Turbulent energy production and entrainment at a highly stratified estuarine front

Author Posting. © American Geophysical Union, 2004. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research 109 (2004): C05004, doi:10.1029/2003JC002094.Rates of turbulent kinetic energy (TKE) production and buoyancy flux in the region immediately seaward (~1 km) of a highly stratified estuarine front at the mouth of the Fraser River (British Columbia, Canada) are calculated using a control volume approach. The calculations are based on field data obtained from shipboard instrumentation, specifically velocity data from a ship mounted acoustic Doppler current profiler (ADCP), and salinity data from a towed conductivity-temperature-depth (CTD) unit. The results allow for the calculation of vertical velocities in the water column, and the total vertical transport of salt and momentum. The vertical turbulent transport quantities (inline equation, inline equation) can then be estimated as the difference between the total transport and the advective transport. Estimated production is on the order of 10−3 m2 s−3, yielding a value of ɛ(νN2)−1 on the order of 104. This rate of TKE production is at the upper limit of reported values for ocean and coastal environments. Flux Richardson numbers in this highly energetic system generally range from 0.15 to 0.2, with most mixing occurring at gradient Richardson numbers slightly less than inline equation. These values compare favorably with other values in the literature that are associated with turbulence observations from regimes characterized by scales several orders of magnitude smaller than are present in the Fraser River.This work was performed as a part of D. MacDonald’s Ph.D. thesis, and was funded by Office of Naval Research grants N000-14-97-10134 and N000-14-97- 10566, National Science Foundation grant OCE-9906787, a National Science Foundation graduate fellowship, and support from the WHOI Academic Programs Office

B cell receptor accessory molecule CD79α : characterisation and expression analysis in a cartilaginous fish, the spiny dogfish (Squalus acanthias)

Copyright © 2013. Published by Elsevier Ltd.Peer reviewedPublisher PD

The T cell receptor/CD3 complex is composed of at least two autonomous transduction modules

Recent studies have demonstrated that the CD3-ζ subunit of the T cell antigen receptor (TCR) complex is involved in signal transduction. However, the function of the remaining invariant subunits, CD3-γ, -δ, and , is still poorly understood. To examine their role in TCR function, we have constructed TCR/CD3 complexes devoid of functional ζ subunit and showed that they are still able to trigger the production of interleukin-2 in response to antigen or superantigen. These data, together with previous results, indicate that the TCR/CD3 complex is composed of at least two parallel transducing units, made of the γδ and ζ chains, respectively, Furthermore, the analysis of partially truncated ζ chains has led us to individualize a functional domain that may have constituted the building block of most of the transducing subunits associated with antigen receptors and some Fc receptors

IL-18 ; a cytokine translates a stress into medical science

Psychological/physical stresses have been reported to exacerbate auto-immune and inflammatory diseases. To clarify a mechanism by which non-inflammatory stresses disrupt host defenses, responses to immobilization stress in mice were investigated, focusing on the role of a multifunctional cytokine, interleukin-18 (IL-18). In the adrenal cortex, the stress induced IL-18 precursor proteins (pro-IL-18) via ACTH and a superoxide-mediated caspase-1 activation pathway, resulting in conversion of pro-IL-18 to the mature form which was released into plasma. Inhibitors of caspase-1, reactive oxygen species and P38 MAPK prevented stress-induced accumulation of plasma IL-18. These inhibitors also blocked stress-induced IL-6 expression. This, together with the observation that IL-6was not induced in stressed-IL-18 deficient mice, showed that IL-6 induction by stress is dependent on IL-18. In stressed organisms, IL-18 may influence pathological and physiological processes. Controlling the caspase-1 activating pathway to suppress IL-18 levels may provide preventative means against stress-related disruption of host defenses

Glucocorticoid-induced TNF receptor-triggered T cells are key modulators for survival/death of neural stem/progenitor cells induced by ischemic stroke

Increasing evidences show that immune response affects the reparative mechanisms in injured brain. Recently, we have demonstrated that CD4+T cells serve as negative modulators in neurogenesis after stroke, but the mechanistic detail remains unclear. Glucocorticoid-induced tumor necrosis factor (TNF) receptor (GITR), a multifaceted regulator of immunity belonging to the TNF receptor superfamily, is expressed on activated CD4+T cells. Herein, we show, by using a murine model of cortical infarction, that GITR triggering on CD4+T cells increases poststroke inflammation and decreases the number of neural stem/progenitor cells induced by ischemia (iNSPCs). CD4+GITR+T cells were preferentially accumulated at the postischemic cortex, and mice treated with GITR-stimulating antibody augmented poststroke inflammatory responses with enhanced apoptosis of iNSPCs. In contrast, blocking the GITR–GITR ligand (GITRL) interaction by GITR–Fc fusion protein abrogated inflammation and suppressed apoptosis of iNSPCs. Moreover, GITR-stimulated T cells caused apoptosis of the iNSPCs, and administration of GITR-stimulated T cells to poststroke severe combined immunodeficient mice significantly reduced iNSPC number compared with that of non-stimulated T cells. These observations indicate that among the CD4+T cells, GITR+CD4+T cells are major deteriorating modulators of poststroke neurogenesis. This suggests that blockade of the GITR–GITRL interaction may be a novel immune-based therapy in stroke