Effects of somatostatin on the hepatic adenylate cyclase system in the rat.
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Adenosine Triphosphate↗
Biomedical subjects
G Higdon
Publications and source records attributed to G Higdon.
Black teachers' perceptions of the ideal pupil.
Torrance's Ideal Child Checklist was administered to 76 black teachers. A comparison of their 10 most and least valued traits with those of the expert panel on the creative personality showed that the two groups agreed only once on the 10 most valued traits and three times on the 10 least valued traits.
Black or African American↗
School conformity and its relationship to creativity.
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Adolescent↗
Development of glucagon sensitivity in neonatal rat liver.
The ontogenesis of the hepatic glucagon-sensitive adenylate cyclase system has been studied in the rat. With a partially purified liver membrane preparation, fetal adenylate cyclase was less responsive to glucagon than the enzyme from neonatal or adult livers. Similar results were obtained in gently prepared liver homogenates, suggesting that destruction of essential components of the fetal liver membrane did not account for the relative unresponsiveness of the adenylate cyclase enzyme to glucagon. Investigation of other factors that might account for diminished fetal hepatic responsiveness to glucagon indicate (a) minimal glucagon degradation by fetal membranes relative to 8-day or adult tissue; and (b) available adenylate cyclase enzyme, as suggested by a 13-fold increase over basal cyclic AMP formation with NaF in fetal liver membranes. These results indicate that neither enhanced glucagon degradation nor adenylate cyclase enzyme deficiency accounts for the relative insensitivity of the fetal hepatic adenylate cyclase system to glucagon. In early neonatal life, hepatic adenylate cyclase responsiveness to glucagon rapidly developed and was maximal 6 days after birth. These changes were closely paralleled by a fivefold increase in glucagon binding and the kinetically determined Vmax for cyclic AMP formation. These observations suggest that (a) fetal hepatic unresponsiveness to glucagon may be explained by a limited number of glucagon receptor sites; (b) during the neonatal period, the development of glucagon binding is expressed primarily as an increase in adenylate cyclase Vmax; (c) the ontogenesis of hepatic responsiveness to glucagon may be important in the resolution of neonatal hypoglycemia.
Adenylyl Cyclases↗