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  • 1
    Publication Date: 2018-02-10
    Description: Resolution of inflammation is an active process that leads to tissue homeostasis and involves multiple cellular and molecular mechanisms. Myeloid-derived suppressor cells (MDSCs) have recently emerged as important cellular components in the resolution of inflammation because of their activities to suppress T cell activation. In this article, we show that HLA-DR – CD11b + CD33 + CD14 + human MDSCs and CD11b + Ly6G – Ly6C + mouse MDSCs markedly increased in patients and mice during and before the resolution phase of autoimmune uveoretinitis. CD11b + Ly6C + monocytes isolated from autoimmune uveoretinitis mice were able to suppress T cell proliferation in culture, and adoptive transfer of the cells accelerated the remission of autoimmune uveoretinitis in mice. Alternatively, depletion of CD11b + Ly6C + monocytes at the resolution phase, but not CD11b + Ly6G + granulocytes, exacerbated the disease. These findings collectively indicate that monocytic MDSCs serve as regulatory cells mediating the resolution of autoimmune uveoretinitis.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
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  • 2
    Publication Date: 2014-10-23
    Description: The holotype of Deinocheirus mirificus was collected by the 1965 Polish-Mongolian Palaeontological Expedition at Altan Uul III in the southern Gobi of Mongolia. Because the holotype consists mostly of giant forelimbs (2.4 m in length) with scapulocoracoids, for almost 50 years Deinocheirus has remained one of the most mysterious dinosaurs. The mosaic of ornithomimosaur and non-ornithomimosaur characters in the holotype has made it difficult to resolve the phylogenetic status of Deinocheirus. Here we describe two new specimens of Deinocheirus that were discovered in the Nemegt Formation of Altan Uul IV in 2006 and Bugiin Tsav in 2009. The Bugiin Tsav specimen (MPC-D 100/127) includes a left forelimb clearly identifiable as Deinocheirus and is 6% longer than the holotype. The Altan Uul IV specimen (MPC-D 100/128) is approximately 74% the size of MPC-D 100/127. Cladistic analysis indicates that Deinocheirus is the largest member of the Ornithomimosauria; however, it has many unique skeletal features unknown in other ornithomimosaurs, indicating that Deinocheirus was a heavily built, non-cursorial animal with an elongate snout, a deep jaw, tall neural spines, a pygostyle, a U-shaped furcula, an expanded pelvis for strong muscle attachments, a relatively short hind limb and broad-tipped pedal unguals. Ecomorphological features in the skull, more than a thousand gastroliths, and stomach contents (fish remains) suggest that Deinocheirus was a megaomnivore that lived in mesic environments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Yuong-Nam -- Barsbold, Rinchen -- Currie, Philip J -- Kobayashi, Yoshitsugu -- Lee, Hang-Jae -- Godefroit, Pascal -- Escuillie, Francois -- Chinzorig, Tsogtbaatar -- England -- Nature. 2014 Nov 13;515(7526):257-60. doi: 10.1038/nature13874. Epub 2014 Oct 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geological Museum, Korea Institute of Geoscience and Mineral Resources, Daejeon 305-350, South Korea. ; Paleontological Center, Mongolian Academy of Sciences, Ulaanbaatar 210-351, Mongolia. ; Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2E9, Canada. ; Hokkaido University Museum, Hokkaido University, Sapporo 060-0810, Japan. ; Earth and History of Life, Royal Belgian Institute of Natural Sciences, Rue Vautier 29, 1000 Bruxelles, Belgium. ; Eldonia, 9 Avenue des Portes Occitanes, 3800 Gannat, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25337880" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Size ; Dinosaurs/*anatomy & histology/*classification ; *Fossils ; Mongolia ; Phylogeny ; Skeleton ; Skull/anatomy & histology ; Spine/anatomy & histology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2018-09-08
    Description: Background/Aim: High expression of the Bcl-2-interacting cell death suppressor (BIS), an anti-apoptotic protein, in various human cancers is linked to a poor outcome. The purpose of this study was to clarify whether BIS is associated with the migration and invasive characteristics of A549 cells. Materials and Methods: BIS-knockout (KO) cells were prepared by the CRISPR/Cas9 method. The aggressive behaviors of A549 cells were analyzed by wound healing and a transwell invasion assay as well as 3D spheroid culture. Results: BIS depletion resulted in significant inhibition of the migration and invasive potential of A549 cells which was accompanied by an increased ratio of E-cadherin/N-cadherin and a decrease in the mRNA levels of Zeb1, Snail, Slug and MMP-2. NF-ĸB activity was suppressed in BIS-KO A549 cells due to the decrease in p65 protein levels, but not in mRNA levels. Conclusion: BIS regulates cell invasion and the induction of the epithelial-mesenchymal transition (EMT) phenotype in A549 cells probably via the NF-ĸB signaling pathway.
