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Biomedical subjects

R Farkas

Publications and source records attributed to R Farkas.

52 records · Page 3Linked to original sources
PubMed1991

Appearance of the T-cell marker CD8 on B chronic lymphatic leukemia cells in long-term cultures.

Long-term cultures of highly purified B chronic lymphatic leukemia cells (B-CLL), were established. The B-CLL lymphocytes acquired the CD8 T cell marker in long-term cultures while still retaining their surface immunoglobulins. In confirmation of previous results, the cultured B-CLL lymphocytes released factor(s) into the culture medium that suppressed the allogeneic mixed-lymphocyte reaction. No correlation was found between the appearance of the CD8 T cell surface marker and onset of suppressor activity.

Antigens, Surface↗
PubMed1987

Long-term cultures of chronic lymphocytic leukemia B cells generate B suppressor cells.

B suppressor cells (Bs) were generated by stimulation with PHA-P or concanavalin A of B cells from peripheral blood of B-cell chronic lymphocytic leukemia (B-CLL) patients. They suppressed well allogeneic mixed lymphocyte reactions. Long-term colonies of B cells from B-CLL were established for up to 6 weeks in liquid media, with B cells acquiring properties of suppressor cells while being cultured. Two types of cultures were observed: cells either grew in compact multicellular colonies or formed diffuse monolayers. Cells that remained alive in cultures for a number of weeks, but did not multiply, did not develop suppressive characteristics. Bs cells retained their phenotypic markers in cultures. Mitosis and lymphoblasts, but no differentiation into plasma cells, were observed. PHA-P-generated Bs were cultured in long-term colonies, retaining their suppressor properties. The establishment of long-term cultures of B-CLL cells may facilitate a better understanding of the nature and characteristics of normal and leukemic B cells.

Aged↗
PubMed1986

Generation of B suppressor cells by phytohaemagglutinin.

Activation by phytohaemagglutinin-P (PHA-P) of B cells from peripheral blood of healthy subjects generated B suppressor cells which inhibited allogeneic mixed lymphocyte reactions (MLR) and PHA-induced DNA synthesis. Their action was direct, that is, not mediated through the induction of T suppressor cells. The finding that B cells can be induced by PHA to become highly effective suppressor cells may have important clinical and experimental implications.

B-Lymphocytes↗
PubMed1982

Myocardial rupture after myocardial infarction. Detection by multi-gated image-acquisition scintigraphy.

Myocardial rupture following infarction usually is an acute and dramatic event. Rarely, it may take a subacute course, allowing surgical treatment. We report herein a case of subacute rupture of the heart in a 54 year old patient with acute myocardial infarction. The rupture was diagnosed by the appearance of a radiopaque halo around the heart during radionuclide ventriculography. The patient subsequently underwent surgical resection of a large anterolateral aneurysm and a 2 inch long rupture of the myocardium and survived. Clinical suspicion, prompt diagnosis, and surgical intervention are important in the management of this relatively unusual complication of infarction.

Heart Aneurysm↗
PubMed1981

Monocyte-mediated regulation of cellular immunity in humans: loss of suppressor activity with ageing.

The effect of ageing on cellular immunity in humans was investigated. Human T cell cytotoxicity (CMC) measured by an in vitro xenogeneic assay was found previously to be depressed in individuals greater than 60 years old (group 2) compared to individuals less than 50 years old (group 1). Removal of plastic-adherent cells prior to sensitization in the xenogeneic CMC assay of human peripheral blood mononuclear cells (HPBM) resulted in a significantly higher rise (P less than 0.001, Wilcoxon rank test) in CMC activity in group 1 compared to group 2. Replacement of plastic-adherent cells (greater than 35% monocytes) to HPBM depleted of monocytes returned the CMC activity to the level observed with unseparated HPBM. Separation of HPBM on Percoll density gradients into monocyte-enriched (less than 75%) and monocyte-depleted (less than 3%) fractions indicated that monocytes were responsible for suppressing CMC in group 1. These results are consistent with the hypothesis that monocyte suppressor function for CMC response declines in ageing humans. When indomethacin (1 microgram/ml) was added to HPBM the Con A- and PHA-induced DNA synthetic response rose in groups 1 and 2. Indomethacin induced a significantly larger (P less than 0.01) rise in suboptimal PHA mitogenesis in group 1 compared to group 2. Individuals whose CMC response rose following adherent cell depletion were examined for the effect of indomethacin on the CMC response of their HPBM. In nine of 13 cases, addition of indomethacin also resulted in increased CMC activity.

Adult↗
PubMed1979

Decreased aminotransferase activity of serum and various tissues in the rat after cefazolin treatment.

Treatment of rats with cefazolin in vivo significantly suppressed activity of alanine and aspartate aminotransferases in serum and in the liver, brain, kidney, and heart. Simultaneous administration of pyridoxal further reduced enzyme activity except in the liver, where there was no change. Pyridoxal 5'-phosphate partly reversed the decreased enzyme activity in the serum, liver, and kidney, but did not return it to the amount observed in the control animals; enzyme activity remained suppressed in the brain and heart. The effect of cefazolin was dose related, but there was no sex-related difference. In contrast to its action on am-notransferase activity, cefazolin elicited no effect on alkaline phosphatase (pyridoxal-5'-phosphate hydrolase) in serum or on pyruvate carboxylase in the liver, heart, and kidney. Cefazolin exposed to the hepatic microsomal mixed-function oxidase system in vitro was partly converted into metabolites that inhibited serum alanine aminotransferase activity in vitro. The latter inhibition was reversed by the addition of pyridoxal 5'-phosphate.

Alanine Transaminase↗
PubMedDate not supplied

Ultrastructural changes of Drosophila larval and prepupal salivary glands cultured in vitro with ecdysone.

Alterations in the ultrastructure of in vitro cultured larval salivary glands of Drosophila melanogaster in response to the steroid hormone ecdysone were studied in relation to complex changes in puffing patterns. We found that the changes in the fine structure of cultured glands reflected progression of the puffing pattern, and they paralleled those seen in vivo. We observed that glue secretion by exocytosis, the main function of salivary glands, took place between puff stage 5 (PS5) and PS7. Glue could not be expectorated under culture conditions but was slowly released from the lumen through a duct into the medium. After the cultured glands reached PS13/PS14, further progress of puffing and fine structural alterations required that the ecdysteroid titer be transiently extremely low or absent. Under in vitro conditions we did not observe the putative new secretory program(s) described for glands in vivo after PS12. However, ultrastructural changes which unambiguously indicated that an autohistolytic process had begun in vitro started to appear after PS17. Many salivary gland cells developed numerous features of progressive self-degradation between PS18 and PS21. Actual degradation of salivary glands in vivo seemed to be rapid, but in vitro degradation was never completed, probably due to a lack of exogenous factors from the hemolymph. Manipulations of ecdysone titer in vitro in the culture medium, known during the larval puffing cycle to cause premature induction of developmentally specific puffing patterns, did not affect the normal development of ultrastructural features of the cytoplasm and nucleus.

Animals↗