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Evangelia Charmandari

Pediatric and Reproductive Endocrinology Branch

National Institute of Child Health and Human Development

National Institutes of Health

Bethesda

USA

[email]@mail.nih.gov

Name/email consistency: high

 
 
 
 
 
 
 

Affiliations

  • Pediatric and Reproductive Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, USA. 2002 - 2006
  • Department of Pediatric Endocrinology, Great Ormond Street Hospital for Children, 9th Floor, Southwood Building. 2005
  • London Centre for Paediatric Endocrinology, University College London, United Kingdom W1N 8AA. 2001 - 2003
  • London Centre for Paediatric Endocrinology, Great Ormond Street Hospital and The Institute of Child Health, University College London, London WC1N 3JH, UK. 2001

References

  1. Functional characterization of the natural human glucocorticoid receptor (hGR) mutants hGRalphaR477H and hGRalphaG679S associated with generalized glucocorticoid resistance. Charmandari, E., Kino, T., Ichijo, T., Zachman, K., Alatsatianos, A., Chrousos, G.P. J. Clin. Endocrinol. Metab. (2006) [Pubmed]
  2. Metabolic syndrome manifestations in classic congenital adrenal hyperplasia: do they predispose to atherosclerotic cardiovascular disease and secondary polycystic ovary syndrome?. Charmandari, E., Chrousos, G.P. Ann. N. Y. Acad. Sci. (2006) [Pubmed]
  3. The human glucocorticoid receptor (hGR) beta isoform suppresses the transcriptional activity of hGRalpha by interfering with formation of active coactivator complexes. Charmandari, E., Chrousos, G.P., Ichijo, T., Bhattacharyya, N., Vottero, A., Souvatzoglou, E., Kino, T. Mol. Endocrinol. (2005) [Pubmed]
  4. Adrenocorticotropin hypersecretion and pituitary microadenoma following bilateral adrenalectomy in a patient with classic 21-hydroxylase deficiency. Charmandari, E., Chrousos, G.P., Merke, D.P. J. Pediatr. Endocrinol. Metab. (2005) [Pubmed]
  5. Endocrinology of the stress response. Charmandari, E., Tsigos, C., Chrousos, G. Annu. Rev. Physiol. (2005) [Pubmed]
  6. A novel point mutation in the ligand-binding domain (LBD) of the human glucocorticoid receptor (hGR) causing generalized glucocorticoid resistance: the importance of the C terminus of hGR LBD in conferring transactivational activity. Charmandari, E., Raji, A., Kino, T., Ichijo, T., Tiulpakov, A., Zachman, K., Chrousos, G.P. J. Clin. Endocrinol. Metab. (2005) [Pubmed]
  7. Glucocorticoids and their actions: an introduction. Charmandari, E., Kino, T., Chrousos, G.P. Ann. N. Y. Acad. Sci. (2004) [Pubmed]
  8. Familial/sporadic glucocorticoid resistance: clinical phenotype and molecular mechanisms. Charmandari, E., Kino, T., Chrousos, G.P. Ann. N. Y. Acad. Sci. (2004) [Pubmed]
  9. Classic congenital adrenal hyperplasia and puberty. Charmandari, E., Brook, C.G., Hindmarsh, P.C. Eur. J. Endocrinol. (2004) [Pubmed]
  10. Pediatric stress: hormonal mediators and human development. Charmandari, E., Kino, T., Souvatzoglou, E., Chrousos, G.P. Horm. Res. (2003) [Pubmed]
  11. Sexual dimorphism in the synchrony of joint growth hormone and cortisol dynamics in children with classic 21-hydroxylase deficiency. Charmandari, E., Pincus, S.M., Matthews, D.R., Johnston, A., Brook, C.G., Hindmarsh, P.C. J. Pediatr. Endocrinol. Metab. (2003) [Pubmed]
  12. Why is management of patients with classical congenital adrenal hyperplasia more difficult at puberty?. Charmandari, E., Brook, C.G., Hindmarsh, P.C. Arch. Dis. Child. (2002) [Pubmed]
  13. Children with classic congenital adrenal hyperplasia have elevated serum leptin concentrations and insulin resistance: potential clinical implications. Charmandari, E., Weise, M., Bornstein, S.R., Eisenhofer, G., Keil, M.F., Chrousos, G.P., Merke, D.P. J. Clin. Endocrinol. Metab. (2002) [Pubmed]
  14. Oral hydrocortisone administration in children with classic 21-hydroxylase deficiency leads to more synchronous joint GH and cortisol secretion. Charmandari, E., Pincus, S.M., Matthews, D.R., Johnston, A., Brook, C.G., Hindmarsh, P.C. J. Clin. Endocrinol. Metab. (2002) [Pubmed]
  15. Treatment with flutamide decreases cortisol clearance: implications for therapy in congenital adrenal hyperplasia. Charmandari, E., Johnston, A., Honour, J.W., Brook, C.G., Hindmarsh, P.C. J. Pediatr. Endocrinol. Metab. (2002) [Pubmed]
  16. Congenital adrenal hyperplasia due to 21-hydroxylase deficiency: alterations in cortisol pharmacokinetics at puberty. Charmandari, E., Hindmarsh, P.C., Johnston, A., Brook, C.G. J. Clin. Endocrinol. Metab. (2001) [Pubmed]
  17. Congenital adrenal hyperplasia: management during critical illness. Charmandari, E., Lichtarowicz-Krynska, E.J., Hindmarsh, P.C., Johnston, A., Aynsley-Green, A., Brook, C.G. Arch. Dis. Child. (2001) [Pubmed]
  18. Serum cortisol and 17-hydroxyprogesterone interrelation in classic 21-hydroxylase deficiency: is current replacement therapy satisfactory?. Charmandari, E., Matthews, D.R., Johnston, A., Brook, C.G., Hindmarsh, P.C. J. Clin. Endocrinol. Metab. (2001) [Pubmed]
  19. Kinetics and effect of percutaneous administration of dihydrotestosterone in children. Charmandari, E., Dattani, M.T., Perry, L.A., Hindmarsh, P.C., Brook, C.G. Horm. Res. (2001) [Pubmed]
 
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