01958nam0 2200409 i 450 CFI030965420231121125450.08813195060IT96-2472 19990920d1995 ||||0itac50 baitaitz01i xxxe z01nCittadinanza europea e extracomunitari: il fenomeno dell'immigrazione nel processo di integrazione europeaa cura di Anna Bedeschi e Gigliola LanducciPadovaCEDAM1995VIII, 378 p.24 cmUniversità degli studi di Padova, Dipartimento di studi internazionali7Relazioni presentate al Convegno tenuto a Padova nel 1993.Tit. sul dorso: Cittadinanza europea e extracomunitari.CFI0310487001CFI01172422001 Università degli studi di Padova, Dipartimento di studi internazionali771201Università degli studi di Padova : Dipartimento di studi internazionaliCFIV077905Cittadinanza europea e extracomunitari.CFI0310487Diritto internazionaleFIRRMLC002887IPaesi della Comunita economica europeaImmigrazioneFIRRMLC124966I304.8421Landucci, GigliolaMILV075930Bedeschi Magrini, AnnaMILV158332Bedeschi, AnnaCFIV166190Bedeschi Magrini, AnnaITIT-0119990920IT-RM0289 IT-FR0098 Biblioteca Statale A. BaldiniRM0289 Biblioteca Area Giuridico EconomicaFR0098 CFI0309654Biblioteca Area Giuridico Economica 53DSG 07/0154 53VM 0000222505 VM barcode:19451-10. - Inventario:2502VMA 2001042320121204 04 53Cittadinanza europea e extracomunitari690377UNICAS02992nam 2200421z- 450 991022004300332120210211(CKB)3800000000216347(oapen)https://directory.doabooks.org/handle/20.500.12854/46856(oapen)doab46856(EXLCZ)99380000000021634720202102d2016 |y 0engurmn|---annantxtrdacontentcrdamediacrrdacarrierEssential Pathways and Circuits of Autism PathogenesisFrontiers Media SA20161 online resource (181 p.)Frontiers Research Topics2-88919-905-3 The Centers for Disease Control and Prevention estimate that 1 in 68 children in the United states is afflicted with autism spectrum disorders (ASD), yet at this time, there is no cure for the disease. Autism is characterized by delays in the development of many basic skills, most notably the ability to socialize and adapt to novelty. The condition is typically identified in children around 3 years of age, however the high heritability of autism suggests that the disease process begins at conception. The identification of over 500 ASD risk genes, has enabled the molecular genetic dissection of the pathogenesis of the disease in model organisms such as mice. Despite the genetic heterogeneity of ASD etiology, converging evidence suggests that these disparate genetic lesions may result in the disruption of a limited number of key biochemical pathways or circuits. Classification of patients into groups by pathogenic rather than etiological categories, will likely aid future therapeutic development and clinical trials. In this set of papers, we explore the existing evidence supporting this view. Specifically, we focus on biochemical cascades such as mTOR and ERK signaling, the mRNA network bound by FMRP and UBE3A, dorsal and ventral striatal circuits, cerebellar circuits, hypothalamic projections, as well as prefrontal and anterior cingulate cortical circuits. Special attention will be given to studies that demonstrate the necessity and/or sufficiency of genetic disruptions (e.g. by molecular deletion and/or replacement) in these pathways and circuits for producing characteristic behavioral features of autism. Necessarily these papers will be heavily weighted towards basic mechanisms elucidated in animal models, but may also include investigations in patients.NeurosciencesbicsscCell signalingCerebellumHypothalamusmTORNeurodevelopmental disordersOxytocinStriatumNeurosciencesGul Dolenauth1331049Mustafa SahinauthBOOK9910220043003321Essential Pathways and Circuits of Autism Pathogenesis3040073UNINA