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R A Cooper

Publications and source records attributed to R A Cooper.

At least 217 records · Page 12Linked to original sources
PubMed1983

Phorbol ester modulation of T-cell antigens in the Jurkat lymphoblastic leukemia cell line.

The effect of phorbol dibutyrate (PDB) on the cell surface antigens of the human T-cell acute lymphoblastic leukemia cell line, Jurkat, was studied with OKT monoclonal antibodies by indirect immunofluorescence assay. Cells were analyzed in an Ortho Spectrum III fluorescence-activated flow cytometer. The surface antigen profile of untreated Jurkat cells resembled that of thymocytes; high levels of T3, T4, T6, T8, T9, T10, and T11 antigens were detected. Although 89% of cells were positive for T11, the putative sheep erythrocyte receptor, only 12% were able to form erythrocyte (sheep) rosettes. Exposure of the cells to 1.0 microM PDB for up to 7 days resulted in a rapid loss in T4 expression and a slower decrease in T6 reactivity, while the percentage of cells positive for T3, T8, T10, and T11 remained high. T4 reappeared on the cell surface when PDB was removed by washing. T11 antigen density increased 70%, and this was accompanied by an increase in the percentage of erythrocyte-rosetting cells from 12 to 55%. These changes in cell surface antigens induced by PDB suggested differentiation to a more mature state (i.e., a precursor cytotoxic-suppressor T-lymphocyte, T3+T8+T10+T11+). However, the reversibility of the change in T4 expression indicated that T4 loss was not a manifestation of terminal differentiation but rather was consistent with a phorbol ester-induced modulation of the cell surface T4 antigen.

Antigens, Surface↗
PubMed1982

An Escherichia coli mutant defective in the NAD-dependent succinate semialdehyde dehydrogenase.

Escherichia coli mutants, unable to grow on 4-hydroxyphenylacetate, have been isolated and found to be defective in the NAD-dependent succinate semialdehyde dehydrogenase. When the mutants are grown with 4-aminobutyrate as sole nitrogen source an NAD-dependent succinate semialdehyde dehydrogenase seen in the parental strain is absent but, as in the parental strain, an NADP-dependent enzyme is induced. Growth of the mutants is inhibited by 4-hydroxyphenylacetate due to the accumulation of succinate semialdehyde. The mutants are more sensitive to inhibition by exogenous succinate semialdehyde than is the parental strain. Secondary mutants able to grow in the presence of 4-hydroxyphenylacetate but still unable to use it as sole carbon source were defective in early steps of 4-hydroxyphenylacetate catabolism and so did not form succinate semialdehyde from 4-hydroxyphenylacetate. The gene encoding the NAD-dependent succinate semialdehyde dehydrogenase of Escherichia coli K-12 was located at min 34.1 on the genetic map.

Aldehyde Oxidoreductases↗
PubMed1982

Phorbol ester induction of leukemic cell differentiation is a membrane-mediated process.

Phorbol esters are potent inducers of macrophage-like differentiation in the HL-60 promyelocytic leukemia cell line. The sequence of events by which they bring about this transition is poorly understood. However, it is known that phorbol esters bind to the surface membrane of HL-60 cells and to various other cells as well. Our studies were directed toward determining the biologic importance of this membrane association. [3H]Phorbol dibutyrate (PBu2) was specifically bound by HL-60 cells with a Kd of 23 nM and with 1.9 X 10(5) binding sites for [3H]PBu2 per cell. There was no internalization of bound [3H]PBu2. Specific binding was fully reversible upon washing in fresh medium, and [3H]PBu2 added thereafter bound normally to its receptor. Within 10 min of binding, PBu2 stimulated [14C]choline incorporation into phosphatidylcholine, with a rapid return to normal upon removal of the PBu2. Membrane-bound PBu2 progressively inhibited DNA synthesis, with 70% inhibition by 8 hr. This process was interrupted if the PBu2 was removed, and little recovery of DNA synthesis occurred in previously inhibited cells. Between 8 and 16 hr, PBu2 induced adherence of cells to plastic, but only in those cells in which phosphatidylcholine synthesis was stimulated, and this process was also interrupted if PBu2 was removed prior to 16 hr. Similarly, nonspecific esterase, which develops after 72 hr of incubation, was induced in cells exposed to PBu2 for the initial 16 hr but not in cells exposed for 5 hr. These studies demonstrate that phorbol esters exert their effects while retained at the cell surface. Inhibition of cell growth and the acquisition of surface and enzymatic properties that characterize macrophages are separable events, each of which proceeds through a receptor-mediated, transmembrane process. The stimulation of phosphatidylcholine synthesis appears to be a part of that process.