    Print ISSN: 0250-7005
    Electronic ISSN: 1791-7530
    Topics: Medicine
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  • 4
    Publication Date: 2016-05-03
    Description: We analysed whole-genome sequences of 560 breast cancers to advance understanding of the driver mutations conferring clonal advantage and the mutational processes generating somatic mutations. We found that 93 protein-coding cancer genes carried probable driver mutations. Some non-coding regions exhibited high mutation frequencies, but most have distinctive structural features probably causing elevated mutation rates and do not contain driver mutations. Mutational signature analysis was extended to genome rearrangements and revealed twelve base substitution and six rearrangement signatures. Three rearrangement signatures, characterized by tandem duplications or deletions, appear associated with defective homologous-recombination-based DNA repair: one with deficient BRCA1 function, another with deficient BRCA1 or BRCA2 function, the cause of the third is unknown. This analysis of all classes of somatic mutation across exons, introns and intergenic regions highlights the repertoire of cancer genes and mutational processes operating, and progresses towards a comprehensive account of the somatic genetic basis of breast cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nik-Zainal, Serena -- Davies, Helen -- Staaf, Johan -- Ramakrishna, Manasa -- Glodzik, Dominik -- Zou, Xueqing -- Martincorena, Inigo -- Alexandrov, Ludmil B -- Martin, Sancha -- Wedge, David C -- Van Loo, Peter -- Ju, Young Seok -- Smid, Marcel -- Brinkman, Arie B -- Morganella, Sandro -- Aure, Miriam R -- Lingjaerde, Ole Christian -- Langerod, Anita -- Ringner, Markus -- Ahn, Sung-Min -- Boyault, Sandrine -- Brock, Jane E -- Broeks, Annegien -- Butler, Adam -- Desmedt, Christine -- Dirix, Luc -- Dronov, Serge -- Fatima, Aquila -- Foekens, John A -- Gerstung, Moritz -- Hooijer, Gerrit K J -- Jang, Se Jin -- Jones, David R -- Kim, Hyung-Yong -- King, Tari A -- Krishnamurthy, Savitri -- Lee, Hee Jin -- Lee, Jeong-Yeon -- Li, Yilong -- McLaren, Stuart -- Menzies, Andrew -- Mustonen, Ville -- O'Meara, Sarah -- Pauporte, Iris -- Pivot, Xavier -- Purdie, Colin A -- Raine, Keiran -- Ramakrishnan, Kamna -- Rodriguez-Gonzalez, F German -- Romieu, Gilles -- Sieuwerts, Anieta M -- Simpson, Peter T -- Shepherd, Rebecca -- Stebbings, Lucy -- Stefansson, Olafur A -- Teague, Jon -- Tommasi, Stefania -- Treilleux, Isabelle -- Van den Eynden, Gert G -- Vermeulen, Peter -- Vincent-Salomon, Anne -- Yates, Lucy -- Caldas, Carlos -- Veer, Laura Van't -- Tutt, Andrew -- Knappskog, Stian -- Tan, Benita Kiat Tee -- Jonkers, Jos -- Borg, Ake -- Ueno, Naoto T -- Sotiriou, Christos -- Viari, Alain -- Futreal, P Andrew -- Campbell, Peter J -- Span, Paul N -- Van Laere, Steven -- Lakhani, Sunil R -- Eyfjord, Jorunn E -- Thompson, Alastair M -- Birney, Ewan -- Stunnenberg, Hendrik G -- van de Vijver, Marc J -- Martens, John W M -- Borresen-Dale, Anne-Lise -- Richardson, Andrea L -- Kong, Gu -- Thomas, Gilles -- Stratton, Michael R -- Nature. 2016 May 2. doi: 10.1038/nature17676.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. ; East Anglian Medical Genetics Service, Cambridge University Hospitals NHS Foundation Trust, Cambridge CB2 9NB, UK. ; Division of Oncology and Pathology, Department of Clinical Sciences Lund, Lund University, Lund SE-223 81, Sweden. ; Theoretical Biology and Biophysics (T-6), Los Alamos National Laboratory, Los Alamos, NM 87545, New Mexico, USA. ; Center for Nonlinear Studies, Los Alamos National Laboratory, Los Alamos, New Mexico 87545, USA. ; Department of Human Genetics, University of Leuven, B-3000 Leuven, Belgium. ; Department of Medical Oncology, Erasmus MC Cancer Institute and Cancer Genomics Netherlands, Erasmus University Medical Center, Rotterdam 3015CN, The Netherlands. ; Radboud University, Department of Molecular Biology, Faculty of Science, 6525GA Nijmegen, The Netherlands. ; European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. ; Department of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, Oslo 0310, Norway. ; K. G. Jebsen Centre for Breast Cancer Research, Institute for Clinical Medicine, University of Oslo, Oslo 0310, Norway. ; Department of Computer Science, University of