Control of reproduction and of undesirable social and sexual behaviour in dogs and cats.
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Biomedical subjects
H A Gerber
Publications and source records attributed to H A Gerber.
Autoradiographic study of the localization of 2,2', 4,4', 5,5'-hexachlorobiphenyl in liver and skin tissue after in vitro uptake.
Cellular distribution of the lipophilic environmental pollutant, 2,2', 4,4', 5,5'-hexachlorobiphenyl (6-CB), was determined by autoradiography after in vitro uptake of the 14C-labeled compound into liver and skin tissue preparation. Light microscopic data of cryostat sections showed that 6-CB is homogeneously distributed in liver tissue. In skin the distribution pattern depended on the conditions of incubation. If skin slices were incubated with 6-CB prior to preparation of cryostat thin sections, the epidermis was practically free of 6-CB and the radioactivity was found mainly in the stratum reticulare of the dermis. If, however, cryostat sections of skin were directly incubated, 6-CB was more homogeneously distributed with an accumulation in the epidermis. Liver and skin sections delipidated with acetone or 95% ethanol prior to incubation with 6-CB took up very little of the compound. Delipidation of sections preincubated with 6-CB resulted in total extraction of 6-CB. The results suggest that human stratum corneum is a barrier to the penetration of 6-CB and that this compound is located in lipid structures of liver and skin.
Animals↗
Characterization of human skin-derived CD1a-positive lymph cells.
The phenotype and function of CD1a+ lymph cells is of considerable interest. By means of microsurgical lymph cannulation human lymph derived from normal skin was sampled. Cells were isolated and processed for immunocytochemistry, electron microscopy, flow cytometry and functional assays. The majority of the cells, (62%), were T cells. The other cells comprised CD1a+ cells (7%), monocytes/macrophages (8%), and B cells (1%); the remainder were erythrocytes or uncharacterized cells. The CD1a+ cells reacted with antibodies against protein S-100, HLA-DR, the Lag antigen, CD4, CD11a, CD11b, CD18, CD25, CD40, CD54, CD80 and CD86. Interestingly, a small prolow portion the of CD1a+ cells (about 5%) reacted with an antibody to CD14. The CD1a+ cells did not react with an antibody against human follicular dendritic cells nor were they CD19-, CD23-, E-cadherin- or factor XIIIa-positive. Both allogenic and antigen-specific T cell proliferation stimulated by antigen-presenting lymph cells were strongly inhibited by adding anti-CD80 and anti-CD86 antibodies. By electron microscopy Birbeck granules were detected in only 22% of the CD1a+ lymph cells and these cells exhibited an extensive ruffling of the surface. These findings demonstrate that CD1a+ lymph cells, which do not express the dermal dendritic cell marker factor XIIIa, resemble dendritic cells formerly designated as 'veiled' as well as lymphoid dendritic cells, suggesting that after migration to the regional lymphoid organs, Langerhans cells form a more differentiated population of dendritic cells specialized in sensitizing T lymphocytes. Our results add further support to the view that resident Langerhans cells may be precursors of lymphoid dendritic cells acquiring the final phenotype in the microenvironment of the lymph node.
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