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  • Electronic Resource  (2)
  • 2005-2009  (1)
  • 1980-1984  (1)
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  • Electronic Resource  (2)
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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 22 (2005), S. 0 
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The atherosclerotic process is regulated by inflammatory mechanisms, which also appear to be involved in the modulation of insulin-resistance, a key player in the pathogenesis of the metabolic syndrome (MS). The interaction between components of the clinical phenotype of the MS with its biological phenotype (insulin resistance, dyslipidaemia, etc.) contributes to the development of a pro-inflammatory state characterized by an increased oxidative stress (i.e. oxidized lipoproteins) and a chronic, subclinical vascular inflammation, as also suggested by the increased C reactive protein (CRP) concentration found in patients with MS. The subclinical inflammatory state peculiar of the MS modulates the atherosclerotic process at different stages, resulting in: (i) endothelial dysfunction and increased expression of endothelial adhesion molecules; (ii) an enhanced recruitment of monocytes within the arterial wall, in the early stages of the atherosclerotic process; leading to (iii) the formation of an unstable atherosclerotic plaque, rich in inflammatory cells, which is the culprit lesion in the vast majority of both coronary and cerebrovascular events observed in with MS.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary We have used a cDNA clone for human apolipoprotein CII (apo CII) to study the apo CII genes in two independent individuals with familial apo CII deficiency. With all the restriction enzymes so far used, gene fragments hybridising with apo CII cDNA are observed that are indistinguishable from normal samples. This demonstrates that in neither of these individuals is the defect due to a major deletion of DNA in or around the apo CII gene. We have used a common polymorphism of the apo CII gene detected with the enzyme TaqI to follow the inheritance of the gene in the families of these apo CII deficient individuals. The pattern of inheritance that we observe is consistent with the defect causing apo CII deficiency being in, or closely linked to the apo CII structural gene.
    Type of Medium: Electronic Resource
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