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S A Morris

Publications and source records attributed to S A Morris.

97 records · Page 6Linked to original sources
PubMed1976

Problems in management of primary bilateral germ cell testicular tumors: report of 3 cases and review of literature.

Bilateral primary germ cell tumors are uncommon but not rare in men with primary testicular tumors. In our series of 78 cases of germ cell tumors 3 (3.8 per cent) were bilateral. In the management of a second neoplasm the same general principles apply as those for the first tumor but one must be aware of the potential complications of radiotion therapy when the total dose for cure of the first and second neoplasms exceeds the tolerance dose of normal tissue and therapy must be modified accordingly. Prognosis is not necessarily poor when a second primary tumor develops and complications can be reduced to a low level with appropriate therapy. Our outline for therapy is presented.

Adult↗
PubMed1975

Antibody-dependent cytotoxicity: modulation by the cytochalasins and microtubule-disruptive agents.

Cytochalasin B was shown to inhibit lysis of antibody-coated target cells by effector cells from rabbit spleen and lymph node. The inhibitory activity was dose-dependent and reversible. At low concentrations of cytochalasin B (0.15 to 0.3 mug/ml) enhancement of antibody-dependent cytotoxicity was observed. The drug appeared to act at an early stage of the lytic pathway after effector cell-target cell interaction, but before triggering of the cytotoxic event. Cytochalasin A was shown to be a more potent but similarly reversible inhibitor of antibody-dependent cytotoxicity. No enhancement of cytotoxicity was seen at non-inhibitory concentrations of cytochalasin A. The microtubule-disruptive agents colchicine (10-4 M), vinblastine (10-5 M) and colcemid (10-6 M) did not influence antibody-dependent cytotoxicity at concentrations which were not toxic to the effector cells. Our results suggest that antibody-dependent cytotoxicity is a surface membrane-initiated process and microtubule-associated functions are not essential.

Animals↗
PubMedDate not supplied

Myocardial expression of endothelin-1 in murine Trypanosoma cruzi infection.

Chagas' disease, caused by Trypanosoma cruzi, is an important cause of myocarditis and chronic cardiomyopathy and is accompanied by microvascular spasm and myocardial ischemia. We reported previously that infection of cultured endothelial cells with T. cruzi increased the synthesis of biologically active endothlein-1 (ET-1). In the present study, we examined the role of ET-1 in the cardiovascular system of CD1 mice infected with the Brazil strain of T. cruzi and C57BL/6 mice infected with the Tulahuen strain during acute infection. In the myocardium of infected mice myonecrosis and multiple pseudocysts were observed. There was also an intense vasculitis of the aorta, coronary artery, smaller myocardial vessels and the endocardial endothelium. Immunohistochemistry studies employing anti-ET-1 antibody revealed increased expression of ET-1 that was most intense in the endocardial and vascular endothelium. Elevated levels of mRNA for preproET-1, endothelin converting enzyme and ET-1 were observed in the same myocardial samples. Plasma ET-1 levels were significantly elevated in infected CD1 mice 10-15 days post infection. These observations suggest that increased levels of ET-1 are a consequence of the initial invasion of the cardiovascular system and provide a mechanism for infection-associated myocardial dysfunction.

Animals↗
PubMedDate not supplied

Intracellular Ca2+ homeostasis in trypomastigotes of Trypanosoma cruzi.

Trypomastigotes of Trypanosoma cruzi maintain an intracellular Ca2+ concentration ([Ca2+]i) of 64 +/- 30 nM. Equilibration of trypomastigotes in an extracellular buffer containing 0.5 mM [Ca2+]o (preloaded cells) increased [Ca2+]i < 20 nM whereas total cell Ca2+ increased by 1.5 to 2.0 pmole/cell. This amount of Ca2+ would be expected to increase [Ca2+]i to > 10 microM suggesting active sequestration of Ca2+. We tested the hypothesis that maintenance of [Ca2+]i involved both the sequestration into intracellular storage sites and extrusion into the extracellular space. Pharmacological probes known to influence [Ca2+]i through well characterized pathways in higher eukaryotic cells were employed. [Ca2+]i responses in the presence or absence of [Ca2+]o were measured to asses the relative contribution of sequestration or extrusion processes in [Ca2+]i homeostasis. In the presence of 0.5 mM [Ca2+]o, the ability of several agents to increase [Ca2+]i was magnified in the order ionomycin >>> nigericin > thapsigargin > monensin > valinomycin. In contrast, preloading markedly enhanced the increase in [Ca2+]i observed only in response to monensin. Manoalide, an inhibitor of phospholipase A2, enhanced the accumulation of [Ca2+]i due to all agents tested, particularly ionomycin and thapsigargin. Our results suggest that sequestration of [Ca2+]i involved storage sites sensitive to monensin and ionomycin whereas extrusion of Ca2+ may involve phospholipase A2 activity. A Na+/Ca2+ exchange mechanism did not appear to contribute to Ca2+ homeostasis.

Animals↗