Barotropic Rossby waves radiating from tropical instability waves in the Pacific Ocean

Author Posting. © American Meteorological Society, 2011. This article is posted here by permission of American Meteorological Society for personal use, not for redistribution. The definitive version was published in Journal of Physical Oceanography 41 (2011): 1160–1181, doi:10.1175/2011JPO4547.1.Tropical instability waves are triggered by instabilities of the equatorial current systems, and their sea level signal, with peak amplitude near 5°N, is one of the most prominent features of the dynamic topography of the tropics. Cross-spectral analysis of satellite altimetry observations shows that there is sea level variability in the Pacific Ocean as far north as Hawaii (i.e., 20°N) that is coherent with the sea level variability near 5°N associated with tropical instability waves. Within the uncertainty of the analysis, this off-equatorial variability obeys the dispersion relation for nondivergent, barotropic Rossby waves over a fairly broad range of periods (26–38 days) and zonal wavelengths (9°–23° of longitude) that are associated with tropical instability waves. The dispersion relation and observed wave properties further suggest that the waves are carrying energy away from the instabilities toward the North Pacific subtropical gyre, which, together with the observed coherence of the sea level signal of the barotropic waves with that of the tropical instability waves, suggests that the barotropic Rossby waves are being radiated from the tropical instability waves. The poleward transport of kinetic energy and westward momentum by these barotropic Rossby waves may influence the circulation in the subtropics.Funding for this research came from WHOI’s TropicalResearch Initiative, the Charles D. Hollister Fund for Assistant Scientist Support, the John E. and Anne W. Sawyer Endowed Fund in Special Support of Scientific Staff, and Grant OCE-0845150 from the National Science Foundation

Dynamics of Membrane Trafficking Downstream of B and T Cell Receptor Engagement: Impact on Immune Synapses

The onset of an adaptive immune response requires the activation of T and B lymphocytes by antigen-presenting cells, through a specialized form of intercellular communication, known as the immunological synapse (IS). In B lymphocytes the IS promotes efficient recognition and acquisition of membrane-bound Ags, while in T cells, it modulates the T cell response upon exposure to peptide-major histocompatibility complexes. In this review, we highlight the similarities that determine B and T cell activation, focusing on immune receptor downstream signaling events that lead to synapse formation. We stress the notion that polarization of T and B lymphocytes characterized by global changes in cytoskeleton and membrane trafficking modulates synapse structure and function, thus determining lymphocyte effector functions and fate

Adaptor SKAP-55 Binds p21ras Activating Exchange Factor RasGRP1 and Negatively Regulates the p21ras-ERK Pathway in T-Cells

While the adaptor SKAP-55 mediates LFA-1 adhesion on T-cells, it is not known whether the adaptor regulates other aspects of signaling. SKAP-55 could potentially act as a node to coordinate the modulation of adhesion with downstream signaling. In this regard, the GTPase p21ras and the extracellular signal-regulated kinase (ERK) pathway play central roles in T-cell function. In this study, we report that SKAP-55 has opposing effects on adhesion and the activation of the p21ras -ERK pathway in T-cells. SKAP-55 deficient primary T-cells showed a defect in LFA-1 adhesion concurrent with the hyper-activation of the ERK pathway relative to wild-type cells. RNAi knock down (KD) of SKAP-55 in T-cell lines also showed an increase in p21ras activation, while over-expression of SKAP-55 inhibited activation of ERK and its transcriptional target ELK. Three observations implicated the p21ras activating exchange factor RasGRP1 in the process. Firstly, SKAP-55 bound to RasGRP1 via its C-terminus, while secondly, the loss of binding abrogated SKAP-55 inhibition of ERK and ELK activation. Thirdly, SKAP-55−/− primary T-cells showed an increased presence of RasGRP1 in the trans-Golgi network (TGN) following TCR activation, the site where p21ras becomes activated. Our findings indicate that SKAP-55 has a dual role in regulating p21ras-ERK pathway via RasGRP1, as a possible mechanism to restrict activation during T-cell adhesion

Osteoporosis in the community. Sensitivity of self-reported estimates and medication use of those diagnosed with the condition

