{"response":{"docs":[{"system_create_dtsi":"2017-10-27T02:31:31Z","system_modified_dtsi":"2018-08-01T18:36:51Z","has_model_ssim":["Article"],"id":"bc386t13k","accessControl_ssim":["4d06e4fe-452c-4112-9019-e24ceb8ced29"],"hasRelatedMediaFragment_ssim":["bc386t14v"],"hasRelatedImage_ssim":["bc386t14v"],"depositor_ssim":["cancelje@ucmail.uc.edu"],"depositor_tesim":["cancelje@ucmail.uc.edu"],"title_tesim":["Overnight, room temperature hold of whole blood followed by 42-day storage of red blood cells in additive solution-7"],"date_uploaded_dtsi":"2017-02-08T00:00:00Z","date_modified_dtsi":"2017-04-10T00:00:00Z","isPartOf_ssim":["admin_set/default"],"proxy_depositor_ssim":["peckjd@mail.uc.edu"],"journal_title_tesim":["Overnight, room temperature hold of whole blood followed by 42-day storage of red blood cells in additive solution-7"],"college_tesim":["Medicine"],"department_tesim":["Hoxworth Blood Center"],"note_tesim":["This work was part of a pilot \"mediated-deposit model\" where library staff found potential works, later submitted for faculty review"],"creator_tesim":["Szczerpiorkowski, Z. 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This study evaluated the storage\nand in vivo recovery characteristics of ONH red blood\ncells (RBCs) stored in additive solution-7 (AS-7)."],"license_tesim":["http://rightsstatements.org/vocab/InC/1.0/"],"date_created_tesim":["2014-10"],"source_tesim":["Overnight, room temperature hold of whole blood followed by 42-day storage of red blood cells in additive solution-7"],"thumbnail_path_ss":"/downloads/bc386t14v?file=thumbnail","suppressed_bsi":false,"actionable_workflow_roles_ssim":["admin_set/default-default-depositing"],"workflow_state_name_ssim":["deposited"],"member_ids_ssim":["bc386t14v"],"file_set_ids_ssim":["bc386t14v"],"visibility_ssi":"open","admin_set_tesim":["Default Admin Set"],"sort_title_ssi":"OVERNIGHT ROOM TEMPERATURE HOLD OF WHOLE BLOOD FOLLOWED BY 42DAY STORAGE OF RED BLOOD CELLS IN ADDITIVE SOLUTION7","human_readable_type_tesim":["Article"],"read_access_group_ssim":["public"],"edit_access_person_ssim":["cancelje@ucmail.uc.edu"],"nesting_collection__pathnames_ssim":["bc386t13k"],"nesting_collection__deepest_nested_depth_isi":1,"_version_":1697073437089988608,"timestamp":"2021-04-15T02:55:50.008Z","score":0.00049999997},{"system_create_dtsi":"2017-10-27T02:31:27Z","system_modified_dtsi":"2018-08-01T18:36:55Z","has_model_ssim":["Article"],"id":"bc386t111","accessControl_ssim":["88e34224-a0e1-4419-af18-4ca2a861ad97"],"hasRelatedMediaFragment_ssim":["bc386t129"],"hasRelatedImage_ssim":["bc386t129"],"depositor_ssim":["cancelje@ucmail.uc.edu"],"depositor_tesim":["cancelje@ucmail.uc.edu"],"title_tesim":["Vasculopathy associated hyperangiotensinemia mobilizes hematopoietic stem cells/progenitors through endothelial AT2R and cytoskeletal dysregulation"],"date_uploaded_dtsi":"2017-02-08T00:00:00Z","date_modified_dtsi":"2017-04-10T00:00:00Z","isPartOf_ssim":["admin_set/default"],"proxy_depositor_ssim":["peckjd@mail.uc.edu"],"journal_title_tesim":["Vasculopathy associated hyperangiotensinemia mobilizes hematopoietic stem cells/progenitors through endothelial AT2R and cytoskeletal dysregulation"],"college_tesim":["Medicine"],"department_tesim":["Hoxworth Blood Center"],"note_tesim":["This work was part of a pilot \"mediated-deposit model\" where library staff found potential works, later submitted for faculty review"],"creator_tesim":["Inagami, T.","Hill, S. 