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 Publications
  Lipoprotein (a) is elevated in patients with renovascular hypertension, but not in patients with primary aldosteronism
  Adrenal cortico-medullary interactions: pheochromocytoma-associated cortical hyperplasia and benign neoplasia
  Central blood pressure measurement may improve risk stratification
  Rapid cortisol measurement aids in real-time confirmation of successful cannulation during adrenal venous samplings (Meeting Abstract)
  Further evidence for linkage of familial hyperaldosteronism type II at chromosome 7p22 in Italian as well as Australian and South American families
  Genetic Basis of Familial Hyperaldosteronism Type II: Further Evidence of Linkage at Chromosome 7P22 (Conference Abstract)
  Clinical, biomedical and radiological overlap between familial hyperaldosteronism type I and II: importance of genetic testing
  No evidence of mutations in RBAK and PMS2 in association with familial hyperaldosteronism type II
  Prevalence of primary aldosteronism among Chinese hypertensive patients
  Case detection, diagnosis, and treatment of patients with primary aldosteronism: an Endocrine Society clinical practice guidelines
  Examination of chromosome 7p22 candidate genes RBaK, PMS2 and GNA12 in familial hyperaldosteronism type II
  Rapid cortisol measurement aids in real-time confirmation of successful cannulation during adrenal venous sampling (AVS)
  Aldosterone excess, hypertension, and chromosome 7p22 - Evidence continues to mount
  Can liquid chromatography-tandem mass spectrometry solve the problem of aldosterone measurement?
  Cardiovascular effects of unilateral adrenalectomy are superior to those of aldosterone antagonist treatment in primary aldosteronism.
  Genetic forms of primary aldosteronism
  Primary aldosteronism: the case for screening
  Aldosterone assays: An urgent need for improvement
  Examination of candidate genes at chromosome 7p22 in familial hyperaldosteronism type II
  Further evidence of linkage at 7p22 with familial hyperaldosteronism type II and exclusion of genetic defects in the RBAK coding regions
  Monogenic mineralocorticoid hypertension
  No evidence for coding region mutations in the retinoblastoma-associated Kruppel-associated box protein gene (RBaK) causing familial hyperaldosteronism type II
  Primary mineralocorticoid excess syndromes
  The expanding role of aldosterone excess in cardiovascular disease
  The hypertensive account
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