Carboxylesterase↗
PubMed1982

Acromegaly and the heart--echocardiographic and nuclear imaging studies.

Left ventricular mass (LV mass) and function were assessed in 16 acromegalic patients by echocardiography, and rest and exercise gated blood pool scanning (GBPS) respectively. At the time of study, five patients had active acromegaly, five were hypertensive and three had coexisting coronary artery disease. Increased LV mass was found in six (38%) patients, of whom four were hypertensive and two others had active acromegaly of long duration. One normotensive patient, who did not have coronary disease, had increased LV mass associated with persistently elevated growth hormone (GH) levels for the previous 11 years. Abnormal LV function, as detected by GBPS, occurred only in the three patients with coronary disease. Thus, acromegaly is associated with increased LV mass in hypertensive patients and normotensive patients who have prolonged elevation of GH levels prior to adequate treatment. We found no detectable impairment of LV function, at rest or exercise unless other cardiac disease was present.

Acromegaly↗
PubMed1982

Vaginography.

Explore the source record for details and available documents.

Aged↗
PubMed1982

Decreased synthesis of high-molecular-weight glycopeptides in human promyelocytic leukemic cells (HL-60) during phorbol ester-induced macrophage differentiation.

The human promyelocytic leukemia ell line, HL-60, synthesized a class of high-molecular-weight (M.W. 5000 to 7000), N-linked glycopeptides as the major class of protein-bound carbohydrates. Small glycopeptides (M.W. 2500 to 3500), typical of most mammalian cells except erythrocytes, represented a minor component in these cells. The large glycopeptides were labeled efficiently with fucose, glucosamine, and galactose but only poorly with mannose. They were found not to be glycolipids, glycosaminoglycans, or mucin-type glycopeptides and were not susceptible to exoglycosidases, but they were partially degraded by endo-beta-galactosidases. These characteristics are similar to those of the large glycopeptides synthesized by erythrocytes, by another human myeloid leukemia cell line (K562), and by human and murine teratocarcinoma cells. High-molecular-weight glycopeptides predominated on another human myeloid leukemia cell line KG1, but they were expressed at low levels on both a human monocytic leukemia cel line (THP-1) and a human T-lymphoblastoid cell line (Jurkat). When HL-60 cells were induced to differentiate into macrophage-like cells with phorbol esters, the proportion of large glycopeptides decreased, and the production of small glycopeptides predominated. This shift was observed within the first several hr after exposure to phorbol esters and was temporally related to the acquisition of adherent properties by the induced cells. In contrast, when HL-60 cells were induced to differentiate into granulocytes by dimethyl sulfoxide, hypoxanthine, or retinoic acid, they continued to synthesize glycopeptides similar to uninduced cells. Human peripheral blood granulocytes synthesized primarily large glycopeptides, whereas monocytes and lymphocytes synthesized mostly small glycopeptides. These results indicate that the synthesis of high-molecular-weight glycopeptides is a property of human myeloid leukemia cell lines and that it persists throughout myeloid differentiation. A proportionate decrease in the synthesis of these large glycopeptidase is a part of the differentiation program for monocytes and macrophages.

Cell Adhesion↗
PubMed1982

Morphologic changes reflecting early and late effects of irradiation of the distal lung of the mouse: a review.

