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Biomedical subjects

A Hellman

Publications and source records attributed to A Hellman.

At least 37 records · Page 2Linked to original sources
PubMed1981

Induction of type-C retrovirus by the tumor promotor TPA.

The tumor promotor 12-0-tetradecanoyl-phorbol-13-acetate (TPA) induced endogenous murine xenotropic type-C retrovirus from A1-2 cells, derived from the BALB/c mouse, as determined by infectious center focus-forming assay on permissive normal rat kidney (NRK) cells. Kinetic dose-response studies showed that the number of cells induced to release virus was dependent on TPA concentration and the time of assay following TPA exposure. Maximal induction occurred when cells were treated with 80 ng/ml of TPA for 24 h and assayed at 24 or 48 h. A 30-min pulsed TPA exposure and 200 ng/ml induced virus levels approximating those observed after a continuous 24-h exposure to 80 ng/ml. The combination of TPA at concentrations of 10 and 20 ng/ml and a suboptimal level of 5-iodo-2-deoxyuridine (IdUrd) enhanced retrovirus induction threefold above that seen by the optimum IdUrd concentration alone. The protease inhibitors, antipain and leupeptin, decreased virus induction by TPA, a protease inducer. The capacity of TPA to induce type-C retrovirus complements results demonstrating the enhancement of Epstein-Barr virus (EBV) and murine mammary tumor virus (MMTV) synthesis by TPA.

Animals↗
PubMed1981

Vascular and metabolic effects of methylprednisolone and phenoxybenzamine during controlled hypotension in the dog.

The relationship between central haemodynamics and vascular and metabolic parameters in skeletal muscle was studied in dogs subjected to controlled haemorrhagic hypotension and treated with cumulative doses of methylprednisolone (4-32 mg x kg-1), (or saline in the control group), followed by phenoxybenzamine. There were no significant haemodynamic or metabolic changes between the groups during the injections of steroid or saline. The alpha-adrenergic receptor blockade caused, as found earlier, a pronounced vasodilation in the steroid group, which was parallelled by an increase in muscle blood flow in the same order of magnitude. There was no clearcut relationship between metabolic and vascular effects in the groups. Despite the significant difference in blood flow between the groups after phenoxybenzamine, only small and insignificant differences were seen in muscle metabolites, with the exception of muscle lactate which showed higher values in the steroid group. The study provides further evidence in support of the hypothesis that the haemodynamic effects of the combination of methylprednisolone and phenoxybenzamine are of neurogenic origin.

Animals↗
PubMed1980

Effects of hydrocortisone, phenoxybenzamine and propranolol on the blood plasma levels of adrenaline and noradrenaline during hemorrhagic hypotension in the dog.

The adrenergic aspects of the mechanism(s) of the vasodilating action of phenoxybenzamine and massive doses of hydrocortisone were studied in anesthetized dogs subjected to controlled hemorrhagic shock. During the predrug hypotension period with decreased cardiac output and heart rate, the plasma adrenaline and noradrenaline levels were both increased. Phenoxybenzamine injected alone augmented the cardiac output and heart rate and reduced the plasma adrenaline without changing the plasma noradrenaline concentration. However, if the adrenergic alpha-receptor blocker was administered in combination with massive doses of hydrocortisone, the degree of vasodilation increased further with a concomitant increase in the concentrations of the two plasma catecholamines. Thus there seems to be no clear-cut relationship between hemodynamic changes and plasma catecholamines. The present findings illustrate the extreme complexity of plasma catecholamine kinetics during hypovolemic shock.

Animals↗
PubMed1980

Effects of adrenergic neuron and ganglion blockers on hemodynamics and plasma catecholamine levels after corticosteroids during hemorrhagic shock in the dog.

