Biodegradation of aromatic hydrocarbons by Haloarchaea and their use for the reduction of the chemical oxygen demand of hypersaline petroleum produced water

AbstractTen halophilic Archaea (Haloarchaea) strains able to degrade aromatic compounds were isolated from five hypersaline locations; salt marshes in the Uyuni salt flats in Bolivia, crystallizer ponds in Chile and Cabo Rojo (Puerto Rico), and sabkhas (salt flats) in the Persian Gulf (Saudi Arabia) and the Dead Sea (Israel and Jordan). Phylogenetic identification of the isolates was determined by 16S rRNA gene sequence analysis. The isolated Haloarchaea strains were able to grow on a mixture of benzoic acid, p-hydroxybenzoic acid, and salicylic acid (1.5mM each) and a mixture of the polycyclic aromatic hydrocarbons, naphthalene, anthracene, phenanthrene, pyrene and benzo[a]anthracene (0.3mM each). Evaluation of the extent of degradation of the mixed aromatic hydrocarbons demonstrated that the isolates could degrade these compounds in hypersaline media containing 20% NaCl. The strains were shown to reduce the COD of hypersaline crude oil reservoir produced waters significantly beyond that achieved using standard hydrogen peroxide treatment alone

Sand in the wheels, or oiling the wheels, of international finance? : New Labour's appeal to a 'new Bretton Woods'

Tony Blair’s political instinct typically is to associate himself only with the future. As such, his explicit appeal to ‘the past’ in his references to New Labour’s desire to establish a “new Bretton Woods” is sufficient in itself to arouse some degree of analytical curiosity (see Blair 1998a). The fact that this appeal was made specifically in relation to Bretton Woods is even more interesting. The resonant image of the international economic context established by the original Bretton Woods agreements invokes a style and content of policy-making which Tony Blair typically dismisses as neither economically nor politically consistent with his preferred vision of the future (see Blair 2000c, 2001b)

Cell-specific discrimination of desmosterol and desmosterol mimetics confers selective regulation of LXR and SREBP in macrophages.

Activation of liver X receptors (LXRs) with synthetic agonists promotes reverse cholesterol transport and protects against atherosclerosis in mouse models. Most synthetic LXR agonists also cause marked hypertriglyceridemia by inducing the expression of sterol regulatory element-binding protein (SREBP)1c and downstream genes that drive fatty acid biosynthesis. Recent studies demonstrated that desmosterol, an intermediate in the cholesterol biosynthetic pathway that suppresses SREBP processing by binding to SCAP, also binds and activates LXRs and is the most abundant LXR ligand in macrophage foam cells. Here we explore the potential of increasing endogenous desmosterol production or mimicking its activity as a means of inducing LXR activity while simultaneously suppressing SREBP1c-induced hypertriglyceridemia. Unexpectedly, while desmosterol strongly activated LXR target genes and suppressed SREBP pathways in mouse and human macrophages, it had almost no activity in mouse or human hepatocytes in vitro. We further demonstrate that sterol-based selective modulators of LXRs have biochemical and transcriptional properties predicted of desmosterol mimetics and selectively regulate LXR function in macrophages in vitro and in vivo. These studies thereby reveal cell-specific discrimination of endogenous and synthetic regulators of LXRs and SREBPs, providing a molecular basis for dissociation of LXR functions in macrophages from those in the liver that lead to hypertriglyceridemia

Reverse genetics in Chlamydomonas: a platform for isolating insertional mutants

A method was developed to identify insertional mutants of Chlamydomonas reinhardtii disrupted for selected target genes. The approach relies on the generation of thousands of transformants followed by PCR-based screenings that allow for identification of strains harboring the introduced marker gene within specific genes of interest. Our results highlight the strengths and limitations of two independent screens that differed in the nature of the marker DNA used (PCR-amplified fragment containing the plasmid-free marker versus entire linearized plasmid with the marker) and in the strategies used to maintain and store transformants

Activation of Steroid and Xenobiotic Receptor (SXR, NR1I2) and Its Orthologs in Laboratory Toxicologic, and Genome Model Species

Background: Nuclear receptor subfamily 1, group I, member 2 (NR1I2), commonly known as steroid xenobiotic receptor (SXR) in humans, is a key ligand-dependent transcription factor responsible for the regulation of xenobiotic, steroid, and bile acid metabolism. The ligand-binding domain is principally responsible for species-specific activation of NR1I2 in response to xenobiotic exposure. Objectives: Our objective in this study was to create a common framework for screening NR1I2 orthologs from a variety of model species against environmentally relevant xenobiotics and to evaluate the results in light of using the species as predictors of xenobiotic disposition and for assessment of environmental health risk. Methods: Sixteen chimeric fusion plasmid vectors expressing the Gal4 DNA-binding domain and species-specific NR1I2 ligand-binding domain were screened for activation against a spectrum of 27 xenobiotic compounds using a standardized cotransfection receptor activation assay. Results: NR1I2 orthologs were activated by various ligands in a dose-dependent manner. Closely related species show broadly similar patterns of activation; however, considerable variation to individual compounds exists, even among species varying in only a few amino acid residues. Conclusions: Interspecies variation in NR1I2 activation by various ligands can be screened through the use of in vitro NR1I2 activation assays and should be taken into account when choosing appropriate animal models for assessing environmental health risk