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The Ang-II effect can be reversed pharmacologically and\ngenetically by inhibiting Ang-II production or signaling through BMEC AT2R, HSCP AT1R/\nAT2R or HSC/P RhoA, but not by interfering with other vascular tone mediators.\nHyperangiotensinemia and high counts of circulating HSC/P seen in sickle cell disease (SCD) as a\nresult of vascular damage, is significantly decreased by Ang-II inhibitors. Our data define for the\nfirst time the role of Ang-II HSC/P traffic regulation and redefine the hematopoietic consequences\nof anti-angiotensin therapy in SCD."],"license_tesim":["http://rightsstatements.org/vocab/InC/1.0/"],"date_created_tesim":["2015-01"],"source_tesim":["Vasculopathy associated hyperangiotensinemia mobilizes hematopoietic stem cells/progenitors through endothelial AT2R and cytoskeletal dysregulation"],"thumbnail_path_ss":"/downloads/bc386t129?file=thumbnail","suppressed_bsi":false,"actionable_workflow_roles_ssim":["admin_set/default-default-depositing"],"workflow_state_name_ssim":["deposited"],"member_ids_ssim":["bc386t129"],"file_set_ids_ssim":["bc386t129"],"visibility_ssi":"open","admin_set_tesim":["Default Admin Set"],"sort_title_ssi":"VASCULOPATHY ASSOCIATED HYPERANGIOTENSINEMIA MOBILIZES HEMATOPOIETIC STEM CELLSPROGENITORS THROUGH ENDOTHELIAL AT2R AND CYTOSKELETAL DYSREGULATION","human_readable_type_tesim":["Article"],"read_access_group_ssim":["public"],"edit_access_person_ssim":["cancelje@ucmail.uc.edu"],"nesting_collection__pathnames_ssim":["bc386t111"],"nesting_collection__deepest_nested_depth_isi":1,"_version_":1697103323650326528,"timestamp":"2021-04-15T10:50:52.053Z","score":0.00049999997},{"system_create_dtsi":"2017-10-27T02:31:23Z","system_modified_dtsi":"2018-08-01T18:36:55Z","has_model_ssim":["Article"],"id":"bc386t090","accessControl_ssim":["1ccf01ad-da31-40b5-a0b4-9f22bc0db581"],"hasRelatedMediaFragment_ssim":["bc386t10r"],"hasRelatedImage_ssim":["bc386t10r"],"depositor_ssim":["cancelje@ucmail.uc.edu"],"depositor_tesim":["cancelje@ucmail.uc.edu"],"title_tesim":["Myeloid Malignancies with Chromosome 5q Deletions Acquire a Dependency on an Intrachromosomal NF-kB Gene Network"],"date_uploaded_dtsi":"2017-02-08T00:00:00Z","date_modified_dtsi":"2017-04-10T00:00:00Z","isPartOf_ssim":["admin_set/default"],"proxy_depositor_ssim":["peckjd@mail.uc.edu"],"journal_title_tesim":["Myeloid Malignancies with Chromosome 5q Deletions Acquire a Dependency on an Intrachromosomal NF-kB Gene Network"],"college_tesim":["Medicine"],"department_tesim":["Hoxworth Blood Center"],"note_tesim":["This work was part of a pilot \"mediated-deposit model\" where library staff found potential works, later submitted for faculty review"],"creator_tesim":["Komurov, K.","Maciejewski, J. P.","Bolanos, L.","Grimes, H. L.","Cancelas, Jose A.","Chen, X.","Barker, B.","Weirauch, M. T.","Jerez, A.","Liu, X.","Makishima, H.","Christie, S.","Starczynowski, D. T.","Rao, D. S.","Fang, J."],"publisher_tesim":["Cell