George William Moll

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Familial male-limited precocious puberty is a male-limited autosomal dominant condition. It is characterized by increased testosterone synthesis in the absence of testicular stimulation by luteinizing hormone (LH). We hypothesised that an abnormal configuration of the LH receptor might autonomously activate G protein coupling, and thereby cause the(More)
Herein, we report mutation analysis of the LH receptor gene in 17 males with LH-independent precocious puberty, of which 8 were familial and 9 had a negative family history. A total of 7 different mutations (all previously reported) were detected in 12 patients. Among 10 European familial male-limited precocious puberty (FMPP) patients who had a LH receptor(More)
We designed a prospective study of height potential in girls with idiopathic precocious puberty, comparing the presenting features of girls with and without evidence of reduced adult height potential. The 14 girls with impaired adult height prognoses (group 1) were reexamined after treatment with a gonadotropin releasing hormone agonist, nafarelin. The(More)
OBJECTIVE To describe the clinical course and the utility of computerized tomography (CT) and magnetic resonance imaging (MRI) in the successful management of an often fatal fungal infection in a 12-year-old patient with insulin-dependent diabetes mellitus (IDDM). CASE The patient was admitted to The University of Mississippi Medical Center (UMC) for the(More)
We tested the concept that estrogen directly stimulates growth hormone (GH) production by determining whether low-dose treatment with ethinyl estradiol increases the GH reserve, as assessed by levodopa administration, without inhibiting somatomedin-C (Sm-C) levels. Twenty-three prepubertal short normal children underwent levodopa tests before and after(More)
We have employed plasma free testosterone concentrations to diagnose polycystic ovary syndrome in adolescence after demonstrating that mature plasma free androgen levels are achieved by midpuberty. Among 43 female volunteers, 10 to 16 years of age, followed up in a mixed longitudinal-cross-sectional study, we found that three (7%) had elevated plasma free(More)
Inherited thyroxine-binding globulin (TBG) deficiency is caused by mutations in the TBG gene located on the X-chromosome. We now describe two families (K and H) with X-linked complete TBG deficiency without mutations in the coding or promoter regions of the TBG gene. The propositi of both families presented with euthyroid hypothyroxinemia and were found to(More)