The hypothalamus and the regulation of food intake.
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Biomedical subjects
Publications and source records attributed to C J Smith.
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Exposure of insulin-responsive, differentiated 3T3-L1 cells (adipocytes) to 0.1 to 1.0 microgram/ml of insulin for 3 to 48 h resulted in a persistent state of enhanced 2-deoxy-D-glucose and 3-O-methyl-D-glucose uptake. Elevated basal transport activity was retained under conditions where 125I-insulin binding activity remained unchanged and exchangeable insulin was dissociated from cell surface receptors. The appearance of enhanced hexose transport activity was prevented by cycloheximide and could be distinguished from the activation of the glucose transport system observed in these and other cells during glucose deprivation. Rigorously washed adipocytes, exhibiting insulin-induced elevations in basal transport activity, were refractory to further stimulation by insulin during hexose uptake assays. Insulin-unresponsive 3T3-L1 preadipocytes failed to increase hexose uptake activity when treated under conditions that elicited an optimal response in adipocytes.
The deltoscapular flap is described as an additional source of regional skin for head and neck reconstruction; this flap behaves in the manmer of an arterially based axial skin flap. On three occasions, I have used this back flap that is almost a mirror image of the deltopectoral flap.
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Three commercially available purified phytohaemagglutinin (PHA) preparations have been examined both chemically and biologically. Marked differences were observed in both composition and mitogenic effect on lymphocytes; the existence of at least two distinct mitogenic fractions in PHA was confirmed.
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Serum half-lives of unfractionated rat alpha-fetoprotein (AFP), concanavalin A (Con A)-nonreactive AFP, and Con A-reactive AFP in normal 45- to 55-day-old male and female F344 rats were determined to be 19 hours. No significant differences were seen between the half-lives of unfractionated AFP and either of the two Con A-affinity molecular variants of AFP studied. No evidence of interconversion of the Con A-affinity AFP variants during 24 hours in the circulation was found. These results supported the conclusion that the proportions of Con A-affinity molecular variants of AFP in the sera of fetal, newborn, and hematoma-bearing rats result from differences in the relative synthesis rates of the two variants.
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Alpha-fetoprotein and albumin were quantified in the sera and amniotic fluids from control, Vitamin A-treated non-exencephalic and Vitamin A-treated exencephalic rat fetuses. Exencephaly was associated with amniotic fluid alpha-fetoprotein concentrations which were significantly elevated over those of Vitamin A-treated non-exencephalic and of untreated fetuses. Amniotic fluid albumin concentrations also were higher in the exencephalic fetuses than in the non-exencephalic fetuses. Serum alpha-fetoprotein and albumin concentrations were lower in the exencephalic than in the non-exencephalic fetuses. The results are cosistent with simple diffusion across a defective barrier as the cause of elevated amniotic fluid alpha-fetoprotein concentrations in the presence of open neural tube defects. This experimental model of neural tube defects result in changes in amniotic fluid alpha-fetoprotein similar to those changes found in human amniotic fluid alpha-fetoprotein concentrations in the presence of neural tube defects.
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Hepatomas secreting large amounts of alpha-fetoprotein were induced in Fischer rats by the continuous feeding of 0.06% 3'-methyl-4-dimethylaminoazobenzene. Serum alpha-fetoprotein concentrations in the 59 hepatoma-bearing rats ranged from 92--3260 microgram/ml (mean, 972 microgram/ml; median, 830 microgram/ml) at the time of primary tumor transplantation.