Laboratory values in severely stunted mental defectives.
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17-Hydroxycorticosteroids↗
Biomedical subjects
H D Mosier
Publications and source records attributed to H D Mosier.
Physical growth in mental defectives. A study in an institutionalized population.
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Adolescent↗
Growth promoting peptides in diabetic and non-diabetic pregnancy: interactions with trophoblastic receptors and serum carrier proteins.
Infantile macrosomia in diabetic pregnancy (DP) is commonly attributed to fetal hyperinsulinism. However, insulin-like growth factors in the mother and the fetus, their binding proteins and their placental receptors may also play roles in the process of fetal overgrowth. We measured levels of maternal and cord serum IGF-I, IGF-II, C-peptide, IGFBP-1, IGFBP-2 and IGFBP-3 in 8 White Class B insulin dependent DP and 8 non-diabetic pregnancies (NP). These results were correlated with the concentration and affinity of placental trophoblastic membrane receptors (TR) for insulin (IN), IGF-I and IGF-II as well as with infant and placenta weights and maternal body mass indices. Significant respective differences between the diabetic and non-diabetic groups were found in mean infant weight, 4248 +/- 114 vs 3555 +/- 119 g (p < 0.001), placental weight 765 +/- 51 vs 575 +/- 24 g (p < 0.01), maternal body mass index 32.8 +/- 3.8 vs 21.3 +/- 1.2 (p < 0.02), cord serum IGF-I 136.8 +/- 6.6 vs 85.9 +/- 5.7 ng/ml (p < 0.01), cord serum C-peptide 18.7 +/- 3.5 vs 9.0 +/- 1.7 ng/ml (p < 0.025), cord serum IGFBP-1 21.9 +/- 4.7 vs 133.2 +/- 43.2 ng/ml (p < 0.025), cord serum IGFBP-2 672.0 +/- 76 vs 1206 +/- 220 ng/ml (p < 0.05) and cord serum IGFBP-3 11.5 +/- 1.0 vs 5.6 +/- 0.6 ng/ml (p < 0.001). No significant differences were found between DP and NP with respect to cord serum IGF-II, maternal serum IGF-I, IGF-II, C-peptide, IGFBP-1, IGFBP-2 and IGFBP-3, and the concentration and affinity of TR for IN, IGF-I and IGF-II. Analysis of variance revealed an interaction between infant weight and the weight of the placenta (p < 0.01), cord IGF-I (p < 0.02), cord C-peptide (p < 0.01) and cord IGFBP-3 (p < 0.01). Regression analysis revealed significant correlations of cord IGF-I with cord values of IGFBP-2 (r = -0.52, p = 0.04) and IGFBP-3 (r = 0.66, p < 0.005). Maternal serum IGF-I significantly correlated only with maternal IGFBP-3 (r = 0.65, p < 0.01). These results suggest that increased fetal production of insulin and IGF-I may contribute to the development of infantile macrosomia in DP. Concomitant changes in fetal production of IGFBPs, particularly IGFBP-2 and IGFBP-3, may modulate the action of insulin and IGFs. The lack of change in number or binding affinity of placental trophoblastic receptors for insulin, IGF-I and IGF-II tends to exclude a significant regulatory role of these receptors in the production of fetal macrosomia.
Adult↗
Successive resetting of the set point for target body size.
Previous studies support the existence of a central set point for target body size. The set point is a hypothetical fixed reference for body size. The present experiments were carried out to determine whether target body size and, by implication, the putative set point can be consecutively reset or whether, once set by an extraneous factor, it is refractory to another extraneous factor. Male and female rats were given 6.0 Gy whole head X-irradiation at two days of age or were sham-irradiated as controls. Significant permanent reduction of body weight, tibia length, and pituitary weight resulted from head-irradiation in both males and females; gonad weight was reduced in males but not significantly in females. At 41 days of age the irradiated animals were injected sc with cortisone acetate, 1 mg/25 g body weight/day, or saline. During cortisone treatment the head-irradiated rats had a decrease in body weight velocity; the effect was greater in males than in females. Following treatment growth velocity approached normal in treated males, and slightly exceeded normal in treated females. Treated males had significantly reduced body weight, tail length, and tibia length at the end of the study. Treated females showed a similar pattern of body weight growth to the treated males, but there was not a significant long term reduction of body weight or change in tail length or tibia length. Final pituitary and gonad size was not affected by cortisone treatment in either sex. The results indicate that the reset of target size after head-irradiation does not result from damage to putative control.(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
Corneal sulfate incorporation during fasting in rats.
Fasting is known to decrease sulfate incorporation as well as other growth functions in cartilage. The present study compared corneal sulfation in vivo and in vitro, with sulfation in cartilage of rats undergoing total food deprivation for 48 hours and refeeding for periods up to 28 days. Sulfate incorporation by cartilage decreased both in vivo and in vitro during the fast and recovered to normal values by 7 days of refeeding. Corneal sulfation increased in vivo during the fast. After 7 days of refeeding corneal sulfation in vivo dropped below the control value and remained below the control level. At later recovery periods corneal sulfation in vivo was normal. Corneal sulfation in vitro decreased during the fast. Normal cartilage showed a decrease in sulfate incorporation in vivo and in vitro with increasing age. Corneal sulfation in vitro followed this pattern, but corneal sulfation in vivo did not. We conclude that the effect of fasting on sulfate metabolism of corneal stroma is qualitatively different from that of cartilage.
Animals↗
Decreased reverse T3 levels in neonates with central hypothyroidism.
Concern arises when a sick infant is found to have a low serum T4, normal thyroid hormone binding, and a nonelevated thyroid-stimulating hormone. Hypothyroxinemia in this situation can result from either euthyroid sick syndrome or central hypothyroidism. To help distinguish between these diagnostic possibilities, we have measured reverse T3 and other thyroid function chemistries in six neonates who have central hypothyroidism in association with hypopituitarism. We found that these infants all had reverse T3 levels that were much lower than reported normal levels for premature and term neonates. This finding suggests that low reverse T3 levels can help to distinguish infants with central hypothyroidism from sick and well infants who tend to have relatively elevated reverse T3 levels.
Diagnosis, Differential↗