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Biomedical subjects

B Beckman

Publications and source records attributed to B Beckman.

33 records · Page 2Linked to original sources
PubMed1983

Erythropoietin production in human renal carcinoma cells passaged in nude mice and in tissue culture.

Renal cell carcinoma tissues from two patients, one with and one without erythrocytosis, were successfully transplanted into athymic nude mice. Transplantations of the erythrocytic tumor through six successive generations of nude mice produced a significant (P less than 0.001) elevation in mean hematocrit from 36.5 +/- 2.1% (range 32-42%) to 53.7 +/- 5.1% (range 40-63%), in comparison with a non-erythrocytic tumor which showed a progressive fall in hematocrit from 46.5 +/- 2.0% (range 41-50%) to 36.8 +/- 1.6% (range 33-40%). Non-grafted control nude mice maintained stable hematocrit levels from an initial level of 45 +/- 0.5% to 46.5 +/- 1.2% when studied over the same time interval. Similarly red cell mass values in the mice transplanted with the erythrocytic tumor (5.04 +/- 1.85 ml/100 g) were considerably higher than in both the non-grafted nude mice (3.39 +/- 0.81 ml/100 g) and the non-erythrocytic tumor-grafted mice (3.8 +/- 0.3 ml/100 g) after 6 generations of transplants. Plasma erythropoietin levels in the erythrocytic tumor-grafted mice (169.4 +/- 83.1 mU/ml) were significantly (P less than 0.02) higher than in the non-grafted controls (22.2 +/- 9.5 mU/ml), and furthermore the erythropoietin levels in the tumor extracts were significantly (P less than 0.02) higher in the tumors from erythrocytic mice (range 54.7 to 234.6 mU/g tumor) than in the tumors from non-erythrocytic mice (range 0.3 to 1.9 mU/g tumor). In vitro monolayer cultures of these tumors confirmed the higher erythropoietin levels in the erythrocytic renal carcinoma (138 mU/ml) as compared with culture media of non-erythrocytic tumors (15-91 mU/ml) using the fetal mouse liver assay (59Fe incorp. into heme). The present studies indicate autonomous erythropoietin production by human renal cell carcinomas both in vivo in nude mice and in vitro in tissue cultures.

Animals↗
PubMed1982

Mixed myeloid-Lymphoid colonies in a patient with polycythemia vera.

Peripheral blood mononuclear cells from a patient with polycythemia vera were cultured in a methylcellulose system employing human serum. Electron microscopy documented the appearance of mixed colonies containing lymphocytes, granulocytes, megakaryocytes, and erythrocytes. In vitro culture characteristics were similar to those seen for other patients with polycythemia ver, ie, colonies grew in the absence of added erythropoietin or other pathway-specific regulators. Plating efficiency was linearly related to the number of cells plated, which supports the concept that each colony arose from a single cell. The appearance of mixed myeloid-lymphoid colonies points to the existence of a primitive stem cell capable of giving rise to multiple hematopoietic cell lines.

Aged↗
PubMed1982

Erythropoietin-independent erythroid colony formation in patients with erythroleukaemia (M6) and related disorders.

In vitro erythropoietin (Ep) responsiveness of human bone marrow mononuclear cells was determined in 12 normal human volunteers and four patients with erythroleukemia (EL), two patients with refractory anaemia with excess blasts (RAEB), and one patient with de novo acute myelogenous leukaemia (AML). The bone marrow cells were cultured in a microtitre methylcellulose system containing 30% human AB serum and human urinary Ep in concentrations ranging from 0 to 2 units/ml. Erythroid colony growth from normal marrow cultures was Ep-dependent. It was augmented by added Ep and inhibited by Ep antiserum. Marrow cells from one patient with EL and one patient with RAEB after transformation to AML had no erythroid colony formation with or without added Ep. All of the remaining patients formed 'spontaneous' or endogenous erythroid colonies (EEC) without the addition of Ep. In three of these (two with EL and one with de novo AML), the erythroid colony formation was augmented by added Ep. In three other patients (one with EL and two with RAEB), erythroid colony growth was unaffected by added Ep or Ep antiserum, and thus appeared to be Ep-independent.