Oslo, Oslo, Norway. ; Gachon Institute of Genome Medicine and Science, Gachon University Gil Medical Center, Incheon, South Korea. ; Translational Research Lab, Centre Leon Berard, 28, rue Laennec, 69373 Lyon Cedex 08, France. ; Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. ; The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands. ; Breast Cancer Translational Research Laboratory, Universite Libre de Bruxelles, Institut Jules Bordet, Bd de Waterloo 121, B-1000 Brussels, Belgium. ; Translational Cancer Research Unit, Center for Oncological Research, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium. ; Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. ; Department of Pathology, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. ; Department of Pathology, Asan Medical Center, College of Medicine, Ulsan University, Ulsan, South Korea. ; Department of Pathology, College of Medicine, Hanyang University, Seoul 133-791, South Korea. ; Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA. ; Morgan Welch Inflammatory Breast Cancer Research Program and Clinic, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard., Houston, Texas 77030, USA. ; Institute for Bioengineering and Biopharmaceutical Research (IBBR), Hanyang University, Seoul, South Korea. ; Institut National du Cancer, Research Division, Clinical Research Department, 52 avenue Morizet, 92513 Boulogne-Billancourt, France. ; University Hospital of Minjoz, INSERM UMR 1098, Bd Fleming, Besancon 25000, France. ; Pathology Department, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK. ; Oncologie Senologie, ICM Institut Regional du Cancer, Montpellier, France. ; The University of Queensland, UQ Centre for Clinical Research and School of Medicine, Brisbane, Queensland 4029, Australia. ; Cancer Research Laboratory, Faculty of Medicine, University of Iceland, 101 Reykjavik, Iceland. ; IRCCS Istituto Tumori "Giovanni Paolo II", Bari, Italy. ; Department of Pathology, Centre Leon Berard, 28 rue Laennec, 69373 Lyon Cedex 08, France. ; Department of Pathology, GZA Hospitals Sint-Augustinus, Antwerp, Belgium. ; Institut Curie, Paris Sciences Lettres University, Department of Pathology and INSERM U934, 26 rue d'Ulm, 75248 Paris Cedex 05, France. ; Cancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK. ; Breast Cancer Now Research Unit, King's College London, London SE1 9RT, UK. ; Breast Cancer Now Toby Robins Research Centre, Institute of Cancer Research, London SW3 6JB, UK. ; Department of Clinical Science, University of Bergen, 5020 Bergen, Norway. ; Department of Oncology, Haukeland University Hospital, 5021 Bergen, Norway. ; National Cancer Centre Singapore, 11 Hospital Drive, 169610, Singapore. ; Singapore General Hospital, Outram Road, 169608, Singapore. ; Equipe Erable, INRIA Grenoble-Rhone-Alpes, 655, Avenue de l'Europe, 38330 Montbonnot-Saint Martin, France. ; Synergie Lyon Cancer, Centre Leon Berard, 28 rue Laennec, Lyon Cedex 08, France. ; Department of Genomic Medicine, UT MD Anderson Cancer Center, Houston, Texas 77230, USA. ; Department of Radiation Oncology, Department of Laboratory Medicine, Radboud University Medical Center, Nijmegen 6525GA, The Netherlands. ; Pathology Queensland, The Royal Brisbane and Women's Hospital, Brisbane, Queensland 4029, Australia. ; Department of Breast Surgical Oncology, University of Texas MD Anderson Cancer Center, 1400 Pressler Street, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27135926" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2018-07-31
    Description: Background/Aim: High expression of the Bcl-2-interacting cell death suppressor (BIS), an anti-apoptotic protein, in various human cancers is linked to a poor outcome. The purpose of this study was to clarify whether BIS is associated with the migration and invasive characteristics of A549 cells. Materials and Methods: BIS-knockout (KO) cells were prepared by the CRISPR/Cas9 method. The aggressive behaviors of A549 cells were analyzed by wound healing and a transwell invasion assay as well as 3D spheroid culture. Results: BIS depletion resulted in significant inhibition of the migration and invasive potential of A549 cells which was accompanied by an increased ratio of E-cadherin/N-cadherin and a decrease in the mRNA levels of Zeb1, Snail, Slug and MMP-2. NF-B activity was suppressed in BIS-KO A549 cells due to the decrease in p65 protein levels, but not in mRNA levels. Conclusion: BIS regulates cell invasion and the induction of the epithelial-mesenchymal transition (EMT) phenotype in A549 cells probably via the NF-B signaling pathway.
