A
Ariel Rösler
Researcher at Hebrew University of Jerusalem
Publications - 31
Citations - 2513
Ariel Rösler is an academic researcher from Hebrew University of Jerusalem. The author has contributed to research in topics: Steroid 11-beta-hydroxylase & Congenital adrenal hyperplasia. The author has an hindex of 20, co-authored 31 publications receiving 2435 citations. Previous affiliations of Ariel Rösler include Ben-Gurion University of the Negev.
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Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1
Sue S. Chang,Stefan Gründer,Aaron Hanukoglu,Ariel Rösler,P.M. Mathew,Israel Hanukoglu,Laurent Schild,Yin Lu,Richard A. Shimkets,Carol Nelson-Williams,Bernard C. Rossier,Richard P. Lifton,Richard P. Lifton +12 more
TL;DR: Investigation of affected offspring of consanguineous union reveals mutations in either the α or β subunits of the amiloride-sensitive epithelial sodium channel in five kindreds that demonstrate the molecular basis and explain the pathophysiology of this disease.
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A Syndrome of Apparent Mineralocorticoid Excess Associated with Defects in the Peripheral Metabolism of Cortisol
Stanley Ulick,L S Levine,Peter Gunczler,G Zanconato,Leyla C. Ramirez,W Rauh,Ariel Rösler,H L Bradlow,Maria I. New +8 more
TL;DR: The decrease in the MCR permitted the maintenance of normal cortisol plasma levels and normal glucocorticoid function at a diminished rate of secretion, and serves as a biochemical marker of this hypertensive syndrome.
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Treatment of men with paraphilia with a long-acting analogue of gonadotropin-releasing hormone.
Ariel Rösler,Eliezer Witztum +1 more
TL;DR: Continuous administration of triptorelin, a long-acting agonist analogue of gonadotropin-releasing hormone, together with supportive psychotherapy, may be an effective treatment for men with severe paraphilia.
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Mutations in the human CYP11B2 (aldosterone synthase) gene causing corticosterone methyloxidase II deficiency
TL;DR: Findings confirm that P450XIB2 is the major enzyme mediating oxidation at position 18 in the adrenal and suggest that a small amount of residual activity undetectable in in vitro assays is sufficient to synthesize normal amounts of aldosterone.
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High frequency of congenital adrenal hyperplasia (classic 11β‐hydroxylase deficiency) among Jews from Morocco
TL;DR: It is proposed that the mutation of 11 beta-hydroxylase deficiency in Jews from Morocco may have originated in either the ancient Jewish settlers or the native Berber tribes who lived in the region of the Atlas Mountains in the southern region of Morocco before the destruction of the Second Temple by the Romans.