The Matsu Wheel: A Cloud-Based Framework for Efficient Analysis and Reanalysis of Earth Satellite Imagery

Project Matsu is a collaboration between the Open Commons Consortium and NASA focused on developing open source technology for cloud-based processing of Earth satellite imagery with practical applications to aid in natural disaster detection and relief. Project Matsu has developed an open source cloud-based infrastructure to process, analyze, and reanalyze large collections of hyperspectral satellite image data using OpenStack, Hadoop, MapReduce and related technologies. We describe a framework for efficient analysis of large amounts of data called the Matsu "Wheel." The Matsu Wheel is currently used to process incoming hyperspectral satellite data produced daily by NASA's Earth Observing-1 (EO-1) satellite. The framework allows batches of analytics, scanning for new data, to be applied to data as it flows in. In the Matsu Wheel, the data only need to be accessed and preprocessed once, regardless of the number or types of analytics, which can easily be slotted into the existing framework. The Matsu Wheel system provides a significantly more efficient use of computational resources over alternative methods when the data are large, have high-volume throughput, may require heavy preprocessing, and are typically used for many types of analysis. We also describe our preliminary Wheel analytics, including an anomaly detector for rare spectral signatures or thermal anomalies in hyperspectral data and a land cover classifier that can be used for water and flood detection. Each of these analytics can generate visual reports accessible via the web for the public and interested decision makers. The result products of the analytics are also made accessible through an Open Geospatial Compliant (OGC)-compliant Web Map Service (WMS) for further distribution. The Matsu Wheel allows many shared data services to be performed together to efficiently use resources for processing hyperspectral satellite image data and other, e.g., large environmental datasets that may be analyzed for many purposes

Probing Colored Particles with Photons, Leptons, and Jets

If pairs of new colored particles are produced at the Large Hadron Collider, determining their quantum numbers, and even discovering them, can be non-trivial. We suggest that valuable information can be obtained by measuring the resonant signals of their near-threshold QCD bound states. If the particles are charged, the resulting signatures include photons and leptons and are sufficiently rich for unambiguously determining their various quantum numbers, including the charge, color representation and spin, and obtaining a precise mass measurement. These signals provide well-motivated benchmark models for resonance searches in the dijet, photon+jet, diphoton and dilepton channels. While these measurements require that the lifetime of the new particles be not too short, the resulting limits, unlike those from direct searches for pair production above threshold, do not depend on the particles' decay modes. These limits may be competitive with more direct searches if the particles decay in an obscure way.Comment: 39 pages, 9 figures; v2: more recent searches include

Canvass: a crowd-sourced, natural-product screening library for exploring biological space

