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A Alter

Publications and source records attributed to A Alter.

12 recordsLinked to original sources

Stimulation of human T cell colony growth by a lymphocyte colony enhancement factor derived from lymphocyte subpopulations.

Blood mononuclear cells (MNC) develop into T cell colonies when the cells are sensitized with PHA and seeded in a two-layer soft agar system. Conditioned medium (CM) derived from MNC enhanced lymphocyte colony formation when it was added to the culture system. CFU-TL appear to be stimulated into colony formation by molecules secreted by lymphocyte subpopulations contained in the seeded cells. In this study, human peripheral blood MNC were fractionated by a battery of techniques into adherent, E+, CD4+, CD8+, B and null cells. CM was prepared from each of the subpopulations and its effects on T cell colony growth assayed. All the lymphocyte subpopulations were found to generate lymphocyte colony enhancement factor (LCEF). After several purification procedures, CM prepared from CD4 and CD8+, displayed LCEF activity corresponding to proteins of molecular weight 30-40 and 100-140 kD.

Antigens, CD

Characterization of the interference of T cell activation by reserpine.

It has been suggested that reserpine blocks expression of delayed hypersensitivity (DH) reactions by depleting tissue mast cells of serotonin, thereby preventing a T cell-dependent release of mast cell serotonin necessary to localize and to amplify the DH response. However, reserpine blocks expression of DH in mast cell-deficient mice. Recently, we showed that the ability of reserpine to interfere with the expression of contact sensitivity was independent of an effect on mast cells, but reflected an effort of the drug on effector T cell function. In the present study we evaluated the mechanisms by which reserpine abrogates the expression of T cell functions. By using human peripheral blood mononuclear cells or enriched T cell populations we found that the drug inhibited, in a dose-dependent fashion, the proliferation of T cells after mitogen stimulation. Reserpine also interfered with the mitogen-induced IL-2 production by these cells, but the IL-2 receptor expression, as measured by immunofluorescence, was unaffected. Despite this, in the continuous presence of reserpine, exogenous IL-2 did not bypass reserpine inhibition of PHA-induced proliferation. By using the fluorescent indicator quin-2 we have demonstrated that preincubation with reserpine prevented the increase of cytosolic free calcium, which accompanies PHA-induced proliferative responses of human T lymphocytes. These results identify the sites of action of reserpine in human T lymphocytes and are sufficient to explain its ability to block cell-mediated immune responses in vitro and in vivo.

Antigens, CD

Biochemical and histological anomalies in the rat hepatic tissue following administration of bichromate and nickel in ionized form.

Administration of bichromate ions at a dose of 60 mg/kg body wt to female rats, reduced dramatically both hepatic microsomal cytochrome P-450 content and the monooxygenase activities assayed, namely: N-demethylation of aminopyrine and O-demethylation of p-nitroanisole. At the same dose the bichromate ion treatment caused a substantial decrease in cytochrome b5 content, but there was no significant reduction in NADPH-cytochrome c reductase activity. Administration of phenobarbital to bichromate ion pretreated rats did not induce a significant increase in cytochrome P-450 content nor in aminopyrine N-demethylase activity. Administration of nickel ions at a dose of 60 mg/kg body wt to female rats did not reduce to a significant level the content or the activity of any of the hepatic microsomal enzymes mentioned above, but did interfere in the de novo synthesis of cytochrome P-450 following phenobarbital treatment. The concentrations of nickel residues in the hepatic tissue of treated rats were only 5.8 times higher compared to the control rats, while those of chromium were 42 times higher than in control rats. Histological changes associated with the increase of bichromate concentration in treated rats were the formation of necrotic areas in the hepatic tissue and partial disintegration of the glomeruli and tubules in the kidney.

Aminopyrine N-Demethylase

Corrosion in metal implants embedded in various locations of the body in rats.

Corrosion in metal implants (stainless steel 316L) was followed up in 25 rats for periods of 1.5 to 14.0 months after insertion into the femur, back muscles, or as an external fixation of the tibia using light and scanning electron microscopy. In the implants buried in the back muscles and as an external fixation, mainly "face" and pitting corrosion were detected in 90% of the implants, while in the intramedullary implants crevice, pitting and various "holes" of irregular shape were evident in all implants. Calcium and phosphate deposits were also found on the intrafemoral implants. The corrosion in the implants was detected as early as 1.5 months but was quite variable. However, a progressive increase in the corrosion occurred concomitant with the length of time after implantation. The question is whether stainless steel metal implants presently in clinical use can be considered innocuous.

Animals

Detection of retroperitoneal hemorrhage after translumbar aortography by computerized tomography.

Thirty-seven patients were examined by CT scan within 24 hours of translumbar aortography. Eighteen of them had signs of hemorrhage, of which psoas asymmetry was the most common. Para-aortic densities and obliteration of the aorta were the next most frequent manifestations. CT scanning can be a useful tool in selected cases to detect or follow hemorrhage after aortography by the translumbar approach.

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