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Autor:
Lucignani G. 1, Panzacchi A. 2, Bosio L. 2, Moresco R.M. 2, 3, Ravasi L. 1, Coppa I. 2, Chiumello G. 2, 4, Frey K. 5, Koeppe R. 5, Fazio F. 2
Publikováno v:
NeuroImage (Orlando Fla., Print) 22 (2004): 22–28. doi:10.1016/j.neuroimage.2003.10.050
info:cnr-pdr/source/autori:Lucignani G. 1, Panzacchi A. 2, Bosio L. 2, Moresco R.M. 2,3, Ravasi L. 1, Coppa I. 2, Chiumello G. 2,4, Frey K. 5, Koeppe R. 5, Fazio F. 2,3/titolo:GABAA receptor abnormalities in prader-willi syndrome assessed with positron emission tomography and [11C]flumazenil./doi:10.1016%2Fj.neuroimage.2003.10.050/rivista:NeuroImage (Orlando Fla., Print)/anno:2004/pagina_da:22/pagina_a:28/intervallo_pagine:22–28/volume:22
info:cnr-pdr/source/autori:Lucignani G. 1, Panzacchi A. 2, Bosio L. 2, Moresco R.M. 2,3, Ravasi L. 1, Coppa I. 2, Chiumello G. 2,4, Frey K. 5, Koeppe R. 5, Fazio F. 2,3/titolo:GABAA receptor abnormalities in prader-willi syndrome assessed with positron emission tomography and [11C]flumazenil./doi:10.1016%2Fj.neuroimage.2003.10.050/rivista:NeuroImage (Orlando Fla., Print)/anno:2004/pagina_da:22/pagina_a:28/intervallo_pagine:22–28/volume:22
Prader-Willi syndrome (PWS) is a multi-system disorder characterized clinically by abnormal mental and physical development. PWS patients have a deletion in an imprinted region on paternal chromosome 15 (15q11-13), maternal disomy for this segment, o