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Biomedical subjects

R G Coffey

Publications and source records attributed to R G Coffey.

At least 55 records · Page 3Linked to original sources
PubMed1976

Effects of concanavalin A and a succinylated derivative on lymphocyte proliferation and cyclic nucleotide levels.

To better define cell surface-related changes involved in lymphocyte activation, we studied native concanavalin A (Con A) and succinylated concanavalin A (Suc-Con A) for their effects on proliferation and cyclic nucleotide levels of human peripheral blood lymphocytes. At optimal mitogenic concentrations, the two forms of Con A induce equivalent proliferation; however, the mitogenic activity of Con A progressively decreases above 50 mug/ml. In contrast, the mitogenic activity of Suc-Con A is not decreased even at 250 mug/ml.

Cell Division↗
PubMed1976

Isoprinosine augmentation of phytohemagglutinin-induced lymphocyte proliferation.

The need for agents designed to modify immune response in the treatment of patients with viral infection, immunodeficiency, or cancer prompted the present study on the mechanisms of action of isoprinosine, a compound developed for antiviral use and whose therapeutic activity may involve the immune system. The effect of isoprinosine on in vitro proliferation of human peripheral blood lymphocytes stimulated by phytohemagglutinin (PHA) and on lymphocyte levels of cyclic adenosine 3',5'-monophosphate and cyclic guanosine 3',5'-monophosphate was analyzed. Over a concentration range from 0.2 to 250 mug/ml, isoprinosine augmented PHA-induced proliferation; maximal stimulation was observed between 25 to 50 mug/ml. Isoprinosine in the absence of PHA had no effect on proliferation. The relative lack of effect of isoprinosine during a 90-min exposure and the lack of effect on lymphocyte cyclic nucleotide levels indicate that isoprinosine potentiates the PHA response by a mechanism different than a number of hormonal agents and such immunopotentiators as levamisole, polyadenylic-acid, and endotoxin. Further evaluation of isoprinosine as an immunopotentiator is indicated.

Cyclic AMP↗
PubMed1975

Norepinephrine stimulation of lymphocyte ATPase by an alpha adrenergic receptor mechanism.

The effects of norepinephrine in interaction with adrenergic blocking compounds were studied on membrane adenosine triphosphatase (ATPase) activities of human lymphocytes and lymphoblasts. Sodium-potassium ion exchange pump activity was assayed by 86-Rb uptake and ATPase activity of membrane fractions was assayed by ADP and inorganic phosphate generation. The results of these studies indicate that norepinephrine acts by an alpha adrenergic mechanism to enhance membrane sodium-potassium ion exchange pump activity and ATPase activity. The pharmacologic and ionic dissection of the adrenergic sensitivity of ATPase activity indicates that this alpha adrenergic mechanism is related to membrane ATPase activities in addition to that associated with the ion exchange pump. Analysis of fractions obtained by sucrose gradients indicates that the action of norepinephrine is localized in the plasma membrane. Beta adrenergic stimulation was observed to inhibit ATPase activity. The complexity of adrenergic effects on membrane ATPase suggests interactions of hormone modulation of membrane nucleotide cyclases and transport-related ATPase enzymes.

Biological Transport↗
PubMed1975

Increased adenosine triphosphatase activity in platelets of asthmatic children.

Adenosine triphosphatase (ATPase) activities were compared in platelets of asthmatic and nonasthmatic children. Significantly elevated Mg2+- and Ca2+-dependent ATPase activities were found in particulate and soluble fractions of platelets from nonsteroid-treated asthmatic children compared to steroid-treated asthmatic and nonasthmatic children. The most pronounced increase (greater than twofold) occurred in the Ca2+-ATPase of the soluble fraction which contains platelet contractile protein. Intact cell surface of ecto ATPase activity was not significantly increased in platelets of asthmatic children. The findings are consistent with adrenergic imbalance in asthma involving depressed adenylate cyclase activity (beta-adrenergic) and increased ATPase activity (alpha-adrenergic) and may relate to abnormal platelet aggregation patterns.

Adenosine Diphosphate↗
PubMed1974

Increased adenosine triphosphatase in leukocytes of asthmatic children.

Adenosine triphosphatase (ATPase) activities were compared in leukocytes of asthmatic and nonasthmatic children. Both Mg(2+)- and Ca(2+)-dependent ATPase activities were significantly elevated in two membrane fractions (59 to 66%) and in a superntant fraction (68 to 72%) prepared from sonicated leukocytes of asthmatic subjects. Intact cell surface or ecto ATPase was also elevated (67 to 76%) in asthmatic leukocytes. Alternate day glucocorticosteroid therapy was associated with leukocyte ATPase activities intermediate between those for asthmatics not receiving steroids and for nonasthmatic control subjects. Incubation of normal leukocytes with 10(-8) M hydrocortisone or leukocyte membranes with 10(-4)-10(-3) M hydrocortisone in vitro also resulted in decreased ATPase activities. The elevated leukocyte ATPase activities appear to relate to the adrenergic imbalance in asthma previously characterized by reduced beta adrenergic responsiveness of adenylate cyclase and suggest the possibility of more than one enzymatic abnormality intrinsic to the asthmatic condition.

Adenosine Triphosphatases↗