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  • American Association for the Advancement of Science (AAAS)  (6)
  • Wiley-Blackwell  (4)
  • 1
    Publication Date: 2013-08-31
    Description: Invasion of microbial DNA into the cytoplasm of animal cells triggers a cascade of host immune reactions that help clear the infection; however, self DNA in the cytoplasm can cause autoimmune diseases. Biochemical approaches led to the identification of cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS) as a cytosolic DNA sensor that triggers innate immune responses. Here, we show that cells from cGAS-deficient (cGas(-/-)) mice, including fibroblasts, macrophages, and dendritic cells, failed to produce type I interferons and other cytokines in response to DNA transfection or DNA virus infection. cGas(-/-) mice were more susceptible to lethal infection with herpes simplex virus 1 (HSV1) than wild-type mice. We also show that cGAMP is an adjuvant that boosts antigen-specific T cell activation and antibody production in mice.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3863637/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3863637/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Xiao-Dong -- Wu, Jiaxi -- Gao, Daxing -- Wang, Hua -- Sun, Lijun -- Chen, Zhijian J -- 5T32AI070116/AI/NIAID NIH HHS/ -- AI-093967/AI/NIAID NIH HHS/ -- R01 AI093967/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Sep 20;341(6152):1390-4. doi: 10.1126/science.1244040. Epub 2013 Aug 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23989956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/biosynthesis ; DNA, Viral/genetics/immunology ; Dendritic Cells/immunology ; Fibroblasts/immunology ; Herpes Simplex/*immunology ; *Herpesvirus 1, Human ; Interferon Regulatory Factor-3/genetics ; Interferon-beta/*biosynthesis/genetics ; Lymphocyte Activation ; Macrophages/immunology ; Mice ; Mice, Knockout ; Nucleotidyltransferases/genetics/*immunology ; Signal Transduction ; T-Lymphocytes/immunology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1996-11-08
    Description: A recently assembled data set of inner core-sensitive free oscillation splitting measurements and body wave differential travel times provides constraints on the patterns of anisotropy in the Earth's inner core. Applying a formalism that allows departures from radial symmetry and cylindrical anisotropy results in models with P-wave velocity distributions whose strength and pattern are incompatible with frozen-in anisotropy, but rather suggest a simple large-scale convection regime in the inner core.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Romanowicz -- Li -- Durek -- New York, N.Y. -- Science. 1996 Nov 8;274(5289):963-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉B. Romanowicz, Seismographic Station and Department of Geology and Geophysics, University of California at Berkeley, Berkeley, CA 94720, USA. X.-D. Li and J. Durek, Seismographic Station, University of California at Berkeley, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8875934" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2009-03-28
    Description: The spread of HIV between immune cells is greatly enhanced by cell-cell adhesions called virological synapses, although the underlying mechanisms have been unclear. With use of an infectious, fluorescent clone of HIV, we tracked the movement of Gag in live CD4 T cells and captured the direct translocation of HIV across the virological synapse. Quantitative, high-speed three-dimensional (3D) video microscopy revealed the rapid formation of micrometer-sized "buttons" containing oligomerized viral Gag protein. Electron microscopy showed that these buttons were packed with budding viral crescents. Viral transfer events were observed to form virus-laden internal compartments within target cells. Continuous time-lapse monitoring showed preferential infection through synapses. Thus, HIV dissemination may be enhanced by virological synapse-mediated cell adhesion coupled to viral endocytosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756521/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756521/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hubner, Wolfgang -- McNerney, Gregory P -- Chen, Ping -- Dale, Benjamin M -- Gordon, Ronald E -- Chuang, Frank Y S -- Li, Xiao-Dong -- Asmuth, David M -- Huser, Thomas -- Chen, Benjamin K -- 5R24 CA095823-04/CA/NCI NIH HHS/ -- AI074420-02/AI/NIAID NIH HHS/ -- DP1 DA028866/DA/NIDA NIH HHS/ -- R01 AI074420/AI/NIAID NIH HHS/ -- R01 AI074420-01A2/AI/NIAID NIH HHS/ -- R01 AI074420-02/AI/NIAID NIH HHS/ -- S10RR09145-01/RR/NCRR NIH HHS/ -- ULRR024146/PHS HHS/ -- New York, N.Y. -- Science. 2009 Mar 27;323(5922):1743-7. doi: 10.1126/science.1167525.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases, Department of Medicine, Immunology Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19325119" target="_blank"〉PubMed〈/a〉
