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   <subfield code="a">10.1007/s00246-011-9980-1</subfield>
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   <subfield code="a">The Myocardium of Fetuses with Endocardial Fibroelastosis Contains Fewer B and T Lymphocytes than Normal Control Myocardium</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Nisha Fernandes, Glenn Taylor, Cedric Manlhiot, Brian McCrindle, Michael Ho, Steven Miner, Adelle Atkinson, Edgar Jaeggi, Lynne Nield]</subfield>
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   <subfield code="a">The observation that endocardial fibroelastosis (EFE) can result from an immune response to maternal autoantibody deposition in the fetal myocardium raises the possibility that the fetal immune system may contribute to the pathogenesis of idiopathic EFE and dilated cardiomyopathy (DCM). This study sought to characterize myocardial immune cell presence in fetuses and neonates with idiopathic EFE+DCM, in those with EFE+structural heart disease, and in normal control subjects. Paraffin tissue sections from fetuses identified from the pathology database were stained for B cell, T cell, macrophage, and general hematopoietic cell surface markers. Of the 14 fetuses included in the study, 5 had EFE+DCM, 4 had EFE+structural heart disease, and 5 were normal control fetuses. The EFE+DCM group had fewer B cells than the control group (0.15 vs. 0.44cells/mm2; p=0.005). The EFE+heart disease group had both fewer B cells (0.18 vs. 0.44cells/mm2; p=0.08) and T cells (0.29 vs. 0.80 cells/mm2; p=0.04) than the control group. The CD4/CD8 ratio was similar in the EFE+DCM and EFE+heart disease groups (1.0 vs. 0.9; p=0.17) but higher in the EFE+DCM group than in the control group (0.9 vs. 0.3; p=0.03). The myocardium of fetuses with EFE contains fewer B and T lymphocytes than normal control fetuses.</subfield>
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   <subfield code="a">Springer Science+Business Media, LLC, 2011</subfield>
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   <subfield code="a">Dilated cardiomyopathy</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Endocardial fibroelastosis</subfield>
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   <subfield code="a">Immune cells</subfield>
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   <subfield code="a">Fernandes</subfield>
   <subfield code="D">Nisha</subfield>
   <subfield code="u">The Hospital for Sick Children, Labatt Family Heart Centre, University of Toronto, M5G 1X8, Toronto, ON, Canada</subfield>
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   <subfield code="a">Taylor</subfield>
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   <subfield code="u">The Hospital for Sick Children, Division of Pathology, University of Toronto, M5G 1X8, Toronto, ON, Canada</subfield>
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   <subfield code="a">Manlhiot</subfield>
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   <subfield code="u">The Hospital for Sick Children, Labatt Family Heart Centre, University of Toronto, M5G 1X8, Toronto, ON, Canada</subfield>
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   <subfield code="a">McCrindle</subfield>
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   <subfield code="u">The Hospital for Sick Children, Labatt Family Heart Centre, University of Toronto, M5G 1X8, Toronto, ON, Canada</subfield>
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   <subfield code="a">Ho</subfield>
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   <subfield code="u">The Hospital for Sick Children, Division of Pathology, University of Toronto, M5G 1X8, Toronto, ON, Canada</subfield>
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   <subfield code="a">Miner</subfield>
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   <subfield code="u">Southlake Regional Health Centre, Newmarket, ON, Canada</subfield>
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   <subfield code="a">Atkinson</subfield>
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   <subfield code="u">The Hospital for Sick Children, Division of Immunology and Allergy, University of Toronto, M5G 1X8, Toronto, ON, Canada</subfield>
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   <subfield code="a">Jaeggi</subfield>
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   <subfield code="u">The Hospital for Sick Children, Labatt Family Heart Centre, University of Toronto, M5G 1X8, Toronto, ON, Canada</subfield>
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   <subfield code="a">Nield</subfield>
   <subfield code="D">Lynne</subfield>
   <subfield code="u">The Hospital for Sick Children, Labatt Family Heart Centre, University of Toronto, M5G 1X8, Toronto, ON, Canada</subfield>
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   <subfield code="t">Pediatric Cardiology</subfield>
   <subfield code="d">Springer-Verlag</subfield>
   <subfield code="g">32/8(2011-12-01), 1088-1095</subfield>
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