Aged↗
PubMed1980

Effects of beta adrenergic agents and prostaglandin E1 on erythroid colony (CFU-E) growth and cyclic AMP formation in Friend erythroleukemic cells.

The formation of erythroid colonies from bone marrow and spleen cells infected with the polycythemic strain of the Friend virus (FV-P) was characterized in an in vitro methyl cellulose colony-forming system in response to prostaglandin E1 and the beta-2 adrenergic agonist, albuterol. Both drugs markedly inhibited the formation of CFU-E colonies of FV-P-infected bone marrow and spleen in the absence or presence of erythropoietin. The albuterol-mediated inhibition of CFU-E colonies (FV-P-infected) was selectively blocked by butoxamine, a beta-2 antagonist. Adenylate cyclase (AC) activity was also determined in FV-P spleen membrane preparations in response to albuterol and PGE1. Both agents stimulated enzyme activity, and butoxamine blocked the stimulation seen with albuterol. The ability of albuterol and PGE1 to stimulate AC activity in the FV-P-infected cells suggests that the effects of these agents on CFU-E formation may be mediated by specific beta-2 adrenergic and PG receptors through the adenylate cyclase-cyclic AMP system.

Adenylyl Cyclases↗
PubMed1980

Decreased erythroid colony-forming cell response of XTfm/Y mice to testosterone and 5 beta-dihydrotestosterone.

Although certain tissue of XTfm/Y mice are known to be deficient in androgen-binding sites, the defect has not been documented for bone marrow. To study the bone marrow response to testosterone and its metabolites, we compared the responses of the erythroid colony-forming cell (CFU-E) in these mice and their wild counter-parts, XTa/Y mice, using an in vitro methyl cellulose system in the presence of erythropoietin. Testosterone or 5 beta-dihydrotestosterone (5 beta-DHT) treatment (5 mg/kg) of Ta/Y mice in vivo before femoral bone marrow culture resulted in a significant increase in CFU-E colonies. However, similar in vivo treatment of Tfm/Y mice with testosterone or 5 beta-DHT had no effect on CFU-E colony formation. 5 alpha-DHT had no significant effect on Ta/Y or Tfm/Y mouse bone marrow. Testosterone or 5 beta-DHT added directly to Ta/Y marrow cultures caused an enhancement of CFU-E colony numbers compared with erythropoietin alone. 5 alpha-DHT inhibited colony formation at high concentrations. Testosterone had no effect on Tfm/Y erythroid colonies, whereas 5 beta-DHT and 5 alpha-DHT significantly inhibited colony formation. These results indicate that Tfm/Y erythroid bone marrow colonies may have an altered response to testosterone and its metabolites compared to that of Ta/Y erythroid colonies. We postulate that the pattern of androgen receptors in the erythroid progenitor cell compartment of Tfm/Y mice is different from that of Ta/Y mice.

Animals↗
PubMed1979

Influence of albuterol on erythropoietin production and erythroid progenitor cell activation.

The effect of albuterol, a potent beta2-adrenergic agonist, on kidney production of erythropoietin (Ep) was studied. Its effects on erythroid colony (CFU-E) formation in vitro in rabbit bone marrow cultures were also assessed. Albuterol produced a significant increase in plasma Ep levels in conscious rabbits following 7 h intravenous infusion (50 (microgram/kg)/min). This effect was blocked by pretreatment of the rabbits with butoxamine (5 mg/kg ip), a potent beta2-adrenergic blocker. Albuterol in doses of 10(-10) to 10(-8) M in combination with Ep was also found to produce a significant increase in the numbers of CFU-E in the plasma clot culture system of rabbit bone marrow. This effect was blocked completely by DL-propranolol (10(-8) M) and by butoxamine (10(-8) M). The data presented suggest that albuterol, a potent activator of beta2-adrenergic receptors, increases kidney production of Ep in vivo and also produces a direct effect in combination with Ep on the proliferation of the erythroid progenitor cell compartment.

Albuterol↗
PubMed1978

Piccolyte investments for better section cutting.

