caused for altered level and frequency characteristics of the recorded underwater noise, and were correlated to the sound measurements made. The measurements (taken in eight harbors around Northern Europe) were statistically analyzed to identify the primary factors influencing near-field sound propagation around a stationary vessel

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

Data from: Distinguishing social from nonsocial navigation in moving animal groups

Many animals, such as migrating shoals of fish, navigate in groups. Knowing the mechanisms involved in animal navigation is important when it comes to explaining navigation accuracy, dispersal patterns, population and evolutionary dynamics and consequently the design of conservation strategies. When navigating towards a common target, animals could interact socially by sharing available information directly or indirectly, or each individual could navigate by itself and aggregations may not disperse because all animals are moving towards the same target. Here, we present an analysis technique that uses individual movement trajectories to determine the extent to which individuals in navigating groups interact socially, given knowledge of their target. The basic idea of our approach is that the movement direction of individuals arises from a combination of responses to the environment and to other individuals. We estimate the relative importance of these responses, distinguishing between social and non-social interactions. We develop and test our method using simulated groups and demonstrate its applicability to empirical data in a case study on groups of guppies moving towards shelter in a tank. Our approach is generic and can be extended to different scenarios of animal group movement

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