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  • 1
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    Mars surface context cameras past, present and future (2016)
    Wiley
    Details
    Publication Date: 2016-04-09
    Description: Mars has been the focus of robotic space exploration since the 1960s, in which time there have been over 40 missions, some successful, some not. Camera systems have been a core component of all instrument payloads sent to the Martian surface, harnessing some combination of monochrome, color, multispectral, and stereo imagery. Together, these datasets provide the geological context to a mission, which over the decades has included the characterization and spatial mapping of geological units and associated stratigraphy, charting active surface processes such as dust devils and water ice sublimation, and imaging the robotic manipulation of samples via scoops (Viking), drills (Mars Science Laboratory (MSL) Curiosity), and grinders (Mars Exploration Rovers). Through the decades, science context imaging has remained an integral part of increasingly advanced analytical payloads, with continual advances in spatial and spectral resolution, radiometric and geometric calibration, and image analysis techniques. Mars context camera design has encompassed major technological shifts, from single photomultiplier tube detectors to megapixel charged-couple-devices, and from multichannel to Bayer filter color imaging. Here we review the technological capability and evolution of science context imaging instrumentation resulting from successful surface missions to Mars, and those currently in development for planned future missions. This article is protected by copyright. All rights reserved.
    Electronic ISSN: 2333-5084
    Topics: Geosciences , Physics
    Published by Wiley on behalf of The American Geophysical Union (AGU).
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  • 2
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    Tetanus toxoid and CCL3 improve dendritic cell vaccines in mice and glioblastoma patients (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-03-13
    Description: After stimulation, dendritic cells (DCs) mature and migrate to draining lymph nodes to induce immune responses. As such, autologous DCs generated ex vivo have been pulsed with tumour antigens and injected back into patients as immunotherapy. While DC vaccines have shown limited promise in the treatment of patients with advanced cancers including glioblastoma, the factors dictating DC vaccine efficacy remain poorly understood. Here we show that pre-conditioning the vaccine site with a potent recall antigen such as tetanus/diphtheria (Td) toxoid can significantly improve the lymph node homing and efficacy of tumour-antigen-specific DCs. To assess the effect of vaccine site pre-conditioning in humans, we randomized patients with glioblastoma to pre-conditioning with either mature DCs or Td unilaterally before bilateral vaccination with DCs pulsed with Cytomegalovirus phosphoprotein 65 (pp65) RNA. We and other laboratories have shown that pp65 is expressed in more than 90% of glioblastoma specimens but not in surrounding normal brain, providing an unparalleled opportunity to subvert this viral protein as a tumour-specific target. Patients given Td had enhanced DC migration bilaterally and significantly improved survival. In mice, Td pre-conditioning also enhanced bilateral DC migration and suppressed tumour growth in a manner dependent on the chemokine CCL3. Our clinical studies and corroborating investigations in mice suggest that pre-conditioning with a potent recall antigen may represent a viable strategy to improve anti-tumour immunotherapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4510871/" 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/PMC4510871/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitchell, Duane A -- Batich, Kristen A -- Gunn, Michael D -- Huang, Min-Nung -- Sanchez-Perez, Luis -- Nair, Smita K -- Congdon, Kendra L -- Reap, Elizabeth A -- Archer, Gary E -- Desjardins, Annick -- Friedman, Allan H -- Friedman, Henry S -- Herndon, James E 2nd -- Coan, April -- McLendon, Roger E -- Reardon, David A -- Vredenburgh, James J -- Bigner, Darell D -- Sampson, John H -- 1UL2 RR024128-01/RR/NCRR NIH HHS/ -- P01 CA154291/CA/NCI NIH HHS/ -- P01-CA154291-01A1/CA/NCI NIH HHS/ -- P50 CA108786/CA/NCI NIH HHS/ -- P50 NS020023/NS/NINDS NIH HHS/ -- P50-CA108786/CA/NCI NIH HHS/ -- P50-NS20023/NS/NINDS NIH HHS/ -- R01 CA134844/CA/NCI NIH HHS/ -- R01 CA177476/CA/NCI NIH HHS/ -- R01 NS067037/NS/NINDS NIH HHS/ -- R01-CA134844/CA/NCI NIH HHS/ -- R01-CA177476-01/CA/NCI NIH HHS/ -- R01-NS067037/NS/NINDS NIH HHS/ -- T32 AI052077/AI/NIAID NIH HHS/ -- T32 GM007171/GM/NIGMS NIH HHS/ -- England -- Nature. 2015 Mar 19;519(7543):366-9. doi: 10.1038/nature14320. Epub 2015 Mar 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Preston Robert Tisch Brain Tumor Center, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Division of Neurosurgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA [3] Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; 1] Division of Neurosurgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; 1] Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Department of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; Department of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; Division of Neurosurgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA. ; Division of Surgical Sciences, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA. ; 1] Preston Robert Tisch Brain Tumor Center, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Division of Neurosurgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA. ; Department of Biostatistics and Bioinformatics, Duke University Medical Center, Durham, North Carolina 27710, USA. ; 1] Preston Robert Tisch Brain Tumor Center, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; 1] Preston Robert Tisch Brain Tumor Center, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Division of Neurosurgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA [3] Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA [4] Department of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA [5] Department of Radiation Oncology, Duke University Medical Center, Durham, North Carolina 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25762141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/immunology ; CD4-Positive T-Lymphocytes/drug effects/immunology ; Cancer Vaccines/administration & dosage/*immunology/therapeutic use ; Cell Movement/drug effects ; Chemokine CCL3/*immunology ; Dendritic Cells/cytology/*drug effects/immunology ; Female ; Glioblastoma/drug therapy/*immunology/pathology/*therapy ; Humans ; Immunotherapy/methods ; Lymph Nodes/cytology/drug effects/immunology ; Mice ; Mice, Inbred C57BL ; Phosphoproteins/chemistry/genetics/immunology ; Substrate Specificity ; Survival Rate ; Tetanus Toxoid/*administration & dosage/*pharmacology/therapeutic use ; Treatment Outcome ; Viral Matrix Proteins/chemistry/genetics/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    A chemokine expressed in lymphoid high endothelial venules promotes the adhesion and chemotaxis of naive T lymphocytes (1998)
    National Academy of Sciences
    Details
    Publication Date: 1998-01-06
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    NLRP3 inflammasome induces chemotactic immune cell migration to the CNS in experimental autoimmune encephalomyelitis (2012)
    National Academy of Sciences
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    Publication Date: 2012-06-13
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 5
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    NLRP3 inflammasome enhances immune cell migration [Immunology] (2012)
    National Academy of Sciences
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    Publication Date: 2012-06-27
    Description: The NLRP3 inflammasome is a multiprotein complex consisting of three kinds of proteins, NLRP3, ASC, and pro-caspase-1, and plays a role in sensing pathogens and danger signals in the innate immune system. The NLRP3 inflammasome is thought to be involved in the development of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). However, the mechanism by which the NLRP3 inflammasome induces EAE is not clear. In this study, we found that the NLRP3 inflammasome played a critical role in inducing T-helper cell migration into the CNS. To gain migratory ability, CD4+ T cells need to be primed by NLRP3 inflammasome-sufficient antigen-presenting cells to up-regulate chemotaxis-related proteins, such as osteopontin, CCR2, and CXCR6. In the presence of the NLRP3 inflammasome, dendritic cells and macrophages also induce chemotactic ability and up-regulate chemotaxis-related proteins, such as α4β1 integrin, CCL7, CCL8, and CXCL16. On the other hand, reduced Th17 cell population size in immunized Nlrp3−/− and Asc−/− mice is not a determinative factor for their resistance to EAE. As currently applied in clinical interventions of MS, targeting immune cell migration molecules may be an effective approach in treating MS accompanied by NLRP3 inflammasome activation.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 6
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    Biased agonists of the chemokine receptor CXCR3 differentially control chemotaxis and inflammation (2018)
    The American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2018
    Description: 〈p〉The chemokine receptor CXCR3 plays a central role in inflammation by mediating effector/memory T cell migration in various diseases; however, drugs targeting CXCR3 and other chemokine receptors are largely ineffective in treating inflammation. Chemokines, the endogenous peptide ligands of chemokine receptors, can exhibit so-called biased agonism by selectively activating either G protein– or β-arrestin–mediated signaling after receptor binding. Biased agonists might be used as more targeted therapeutics to differentially regulate physiological responses, such as immune cell migration. To test whether CXCR3-mediated physiological responses could be segregated by G protein– and β-arrestin–mediated signaling, we identified and characterized small-molecule biased agonists of the receptor. In a mouse model of T cell–mediated allergic contact hypersensitivity (CHS), topical application of a β-arrestin–biased, but not a G protein–biased, agonist potentiated inflammation. T cell recruitment was increased by the β-arrestin–biased agonist, and biopsies of patients with allergic CHS demonstrated coexpression of CXCR3 and β-arrestin in T cells. In mouse and human T cells, the β-arrestin–biased agonist was the most efficient at stimulating chemotaxis. Analysis of phosphorylated proteins in human lymphocytes showed that β-arrestin–biased signaling activated the kinase Akt, which promoted T cell migration. This study demonstrates that biased agonists of CXCR3 produce distinct physiological effects, suggesting discrete roles for different endogenous CXCR3 ligands and providing evidence that biased signaling can affect the clinical utility of drugs targeting CXCR3 and other chemokine receptors.〈/p〉
    Print ISSN: 1945-0877
    Electronic ISSN: 1937-9145
    Topics: Biology , Medicine
    Published by The American Association for the Advancement of Science (AAAS)
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  • 7
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    Mars surface context cameras past, present, and future (2016)
    American Geophysical Union
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    Publication Date: 2016-04-01
    Electronic ISSN: 2333-5084
    Topics: Geosciences , Physics
    Published by American Geophysical Union
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  • 8
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    Multiscale and Multispectral Characterization of Mineralogy with the ExoMars 2022 Rover Remote Sensing Payload (2020)
    American Geophysical Union
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    Publication Date: 2020-04-01
    Electronic ISSN: 2333-5084
    Topics: Geosciences , Physics
    Published by American Geophysical Union
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