Five to ten nanograms of labeled angiotensin II rapidly injected in the left ventricle of adult rats was found to induce significant ultrastructural endothelial changes, resulting in net increases in number and size of pinocytotic vesicles as well as widening of intercellular spaces. This effect was followed by preferential localization of the compound in the nuclear zone of vascular and cardiac muscle cells. The selective cellular localization of angiotensin II suggests that this vasoactive agent or some of its metabolic fragments may have specific effects on nuclear function.
Recent investigations in the rat have shown that endothelial cell contraction should be included among the multiple actions of angiotensin II (All) in large arteries. In the current study, after intravenous injections (60 mg/kg) of the azo dye Evans blue, a segment of the rabbit abdominal aorta was isolated between temporary ligatures and injected with 1 X
A well-preserved mummified child from about A.D. 1200 was recovered fron Canyon de Chelly in northeastern Arizona in 1971. Striking skull changes were found and microscopic, ultrastructural, and cytochemical studies confirm the diagnosis of porotic hyperostosis that resulted in spongy bone appearance. We suggest that a possible cause for this condition could be iron deficiency of a severity seldom found in modern societies.
Quilty lesions, as first described by Billingham in 1981, or 'Quilty Effect' (QE) are distinct endomyocardial mononuclear cell infiltrates that have been observed in human heart transplant recipients, as well as in experimental models of heart transplantation. In the present investigations, the pattern and extent of apoptosis (programmed cell death) and myocyte necrosis, as well as specific lymphocyte subsets in Quilty lesions was assessed. Endomyocardial biopsies obtained from 13 patients at 10-3362 days post-transplant were examined. Apoptosis, as identified by DNA nick end-labeling, was found in myocytes at the periphery of Quilty lesions in 11 of 13 cases (85%), and 'early' stages of myocyte necrosis, as demonstrated by specific staining with alpha light chain myosin monoclonal antibodies (mAb), was observed at the same sites in 10 of 13 cases (77%) of both Quilty type A and type B lesions. Apoptosis was not identified in the lymphocyte infiltrates of any of the lesions examined. Lymphocyte subsets were characterized using mAb for T cell receptor (CD3), for helper/inducer T cells (CD4), for cytotoxic/suppressor T cells (CD8) and for mature B cells (CD20). Immunostaining revealed separate clusters of T lymphocytes with less prevalent B cells within the Quilty lesions. CD4+ cells were found in larger numbers than CD8+ cells in all cases. Non-B, non-T large lymphocytes were occasionally present. Except for the extent of the cellular infiltrate, no major cytochemical lymphocyte distribution differences were found between Quilty type A and B lesions. Myocyte apoptosis and early necrosis at the periphery of Quilty lesions suggest that early myocyte injury occurring in B lesions may represent initial or 'abortive stages' of cardiac allograft rejection. Why these lesions do not progress to overt rejection indeed warrant further detailed studies.
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