In radiation of the thorax, the lung has been shown to be a major dose-limiting organ. The early and late responses of the lung to radiation has been reviewed, with primary emphasis on the following cell types: type II pneumocyte, type I pneumocyte, pulmonary endothelial cell and macrophage. The earliest observable and quantifiable cellular response to radiation is exhibited by the type II pneumocytes as a decrease in lamellar bodies and a corresponding increase in surfactant content of the alveolar lavage. By 18-63 weeks following exposure, several type II cells, restored in their lamellar body population, undergo degeneration and sloughing into alveolar spaces. Type I pneumocytes generally exhibit little change, although some investigators describe alveolar denudation due to degenerating type I cells. Macrophages decrease in numbers following irradiation, returning to normal populations by 4 weeks. These changes correspond closely to the changes in alveolar lavage phospholipid phosphorus. Descriptions of radiation-induced damage to endothelial cells are variable. However, blebbing and vacuolation appear to be late developing responses, although altered permeability may be earlier in its expression. Radiation pneumonitis and fibrosis are the two major clinical and experimental responses of the lung to radiation following exposures of greater than 12 Gy. The former appears to involve type II cells, macrophages and pulmonary endothelial cells, and for the latter macrophages, fibroblasts, type II pneumocytes and the pulmonary endothelial cells are involved. The two events are not interdependent, and may not necessarily be interrelated.

Animals↗
PubMed1981

Succinic semialdehyde dehydrogenases of Escherichia coli: their role in the degradation of p-hydroxyphenylacetate and gamma-aminobutyrate.

Two physically and genetically distinct forms of succinic-semialdehyde dehydrogenase have been identified in Escherichia coli B. The two enzymes could be separated by filtration on Sephadex G-150 and their apparent molecular weights were 200 000 and 97 000. The larger enzyme, which is specific for NADP, is induced by growth on gamma-aminobutyrate. Its induction is highly coordinated with that of gamma-aminobutyrate:2-oxoglutarate transaminase, the enzyme which initiates degradation of gamma-aminobutyrate. The smaller enzyme, which is induced by growth on p-hydroxyphenylacetate, has been purified to 98% homogeneity by affinity chromatography in conjunction with conventional methods. Under standard assay conditions this enzyme acts preferentially with NAD but reduces NADP at 15% of the rate observed for NAD, primarily because of a difference in Km. Apparent Km values for succinic semialdehyde and NAD are 13.3 +/- 1.3 microM and 33.7 +/- 1.4 microM, respectively. The subunit molecular weight was estimated to be 55 000, indicating that the native enzyme is dimeric. The NAD-dependent succinic-semialdehyde dehydrogenase is also induced by exposure of cells to exogenous succinic semialdehyde, a treatment which has no effect on the amount of other enzymes of p-hydroxyphenylacetate or gamma-aminobutyrate metabolism. Apparently the gene for this enzyme functions independently from the genes encoding the other enzymes of p-hydroxyphenyl-acetate degradation. As a consequence of its induction mechanism, this NAD-dependent dehydrogenase is also present in extracts of E. coli B grown with gamma-aminobutyrate as sole nitrogen source, in addition to the NADP-specific enzyme involved in gamma-aminobutyrate metabolism. Presumably the NAD-dependent enzyme is gratuitously induced by succinic semialdehyde formed by transamination of gamma-aminobutyrate.

Aldehyde Oxidoreductases↗
PubMed1981

Identification and purification of distinct isomerase and decarboxylase enzymes involved in the 4-hydroxyphenylacetate catabolic pathway of Escherichia coli.

The possible involvement of an isomerase in the 4-hydroxyphenylacetate meta-cleavage pathway has been studied. 5-Carboxymethyl-2-hydroxymuconate has been shown to undergo both spontaneous and enzyme-catalysed isomerisation to give 5-carboxymethyl-2-oxo-hex-3-ene-1,5-dioate, a compound with an absorbance maximum at 246 nm. The latter compound rather than the former is the substrate for a decarboxylase that produces 2-hydroxyhepta-2,4-diene,1,7-dioate. The isomerase and decarboxylase enzymes have been purified to over 90% homogeneity. Mg2+ is required for the decarboxylase reaction but not for the isomerase.

Carbon-Carbon Double Bond Isomerases↗