Biomedical subjects

A B Knight

Publications and source records attributed to A B Knight.

21 records · Page 2Linked to original sources

PubMed1980

Increased levels of multiplication-stimulating activity, an insulin-like growth factor, in fetal rat serum.

Multiplication-stimulating activity (MSA), purified from medium conditioned by the BRL-3A rat liver cell line, previously has been shown to be closely related to the human somatomedins or insulin-like growth factors. A radioimmunoassay was utilized to measure MSA levels in sera from fetal, maternal, and young rats. A serum somatomedin-binding protein was found to interfere in the radioimmunoassay by competing with antibody for binding 125I-labeled MSA. Therefore, prior to radioimmunoassay, sera were filtered on Sephadex G-75 in 1 M acetic acid to dissociate and separate somatomedin activity from the binding protein. Concentrations of MSA by radioimmunoassay were 20- to 100-fold higher in feta rat sera (1.8-4.4 micrograms/ml) than in maternal sera. MSA levels gradually decreased after birth, reaching maternal levels by day 25 of extrauterine life. MSA concentrations in feta rat sera also were found to be correspondingly high by a rat liver membrane radioreceptor assay and a competitive binding protein assay using rat serum somatomedin-binding protein. The findings of higher levels of MSA in fetal than in maternal rat sera and the gradual decline in MSA serum concentrations after birth are in direct contrast to total somatomedin activities measured by biosassay. Thus, MSA may function as a growth factor in the fetal rat whereas other somatomedins may play a role in stimulating growth during extrauterine life.

Age Factors↗

PubMed1980

Maternal pulmonary edema resulting from betamimetic and glucocorticoid therapy.

Four cases are presented of maternal pulmonary edema occurring in patients who had no primary cardiac disease but who were receiving terbutaline and glucocorticoids or terbutaline alone for treatment of premature labor. Fluid overload was the event that triggered this decompensation. The physiologic high-output cardiac state of pregnancy is described and the manner in which betamimetic drugs and corticosteroids exacerbate this situation and cause congestive heart failure is shown. Methods of management to avoid this complication of premature labor therapy are suggested.

Adolescent↗

PubMed1974

Intracellular potassium. A determinant of the sodium-potassium pump rate.

Normal human red cells which have had their intracellular sodium (Na(c)) reduced have a diminished Na-K pump rate, but only if intracellular potassium (K(c)) is high. If most of the K(c) is replaced by tetramethylammonium or choline, both ouabain-sensitive Na efflux and K influx are significantly increased even with Na(c) below normal. Cells with reduced Na(c) and high K(c) have an unchanged Na efflux if external potassium (K(ext)) is removed. In contrast, low-Na, low-K cells have a large ouabain-sensitive Na efflux which shows a normal response to removal of K(ext). Neither low-K nor high-K cells have an altered ouabain-sensitive K efflux. Measurement at constant low Na(c) and varying K(c) shows the pump Na efflux to be an inverse function of K(c). Thus, in low-Na cells, K(c) appears to act as an inhibitor of the pump. Inhibition by high K(c) can be seen even when Na(c) is normal. The effects attributed to K(c) are distinguished experimentally from other variables such as cell volume, adenosine triphosphate concentration, effects of the replacement cations, and the method used to alter intracellular cation concentrations. A role is proposed for K(c), in cooperation with Na(c), in regulating the pump rate of normal human red cells.

Adenosine Triphosphate↗