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  • Book
    Ian M.C. Dixon, Jeffrey T. Wigle, editors.
    Contents:
    Cardiac fibrosis and heart failure-- cause or effect?
    Fibroblast activation in the infarcted myocardium
    Mechanical and matrix regulation of valvular fibrosis
    Bone marrow-derived progenitor cells, micro-RNA, and fibrosis
    The stressful life of cardiac myofibroblasts
    Pathogenic origins of fibrosis in the hypertensive heart disease that accompnaies aldosternoism
    Embryological origin of valve progenitor cells
    Diverse cellular origin of valve progenitor cells
    Diverse cellular origins of cardiac fibroblasts
    Non-canonical regulation of TGF-β1 signaling: a role for Ski/Sno and YAP/TAZ
    Molecular mechanisms of smooth muscle and fibroblast phenotype conversions in the failing heart
    Current and future strategies for the diagnosis and treatment of cardiac fibrosis
    Remodelling of the cardiac extracellular matrix: role of collagen degradation and accumulation in pathogenesis of heart failure
    Matrix metalloproteinase 9 (MMP-9)
    Collagen processing and its role in fibrosis
    Mechanisms of cardiac fibrosis and heart failure
    Mathematical simulations of sphingosine-1-phosphate actions on mammalian ventricular myofibroblasts and myocytes
    Extracellular matrix and cardiac disease: surgical and scientific perspectives
    The role or neurohumoral activation in cardiac fibrosis and heart failure
    Natriuretic peptides: critical regulators of cardiac fibroblasts and the extracellular matrix in the heart
    Cardiac tissue engineering for the treatment of heart failure post-infarction
    Mechanisms in cardiac valve failure and the development of tissue engineered heart valves
    Index.
    Digital Access Springer 2015
  • Article
    Lang JM, Bigel P, Giron C, Faradji A, Oberling F, Mayer S.
    Nouv Presse Med. 1979 Nov 12;8(44):3629-32.
    There is increasing evidence in the literature for persistent deficiency in cell-mediated immunity (CMI) in Hodgkin's diseases during apparent remissions after discontinuation of the treatment. Patients were followed for 6 months to 2 years after all treatments were stopped. There was a high percentage (41.6) of subjects with skin anergy to seven recall antigens, a highly significant (p less than 0,0001) decrease, as compared with controls, in total and active E rosettes independently from the number of lymphocytes, and a highly significant diminution of T-lymphocyte in vitro reactivity to various doses of phyto haemagglutinine (PHA). There was no difference between the patients tested between 6 months and 1 year and those tested more than 2 years after treatment. No correlation between skin tests and active rosettes was found in this series. Finally, the CMI deficiency is some what different in patients on remission and in untreated patients.
    Digital Access Access Options