21 |
Studies on the purported role of lipid methylation in mast cell activationBenyon, R. C. January 1986 (has links)
No description available.
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22 |
The cloning, expression, and characterisation of Streptoccal protein GMurphy, Jonathan Paul January 1991 (has links)
No description available.
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23 |
Site directed mutagenesis of an IgG binding protein based upon Protein A from Staphylococcus aureusFerris, William Frank January 1992 (has links)
No description available.
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24 |
An investigation into the regulation of human IgE synthesisQuint, D. J. January 1988 (has links)
No description available.
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Regulation of IgG subclass production in manScott, Ann Elizabeth January 1990 (has links)
No description available.
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MEDIATORS OF IgE-INDUCED ANAPHYLAXIS: AN IN VITRO STUDY OF MEDIATORS CAUSING CONTRACTION OF RABBIT PULMONARY ARTERYWiese, Anne Carroll Gordon, 1956- January 1987 (has links)
Rabbits were immunized such that antibodies of the IgE class were preferentially produced. Normal rabbit pulmonary artery sections were challenged with supernatant from antigen-treated sensitized blood cells in the presence of antagonists. The hypothesis is that mediators capable of contracting pulmonary arteries are released from blood cells when blood cells are challenged with antigen. Possible mediators are histamine, serotonin, indomethacin and LTD4. Chlorpheniramine (2.6 x 10⁻⁵M) with methysergide (1 x 10⁻⁵ produced a one-hundred-twenty-fold inhibition of contraction. Chlorpheniramine with FPL-55712 (1 x 10⁻⁵M) did not significantly alter the response seen with chlorpheniramine alone. When supernatant obtained from sensitized blood cells pretreated with 1 x 10⁻⁵ indomethacin was used to challenge muscle rings in the presence of chlorpheniramine the response was also not significantly different from response seen with chlorpheniramine alone. Histamine contracted pulmonary artery. Chlorpheniramine (2.6 x 10⁻⁵ inhibited the response six-hundred-fold. Serotonin also contracted pulmonary artery. Methysergide (10⁻⁵M) blocked the response seven-hundred-fold.
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Influence of ultra-endurance exercise on immunoglobulin isotypes and subclassesMcKune, AJ, Smith, LL, Semple, SJ, Wadee, AA 30 January 2005 (has links)
Background: Strenuous exercise is associated with tissue damage. This activates the innate immune system
and local inflammation. Interaction between innate and adaptive immunity is essential for maintaining
health, suggesting that the adaptive immune system may also be altered by exercise.
Objectives: To determine exercise induced changes in the adaptive immune system by measuring the
immunoglobulin isotype and subclass response to an ultra-marathon.
Methods: Venepuncture was performed on 11 experienced volunteers (six men, five women; mean (SD)
age 43 (9.8) years) 24 hours before the projected finishing time and immediately after and 3, 24, and
72 hours after an ultra-marathon (90 km). Serum was stored at 280˚C. IgM, IgD, IgA, IgG, IgG1, 2, 3,
and 4, and total IgE were measured.
Results: The following immunoglobulins were significantly (p(0.05) altered after the race: IgD,
immediately (251%) and 24 hours (241%) after; IgM 24 hours after (223%); total IgG immediately after
(+12%). There were no reports of symptoms of upper respiratory tract infections after the ultra-marathon.
Conclusions: In experienced ultra-endurance runners, alterations in immunoglobulin concentrations after a
race suggest an enhanced immune response, including isotype switching, interactions with the innate
immune system, and a secondary antibody response. These alterations may have a role in the
maintenance of subject health after an ultra-marathon.
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28 |
Insights into the regulation of human IgE : a complete picture in vitroBitsaktsis, Constantine January 2002 (has links)
No description available.
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29 |
Putative strategies for the generation of antibodies and inhibitors of Cathespin SMeighan, Mark A. January 1998 (has links)
No description available.
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30 |
IgA nephropathy and liver disease /Lomax-Smith, Jane. January 1984 (has links) (PDF)
Thesis (Ph. D.)--University of Adelaide, 1986. / Includes bibliographical references (leaves 331-381).
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