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Biomedical subjects

E B Thompson

Publications and source records attributed to E B Thompson.

234 records · Page 13Linked to original sources
PubMed1972

Expression of aryl hydrocarbon hydroxylase induction and suppression of tyrosine aminotransferase induction in somatic-cell hybrids.

Aryl hydrocarbon hydroxylase activity is inducible in mouse 3T3 fibroblasts by benz[alpha]anthracene, whereas no detectable basal or inducible levels of this enzyme occur in rat-hepatoma tissue culture cells. Conversely, tyrosine aminotransferase activity is inducible in hepatoma cells by dexamethasone, whereas only low noninducible levels of this enzyme exist in 3T3 cells. In hybrids formed by fusion of these two parent lines, levels of inducible hydroxylase activity range from the same as, to more than 20-fold greater than, that in the 3T3 parent; aminotransferase levels remain very low and noninducible in all of these same hybrids. A majority of the 1S-chromosomal complement from each parent is retained in most of these hybrids. The kinetics of hydroxylase induction and degradation, responses of hydroxylase induction to actinomycin D and cycloheximide, and the relative thermolability of the control and induced activities are similar in the 3T3 parent and in the hybrids. Failure to inactivate any of the aminotransferase activity in the hybrids with antibody specific for the rat enzyme indicates that all of the basal noninducible aminotransferase activity is derived from the mouse 3T3 parent.

Animals↗
PubMed1971

Expression of tyrosine aminotransferase activity in somatic-cell heterokaryons: evidence for negative control of enzyme expression.

Cells of the tyrosine aminotransferase (EC 2.6.1.5)-inducible line, HTC, were fused with those of the BRL-62 line, which contain little or no enzyme and are unresponsive to the usual steroid inducers. Histochemical examination of the resulting heterokaryons within 24 hr of the fusion showed them to have little or no enzyme and to be unresponsive to steroids. These experiments disclose that the observed negative dominance is universal in the fused cells and that such dominance occurs promptly after fusion, when loss of chromosomes has not occurred.

Animals↗
PubMed1971

Partial purification by affinity chromatography of tyrosine aminotransferase-synthesizing ribosomes from hepatoma tissue culture cells.

This report describes a cell-free protein-synthesizing system derived from hepatoma tissue culture cells in which the synthesis of tyrosine aminotransferase is enhanced in relation to total protein synthesis. The enhancement was achieved by using affinity chromatography to select a specific fraction of ribosomes in which the proportion of tyrosine aminotransferase synthesis is higher than it is in unfractionated ribosomes.

Adsorption↗
PubMedDate not supplied

Glucocorticoid mediated transcriptional repression of c-myc in apoptotic human leukemic CEM cells.

Suppression of c-myc has been implicated as a critical event in some glucocorticoid-evoked apoptotic systems. It is therefore of interest to understand the mechanism of glucocorticoid-regulation of the c-myc gene. In the present study, a detailed analysis of dexamethasone (Dex)-evoked regulation of the human c-myc gene in human leukemic CEM-C7 cells has been performed. Dex suppresses c-myc mRNA and immunoreactive protein expression in clone CEM-C7 and subclone CEM-C7-14 cells. Nuclear run-on assays suggested that the regulation occurred at the level of transcription initiation. The half-life of c-myc mRNA was approximately 30 min and its stability was not affected by Dex treatment. In addition, Dex suppressed luciferase gene expression driven by -2052 to +34 bp c-myc promoter in transfected CEM-C7-14 cells. This result further supports that c-myc gene is suppressed by Dex at the transcriptional level in apoptotic human leukemic cells.

Apoptosis↗
PubMedDate not supplied

Glucocorticoids, oxysterols, and cAMP with glucocorticoids each cause apoptosis of CEM cells and suppress c-myc.

In clones of the CEM human acute lymphoblastic leukemic cell line, glucocorticoids, oxysterols and activators of the cAMP pathway acting synergistically with glucocorticoids, each can cause apoptotic cell death. Morphologically and kinetically, these deaths resemble one another. The kinetics are striking: in each case, after addition of the lethal compound(s), an interval of approximately 24 h follows, during which cell growth continues unabated. During this "prodromal" period, removal of the apoptotic agent leaves the cells fully viable. We hypothesize that a sequence of biochemical events occurs during the prodrome which eventually results in the triggering of the full apoptotic response as evidenced by the activation of caspases and DNA fragmentation. At some point, the process is irreversible and proceeds relatively rapidly to cell death. Suppression of c-Myc seems a universal early event evoked by each of these lethal compounds or combinations, and we conclude that the negative regulation of this proto-oncogene is an important aspect of the critical pre-apoptotic events in these cells.

Apoptosis↗
PubMedDate not supplied

Biological and phytochemical investigation of plants XV. Pteryxia terebinthina var. terebinthina (Umbelliferae).

Aqueous extracts of Pteryxia terebinthina var. terebinthina were shown to possess antiarrhythmic activity. A novel furanocoumarin, pterybinthinone, the known coumarins pteryxin and umbelliferone, and sucrose were isolated from this plant. Attempts to re-isolate a structurally undefined, defibrillatory substance by means of a published protocol were unsuccessful.

Aconitum↗
PubMedDate not supplied

A time-course study of hypothyroidism-induced hypotension: its relation to food deprivation.

Concentrations of 0.05, 0.01 and 0.2% propylthiouracil (PTU), incorporated into standard rat chow, induced hypothyroidism in male Sprague-Dawley rats following 6-8 weeks administration. The concentrations caused a progressive decrease in arterial blood pressure (BP), heart rate (HR), body weight (BW), food intake (FI), levels of triiodothyronine (T3), thyroxine (T4) and an increase in thyrotropin (TSH) levels. There was no clear-cut dose-dependent change in these parameters, since the values obtained for the 3 groups were not significantly different from one another, but were significantly lower than that of control rats (euthyroid). Pair-feeding studies between partial food-deprived euthyroid rats and PTU-induced hypothyroid rats showed that both types of treatment caused a decrease in BW, BP, HR, colonic temperature, levels of T3, T4 and an increase in TSH. The changes were significantly (P less than .05) greater in the hypothyroid than in the food deprived rats at the end of the 6th week and thereafter.

Animals↗