    Print ISSN: 0250-7005
    Electronic ISSN: 1791-7530
    Topics: Medicine
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  • 6
    Publication Date: 2012-01-27
    Description: Matter with a high energy density (〉10(5) joules per cm(3)) is prevalent throughout the Universe, being present in all types of stars and towards the centre of the giant planets; it is also relevant for inertial confinement fusion. Its thermodynamic and transport properties are challenging to measure, requiring the creation of sufficiently long-lived samples at homogeneous temperatures and densities. With the advent of the Linac Coherent Light Source (LCLS) X-ray laser, high-intensity radiation (〉10(17) watts per cm(2), previously the domain of optical lasers) can be produced at X-ray wavelengths. The interaction of single atoms with such intense X-rays has recently been investigated. An understanding of the contrasting case of intense X-ray interaction with dense systems is important from a fundamental viewpoint and for applications. Here we report the experimental creation of a solid-density plasma at temperatures in excess of 10(6) kelvin on inertial-confinement timescales using an X-ray free-electron laser. We discuss the pertinent physics of the intense X-ray-matter interactions, and illustrate the importance of electron-ion collisions. Detailed simulations of the interaction process conducted with a radiative-collisional code show good qualitative agreement with the experimental results. We obtain insights into the evolution of the charge state distribution of the system, the electron density and temperature, and the timescales of collisional processes. Our results should inform future high-intensity X-ray experiments involving dense samples, such as X-ray diffractive imaging of biological systems, material science investigations, and the study of matter in extreme conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vinko, S M -- Ciricosta, O -- Cho, B I -- Engelhorn, K -- Chung, H-K -- Brown, C R D -- Burian, T -- Chalupsky, J -- Falcone, R W -- Graves, C -- Hajkova, V -- Higginbotham, A -- Juha, L -- Krzywinski, J -- Lee, H J -- Messerschmidt, M -- Murphy, C D -- Ping, Y -- Scherz, A -- Schlotter, W -- Toleikis, S -- Turner, J J -- Vysin, L -- Wang, T -- Wu, B -- Zastrau, U -- Zhu, D -- Lee, R W -- Heimann, P A -- Nagler, B -- Wark, J S -- England -- Nature. 2012 Jan 25;482(7383):59-62. doi: 10.1038/nature10746.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, Clarendon Laboratory, University of Oxford, Parks Road, Oxford OX1 3PU, UK. sam.vinko@physics.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22278059" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2018-10-11
    Description: Developing and mature chondrocytes constantly interact with and remodel the surrounding extracellular matrix (ECM). Recent research indicates that integrin-ECM interaction is differentially regulated during cartilage formation (chondrogenesis). Integrin signaling is also a key source of the catabolic reactions responsible for joint destruction in both rheumatoid arthritis and osteoarthritis. However, we do not understand how chondrocytes dynamically regulate integrin signaling in such an ECM-rich environment. Here, we found that developing chondrocytes express integrin-β–like 1 ( Itgbl1 ) at specific stages, inhibiting integrin signaling and promoting chondrogenesis. Unlike cytosolic integrin inhibitors, ITGBL1 is secreted and physically interacts with integrins to down-regulate activity. We observed that Itgbl1 expression was strongly reduced in the damaged articular cartilage of patients with osteoarthritis (OA). Ectopic expression of Itgbl1 protected joint cartilage against OA development in the destabilization of the medial meniscus–induced OA mouse model. Our results reveal ITGBL1 signaling as an underlying mechanism of protection against destructive cartilage disorders and suggest the potential therapeutic utility of targeting ITGBL1 to modulate integrin signaling in human disease.
