1,956 research outputs found

    Humoral and cellular immunopathology of hepatic and cardiac hamster-into-rat xenograft rejection: Marked stimulation of IgM<sup>++bright</sup>/IgD<sup>+dull</sup> splenic B cells

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    Normal Lewis rat serum contains antibodies (IgM > IgG) that bind to hamster leukocytes and endothelial cells. Transplantation of either the heart or liver from hamster rat results in release of hamster hematolymphoid cells from the graft, which lodge in the recipient spleen (cell migration), where recipient T- and B-cell populations initiate DNA synthesis within one day. There is marked stimulation of splenic IgM++(bright)/IgD+(dull) B cells in the marginal zone and red pulp, which account for 48% of the total splenic blast cell population by 4 days after liver transplantation. CD4+ predominant T-cell proliferation in the splenic periarterial lymphatic sheath and paracortex of peripheral lymph nodes occurs almost simultaneously. The effector phase of rejection in cardiac recipients is dominated by complement-fixing IgM antibodies, which increase daily and result in graft destruction in 3 to 4 days, even in animals treated with FK506. In liver recipients, combined antibody and cellular rejection, associated with graft infiltration by OX8+ natural killer, and fewer W3/25+ (CD4) lymphocytes, are responsible for graft failure in untreated recipients at 6 to 7 days. FK506 inhibits the T-cell response in liver recipients and significantly prolongs graft survival, but does not prevent the rise or deposition of IgM antibodies in the graft. However, a single injection of cyclophosphamide 10 days before transplantation effectively depletes the splenic IgM++(bright)/IgD+(dull) cells and in combination with FK506, results in 100% survival of both cardiac and hepatic xenografts for more than 60 days. Although extrapolation of morphological findings to functional significance is fraught with potential problems, we propose the following mechanisms of xenograft rejection. The reaction initially appears to involve primitive host defense mechanisms, including an IgM-producing subpopulation of splenic B cells and natural killer cells. Based on the reaction and distribution of OX8+ and W3/25+ cells, antibody dependent cell cytotoxicity and delayed-type hypersensitivity responses seem worthy of further investigation as possible effector mechanisms. Effective control of xenograft rejection is likely to require a dual pharmaceutical approach, one to contain T-cell immunity and another to blunt the primitive B-cell response

    Mass breast screening is highly inefficient [1]

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    Preformed lymphocytotoxic antibodies: The effects of class, titer and specificity on liver vs. heart allografts

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    The effect on liver and heart allograft survival (ACI rats to Lewis rats) was studied after three methods of recipient presensitization and after different intervals between sensitization and transplantation. With comparable lymphocytotoxic antibody titers, liver allografts always survived longer than heart grafts. The titer, class and specificity of the antibodies varied with the method of sensitization. Four skin grafts produced IgG and IgM lymphocytotoxic antibody titers of 1:2,000 to 4,000. The IgG fraction was shown to have hepatic vascular endothelial specificity by indirect immunofluorescence. These primed recipients hyperacutely rejected both heart and liver allografts, which showed vascular deposition of IgG antibodies. Survival of either kind of graft was inversely proportional to the lymphocytotoxic antibody titer and length of time after placement of the last skin graft. Presensitization with a single heterotopic heart graft produced an even higher mixed IgG and IgM lymphocytotoxic antibody titer of 1:8,000 but with less IgG vascular endothelial specificity. These animals also hyperacutely rejected heart or liver grafts with tissue deposition of IgG but less consistently and with a weaker correlation with lymphocytotoxic antibody titers and time after sensitization. Sensitization with two pretransplant blood transfusions produced the lowest titer (1:500 to 1,000) and the least IgG vascular endothelial specificity. Liver allograft survival was routinely enhanced in these animals, and little effect was seen on heart grafts. Collectively, the experiments showed that the liver is not only resistant to antibody‐mediated rejection relative to the heart but is more easily enhanced. A more precise characterization of preformed antibodies may increase the ability to predict the outcome of liver transplantation in sensitized recipients or guide pretransplant strategies to foster enhancing antibodies. Copyright © 1992 American Association for the Study of Liver Disease

    Electrical conductivity and electromagnetic interference shielding of multiwalled carbon nanotube composites containing Fe catalyst

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    Thin and flexible composite films of raw or purified multiwalled carbon nanotube (MWCNT) with various mass fractions and poly(methylmethacrylate) (PMMA) were synthesized for electromagnetic interference (EMI) shielding material. From scanning electron microscopy and high-resolution transmission electron microscopy photographs, we observed the formation of a conducting network through MWCNTs in an insulating PMMA matrix and the existence of an Fe catalyst in MWCNTs. The dc conductivity (sigma(dc)) of the systems increased with increasing MWCNT mass fraction, showing typical percolation behavior. The measured EMI shielding efficiency (SE) of MWCNT-PMMA composites by using the extended ASTM D4935-99 method (50 MHz-13.5 GHz) increased with increasing MWCNT mass fraction as sigma(dc). The highest EMI SE for raw MWCNT-PMMA composites was similar to27 dB, indicating commercial use for far-field EMI shielding. The contribution of absorption to total EMI SE of the systems is larger than that of reflection. Based on magnetic permeability, we suggest raw MWCNTs and their composites can be used for near-field EMI shielding.open28629
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