Knowing the in vitro effects of morphine on monkey leukocytes would be helpful in extending the utility of a monkey model for psychoneuroimmunological investigations. Morphine effects on T11, Leu2a, and Leu3a antigenic markers on leukocytes from rhesus monkeys and humans were assessed by using single- and two-color cytofluorometric analyses. Kinetics of expression of these markers was determined after modulation of the original complement of T11 markers from the surface of T11(+) cells. Percentages of leukocytes detectable by directly staining these markers before modulation were within the expected range for monkey and human cells. Also, as expected, T11 modulation reduced the percentages of cells expressing T11. This reduction was particularly obvious for T11 in the single-color analyses, with reductions being greater for monkey than human cells. Furthermore, in the single-color analyses, the effects of morphine on kinetics of T11 expression were quite similar for both human and monkey cells. In the two-color analyses, the simultaneous expression of T11 and Leu3a markers was uniform for both monkey and human cells. The effects of morphine on kinetics of expression of these markers varied only slightly between species. On the other hand, the distribution of Leu2a on T11 cells was markedly different for monkey and human T-cells. Whereas all human Leu2a(+) cells expressed similar numbers of T11 receptors, monkey cells with high-density Leu2a expressed fewer T11 markers than those with low-density Leu2a. The effects of morphine on kinetics of Leu2a and T11 expression were at obvious variance between species.(ABSTRACT TRUNCATED AT 250 WORDS)
Incubation of human T lymphocytes with saturating concentrations of combinations of certain anti-CD2 and -CD4 mAb results in reciprocal down-regulation of the cell surface density expression of the respective CD molecules. Such reciprocal down-regulation occurs at 0 degrees C in the presence of sodium azide and appears selective for CD2 and CD4 molecules because mAb identifying various other CD T cell surface molecules (anti-Leu2a, -OK-CLL, -W6/32, -beta 2-microglobulin, -4B4) do not modulate CD2 or CD4 R density, and because anti-CD2 mAb (anti-OKT11 and -D66 clone-1) do not alter CD8 R density (anti-OKT8, -Leu2a) and vice versa. Down-regulation of CD2 by mAb specific to CD4 is epitope-specific but does not vary on the basis of the antibody isotype used. The anti-CD4 mAb, Leu3a, was the strongest CD2 down-regulator examined followed by OKT4F. mAb specific to other CD4 epitopes (B, C, D, and E) caused only slight down-regulation of CD2 expression whereas anti-OKT4 and -OKT4A mAb had no significant regulatory effect. Also, mAb specific to the 9.6 (anti-OKT11) and D66 (anti-D66 clone 1) epitopes of the CD2 molecule down-regulated CD4 density detectable with Leu3a, OKT4, and OKT4A anti-CD4 mAb. Down-regulation of CD2 by anti-CD4 mAb also occurred with the transformed T cell line, KE-37, which demonstrates that such effects can occur without mononuclear phagocytic accessory cells. From these data it can be concluded that important T cell immunoregulatory signals may be transmitted intramembranally between CD2 and CD4 glycoproteins.
Multiple birth neonates are unique in sharing similar intrauterine, and commonly the extrauterine, environments. The development of an infectious disease in one infant during the perinatal period assumes special significance in this setting, and the other siblings are often at high risk for a similar disease. Under these circumstances it is important to make a rapid etiologic diagnosis to provide appropriate therapeutic intervention. The immediate, or "stat", autopsy is a diagnostic modality involving the use of multiple procedures for the rapid diagnosis of perinatal infection which may be lifesaving in the setting of multiple birth neonates. This report describes the use of the "stat" autopsy to diagnose a fatal case of disseminated herpes simplex infection in a twin, which lead to the immediate treatment of the surviving sibling with appropriate antiviral medication.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.