    Keywords: CD4-Positive T-Lymphocytes/*physiology/ultrastructure/*virology ; *Cell Adhesion ; Coculture Techniques ; Cytochalasin D/pharmacology ; Endocytosis ; HIV/*physiology/ultrastructure ; Humans ; Imaging, Three-Dimensional ; Jurkat Cells ; Microscopy, Confocal ; Microscopy, Electron, Transmission ; Microscopy, Video ; Receptors, CCR5/metabolism ; Receptors, CXCR4/metabolism ; Recombinant Fusion Proteins/metabolism ; *Virus Internalization ; gag Gene Products, Human Immunodeficiency Virus/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2014-12-20
    Description: Multivalent molecules with repetitive structures including bacterial capsular polysaccharides and viral capsids elicit antibody responses through B cell receptor (BCR) crosslinking in the absence of T cell help. We report that immunization with these T cell-independent type 2 (TI-2) antigens causes up-regulation of endogenous retrovirus (ERV) RNAs in antigen-specific mouse B cells. These RNAs are detected via a mitochondrial antiviral signaling protein (MAVS)-dependent RNA sensing pathway or reverse-transcribed and detected via the cGAS-cGAMP-STING pathway, triggering a second, sustained wave of signaling that promotes specific immunoglobulin M production. Deficiency of both MAVS and cGAS, or treatment of MAVS-deficient mice with reverse transcriptase inhibitors, dramatically inhibits TI-2 antibody responses. These findings suggest that ERV and two innate sensing pathways that detect them are integral components of the TI-2 B cell signaling apparatus.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391621/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391621/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zeng, Ming -- Hu, Zeping -- Shi, Xiaolei -- Li, Xiaohong -- Zhan, Xiaoming -- Li, Xiao-Dong -- Wang, Jianhui -- Choi, Jin Huk -- Wang, Kuan-wen -- Purrington, Tiana -- Tang, Miao -- Fina, Maggy -- DeBerardinis, Ralph J -- Moresco, Eva Marie Y -- Pedersen, Gabriel -- McInerney, Gerald M -- Karlsson Hedestam, Gunilla B -- Chen, Zhijian J -- Beutler, Bruce -- P01 AI070167/AI/NIAID NIH HHS/ -- R01 AI093967/AI/NIAID NIH HHS/ -- R01 CA157996/CA/NCI NIH HHS/ -- U19 AI100627/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 19;346(6216):1486-92. doi: 10.1126/science.346.6216.1486.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8502, USA. ; Department of Pediatrics and Children's Medical Center Research Institute, and McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8502, USA. ; Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8502, USA. Howard Hughes Medical Institute, Department of Molecular Biology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9148, USA. ; Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Nobels vag 16, SE-171 77 Stockholm, Sweden. ; Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8502, USA. Bruce.Beutler@UTSouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25525240" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/*immunology ; Animals ; Antibody Formation ; Antigens, T-Independent/*immunology ; B-Lymphocytes/*immunology ; Cytosol/immunology ; DNA/immunology ; Endogenous Retroviruses/genetics/*immunology ; Lymphocyte Activation ; Membrane Proteins/immunology ; Mice ; Mice, Inbred C57BL ; NF-kappa B/metabolism ; Nucleotides, Cyclic/immunology ; Nucleotidyltransferases/genetics/*immunology ; RNA, Viral/genetics/*immunology ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Electronic Resource
    Electronic Resource
    Chichester [u.a.] : Wiley-Blackwell
    International Journal for Numerical Methods in Engineering 37 (1994), S. 3585-3603 
    ISSN: 0029-5981
    Keywords: Engineering ; Engineering General
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Mathematics , Technology
    Notes: In the paper we present a postprocessed type of a posteriori error estimate and a h-version adaptive procedure for the semidiscrete finite element method in dynamic analysis. In space the super-convergent patch recovery technique is used for determining higher-order accurate stresses and, thus, a spatial error estimate. In time a postprocessing technique is developed for obtaining a local error estimate for one step time integration schemes (the HHT-α method). Coupling the error estimate with a mesh generator, a h-version adaptive finite element procedure is presented for two-dimensional dynamic analysis. It updates the spatial mesh and time step automatically so that the discretization errors are controlled within specified tolerances. Numerical studies on different problems are presented for demonstrating the performances of the proposed adaptive procedure.
    Additional Material: 19 Ill.