The involvement of adrenergic mechanisms in the ability of massive doses of methylprednisolone to potentiate the vasodilatory effects of phenoxybenzamine during controlled hemorrhagic shock was investigated. Dogs were subjected to ligation of the adrenals and, with the exception of the controls, were pretreated with either hexamethonium or bretylium. Despite careful surgery, the adrenal ligation, per se, failed to alter the concentration of plasma catecholamines. Hexamethonium and bretylium, on the other hand, both decreased the levels of plasma catecholamines: noradrenaline to a greater extent than adrenaline. Methylprednisolone was almost ineffective after ganglionic or adrenergic neuron blockade. Furthermore, the degree of vasodilation after methylprednisolone and phenoxybenzamine seemed to correlate better with plasma noradrenaline than with adrenaline. These findings indicate that the ability of methylprednisolone to induce vasodilation in the presence of adrenergic alpha-receptor blockade in hypovolemic shock in the dog relies on an intact release of noradrenaline from postganglionic adrenergic nerve terminals.

Adrenal Medulla↗
PubMed1980

Spontaneous adrenal tumors in the aged, ovariectomized NIH swiss mouse without enhanced retrovirus expression.

A high incidence of adrenal tumors was observed in aged female NIH Swiss mice which had been ovariectomized at 2 to 4 weeks of age but not in nonovariectomized controls. Although tumors weighing more than 1 g were not infrequent in the oldest (> 24 months) animals, adrenal glands did not appear macroscopically abnormal before the age of 18 months. Histologically, however, focal or diffuse abnormalities were found in essentially every gland examined from mice over 12 months of age, including glands of normal size. Since the NIH Swiss mouse has been shown to contain an endogenous xenotropic virus whose expression is under hormonal control, the adrenal tumors were examined in detail for evidence of abnormal viral expression. We were unable, by a variety of techniques, to demonstrate elevated expression of type C virus in these adrenal tumors.

Adrenal Gland Neoplasms↗
PubMed1979

Regulation of endogenous virus production by bromodeoxyuridine and dibutyryl cyclic AMP in Chinese hamster ovary cells.

Either dibutyryl cyclic AMP or bromodeoxyuridine can enhance RNA type-C virus production in Chinese hamster ovary cells. The resultant effect of simultaneous treatment of cells with 1 mM cyclic AMP and 65 muM bromodeoxyuridine is greater than their additive effects when used separately. The increase in virus production does not seem to involve viral gene amplification, but correlates with an increase in viral RNA transcription. The virus is also shown immunologically to be unique to the Chinese hamster cells and does not appear to be a result of external infection by other common laboratory type-C viruses. The control of this endogenous viral genomic expression may therefore by proposed to be under the normal Chinese hamster gene regulatory mechanism.

Animals↗
PubMed1979

Depression of Rauscher leukemia virus envelope glycoprotein gp71 binding by lymphoid cells during leukemogenesis in mice.

The availability of membrane receptors for the 71,000-dalton envelope glycoprotein (gp71) of Rauscher murine leukemia virus on splenic and thymic cells from BALB/c mice during Rauscher murine leukemia virus-induced leukemogenesis was determined utilizing a radiolabeled gp71 binding assay. Shortly after infection, the relative cellular [125I]gp71 binding level decreased, first with splenic cells (at day 7 to 10 after infection) and later with thymic cells (at day 10 to 20 after infection). The dependency of the reduction of binding on the replication of the inoculated virus was demonstrated by regression analyses using cellular gp71 binding level as the dependent variable and infectious virus titer, as well as viral gp71 and p30 levels, of spleens and thymuses from infected mice as independent variables. With each independent variable, the reduction of gp71 binding for both cell types was highly dependent (P less than 0.01) on the level of virus detected in their respective organ. In the early stages of leukemogenesis, the [125I]gp71 binding level declined to approximately 20 to 30% of control values. During this period the rate of reduction of binding was very rapid and, in general was similar for both splenic and thymic cells. Further progression of the disease resulted in little or no further reduction in binding. The application of this technique to monitor host ecotropic virus synthesis and to study cell surface virus receptor control mechanisms in vivo is discussed.

Animals↗