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Biomedical subjects

J S Parks

Publications and source records attributed to J S Parks.

At least 145 records · Page 8Linked to original sources
PubMed1978

Familial hypopituitarism with large sella turcica.

We studied endocrine function in three siblings with short stature and enlargement of the sella turcica. Sellar volumes were 5.9, 3.7 and 4.0 standard deviations above age-specific means. Computed tomography or pneumoencephalography showed full sellae without suprasellar extension. Basal thyrotropin levels were low despite hypothyroidism and increments were less than 3 micromicron per milliliter after thyrotropin-releasing hormone injection. Stimulated growth hormone levels were less than 5 ng per milliliter, declining to less than 2 ng per milliliter after thyroxine treatment. Both thyroxine and growth hormone treatments were required for rapid growth. Impaired thyrotropin responses to thyrotropin-releasing hormone distinguish these patients from most cases of idiopathic or familial deficiency of thyrotropin and growth hormone. Persistent deficiency of growth hormone during thyroxine treatment indicates that the defects is not limited to thyrotropin structure or release. The findings are compatible with either familial neoplasia of the anterior pituitary or a regulatory defect promoting anterior pituitary-cell hyperplasia and inhibiting thyrotropin and growth hormone release.

Adolescent↗
PubMed1977

Basal and stimulated serum growth hormone concentrations in inflammatory bowel disease.

Patients with inflammatory bowel disease (IBD) manifest growth failure which may antecede abdominal symptoms by some years. Eight of ten children with documented IBD had records of decreasing growth velocities. Investigation of growth hormone reserves showed excessive rather than impaired responses. Mean basal GH level was 6.2 +/- 0.75 (SEM) ng/ml. During sleep, the mean GH level rose to 26.0 +/- 4.7 ng/ml and following propranolol-glucagon stimulation, to 46.0 +/- 4.5 ng/ml. All values were significantly higher than levels obtained in a control population of 25 children investigated for short stature who were not GH deficient. The mean peak GH response following insulin in the IBD group (10.8 +/- 3.8 ng/ml), however, did not differ from the mean peak response in the control group (13.5 +/- 3.3 ng/ml). Growth failure in patients with IBD is not the result of GH deficiency and is not an irreversible phenomenon. On the contrary, judicious use of glucocorticoids aimed at the control of the disease usually produces compensatory growth acceleration ("catch-up growth").

Adolescent↗
PubMed1976

Gonadotropin responses to luteinizing releasing factor in boys treated with cyclophosphamide for nephrotic syndrome.

Cyclophosphamide therapy of the nephrotic syndrome has been associated with oligo- and azoospermia and with abnormalities of testicular histology in adults and pubertal boys. In 15 prepubertal boys, no abnormalities of basal serum levels of LH, FSH, or T were found when they were studied 8 months to 7 years after cyclophosphamide therapy. Five boys were pubertal during therapy were found to have elevated mean basal values of gonadotropins with normal testosterone levels and elevated LH responses to LRF; the FSH responses to LRF were elevated in four patients. One of four boys who were prepubertal during therapy but pubertal at the time of testing had an elevated basal LH and LH response to LRF. Three boys who were prepubertal at the times of therapy and testing had normal LH responses to LRF. The LRF test may provide a means of identifying the patient who has sustained testicular injury and who may require testicular biopsy.

Adolescent↗
PubMed1976

Sex differences in binding of human growth hormone to isolated rat hepatocytes.

Since liver is a target for growth hormone action, binding of 125I-labeled human growth hormone to enzymatically isolated rat hepatocytes was studied. Specific binding was shown with hepatocytes from both male and female animals. There was a single class of receptors for human growth hormone on cells from males (affinity constant, Ka = 1.16 x 10(9) liters/mole; sites per cell, q = 6200). In males, bovine growth hormone was almost as potent as human growth hormone in displacing bound 125I-labeled human growth hormone, while ovine prolactin was about 1000 times less potent. Cells from female rats bound more 125I-labeled human growth hormone than cells from males. The cells from females contained at least two classes of receptors for human growth hormone. The receptor of highest affinity had the same affinity for human growth hormone as the single receptor found in males (Ka = 0.96 x 10(9) liters/mole). However, there were three to four times as many of these receptors per cell in females (q = 21,000). In females, bovine growth hormone and ovine prolactin were both about 20 times less potent than human growth hormone. Treatment of male rats with estrone produced cells that show the same binding characteristics as females. These results indicate that human growth hormone binds to a somatogenic receptor in hepatocytes from male rats. In females and estrogen-treated males, the receptors that bind human growth hormone recognize lactogenic as well as somatogenic properties. This suggests that the lactogenic and growth-promoting effects of human growth hormone in the rat are mediated by different receptors.

Animals↗
PubMed1976

Characterization of somatogenic and lactogenic binding sites in isolated rat hepatocytes.

Suspensions of rat hepatocytes isolated enzymatically by the method of Berry and Friend were used to study the binding of 125I-labeled human (hGH) and bovine (bGH) growth hormones and ovine prolactin (oPRL). Displacement of these labeled hormones by their unlabeled analogues was analyzed by means of Scatchard plots and affinity constants (K) and the number of binding sites per cell (q) were calculated. Specificity of binding was studied using hGH, bGH oPRL and rat growth hormone (rGH) and rat prolactin (rPRL). Rat hepatocytes contained two types of binding sites which bound hGH. The first, somatogenic, was specific for the growth-promoting hormones bGH and rGH. The second, lactogenic, was specific for lactogenic hormones, oPRL and rPRL. Human GH, which has both lactogenic and growth-promoting properties in rodents, bound to both sites. The somatogenic binding sites were present in both males and females, and the number of sites was similar in females and in males and was not affected by hypophysectomy. The lactogenic binding sites were present only in females, and the number of lactogenic and somatogenic sites was similar (40,000/cell). The affinity of hGH for the lactogenic binding sites was less than for the somatogenic (0.37 X 10(9) vs. 1 X 10(9)M-1). The lactogenic binding sites were lost when female rats were hypophysectomized and could not be restored by estrogen treatment.

Animals↗
PubMed1975

Low serum triiodothyronine in patients with anorexia nervosa.

Patients with anorexia nervosa can demonstrate clinical and/or laboratory findings suggestive of reduced thyroid hormone secretion. In this study, the thyroxine (T4) and triiodothyronine (T3) serum concentrations, and thyrotropin (TSH) response to intravenous administration of thyrotropin releasing hormone (TRH) were determined in 6 patients (aged 9 to 15 yr) with anorexia nervosa and the results compared to those found in a group of 15 normal subjects. The mean basal TSH concentration and mean maximum increase in TSH after TRH were comparable to those in the normal subjects. The mean T4 concentration (7.2 mug/100 ml) in the anorexia nerovsa group was slightly but significantly lower than in the normal group (9.5 mug/100 ml). Five of the 6 patients had serum T3 concentrations below the lower limits of normal and the mean T3 concentrations (49.7 ng/100 ml) was significantly lower than in the normal group (106 ng/100 ml). The extremely low serum levels of T3 in these patients with anorexia nervosa suggest that peripheral conversion of T4 to T3 is impaired during chronic starvation.

Adolescent↗