[Incidence of transitory hypoglycemia in a random population of newborn infants].
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Biomedical subjects
Publications and source records attributed to A Liotta.
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The concentration of epidermal growth factor (EGF) in mouse submaxillary gland displays a circadian variation, which can be phase-shifted by light-dark reversal, and which is abolished by superior cervical ganglionectomy (SCG). Such circadian variation persists in fasted animals. Peak concentrations occur during light hours, trough concentrations during dark, although peak concentrations in female animals occur 8 h in advance of the time when they are seen in male animals. The nocturnal fall can be reversed by a one hour exposure to light presented during the normal dark period. SCG does not abolish the increase in submaxillary gland EGF concentrations to levels characteristic of the normal male that is seen following testosterone administration to female mice (who normally exhibit much lower EGF concentrations). Plasma EGF concentrations do not exhibit a ciradian variation.
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A sensitive bioassay for the measurement of plasma ACTH is presented. The use of silicic acid adsorption of plasma, with a subsequent acid wash and aqueous acetone desorption, was successful in removing those substances which had interfered with the steroidogenic response of dispersed adrenal cells when unextracted plasma was employed. This extraction procedure extracted 72-76% of ACTH present in plasma. Two pg ACTH1-39 could be consistently detected. Alpha-hACTH1-39 and alpha-pACTH1-39 exhibited equal potencies. Beta-MSH was ineffective at dosage levels up to 2 x 10(8) pg. One x 10(8) pg of ACTH1-10, ACTH4-10, or alpha-MSH had a steroidogenic effect equivalent to that of 40 pg ACTH1-39. ACTH 17-39 and ACTH 11-24 were incapable of stimulating steroid production at doses of 1 x 10(8) pg. Excesses of the latter, but not of the former appeared to be able to antagonize the steroidogenic effect of ACTH1-39. Plasma from normal subjects, bioassayed by this extraction procedure, contained 12-186 pg/ml ACTH at 0400-0800: 14-93 pg/ml ACTH at 1000-1300, and less than 10-34 pg/ml ACTH at 1600-2200. Hypoglycemia and vasopressin administration were followed by increases in plasma ACTH concentratrations. Plasma ACTH concentrations in untreated patients with Cushing's disease (sampled over the period 0900-1300) ranged from 65-220 pg/ml. Three patients with Addison's disease (untreated or 12 h following replacement steroid withdrawal) had ACTH concentrations of 223, 370 and 1226 pg/ml. Markedly elevated ACTH concentrations were observed in a patient with Nelson's syndrome (391 and 835 pg/ml). Bioassayable ACTH was not detected in 2 patients with panhypopituitarism.
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