38 research outputs found

    A lake-centric geospatial database to guide research and inform management decisions in an Arctic watershed in northern Alaska experiencing climate and land-use changes

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    Lakes are dominant and diverse landscape features in the Arctic, but conventional land cover classification schemes typically map them as a single uniform class. Here, we present a detailed lake-centric geospatial database for an Arctic watershed in northern Alaska. We developed a GIS dataset consisting of 4362 lakes that provides information on lake morphometry, hydrologic connectivity, surface area dynamics, surrounding terrestrial ecotypes, and other important conditions describing Arctic lakes. Analyzing the geospatial database relative to fish and bird survey data shows relations to lake depth and hydrologic connectivity, which are being used to guide research and aid in the management of aquatic resources in the National Petroleum Reserve in Alaska. Further development of similar geospatial databases is needed to better understand and plan for the impacts of ongoing climate and land-use changes occurring across lake-rich landscapes in the Arctic

    Infected Cell Killing by HIV-1 Protease Promotes NF-κB Dependent HIV-1 Replication

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    Acute HIV-1 infection of CD4 T cells often results in apoptotic death of infected cells, yet it is unclear what evolutionary advantage this offers to HIV-1. Given the independent observations that acute T cell HIV-1 infection results in (1) NF-κB activation, (2) caspase 8 dependent apoptosis, and that (3) caspase 8 directly activates NF-κB, we questioned whether these three events might be interrelated. We first show that HIV-1 infected T cell apoptosis, NF-κB activation, and caspase 8 cleavage by HIV-1 protease are coincident. Next we show that HIV-1 protease not only cleaves procaspase 8, producing Casp8p41, but also independently stimulates NF-κB activity. Finally, we demonstrate that the HIV protease cleavage of caspase 8 is necessary for optimal NF-κB activation and that the HIV-1 protease specific cleavage fragment Casp8p41 is sufficient to stimulate HIV-1 replication through NF-κB dependent HIV-LTR activation both in vitro as well as in cells from HIV infected donors. Consequently, the molecular events which promote death of HIV-1 infected T cells function dually to promote HIV-1 replication, thereby favoring the propagation and survival of HIV-1

    The Science Performance of JWST as Characterized in Commissioning

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    This paper characterizes the actual science performance of the James Webb Space Telescope (JWST), as determined from the six month commissioning period. We summarize the performance of the spacecraft, telescope, science instruments, and ground system, with an emphasis on differences from pre-launch expectations. Commissioning has made clear that JWST is fully capable of achieving the discoveries for which it was built. Moreover, almost across the board, the science performance of JWST is better than expected; in most cases, JWST will go deeper faster than expected. The telescope and instrument suite have demonstrated the sensitivity, stability, image quality, and spectral range that are necessary to transform our understanding of the cosmos through observations spanning from near-earth asteroids to the most distant galaxies.Comment: 5th version as accepted to PASP; 31 pages, 18 figures; https://iopscience.iop.org/article/10.1088/1538-3873/acb29

    The James Webb Space Telescope Mission

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    Twenty-six years ago a small committee report, building on earlier studies, expounded a compelling and poetic vision for the future of astronomy, calling for an infrared-optimized space telescope with an aperture of at least 4m4m. With the support of their governments in the US, Europe, and Canada, 20,000 people realized that vision as the 6.5m6.5m James Webb Space Telescope. A generation of astronomers will celebrate their accomplishments for the life of the mission, potentially as long as 20 years, and beyond. This report and the scientific discoveries that follow are extended thank-you notes to the 20,000 team members. The telescope is working perfectly, with much better image quality than expected. In this and accompanying papers, we give a brief history, describe the observatory, outline its objectives and current observing program, and discuss the inventions and people who made it possible. We cite detailed reports on the design and the measured performance on orbit.Comment: Accepted by PASP for the special issue on The James Webb Space Telescope Overview, 29 pages, 4 figure

    Primary CD4 T cells from HIV infected patients upregulate HIV replication in response to Casp8p41.

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    <p>Primary CD4 T cells from eight HIV positive or three HIV negative (data not shown) donors were transfected with empty vector control, Casp8FL, or Casp8p41, and p24 antigen production measured in triplicate. The limit of detection for the p24 assay is <5 pg/ml. Results presented represent means of replicates.</p

    HIV protease upregulation of HIV LTR requires caspase 8.

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    <p>(A) The caspase 8 deficient 19.2 cell line was stably transfected with empty vector control, wild type caspase 8 (Casp8WT) or caspase 8 containing the HIV-1 protease resistant cleavage mutation RN at position 355/356 (Casp8RN), and then transfected with HIV-1 protease along with the HIV-LTR-Luc reporter construct. (B) 19.2 cells were transfected with Casp8WT in the presence or absence of Nelfinavir (Nfv) and then with HIV protease along with the HIV-LTR-Luc reporter construct. Results of three independent experiments expressed as fold increase relative to control, normalized to Renilla, +/− SD.</p

    Jurkat T cell upregulate HIV LTR coincident with Casp8p41 expression.

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    <p>(A) Jurkat T cells were acutely infected with HIV IIIb or mock and three days post infection transfected with RFP. RFP positive cells were gated and p24 content analyzed by intracellular staining with p24 FITC. (B) HIV or mock infected Jurkat T cells were transfected with HIV LTR luciferase or HIV LTRΔTAR luciferase reporter constructs with or without Renilla cotransfection and luciferase measured in the presence or absence of the HIV protease inhibitor Nelfinavir (Nfv). (C) HIV IIIb or mock infected Jurkat T cells were analyzed daily for viability HIV LTRΔTAR luciferase/Renilla activity and (D) Casp8p41 content. (E) Casp8p41 was also measured in Day 3 HIV infected cells in the presence or absence of Nfv. All results representative of three or more experiments.</p

    Casp8p41 upregulates HIV LTR.

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    <p>293T cells were transfected with empty vector control, HA-Casp8FL or HA-Casp8p41, along with the HIV-LTR-Luc reporter construct. Transgene expression was confirmed by HA Western Blot. Results expressed as fold increase relative to control, normalized to Renilla. Results of three independent experiments expressed as fold increase relative to control, normalized to Renilla, +/− SD.</p

    Casp8p41 upregulation of HIV LTR is NF-κB dependent.

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    <p>(A) 293T cells were transfected with empty vector control, Casp8FL or Casp8p41 along with HIV-LTR-Luc or with HIV-LTR-Luc with the KB site deleted (HIV-LTR-ΔKB-Luc) as indicated. Results of three independent experiments expressed as fold increase relative to control, normalized to Renilla, +/− SD. Results expressed as luciferase expression per Renilla. *p = <0.05 compared to HIV LTR. (B) 293T cells were transfected with empty vector control HA-Casp8FL or HA-Casp8p41 and analyzed by EMSA in the presence or absence of anti-p50 or anti-p65 antibodies. As a control for the antibodies EMSA's were performed in cells transfected with p50/p65 in the presence or absence of anti-p50 or p65 antibodies. The level of Casp8FL and Casp8p41 expression were determined in parallel.</p

    Casp8p41 upregulation of HIV LTR requires DED.

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    <p>293 T cells were transfected with empty vector control, Casp8p41, or Casp8p41 with one DED deleted (Casp8p41 ΔDED), along with HIV-LTR-Luc, and luciferase measured. Results of three independent experiments expressed as fold increase relative to control, normalized to Renilla, +/− SD.</p
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