3. Electronic Theses and Dissertations (ETDs) - All submissions

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    The role of mononuclear cells in tuberculosis
    (1992-06-03) Sussman, Garth
    Sonicates derived from Mycobacterium tuberculosis suppressed lymphocytes proliferation. Pulsing of monocytes with mycobacterial sonicates resulted in the release of high molecular weight lipids. Both these lipids and those prepared by column fractionation of mycobacterial sonicates suppressed lymphocyte blastogenesis.This effect was due to the activation and not the proliferation of CD8+ lymphocytes by the lipid containing mycobacterial fractions of Mr>200kDa that could be obtained in vitro by column fractions.
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    The effects of interferon on cultured cells persistently infected with viruses
    (1986-09-09) Crespi, Madeleine
    An investigation was done to examine the role of IFN in viral persistence at the cellular level. For this purpose two types of persistent infections were chosen. The first type was cell lines which contained hepatitis B virus (HBV) DNA (PLC/PRF/5 and Hep 3B cells) uninfected control hepatoma cells, (Mahlavu, HA22T and Hep G2 cells) or simian virus 40 (SV40) DNA (C2, C6, Cll cells) and control uninfected (CV-1 cells). In the second type of infection Vero cells persistently infected with SSPE or Sendai virus were used.
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    Cellular iron metabolism in haemochromatotic macrophages
    (1995) Ickinger, Claudia
    HLA-linked haemochromatosis is the result of an inborn error of metabolism inherited as an autosomal recessive gene, closely linked to the HLA locus on chromosome six. In this condition iron absorption is inappropriately high leading to iron overload. Integral to the pathogenesis of this disorder and in contrast to other causes of iron overload, is the relatively modest accumulation of iron within cells of both the small intestine and the reticuloendothelial system and the excessive deposition of iron in parenchymal cells of the liver and other organs. This observation has led to the suggestion that the primary defect(s) could be present in either the gut, the liver, the reticuloendothelial system or all three. Abnormalities in iron uptake by cells, iron transport through and between cells and iron storage in cells have all been suggested as possible mechanisms responsible for the abnormal absorption and distribution of iron in haemochromatosis. Malfunction of the iron transport protein transferrin or its receptor could be responsible for abnormal distribution and iron loading while an abnormality of ferritin iron storage could explain why some cells appear to be unable to store iron and others are iron overloaded.
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    An in vivo and in vitro study of some luminal and cellular factors influencing iron absorption
    (1966-03) Jacobs, Peter
    Although the various factors which influence the absorption of iron from the gastrointestinal tract have been extensively investigated, there still remains uncertainty concerning several basic aspects of this process
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