Piccolyte 115 (beta-pinence polymers) added to Tissuemat, Paraplast or Peel-Away embedding media is recommended for investment of infiltrated tissues. Mixed with paraffin at 3% and 10% and used for double embedding of paraffin infiltrated tissues, Piccolyte 115 permits good, complete sections virtually free of folds or wrinkles in less time and with less effort than with paraffin embedding alone.

Bicyclic Monoterpenes↗
PubMed1975

Stimulation of osmotic water flow in toad bladder by prostaglandin E1. Evidence for different compartments of cyclic AMP.

The effect of prostaglandin E1 (PGE1) on osmotic water flow across toad bladder and cyclic AMP content of the mucosal epithelial cells has been determined under basal conditions and in the presence of either theophylline or antidiuretic hormone (ADH); Under basal conditions and with PGE1 concentrations from 10(-8) to 10(-5) M no evidence of stimulation of water flow was observed, and with 10(-7) M PGE1 a significant inhibition was foundmcyclic AMP content under control conditions was 8 pmol/mg protein. It was 9 at 10(-8) M PGE1, 13 at 10(-7) M, 16 at 10(-6) M, and 23 at 10(-5) M. In the presence of theophylline, 10(-8) and 10(-7) M PGE1 inhibited the theophylline-induced water flow as expected. In contrast, 10(-6) and 10(-5) M PGE1 enhanced the rate of water flow. Theophylline increased cyclic AMP content from 8 to 18 pmol/mg protein. PGE1 in the presence of theophylline caused marked increases in cyclic AMP content; The content was 23 at 10(-7) M, 41 at 10(-6) M, and 130 at 10(-5) M; Thus PGE1 stimulates theophylline-induced water flow at cyclic AMP concentrations somewhere between 23 and 41 pmol/mg. Further evidence along these lines was obtained from experiments in which the effects of PGE1 on ADH-induced water flow were studied. Inhibitory effects of PGE1 were not observed at concentrations of PGE1 which raised the level of intracellular cyclic AMP to 30 pmol/mg protein or higher. These results were obtained despite the fact that all four concentrations of PGE1 tested were found capable of inhibiting ADH-induced water flow under appropriate conditions or, in other words, were inhibiting the adenylate cyclase controlling water flow, Thus the increase in cyclic AMP content in response to PGE1 is not derived from this enzyme. Thus the stimulation of water flow by PGE1 in the presence of theophylline is thought to be caused by cyclic AMP spilling over from one compartment to the water flow compartment. No evidence was obtained to directly suggest spillover into the sodium transport compartment. Furthermore evidence is discussed to suggest that most of the cyclic AMP generated in the tissue does not originate from the enzyme controlling sodium transport. As cyclic AMP-stimulated water flow and sodium transport are thought to occur in one cell type, the granular cells, distinct pools of cyclic AMP are thought to be present in one and the same cell type. Thus one pool controls water flow and one controls sodium transport. With high concentrations of PGE1 in the presence of theophylline or high concentrations of ADH, the adenylate cyclase responsible for water flow is inhibited; However, PGE1 can stimulate a tissue adenylate cyclase to sufficiently high levels that cyclic AMP spills over into the "water flow compartment" and thus stimulates water flow.

Animals↗
PubMed1974

Studies on the mode of action of cholera toxin. Effects on solubilized adenylate cyclase.

To gain further insight into the mechanism of action of cholera toxin, solubilized preparations of adenylate cyclase from control and toxin-treated rat livers were studied. Adenylate cyclase activity was measured in both particulate and solubilized form in rat liver under control conditions and after intravenous injection of cholera toxin. Cholera toxin caused a 3.3-fold activation of adenylate cyclase in the particulate preparation and a 5.8-fold increase in the solubilized preparation. Thus, the ability of cholera toxin to stimulate adenylate cyclase is present even when the enzyme membrane environment is disrupted. Furthermore, the solubilized enzyme, after treatment with cholera toxin, retained its ability to respond to catecholamines, but not to glucagon. In contrast, the control enzyme lost its responsiveness to catecholamines and glucagon after solubilization.

Adenylyl Cyclases↗