Objectives: To assess the sensitivity and specificity of self-reported osteoporosis compared with dual energy X-ray absorptiometry (DXA) defined osteoporosis, and to describe medication use among participants with the condition. Methods: Data were obtained from a population-based longitudinal study and assessed for the prevalence of osteoporosis, falls, fractures and medication use. DXA scans were also undertaken. Results: Overall 3.8% (95% confidence interval (CI) 3.2 to 4.5) of respondents and 8.8% (95% CI 7.5 to 10.3) of those aged ≥ 50 years reported that they had been diagnosed with osteoporosis by a doctor. The sensitivity (those self-reporting osteoporosis and having low bone mineral density (BMD) on DXA) was low (22.7%), although the specificity was high (94.4%). Only 16.1% of those aged ≥ 50 years and with DXA-defined osteoporosis were taking bisphosphonates. Conclusions: The sensitivity of self-reporting to identify osteoporosis is low. Anti-osteoporotic medications are an important part of osteoporosis treatment but opportunities to use appropriate medications were missed and inappropriate medications were used.T. K. Gill, A. W. Taylor, C. L. Hill, P. J. Phillip

Exponential Barycenters of the Canonical Cartan Connection and Invariant Means on Lie Groups

International audienceWhen performing statistics on elements of sets that possess a particular geometric structure, it is desirable to respect this structure. For instance in a Lie group, it would be judicious to have a notion of a mean which is stable by the group operations (composition and inversion). Such a property is ensured for Riemannian center of mass in Lie groups endowed with a bi-invariant Riemannian metric, like compact Lie groups (e.g. rotations). However, bi-invariant Riemannian metrics do not exist for most non compact and non-commutative Lie groups. This is the case in particular for rigid-body transformations in any dimension greater than one, which form the most simple Lie group involved in biomedical image registration. In this paper, we propose to replace the Riemannian metric by an affine connection structure on the group. We show that the canonical Cartan connections of a connected Lie group provides group geodesics which are completely consistent with the composition and inversion. With such a non-metric structure, the mean cannot be defined by minimizing the variance as in Riemannian Manifolds. However, the characterization of the mean as an exponential barycenter gives us an implicit definition of the mean using a general barycentric equation. Thanks to the properties of the canonical Cartan connection, this mean is naturally bi-invariant. We show the local existence and uniqueness of the invariant mean when the dispersion of the data is small enough. We also propose an iterative fixed point algorithm and demonstrate that the convergence to the invariant mean is at least linear. In the case of rigid-body transformations, we give a simple criterion for the global existence and uniqueness of the bi-invariant mean, which happens to be the same as for rotations. We also give closed forms for the bi-invariant mean in a number of simple but instructive cases, including 2D rigid transformations. For general linear transformations, we show that the bi-invariant mean is a generalization of the (scalar) geometric mean, since the determinant of the bi-invariant mean is the geometric mean of the determinants of the data. Finally, we extend the theory to higher order moments, in particular with the covariance which can be used to define a local bi-invariant Mahalanobis distance

An Observational Cohort Study of the Kynurenine to Tryptophan Ratio in Sepsis: Association with Impaired Immune and Microvascular Function

Both endothelial and immune dysfunction contribute to the high mortality rate in human sepsis, but the underlying mechanisms are unclear. In response to infection, interferon-γ activates indoleamine 2,3-dioxygenase (IDO) which metabolizes the essential amino acid tryptophan to the toxic metabolite kynurenine. IDO can be expressed in endothelial cells, hepatocytes and mononuclear leukocytes, all of which contribute to sepsis pathophysiology. Increased IDO activity (measured by the kynurenine to tryptophan [KT] ratio in plasma) causes T-cell apoptosis, vasodilation and nitric oxide synthase inhibition. We hypothesized that IDO activity in sepsis would be related to plasma interferon-γ, interleukin-10, T cell lymphopenia and impairment of microvascular reactivity, a measure of endothelial nitric oxide bioavailability. In an observational cohort study of 80 sepsis patients (50 severe and 30 non-severe) and 40 hospital controls, we determined the relationship between IDO activity (plasma KT ratio) and selected plasma cytokines, sepsis severity, nitric oxide-dependent microvascular reactivity and lymphocyte subsets in sepsis. Plasma amino acids were measured by high performance liquid chromatography and microvascular reactivity by peripheral arterial tonometry. The plasma KT ratio was increased in sepsis (median 141 [IQR 64–235]) compared to controls (36 [28–52]); p<0.0001), and correlated with plasma interferon-γ and interleukin-10, and inversely with total lymphocyte count, CD8+ and CD4+ T-lymphocytes, systolic blood pressure and microvascular reactivity. In response to treatment of severe sepsis, the median KT ratio decreased from 162 [IQR 100–286] on day 0 to 89 [65–139] by day 7; p = 0.0006) and this decrease in KT ratio correlated with a decrease in the Sequential Organ Failure Assessment score (p<0.0001). IDO-mediated tryptophan catabolism is associated with dysregulated immune responses and impaired microvascular reactivity in sepsis and may link these two fundamental processes in sepsis pathophysiology