966 research outputs found

    Spatial and temporal patterns of Pseudo-nitzschia genetic diversity in the North Pacific Ocean from the Continuous Plankton Recorder survey

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    Several species of the marine diatom Pseudo-nitzschia can produce the neurotoxin domoic acid that is responsible for the seafood-borne illness amnesic shellfish poisoning in humans, marine wildlife mortalities and prolonged closures of fisheries resulting in economic losses to coastal communities. Since the year 2000, Pseudo-nitzschia species have been monitored in the Pacific Ocean with the Continuous Plankton Recorder (CPR). We used a combination of scanning electron microscopy with high-throughput and Sanger sequencing of CPR survey samples to compare the diversity of phytoplankton, including Pseudo-nitzschia species, from the north-eastern Pacific Ocean over 3 climatically different years: 2002, 2005 and 2008. A Pseudo-nitzschia-specific primer set targeting a partial region of the large subunit ribosomal DNA (rDNA) revealed spatially separated communities of Pseudo-nitzschia. The coastal region was dominated by a diverse array of P. fraudulenta unique sequences (operational taxonomic units), whereas the offshore region was rich in P. multiseries and contained a wide range of other Pseudo-nitzschia taxa, many not previously observed in this region. In 2008, exceptionally cold sea surface temperatures were recorded, influenced by a strong negative Pacific Decadal Oscillation signal. In that year, a more diverse assemblage of species was present in a spring open water sample, whereas P. fraudulenta was unusually rare from a coastal autumn sample. This is the first application of high-throughput genetic methods to uncover patterns of Pseudo-nitzschia genetic diversity from archival CPR samples, demonstrating the value of using CPR for plankton community analysis in rarely sampled regions of the oceans

    Impacts of climate variability and future climate change on harmful algal blooms and human health

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    This is the final version of the article. Available from BioMed Central via the DOI in this record.Anthropogenically-derived increases in atmospheric greenhouse gas concentrations have been implicated in recent climate change, and are projected to substantially impact the climate on a global scale in the future. For marine and freshwater systems, increasing concentrations of greenhouse gases are expected to increase surface temperatures, lower pH, and cause changes to vertical mixing, upwelling, precipitation, and evaporation patterns. The potential consequences of these changes for harmful algal blooms (HABs) have received relatively little attention and are not well understood. Given the apparent increase in HABs around the world and the potential for greater problems as a result of climate change and ocean acidification, substantial research is needed to evaluate the direct and indirect associations between HABs, climate change, ocean acidification, and human health. This research will require a multidisciplinary approach utilizing expertise in climatology, oceanography, biology, epidemiology, and other disciplines. We review the interactions between selected patterns of large-scale climate variability and climate change, oceanic conditions, and harmful algae.This work was funded in part through grants from the NSF/NIEHS Centers for Oceans and Human Health, grant numbers NSF OCE04-32479 and NIEHS P50 ES012740 (EAL), NSF OCE-0432368 and NIEHS P50 ES012736 (LEF), NIEHS P50 ES012762 and NSF OCE-0434087 (SKM, MSP). SKM, VLT and NJM also were supported in part by the West Coast Center for Oceans and Human Health (WCCOHH) as part of the NOAA Oceans and Human Health Initiative, and this is WCCOHH publication no. 26. The WCCOHH is part of the National Marine Fisheries Service's Northwest Fisheries Science Center, Seattle, Washington

    Quantum Group Structure and Local Fields in the Algebraic Approach to 2D Gravity

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    This review contains a summary of work by J.-L. Gervais and the author on the operator approach to 2d gravity. Special emphasis is placed on the construction of local observables -the Liouville exponentials and the Liouville field itself - and the underlying algebra of chiral vertex operators. The double quantum group structure arising from the presence of two screening charges is discussed and the generalized algebra and field operators are derived. In the last part, we show that our construction gives rise to a natural definition of a quantum tau function, which is a noncommutative version of the classical group-theoretic representation of the Liouville fields by Leznov and Saveliev.Comment: 38 pages, LaTex file. Proceedings of the Vth International Conference on Mathematical Physics, Strings and Quantum gravity, Alushta, Ukraine 199

    Faces of matrix models

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    Partition functions of eigenvalue matrix models possess a number of very different descriptions: as matrix integrals, as solutions to linear and non-linear equations, as tau-functions of integrable hierarchies and as special-geometry prepotentials, as result of the action of W-operators and of various recursions on elementary input data, as gluing of certain elementary building blocks. All this explains the central role of such matrix models in modern mathematical physics: they provide the basic "special functions" to express the answers and relations between them, and they serve as a dream model of what one should try to achieve in any other field.Comment: 10 page

    On Combinatorial Expansions of Conformal Blocks

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    In a recent paper (arXiv:0906.3219) the representation of Nekrasov partition function in terms of nontrivial two-dimensional conformal field theory has been suggested. For non-vanishing value of the deformation parameter \epsilon=\epsilon_1+\epsilon_2 the instanton partition function is identified with a conformal block of Liouville theory with the central charge c = 1+ 6\epsilon^2/\epsilon_1\epsilon_2. If reversed, this observation means that the universal part of conformal blocks, which is the same for all two-dimensional conformal theories with non-degenerate Virasoro representations, possesses a non-trivial decomposition into sum over sets of the Young diagrams, different from the natural decomposition studied in conformal field theory. We provide some details about this intriguing new development in the simplest case of the four-point correlation functions.Comment: 22 page

    Functional Interaction of Parkinson's Disease-Associated LRRK2 with Members of the Dynamin GTPase Superfamily.

