Kenneth C. Copeland

Insulin-Like Growth Factor I in Substrate-Deprived, Growth-Retarded Fetal Rats

ABSTRACT: Plasma, amniotic fluid, and tissue concentrations of IGF-I were examined in nutritionally deprived, growth-retarded fetal rats to determine whether IGF-I concentration serves as a marker for nutritional status. Growth retardation was induced by 72 h of maternal fasting. Twenty-three control and 17 growth-retarded fetuses were individually analyzed and compared. Plasma IGF-I concentrations were significantly lower in test compared with control animals (test 56.8 ± 14.9, control 87.4 ± 17.5 ng/mL, p < 0.01). Amniotic fluid IGF-I concentrations were not different (test 14.0 ± 8.7, control 12.2 ± 2.6 ng/mL). IGF-I concentrations obtained from both placental and hepatic tissues were lower in test compared with control animals [placenta: test 293 ± 25 versus control 655 ± 114 ng/g (p < 0.001); hepatic: test 173 ± 38 versus control 230 ± 51 ng/g (p < 0.01)]. Reductions in fetal, placental, and hepatic weights in test animals were more closely related to changes in placental IGF-I concentration than to either plasma or hepatic IGF-I concentrations. We conclude that fetal plasma IGF-I is a valuable marker for intrauterine substrate deprivation and that the growth-retarded rat fetus is accurately identified and specifically characterized by a low placental concentration of extractable IGF-I.

Neonatal Hyperbilirubinemia and Hypoglycemia in Congenital Hypopituitarism

Christian syndrome in infancy. Br J Dermatol 98:175, 1978 2. Vestermark S: Weber-Christian syndrome in a newborn. Acta Paediatr Scand 55:432, 1966 3. Larkin V, De Sanctis AG, Margulis AE: Relapsing febrile nodular non-suppurative panniculitis (WeberChristian disease); review of the literature with report of a case. Am J Dis Child 67:120, 1944 4. Sanford HN, Eubank DF, Stenn F: Chronic panniculitis with leukopenia (Weber-Christian syndrome). Am J Dis Child 83:156, 1952 5. Forstrom L, Winkelmann RK: Acute panniculitis. A clinical and histopathologic study of 34 cases. Arch Dermatol 113:909, 1977

The baboon as a model for puberty: growth, testis size, plasma testosterone, and somatomedin-C

Physical and hormonal changes of human puberty have been described extensively, yet a nonhuman primate model for pubertal events is lacking. This study is a cross-section analysis of pubertal growth, testis size, and plasma concentration of testosterone (T) and somatomedin-C (SM-C) in the male baboon (Paplo sp.). Baboons (n = 84) with known dates of birth (3 - 272 weeks of age) and 10 adults (> 10 years) were examined by the same investigators for body weight (BWt), crown-rump length (CRL), and testis size. A plasma sample was drawn for determination of T by RIA. A separate group of 26 male baboons, ages 3 weeks to adult, were studied cross-sectionally for SM-C. As in the human, testis size increased only slightly before puberty. By 3 to 3.5 years, there was a marked increase in testis size coincident with or slightly preceding increases in BWt, CRL, and plasma T. Testis size continued to increase slightly after 5 years to adult size. By 3 to 4 years, there was a significant increase in SM-C which declined in adults (0 - 3 yr, M ± SE = 1.00 ± 0.14, n = 12; 3 - 4 yr, 8.46 ± 0.57, n = 10; > 6 yr, 3.90 ± 0.21, n = 4). Regression analyses of BWt, CRL, and testis size vs. age revealed significant changes in slope beginning at about 3 years. In conclusion, these data define the age of puberty and describe pubertal changes in somatic growth and testicular development in the baboon and suggest that this species may be an appropriate nonhuman primate model for human pubertal growth and development. (SM-C tracer supplied by J. Van Wyk.)

Two Novel Homozygous Mutations in the Type II 3β-Hydroxysteroid Dehydrogenase(3β-HSD) Gene Causing Non-Salt Wasting and Salt Wasting 3β-HSD Deficiency Congenital Adrenal Hyperplasia (CAH) and the Utility of Hormonal Profiles for Diagnosising Bonafide 3β-HSD Deficiency CAH• 505

Two Novel Homozygous Mutations in the Type II 3β-Hydroxysteroid Dehydrogenase(3β-HSD) Gene Causing Non-Salt Wasting and Salt Wasting 3β-HSD Deficiency Congenital Adrenal Hyperplasia (CAH) and the Utility of Hormonal Profiles for Diagnosising Bonafide 3β-HSD Deficiency CAH• 505

Telephone Charges and Payments in a Diabetes Clinic 445

OBJECTIVES To determine reimbursement rates after initiation of charges for certain telephone calls in a pediatric diabetes care center. DESIGN A review of charges and payments data during 1996. RESULTS Four hundred seventy-two telephone calls initiated by patients and parents were billed during the study period. These calls regarded treatment of hypoglycemia, hyperglycemia, ketonuria, sick day treatment, and insulin dose changes. Insured patients were charged for 384 telephone calls and indigent patients were charged for 88 telephone calls. Telephone calls from insured patients generated charges of

Estradiol (EE 2 ) and Growth Hormone (GH) Increase Bone Deposition in Girls with Turner's Syndrome † 400

9215 and payments of

DHEA-S, IGF-I, and IGFBP-1 and -3 Relationships to Insulin and Body Fat in Normal Prepubertal Caucasian, African-American, and Hispanic Girls |[dagger]| 427

3074. Insurance payments were

Puberty in the Chimpanzee: Somatomedin-C and Its Relationship to Somatic Growth and Steroid Hormone Concentrations

1677 (18% of charges), and patient payments were

Estrogen stimulates growth hormone and somatomedin-C in castrate and intact female baboons.

1396 (15% of charges). Telephone calls from uninsured patients covered by Texas Medicaid or Chronically Ill and Disabled Children funding generated charges of

Pubertal endocrinology of the baboon: elevated somatomedin-C/insulin-like growth factor I at puberty.

2193 and no payments. CONCLUSIONS Telephone charges were reimbursed by all payors at an overall rate of 27%.