Reports"],"description_tesim":["Chromosome 5q deletions (del[5q]) are common in\nhigh-risk (HR) myelodysplastic syndrome (MDS) and\nacute myeloid leukemia (AML); however, the gene\nregulatory networks that sustain these aggressive\ndiseases are unknown. Reduced miR-146a expression\nin del(5q) HR MDS/AML and miR-146a/ hematopoietic\nstem/progenitor cells (HSPCs) results in\nTRAF6/NF-kB activation. Increased survival and proliferation\nof HSPCs from miR-146alow HR MDS/AML is\nsustained by a neighboring haploid gene, SQSTM1\n(p62), expressed from the intact 5q allele. Overexpression\nof p62 from the intact allele occurs through\nNF-kB-dependent feedforward signaling mediated\nby miR-146a deficiency. p62 is necessary for\nTRAF6-mediated NF-kB signaling, as disrupting the\np62-TRAF6 signaling complex results in cell-cycle arrest\nand apoptosis of MDS/AML cells. Thus, del(5q)\nHR MDS/AML employs an intrachromosomal gene\nnetwork involving loss of miR-146a and haploid overexpression\nof p62 via NF-kB to sustain TRAF6/NF-kB\nsignaling for cell survival and proliferation. Interfering\nwith the p62-TRAF6 signaling complex represents a\ntherapeutic option in miR-146a-deficient and aggressive\ndel(5q) MDS/AML."],"license_tesim":["http://rightsstatements.org/vocab/InC/1.0/"],"date_created_tesim":["2014-09"],"source_tesim":["Myeloid Malignancies with Chromosome 5q Deletions Acquire a Dependency on an Intrachromosomal NF-kB Gene Network"],"thumbnail_path_ss":"/downloads/bc386t10r?file=thumbnail","suppressed_bsi":false,"actionable_workflow_roles_ssim":["admin_set/default-default-depositing"],"workflow_state_name_ssim":["deposited"],"member_ids_ssim":["bc386t10r"],"file_set_ids_ssim":["bc386t10r"],"visibility_ssi":"open","admin_set_tesim":["Default Admin Set"],"sort_title_ssi":"MYELOID MALIGNANCIES WITH CHROMOSOME 5Q DELETIONS ACQUIRE A DEPENDENCY ON AN INTRACHROMOSOMAL NFKB GENE NETWORK","human_readable_type_tesim":["Article"],"read_access_group_ssim":["public"],"edit_access_person_ssim":["cancelje@ucmail.uc.edu"],"nesting_collection__pathnames_ssim":["bc386t090"],"nesting_collection__deepest_nested_depth_isi":1,"_version_":1697085740469452800,"timestamp":"2021-04-15T06:11:23.425Z","score":0.00049999997},{"system_create_dtsi":"2017-10-27T02:31:18Z","system_modified_dtsi":"2018-08-01T18:36:54Z","has_model_ssim":["Article"],"id":"bc386t07f","accessControl_ssim":["199961fe-7545-4e66-987e-4522e8c9138e"],"hasRelatedMediaFragment_ssim":["bc386t08q"],"hasRelatedImage_ssim":["bc386t08q"],"depositor_ssim":["cancelje@ucmail.uc.edu"],"depositor_tesim":["cancelje@ucmail.uc.edu"],"title_tesim":["Pathogenesis of ELANE-Mutant Severe Neutropenia Revealed by Induced Pluripotent Stem Cells"],"date_uploaded_dtsi":"2017-02-08T00:00:00Z","date_modified_dtsi":"2017-04-10T00:00:00Z","isPartOf_ssim":["admin_set/default"],"proxy_depositor_ssim":["peckjd@mail.uc.edu"],"journal_title_tesim":["Pathogenesis of ELANE-mutant severe neutropenia revealed by induced pluripotent stem cells"],"college_tesim":["Medicine"],"department_tesim":["Hoxworth Blood Center"],"note_tesim":["This work was part of a pilot \"mediated-deposit model\" where library staff found potential works, later submitted for faculty review"],"creator_tesim":["Lutzko, C.","Mehta, P.","Kalfa, T.","Aronow, B. 