Seismic oceanography imaging of thermal intrusions in strong frontal regions

The Naval Research Laboratory and collaborating partners carried out two dedicated seismic oceanography field experiments in two very different strong frontal regions. ADRIASEISMIC took seismic oceanography measurements at the confluence of North Adriatic Dense Water advected along the Western Adriatic Current and Modified Levantine Intermediate Water advected around the topographic rim of the Southern Adriatic basin. ARC12 took seismic oceanography measurements in and around the Agulhas Return Current as it curved northwards past the Agulhas Plateau and interacted with a large anticyclone that had collided with the current. Despite one study focused on coastal boundary currents and the other focused on a major Western Boundary Current extension, the complex horizontal structures seen through seismic imaging are tied to the processes of thermal intrusions and interleaving in both systems. Seismic Oceanography provides a unique capability of tracking the fine-scale horizontal extent of these intrusions

The response of the Ligurian and Tyrrhenian Seas to a summer Mistral event: A coupled atmosphere–ocean approach

In this paper the effect of a summer Mistral event on the Ligurian and Tyrrhenian Seas in the northwestern Mediterranean is discussed, using a coupled numerical model and satellite and in situ observations. The focus is on the spatial and temporal distribution of the ocean mixed layer response to the strong winds, and on how this is affected by atmosphere–ocean coupling. The model used is the Coupled Ocean–Atmosphere Mesoscale Prediction System (COAMPS®1), developed at the Naval Research Laboratory. This system includes an atmospheric sigma coordinate, non-hydrostatic model, coupled to a hydrostatic sigma-z level ocean model (Naval Coastal Ocean Model), using the Earth System Modeling Framework (ESMF). The model is run at high (km scale) resolution to capture the fine structure of wind jets and surface cooling. Two non-assimilating numerical experiments, coupled and uncoupled, are run for a 3-day period of a Mistral event, to examine more closely the impact of coupling on the surface flux and sea surface temperature (SST) fields. The cooling of SST up to 3 °C over 72 h in the coupled run significantly reduced the surface momentum and heat fluxes, relative to the uncoupled simulation, where the SST was kept fixed at the initial value. Mixed layer depths increase by as much as 30 m during the event. A heat budget analysis for the ocean is carried out to further explain and investigate the SST evolution. Shear-induced mixing in inertial waves is found to be important to the surface cooling. Effects of coupling on the atmospheric boundary layer are found to be significant, but overall the effect of coupling on the synoptic low pressure system is small

Spring 2009 water mass distribution, mixing and transport in the southern Adriatic after a low production of winter dense waters

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Submarine canyon dynamics - Executive Summary

Discussing submarine canyons dynamics through a multidisciplinary approach allowed to identify both advances in knowledge and remaining gaps concerning the controlling factors underlying the formation, development, ecological functioning and vulnerability of canyons at various time scales. As a result, we identified a number of recommendations for future research and actions that the interested reader will discover in this synthetic chapter, drafted as a collective effort in the months following our meeting. The subsequent chapters, each written by a workshop participant, detail the specificities and dynamics of of submarine canyons within and beyond the Mediterranean domain

Structural insight into molecular mechanism of poly (ethylene terephthalate) degradation

Plastics, including poly(ethylene terephthalate) (PET), possess many desirable characteristics and thus are widely used in daily life. However, non-biodegradability, once thought to be an advantage offered by plastics, is causing major environmental problem. Recently, a PET-degrading bacterium, Ideonella sakaiensis, was identified and suggested for possible use in degradation and/or recycling of PET. However, the molecular mechanism of PET degradation is not known. Here we report the crystal structure of I. sakaiensis PETase (IsPETase) at 1.5 angstrom resolution. IsPETase has a Ser-His-Asp catalytic triad at its active site and contains an optimal substrate binding site to accommodate four monohydroxyethyl terephthalate (MHET) moieties of PET. Based on structural and site-directed mutagenesis experiments, the detailed process of PET degradation into MHET, terephthalic acid, and ethylene glycol is suggested. Moreover, other PETase candidates potentially having high PET-degrading activities are suggested based on phylogenetic tree analysis of 69 PETase-like proteins

Defective Innate Cell Response and Lymph Node Infiltration Specify Yersinia pestis Infection

Since its recent emergence from the enteropathogen Yersinia pseudotuberculosis, Y. pestis, the plague agent, has acquired an intradermal (id) route of entry and an extreme virulence. To identify pathophysiological events associated with the Y. pestis high degree of pathogenicity, we compared disease progression and evolution in mice after id inoculation of the two Yersinia species. Mortality studies showed that the id portal was not in itself sufficient to provide Y. pseudotuberculosis with the high virulence power of its descendant. Surprisingly, Y. pseudotuberculosis multiplied even more efficiently than Y. pestis in the dermis, and generated comparable histological lesions. Likewise, Y. pseudotuberculosis translocated to the draining lymph node (DLN) and similar numbers of the two bacterial species were found at 24 h post infection (pi) in this organ. However, on day 2 pi, bacterial loads were higher in Y. pestis-infected than in Y. pseudotuberculosis-infected DLNs. Clustering and multiple correspondence analyses showed that the DLN pathologies induced by the two species were statistically significantly different and identified the most discriminating elementary lesions. Y. pseudotuberculosis infection was accompanied by abscess-type polymorphonuclear cell infiltrates containing the infection, while Y. pestis-infected DLNs exhibited an altered tissue density and a vascular congestion, and were typified by an invasion of the tissue by free floating bacteria. Therefore, Y. pestis exceptional virulence is not due to its recently acquired portal of entry into the host, but is associated with a distinct ability to massively infiltrate the DLN, without inducing in this organ an organized polymorphonuclear cell reaction. These results shed light on pathophysiological processes that draw the line between a virulent and a hypervirulent pathogen

Cardiac Alpha-Myosin (MYH6) Is the Predominant Sarcomeric Disease Gene for Familial Atrial Septal Defects

Secundum-type atrial septal defects (ASDII) account for approximately 10% of all congenital heart defects (CHD) and are associated with a familial risk. Mutations in transcription factors represent a genetic source for ASDII. Yet, little is known about the role of mutations in sarcomeric genes in ASDII etiology. To assess the role of sarcomeric genes in patients with inherited ASDII, we analyzed 13 sarcomeric genes (MYH7, MYBPC3, TNNT2, TCAP, TNNI3, MYH6, TPM1, MYL2, CSRP3, ACTC1, MYL3, TNNC1, and TTN kinase region) in 31 patients with familial ASDII using array-based resequencing. Genotyping of family relatives and control subjects as well as structural and homology analyses were used to evaluate the pathogenic impact of novel non-synonymous gene variants. Three novel missense mutations were found in the MYH6 gene encoding alpha-myosin heavy chain (R17H, C539R, and K543R). These mutations co-segregated with CHD in the families and were absent in 370 control alleles. Interestingly, all three MYH6 mutations are located in a highly conserved region of the alpha-myosin motor domain, which is involved in myosin-actin interaction. In addition, the cardiomyopathy related MYH6-A1004S and the MYBPC3-A833T mutations were also found in one and two unrelated subjects with ASDII, respectively. No mutations were found in the 11 other sarcomeric genes analyzed. The study indicates that sarcomeric gene mutations may represent a so far underestimated genetic source for familial recurrence of ASDII. In particular, perturbations in the MYH6 head domain seem to play a major role in the genetic origin of familial ASDII