NCATS thanks Dingyin Tao for assistance with compound characterization. This research was supported by the Intramural Research Program of the National Center for Advancing Translational Sciences, National Institutes of Health (NIH). R.B.A. acknowledges support from NSF (CHE-1665145) and NIH (GM126221). M.K.B. acknowledges support from NIH (5R01GM110131). N.Z.B. thanks support from NIGMS, NIH (R01GM114061). J.K.C. acknowledges support from NSF (CHE-1665331). J.C. acknowledges support from the Fogarty International Center, NIH (TW009872). P.A.C. acknowledges support from the National Cancer Institute (NCI), NIH (R01 CA158275), and the NIH/National Institute of Aging (P01 AG012411). N.K.G. acknowledges support from NSF (CHE-1464898). B.C.G. thanks the support of NSF (RUI: 213569), the Camille and Henry Dreyfus Foundation, and the Arnold and Mabel Beckman Foundation. C.C.H. thanks the start-up funds from the Scripps Institution of Oceanography for support. J.N.J. acknowledges support from NIH (GM 063557, GM 084333). A.D.K. thanks the support from NCI, NIH (P01CA125066). D.G.I.K. acknowledges support from the National Center for Complementary and Integrative Health (1 R01 AT008088) and the Fogarty International Center, NIH (U01 TW00313), and gratefully acknowledges courtesies extended by the Government of Madagascar (Ministere des Eaux et Forets). O.K. thanks NIH (R01GM071779) for financial support. T.J.M. acknowledges support from NIH (GM116952). S.M. acknowledges support from NIH (DA045884-01, DA046487-01, AA026949-01), the Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Medical Research Program (W81XWH-17-1-0256), and NCI, NIH, through a Cancer Center Support Grant (P30 CA008748). K.N.M. thanks the California Department of Food and Agriculture Pierce's Disease and Glassy Winged Sharpshooter Board for support. B.T.M. thanks Michael Mullowney for his contribution in the isolation, elucidation, and submission of the compounds in this work. P.N. acknowledges support from NIH (R01 GM111476). L.E.O. acknowledges support from NIH (R01-HL25854, R01-GM30859, R0-1-NS-12389). L.E.B., J.K.S., and J.A.P. thank the NIH (R35 GM-118173, R24 GM-111625) for research support. F.R. thanks the American Lebanese Syrian Associated Charities (ALSAC) for financial support. I.S. thanks the University of Oklahoma Startup funds for support. J.T.S. acknowledges support from ACS PRF (53767-ND1) and NSF (CHE-1414298), and thanks Drs. Kellan N. Lamb and Michael J. Di Maso for their synthetic contribution. B.S. acknowledges support from NIH (CA78747, CA106150, GM114353, GM115575). W.S. acknowledges support from NIGMS, NIH (R15GM116032, P30 GM103450), and thanks the University of Arkansas for startup funds and the Arkansas Biosciences Institute (ABI) for seed money. C.R.J.S. acknowledges support from NIH (R01GM121656). D.S.T. thanks the support of NIH (T32 CA062948-Gudas) and PhRMA Foundation to A.L.V., NIH (P41 GM076267) to D.S.T., and CCSG NIH (P30 CA008748) to C.B. Thompson. R.E.T. acknowledges support from NIGMS, NIH (GM129465). R.J.T. thanks the American Cancer Society (RSG-12-253-01-CDD) and NSF (CHE1361173) for support. D.A.V. thanks the Camille and Henry Dreyfus Foundation, the National Science Foundation (CHE-0353662, CHE-1005253, and CHE-1725142), the Beckman Foundation, the Sherman Fairchild Foundation, the John Stauffer Charitable Trust, and the Christian Scholars Foundation for support. J.W. acknowledges support from the American Cancer Society through the Research Scholar Grant (RSG-13-011-01-CDD). W.M.W.acknowledges support from NIGMS, NIH (GM119426), and NSF (CHE1755698). A.Z. acknowledges support from NSF (CHE-1463819). (Intramural Research Program of the National Center for Advancing Translational Sciences, National Institutes of Health (NIH); CHE-1665145 - NSF; CHE-1665331 - NSF; CHE-1464898 - NSF; RUI: 213569 - NSF; CHE-1414298 - NSF; CHE1361173 - NSF; CHE1755698 - NSF; CHE-1463819 - NSF; GM126221 - NIH; 5R01GM110131 - NIH; GM 063557 - NIH; GM 084333 - NIH; R01GM071779 - NIH; GM116952 - NIH; DA045884-01 - NIH; DA046487-01 - NIH; AA026949-01 - NIH; R01 GM111476 - NIH; R01-HL25854 - NIH; R01-GM30859 - NIH; R0-1-NS-12389 - NIH; R35 GM-118173 - NIH; R24 GM-111625 - NIH; CA78747 - NIH; CA106150 - NIH; GM114353 - NIH; GM115575 - NIH; R01GM121656 - NIH; T32 CA062948-Gudas - NIH; P41 GM076267 - NIH; R01GM114061 - NIGMS, NIH; R15GM116032 - NIGMS, NIH; P30 GM103450 - NIGMS, NIH; GM129465 - NIGMS, NIH; GM119426 - NIGMS, NIH; TW009872 - Fogarty International Center, NIH; U01 TW00313 - Fogarty International Center, NIH; R01 CA158275 - National Cancer Institute (NCI), NIH; P01 AG012411 - NIH/National Institute of Aging; Camille and Henry Dreyfus Foundation; Arnold and Mabel Beckman Foundation; Scripps Institution of Oceanography; P01CA125066 - NCI, NIH; 1 R01 AT008088 - National Center for Complementary and Integrative Health; W81XWH-17-1-0256 - Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Medical Research Program; P30 CA008748 - NCI, NIH, through a Cancer Center Support Grant; California Department of Food and Agriculture Pierce's Disease and Glassy Winged Sharpshooter Board; American Lebanese Syrian Associated Charities (ALSAC); University of Oklahoma Startup funds; 53767-ND1 - ACS PRF; PhRMA Foundation; P30 CA008748 - CCSG NIH; RSG-12-253-01-CDD - American Cancer Society; RSG-13-011-01-CDD - American Cancer Society; CHE-0353662 - National Science Foundation; CHE-1005253 - National Science Foundation; CHE-1725142 - National Science Foundation; Beckman Foundation; Sherman Fairchild Foundation; John Stauffer Charitable Trust; Christian Scholars Foundation)Published versionSupporting documentatio