    Print ISSN: 1946-6234
    Electronic ISSN: 1946-6242
    Topics: Medicine
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  • 8
    Publication Date: 2018-10-23
    Description: In addition to essential roles in protein synthesis, lysyl–tRNA synthetase (KRS) is secreted to trigger a proinflammatory function that induces macrophage activation and TNF-α secretion. KRS has been associated with autoimmune diseases such as polymyositis and dermatomyositis. In this study, we investigated the immunomodulatory effects of KRS on bone marrow–derived dendritic cells (DCs) of C57BL/6 mice and subsequent polarization of Th cells and analyzed the underlying mechanisms. KRS-treated DCs increased the expression of cell surface molecules and proinflammatory cytokines associated with DC maturation and activation. Especially, KRS treatment significantly increased production of IL-12, a Th1-polarizing cytokine, in DCs. KRS triggered the nuclear translocation of the NF-B p65 subunit along with the degradation of IB proteins and the phosphorylation of MAPKs in DCs. Additionally, JNK, p38, and ERK inhibitors markedly recovered the degradation of IB proteins, suggesting the involvement of MAPKs as the upstream regulators of NF-B in the KRS-induced DC maturation and activation. Importantly, KRS-treated DCs strongly increased the differentiation of Th1 cells when cocultured with CD4 + T cells. The addition of anti–IL-12–neutralizing Ab abolished the secretion of IFN- in the coculture, indicating that KRS induces Th1 cell response via DC-derived IL-12. Moreover, KRS enhanced the OVA-specific Th1 cell polarization in vivo following the adoptive transfer of OVA-pulsed DCs. Taken together, these results indicated that KRS effectively induced the maturation and activation of DCs through MAPKs/NF-B–signaling pathways and favored DC-mediated Th1 cell response.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
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  • 9
    Publication Date: 2018-05-01
    Description: Background/Aim: This study investigated the clinical prognostic relevance of the neutrophil-to-lymphocyte ratio (NLR) in patients with human epidermal receptor 2 (HER2)-positive metastatic advanced gastric cancer (AGC) treated with combination chemotherapy including trastuzumab. Patients and Methods: This is a retrospective analysis of 73 patients diagnosed with metastatic AGC who were treated with trastuzumab combination chemotherapy. NLR was calculated as the neutrophil count divided by the lymphocyte count. A cut-off value of 3 was selected, which classified patients into two categories, low (≤3.0) or high (〉3.0). Results: In the univariate analysis, the high-NLR patients showed a significantly shorter progression-free survival (PFS) and overall survival (OS) than the low-NLR patients (PFS, p=0.012, OS, p=0.047). In the multivariate analysis, the high NLR was independently associated with a shorter PFS (p=0.015) and OS (p=0.040). Conclusion: This study found that a high NLR was associated with a shorter PFS and OS in patients with HER2-positive gastric cancer treated with trastuzumab.
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    Electronic ISSN: 1791-7530
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  • 10
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Highly split, visible light emissions at room temperature were observed in the range from 335 to 650 nm in silicon-rich oxide films deposited in the plasma phase of a mixture of silane and oxygen. The mechanism of the light emissions is classified into two categories. The photoluminescence bands at both 365 and 469 nm are related to the intrinsic defects of the E′ center and the neutral oxygen vacancy, respectively. However, the relatively sharp peaks at 403 and 535 nm are correlated with the development of polycrystalline core of Si-enriched parts. © 1996 American Institute of Physics.
    Type of Medium: Electronic Resource
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