F J Hayes

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Aromatase inhibition in the human male reveals a hypothalamic site of estrogen feedback
    F J Hayes
    Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston 02114, USA
    J Clin Endocrinol Metab 85:3027-35. 2000
  2. ncbi request reprint Differential regulation of gonadotropin secretion by testosterone in the human male: absence of a negative feedback effect of testosterone on follicle-stimulating hormone secretion
    F J Hayes
    Reproductive Endocrine Unit of the Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    J Clin Endocrinol Metab 86:53-8. 2001
  3. ncbi request reprint Importance of inhibin B in the regulation of FSH secretion in the human male
    F J Hayes
    Reproductive Endocrine Unit, Department of Medicine, and National Center for Infertility Research, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    J Clin Endocrinol Metab 86:5541-6. 2001
  4. ncbi request reprint Prevalence, phenotypic spectrum, and modes of inheritance of gonadotropin-releasing hormone receptor mutations in idiopathic hypogonadotropic hypogonadism
    M Beranova
    Reproductive Endocrine Unit, Harvard-wide Reproductive Endocrine Sciences Center, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    J Clin Endocrinol Metab 86:1580-8. 2001
  5. ncbi request reprint The fertile eunuch variant of idiopathic hypogonadotropic hypogonadism: spontaneous reversal associated with a homozygous mutation in the gonadotropin-releasing hormone receptor
    N Pitteloud
    Reproductive Endocrine Unit of the Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    J Clin Endocrinol Metab 86:2470-5. 2001
  6. ncbi request reprint Genetics of hypogonadotropic hypogonadism
    S B Seminara
    Reproductive Endocrine Unit, Massachusetts General Hospital, Boston 02114, USA
    J Endocrinol Invest 23:560-5. 2000
  7. ncbi request reprint The importance of autosomal genes in Kallmann syndrome: genotype-phenotype correlations and neuroendocrine characteristics
    L M Oliveira
    Reproductive Endocrine Sciences Center, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA
    J Clin Endocrinol Metab 86:1532-8. 2001

Collaborators

Detail Information

Publications7

  1. ncbi request reprint Aromatase inhibition in the human male reveals a hypothalamic site of estrogen feedback
    F J Hayes
    Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston 02114, USA
    J Clin Endocrinol Metab 85:3027-35. 2000
    ..From these data, we conclude that in the human male, estrogen has dual sites of negative feedback, acting at the hypothalamus to decrease GnRH pulse frequency and at the pituitary to decrease responsiveness to GnRH...
  2. ncbi request reprint Differential regulation of gonadotropin secretion by testosterone in the human male: absence of a negative feedback effect of testosterone on follicle-stimulating hormone secretion
    F J Hayes
    Reproductive Endocrine Unit of the Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    J Clin Endocrinol Metab 86:53-8. 2001
    ..From these data we conclude that in terms of sex steroid feedback, E(2) is the predominant regulator of FSH secretion in the human male...
  3. ncbi request reprint Importance of inhibin B in the regulation of FSH secretion in the human male
    F J Hayes
    Reproductive Endocrine Unit, Department of Medicine, and National Center for Infertility Research, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    J Clin Endocrinol Metab 86:5541-6. 2001
    ..9 +/- 2.0 vs. 66.8 +/- 20.1 IU/liter; P < 0.005). From this human model of acute sex steroid withdrawal, we conclude that Inh B is likely to be the major feedback regulator of FSH secretion in the human male...
  4. ncbi request reprint Prevalence, phenotypic spectrum, and modes of inheritance of gonadotropin-releasing hormone receptor mutations in idiopathic hypogonadotropic hypogonadism
    M Beranova
    Reproductive Endocrine Unit, Harvard-wide Reproductive Endocrine Sciences Center, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    J Clin Endocrinol Metab 86:1580-8. 2001
    ....
  5. ncbi request reprint The fertile eunuch variant of idiopathic hypogonadotropic hypogonadism: spontaneous reversal associated with a homozygous mutation in the gonadotropin-releasing hormone receptor
    N Pitteloud
    Reproductive Endocrine Unit of the Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    J Clin Endocrinol Metab 86:2470-5. 2001
    ..This case thus expands the emerging clinical spectrum of GnRH-R mutations, provides the first genetic basis for the fertile eunuch variant of IHH and documents the occurrence of reversible IHH in a patient with a GnRH-R mutation...
  6. ncbi request reprint Genetics of hypogonadotropic hypogonadism
    S B Seminara
    Reproductive Endocrine Unit, Massachusetts General Hospital, Boston 02114, USA
    J Endocrinol Invest 23:560-5. 2000
    ..As these mutations account for less than 20% of all IHH cases, discovery of additional gene mutations will continue to advance our understanding of this intriguing syndrome...
  7. ncbi request reprint The importance of autosomal genes in Kallmann syndrome: genotype-phenotype correlations and neuroendocrine characteristics
    L M Oliveira
    Reproductive Endocrine Sciences Center, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA
    J Clin Endocrinol Metab 86:1532-8. 2001
    ..Taken together, these findings suggest that autosomal genes account for the majority of familial cases of KS, and that unique neuroendocrine phenotypes consistent with some GnRH neuronal migration may exist in these patients...