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    Mutations in LRRK2 cause autosomal dominant Parkinson's disease (PD). LRRK2 encodes a multi-domain protein containing GTPase and kinase domains, and putative protein-protein interaction domains. Familial PD mutations alter the GTPase and kinase activity of LRRK2 in vitro. LRRK2 is suggested to regulate a number of cellular pathways although the underlying mechanisms are poorly understood. To explore such mechanisms it has proved informative to identify LRRK2-interacting proteins, some of which serve as LRRK2 kinase substrates. Here, we identify common interactions of LRRK2 with members of the dynamin GTPase superfamily. LRRK2 interacts with dynamin 1-3 that mediate membrane scission in clathrin-mediated endocytosis and with dynamin-related proteins that mediate mitochondrial fission (Drp1) and fusion (mitofusins and OPA1). LRRK2 partially co-localizes with endosomal dynamin-1 or with mitofusins and OPA1 at mitochondrial membranes. The subcellular distribution and oligomeric complexes of dynamin GTPases are not altered by modulating LRRK2 in mouse brain, whereas mature OPA1 levels are reduced in G2019S PD brains. LRRK2 enhances mitofusin-1 GTP binding, whereas dynamin-1 and OPA1 serve as modest substrates of LRRK2-mediated phosphorylation in vitro. While dynamin GTPase orthologs are not required for LRRK2-induced toxicity in yeast, LRRK2 functionally interacts with dynamin-1 and mitofusin-1 in cultured neurons. LRRK2 attenuates neurite shortening induced by dynamin-1 by reducing its levels, whereas LRRK2 rescues impaired neurite outgrowth induced by mitofusin-1 potentially by reversing excessive mitochondrial fusion. Our study elucidates novel functional interactions of LRRK2 with dynamin superfamily GTPases that implicate LRRK2 in the regulation of membrane dynamics important for endocytosis and mitochondrial morphology

    Loss of the laminin subunit alpha-3 induces cell invasion and macrophage infiltration in cutaneous squamous cell carcinoma

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    Background Cutaneous squamous cell carcinoma (cSCC) is a common cancer that invades the dermis through the basement membrane. The role of the basement membrane in poorly differentiated cSCC is not well understood.Objectives To study the effect that loss of the laminin subunit alpha-3 (alpha 3) chain from the tumour microenvironment has on tumour invasion and inflammatory cell recruitment.Methods We examined the role of the basement membrane proteins laminin subunits alpha 3, beta 3 and gamma 2 in SCC invasion and inflammatory cell recruitment using immunohistochemistry, short hairpin RNA knockdown, RNA-Seq, mouse xenograft models and patient tumour samples.Results Analysis of SCC tumours and cell lines using antibodies specific to laminin chains alpha 3, beta 3 and gamma 2 identified a link between poorly differentiated SCC and reduced expression of laminin alpha 3 but not the other laminin subunits investigated. Knockdown of laminin alpha 3 increased tumour invasion both in vitro and in vivo. Western blot and immunohistochemical staining identified increased phosphorylated myosin light chain with loss of laminin alpha 3. Inhibition of ROCK (rho-associated protein kinase) but not Rac1 significantly reduced the invasive potential of laminin alpha 3 knockdown cells. Knockdown of laminin subunits alpha 3 and gamma 2 increased monocyte recruitment to the tumour microenvironment. However, only the loss of laminin alpha 3 correlated with increased tumour-associated macrophages both in xenografted tumours and in patient tumour samples.Conclusions These data provide evidence that loss of the laminin alpha 3 chain in cSCC has an effect on both the epithelial and immune components of cSCC, resulting in an aggressive tumour microenvironment

    Paintable Battery

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    If the components of a battery, including electrodes, separator, electrolyte and the current collectors can be designed as paints and applied sequentially to build a complete battery, on any arbitrary surface, it would have significant impact on the design, implementation and integration of energy storage devices. Here, we establish a paradigm change in battery assembly by fabricating rechargeable Li-ion batteries solely by multi-step spray painting of its components on a variety of materials such as metals, glass, glazed ceramics and flexible polymer substrates. We also demonstrate the possibility of interconnected modular spray painted battery units to be coupled to energy conversion devices such as solar cells, with possibilities of building standalone energy capture-storage hybrid devices in different configurations

    Long-term (trophic) purinergic signalling: purinoceptors control cell proliferation, differentiation and death

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    The purinergic signalling system, which uses purines and pyrimidines as chemical transmitters, and purinoceptors as effectors, is deeply rooted in evolution and development and is a pivotal factor in cell communication. The ATP and its derivatives function as a 'danger signal' in the most primitive forms of life. Purinoceptors are extraordinarily widely distributed in all cell types and tissues and they are involved in the regulation of an even more extraordinary number of biological processes. In addition to fast purinergic signalling in neurotransmission, neuromodulation and secretion, there is long-term (trophic) purinergic signalling involving cell proliferation, differentiation, motility and death in the development and regeneration of most systems of the body. In this article, we focus on the latter in the immune/defence system, in stratified epithelia in visceral organs and skin, embryological development, bone formation and resorption, as well as in cancer. Cell Death and Disease (2010) 1, e9; doi:10.1038/cddis.2009.11; published online 14 January 201
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