{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe provided abstracts focus on Williams syndrome and the effects of hemizygous deletions in the 7q11.23 region, emphasizing the role of genes such as CYLN2 in neurodevelopmental dysfunction. Notably, none of the excerpts mention SNORD116‐30 or any small nucleolar RNAs, and therefore they do not provide any direct or inferred information regarding the function or role of SNORD116‐30 in either neural development or the pathogenesis of Williams syndrome."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n \nIn the first abstract, the investigation centers on the consequences of CYLN2 haploinsufficiency in mice, which results in growth deficiencies, hippocampal dysfunction, and motor coordination deficits, alongside altered distribution of microtubule‐associated proteins. This study does not allude to any snoRNA, including SNORD116‐30."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n\nFurthermore, the second abstract discusses the contribution of several genes, particularly CYLN2 and GTF2IRD1, to the cognitive and motor deficits observed in Williams syndrome patients. The analysis of gene‐specific knockout mouse models reinforces the role of these genes in brain structure alterations and neural performance, yet it does not provide any data or mention regarding SNORD116‐30."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Casper C Hoogenraad, Bas Koekkoek, Anna Akhmanova, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Targeted mutation of Cyln2 in the Williams syndrome critical region links CLIP-115 haploinsufficiency to neurodevelopmental abnormalities in mice."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Nat Genet (2002)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/ng954"}], "href": "https://doi.org/10.1038/ng954"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12195424"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12195424"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "J M van Hagen, J N van der Geest, R S van der Giessen, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Contribution of CYLN2 and GTF2IRD1 to neurological and cognitive symptoms in Williams Syndrome."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Neurobiol Dis (2007)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.nbd.2006.12.009"}], "href": "https://doi.org/10.1016/j.nbd.2006.12.009"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "17270452"}], "href": "https://pubmed.ncbi.nlm.nih.gov/17270452"}]}]}]}