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Similarly, high-dose G-CSF (or downstream signaling through AKT/BCL2) rescues\nthe dysgranulopoietic defect in SCN patient–derived iPSCs through C/EBPβ-dependent emergency granulopoiesis. In\ncontrast, sivelestat, an NE-specific small-molecule inhibitor, corrected dysgranulopoiesis by restoring normal intracellular\nNE localization in primary granules; ameliorating UPR/ER stress; increasing expression of CEBPA, but not CEBPB; and\npromoting promyelocyte survival and differentiation. Together, these data suggest that SCN disease pathogenesis includes\nNE mislocalization, which in turn triggers dysfunctional survival signaling and UPR/ER stress. This paradigm has the\npotential to be clinically exploited to achieve therapeutic responses using lower doses of G-CSF combined with targeting to\ncorrect NE mislocalization."],"license_tesim":["http://rightsstatements.org/vocab/InC/1.0/"],"date_created_tesim":["2015-07"],"source_tesim":["Pathogenesis of ELANE-mutant severe neutropenia revealed by induced pluripotent stem cells"],"thumbnail_path_ss":"/downloads/bc386t08q?file=thumbnail","suppressed_bsi":false,"actionable_workflow_roles_ssim":["admin_set/default-default-depositing"],"workflow_state_name_ssim":["deposited"],"member_ids_ssim":["bc386t08q"],"file_set_ids_ssim":["bc386t08q"],"visibility_ssi":"open","admin_set_tesim":["Default Admin Set"],"sort_title_ssi":"PATHOGENESIS OF ELANEMUTANT SEVERE NEUTROPENIA REVEALED BY INDUCED PLURIPOTENT STEM CELLS","human_readable_type_tesim":["Article"],"read_access_group_ssim":["public"],"edit_access_person_ssim":["cancelje@ucmail.uc.edu"],"nesting_collection__pathnames_ssim":["bc386t07f"],"nesting_collection__deepest_nested_depth_isi":1,"_version_":1697079758815232000,"timestamp":"2021-04-15T04:36:18.875Z","score":0.00049999997},{"system_create_dtsi":"2017-10-27T02:31:13Z","system_modified_dtsi":"2018-08-01T18:36:54Z","has_model_ssim":["Article"],"id":"bc386t05w","accessControl_ssim":["aa4e940c-86e9-4afe-9c54-7c92942af259"],"hasRelatedMediaFragment_ssim":["bc386t065"],"hasRelatedImage_ssim":["bc386t065"],"depositor_ssim":["cancelje@ucmail.uc.edu"],"depositor_tesim":["cancelje@ucmail.uc.edu"],"title_tesim":["P62 is Required for Stem Cell/Progenitor Retention through Inhahvition of IKK/NF-kB/CcI14 Signaling at the Bone Marrow Macrophage-Osteoblast Niche"],"date_uploaded_dtsi":"2017-02-08T00:00:00Z","date_modified_dtsi":"2017-04-10T00:00:00Z","isPartOf_ssim":["admin_set/default"],"proxy_depositor_ssim":["peckjd@mail.uc.edu"],"journal_title_tesim":["p62 Is Required for Stem Cell/Progenitor Retention through Inhibition of IKK/NF-kB/Ccl4 Signaling at the Bone Marrow Macrophage-Osteoblast Niche"],"college_tesim":["Medicine"],"department_tesim":["Hoxworth Blood Center"],"note_tesim":["This work was part of a pilot \"mediated-deposit model\" where library staff found potential works, later submitted for faculty review"],"creator_tesim":["Moscat, J.","Nayak, R. 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