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  • 6
    Electronic Resource
    Electronic Resource
    Chichester [u.a.] : Wiley-Blackwell
    International Journal for Numerical Methods in Engineering 39 (1996), S. 2131-2152 
    ISSN: 0029-5981
    Keywords: discontinuous Galerkin finite element method ; predictor-multicorrector ; adaptive time integration ; structural dynamics ; Engineering ; Engineering General
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Mathematics , Technology
    Notes: This paper studies a time-discontinuous Galerkin finite element method for structural dynamic problems, by which both displacements and velocities are approximated as piecewise linear functions in the time domain and may be discontinuous at the discrete time levels. A new iterative solution algorithm which involves only one factorization for each fixed time step size and a few iterations at each step is presented for solving the resulted system of coupled equations. By using the jumps of the displacements and the velocities in the total energy norm as error indicators, an adaptive time-stepping procedure for selecting the proper time step size is described. Numerical examples including both single-DOF and multi-DOF problems are used to illustrate the performance of these algorithms. Comparisons with the exact results and/or the results by the Newmark integration scheme are given. It is shown that the time-discontinuous Galerkin finite element method discussed in this study possesses good accuracy (third order) and stability properties, its numerical implementation is not difficult, and the higher computational cost needed in each time step is compensated by use of a larger time step size.
    Additional Material: 20 Ill.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Chichester : Wiley-Blackwell
    Communications in Numerical Methods in Engineering 9 (1993), S. 273-292 
    ISSN: 1069-8299
    Keywords: Engineering ; Engineering General
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Mathematics , Technology
    Notes: A simple a posteriori local error estimator for time discretization in structural dynamic analysis is presented. It is derived from the difference of the solutions between an ordinary integration method (the Newmark scheme) and another higher-order one which assumes that the derivatives of accelerations vary linearly within each time step. It may be obtained directly without resolving new equations, so the additional computational cost is small and the implementation is convenient. Furthermore, it is shown that this error estimator may also be obtained by Taylor expansion or by a post-processing technique. Accordingly, an adaptive time-stepping procedure, which automatically adjusts the time-step size so that the local error at each time step is within a prescribed accuracy, is described. Numerical examples, including two single-DOF problems, a two-DOF problem and a multi-DOF model, are presented. The results show that the presented local error estimator is simple, reliable and accurate.
    Additional Material: 9 Ill.
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  • 8
    Electronic Resource
    Electronic Resource
    Chichester : Wiley-Blackwell
    Communications in Numerical Methods in Engineering 10 (1994), S. 313-320 
    ISSN: 1069-8299
    Keywords: Engineering ; Engineering General
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Mathematics , Technology
    Notes: In the paper we present a superconvergent patch recovery technique for obtaining higher-order-accurate finite-element solutions and thus a postprocessed type of L2 norm error estimate. Two modifications make our procedure different from the one proposed by Zienkiewicz and Zhu (1992), in which higher-order-accurate derivatives of the finite-element solution at nodes are determined. Firstly, the recovery process is made for element, not for nodes. An ‘element patch’, which represents the union of an element under consideration and the surrounding elements, is introduced. Secondly, the local error estimate is calculated directly from the improved solution for this element. Numerical tests on both 1D and 2D model problems show that this method can provide an asymptotically exact a posteriori L2 norm error estimate if the used element possesses superconvergent points for the solutions.
    Additional Material: 7 Ill.
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  • 9
    Publication Date: 2019
    Description: 〈p〉Cancer cells often encounter oxidative stress. However, it is unclear whether normal and cancer cells differentially respond to oxidative stress. Here, we demonstrated that under oxidative stress, hepatocellular carcinoma (HCC) cells exhibit increased antioxidative response and survival rates compared to normal hepatocytes. Oxidative stimulation induces HCC-specifically expressed fructokinase A (KHK-A) phosphorylation at S80 by 5'-adenosine monophosphate-activated protein kinase. KHK-A in turn acts as a protein kinase to phosphorylate p62 at S28, thereby blocking p62 ubiquitination and enhancing p62’s aggregation with Keap1 and Nrf2 activation. Activated Nrf2 promotes expression of genes involved in reactive oxygen species reduction, cell survival, and HCC development in mice. In addition, phosphorylation of KHK-A S80 and p62 S28 and nuclear accumulation of Nrf2 are positively correlated in human HCC specimens and with poor prognosis of patients with HCC. These findings underscore the role of the protein kinase activity of KHK-A in antioxidative stress and HCC development.〈/p〉
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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  • 10
    Publication Date: 2019
    Description: 〈p〉How somatic mutations accumulate in normal cells is poorly understood. A comprehensive analysis of RNA sequencing data from ~6700 samples across 29 normal tissues revealed multiple somatic variants, demonstrating that macroscopic clones can be found in many normal tissues. We found that sun-exposed skin, esophagus, and lung have a higher mutation burden than other tested tissues, which suggests that environmental factors can promote somatic mosaicism. Mutation burden was associated with both age and tissue-specific cell proliferation rate, highlighting that mutations accumulate over both time and number of cell divisions. Finally, normal tissues were found to harbor mutations in known cancer genes and hotspots. This study provides a broad view of macroscopic clonal expansion in human tissues, thus serving as a foundation for associating clonal expansion with environmental factors, aging, and risk of disease.〈/p〉
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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