By Herman Friedman (auth.), Herman Friedman, Toby K. Eisenstein, John Madden, Burt M. Sharp (eds.)
This quantity represents the lawsuits of the Symposium on AIDS, medicinal drugs of Abuse and the Neuroimmune Axis. This assembly used to be held in San Diego, California, November 11-13, 1995. As within the earlier symposia during this sequence, efficient experiences have been reviewed in regards to the dating among the fearful and the immune structures concerning the dating among medicines of abuse and infections, particularly infections by way of the immunode ficiency virus that motives AIDS. lately, a number of investigators have all started to explain the position of illicit medicines and their endogenous opposite numbers at the brain-immune axis. it's well known that the neuroendocrine approach is in detail taken with the results and manifestations of the interactions of substances of abuse and the immune method. The assembly on which the chapters during this ebook are dependent introduced jointly many organic scientists from an array of assorted clinical disciplines whose paintings is targeted at the results of gear of abuse at the neuroendocrine-immune axis and its relationships to immunodeficiency brought on by the AIDS virus. As some time past, the symposium used to be targeted in targeting the . brain-immune axis from the perspective of gear of abuse instead of from the point of view of immunity or the mind itself.
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Extra info for AIDS, Drugs of Abuse, and the Neuroimmune Axis
Chang et aI. of ACTH from the anterior pituitary, and increases the subsequent release of glucocorticoids from the adrenal gland. FOS functions as a transcriptional factor by forming a complex with the JUN protein which then binds to AP-I sites on target genes. 23 The gene for the precursor of CRF contains many AP-I sites. It is possible, therefore, that the desensitization of IL-I-j3-induced FOS responsiveness may extend to the gene regulation of CRF and, in tum, to the regulation of the HPA axis.
26 Since chronic exposure to morphine attenuates the IL-Ij3-induced FOS immunoreactivity in the PVN, which may regulate CRF expression in the hypothalamus, one can argue that chronic exposure to morphine could suppress the CRFmediated activation of the HPA axis by attenuating the IL-Ij3-induced FOS-mediated pathways in the PVN. 5. BOTH FMLP AND IL-l~ INCREASE LEUKOCYTE-ENDOTHELIAL ADHESION (LEA) IN THE RAT MESENTERY To study the actions of morphine directly on the immune system, we examined the modulatory effects of chronic exposure to morphine on leukocyte-endothelium adhesion (LEA) in the rat mesentery.
44:127-142. 29. L. E. 1991 Extracellular calcium results in a conformational change in Mac-I (CD II blCD 18) on neutrophils: Differentiation of adhesion and phagocytosis functions of Mac-I. J. , 146:685-691. 30. w. 1993 Endothelial adhesion molecules and their role in inflammation. Canadian J. ofPhysiol. , 71:76-87. 31. , Avdi, N. M. 1989 Adherence of neutrophils to cultured human microvascular endothelial cells. Stimulation by chemotactic peptides and lipid mediators and dependence upon the Mac-I, LFA-l, P 150,95 glycoprotein family.
AIDS, Drugs of Abuse, and the Neuroimmune Axis by Herman Friedman (auth.), Herman Friedman, Toby K. Eisenstein, John Madden, Burt M. Sharp (eds.)