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1 Albright hereditary osteodystrophy (AHO), a disorder cha
2 Albright hereditary osteodystrophy (AHO), an autosomal d
3 Albright's Hereditary Osteodystrophy (AHO) was the first
4 den Dystonia Rating Scale-Motor Scale, Barry Albright Dystonia Scale), disability (Burke Fahn Marsden
5 otal score of at least 3 points on the Barry-Albright Dystonia (BAD) scale, and no evidence of iron d
6 kinson's Disease Rating Scale (UPDRS), Barry-Albright Dystonia (BAD) scale, Schwab and England Activi
8 d hyperphosphatemia but without evidence for Albright hereditary osteodystrophy who has paternal unip
9 n the 1940s with the demonstration by Fuller Albright that treatment with oestrogen could reverse the
10 ings potentially have implications for human Albright hereditary osteodystrophy, a condition caused b
12 ha-inactivating mutations lead to obesity in Albright hereditary osteodystrophy (AHO) patients, but o
13 reports of mild heterotopic ossification in Albright's hereditary osteodystrophy (AHO) and a recent
18 ently, IPMNs have been described as a McCune-Albright syndrome-associated tumor, present in about 15%
19 of polyostotic fibrous dysplasia and McCune-Albright syndrome among patients operated on for presump
20 ts with fibrous dysplasia of bone and McCune-Albright syndrome generated more basal cAMP accumulation
22 utations) and hormone hypersecretion (McCune-Albright syndrome caused by gain-of-function mutations).
23 ary mucinous neoplasms (IPMNs) and in McCune-Albright syndrome, characterized by fibrous dysplasia, p
25 predisposing to pituitary neoplasias: McCune-Albright syndrome, multiple endocrine neoplasia type 1,
26 e of a syndromic IPMN as a feature of McCune-Albright syndrome, this observation is further evidence
28 Because of its similarities to the McCune-Albright syndrome and other features, such as paradoxica
31 nd bone age advancement in girls with McCune-Albright syndrome (MAS), despite ovarian enlargement.
33 have been identified in patients with McCune-Albright syndrome, but the mechanism leading to the spec
39 ors of this Special Feature, CSTL alumni Tom Albright and Jennifer Mnookin have recruited articles at
42 an homologue GNAS1, mutated in patients with Albright hereditary osteodystrophy, is also imprinted.