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Biomedical subjects

C M Foster

Publications and source records attributed to C M Foster.

41 records · Page 3Linked to original sources
PubMed1984

Absence of pubertal gonadotropin secretion in girls with McCune-Albright syndrome.

Precocious puberty in girls with McCune-Albright syndrome has been attributed in some cases to early activation of the hypothalamic-pituitary-gonadal axis and in other cases to sex steroid secretion by apparently autonomous ovarian cysts. We evaluated serum gonadotropins and sex steroids in six girls (aged 1-9 yr) with McCune-Albright syndrome. The children had Tanner stage II-IV pubertal development. In five patients, nocturnal gonadotropin concentrations and the gonadotropin response to LHRH were within the normal range for prepubertal children. Thus, the precocious puberty in these patients could not be explained by activation of the hypothalamic-pituitary-ovarian axis. One child had high amplitude nocturnal pulses of serum LH and a LH-predominant response to LHRH. She was the oldest of the six girls and had a bone age of 13.5 yr which is within the range in which hypothalamic-pituitary-ovarian activation normally occurs. The children all had ovarian enlargement and ovarian cysts determined by ultrasound. It appears that precocious puberty in McCune-Albright syndrome may result from ovarian estrogen secretion in the absence of normal pubertal activation of the hypothalamic-pituitary-ovarian axis.

Adolescent↗
PubMed1984

Variable response to a long-acting agonist of luteinizing hormone-releasing hormone in girls with McCune-Albright syndrome.

Six girls with McCune-Albright syndrome were treated for at least 2 months with the long-acting LHRH agonist D-Trp6-Pro9-NEt-LHRH, which previously was found to be an effective treatment for true precocious puberty. Nocturnal and LHRH-stimulated serum gonadotropin levels and plasma estradiol levels were measured before treatment and after 2-3 months of treatment. Five of the six girls had no decrease in serum gonadotropin or plasma estradiol levels during therapy, and their pubertal signs were unaffected by treatment. All five of these girls had serum gonadotropin levels that were within or below the normal prepubertal range. The sixth girl, who had gonadotropin levels in the normal pubertal range before treatment, had decreased serum gonadotropin and plasma estradiol levels during 1 yr of LHRH analog therapy. This was associated with cessation of menses and regression of secondary sexual changes. The failure of LHRH analog to modify the course of precocious puberty in the five patients with prepubertal serum gonadotropin concentrations is further evidence that the mechanism of precocious puberty in most girls with McCune-Albright syndrome differs from that in patients with true precocious puberty.

Child↗
PubMed1983

Covalent labeling of rat thymocyte and human lymphoid glucocorticoid receptor.

Lymphoid cells contain specific receptors for glucocorticoids. We have used [3H]dexamethasone-21-mesylate to label covalently glucocorticoid receptors in rat thymic lymphocytes and in neoplastic cells obtained from patients with acute lymphoblastic leukemia and malignant lymphoma. The covalently labeled glucocorticoid receptors were identified by polyacrylamide gel electrophoresis (in the presence of 0.1% sodium dodecyl sulfate). In cytosolic fractions prepared from rat thymic lymphocytes, [3H]-dexamethasone-21-mesylate labels a protein (Mr approximately equal to 95,000) which was identified as the glucocorticoid receptor by the following criteria: (a) labeling of this moiety is inhibited by treatment with a 100-fold molar excess of glucocorticoids, such as dexamethasone and triamcinolone acetonide; and (b) the covalently labeled Mr approximately equal to 95,000 protein is activated (by heating at 20 degrees for 30 min) to a form that binds to DNA-cellulose. When intact thymocytes are treated with [3H]dexamethasone-21-mesylate, an Mr approximately equal to 95,000 moiety is also labeled covalently. Approximately 35% of the glucocorticoid receptors can be labeled covalently when intact thymocytes are treated with 100 nM [3H]dexamethasone-21-mesylate for 30 min at 4 degrees. Neoplastic cells from acute lymphoblastic leukemia and malignant lymphoma were treated with [3H]dexamethasone-21-mesylate. In all samples, an Mr approximately equal to 95,000 moiety was labeled covalently; labeling was inhibited by excess glucocorticoid. Smaller moieties were also identified by competition experiments; these may represent proteolytic fragments of the Mr approximately equal to 95,000 receptor. Thus, in rat and human lymphoid cells, [3H]dexamethasone-21-mesylate can be used to label covalently the glucocorticoid receptor.

Affinity Labels↗
PubMed1978

Postpartum cytomegalovirus infection. A hazard of multiple transfusions.

A patient whose postpartum course included the defibrination syndrome and Bacteroides septicemia developed recurrent high fever. Cytomegalovirus infection was suspected on the basis of the clinical features and a history of massive blood transfusion, and was confirmed by subsequent observations. Recognition of this disease and its typically benign course averts the need for extensive diagnostic procedures, exploration, and empiric drug therapy trials.

Adult↗