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1 disorders such as schizophrenia, autism, and Williams syndrome.
2 and effects of specific genes hemideleted in Williams syndrome.
3 the general population and individuals with Williams syndrome.
4 pmental morphologic feature between FraX and Williams syndrome.
5 ndaries were more variable in the group with Williams syndrome.
6 on-deficit-hyperactivity disorder (ADHD) and Williams syndrome.
7 al and behavioral phenotype of patients with Williams syndrome.
8 s one of about 20 genes typically deleted in Williams syndrome.
9 commonly deleted in the congenital disorder, Williams syndrome.
10 phenotype of the usually sporadic condition Williams syndrome.
11 tu hybridization, useful in the diagnosis of Williams syndrome.
12 Dravet, Fragile X, Prader-Willi, Turner, and Williams syndromes.
13 es relevant to autism spectrum disorders and Williams' syndrome.
14 mygdala coupling, both of which characterize Williams' syndrome.
15 keletal dynamics and is a candidate gene for Williams' syndrome.
16 n's syndrome (16%), Noonan's syndrome (15%), Williams' syndrome (12%), and 22q11.2 deletion syndrome
17 dings from two experiments with infants with Williams syndrome (a phenotype selected to bolster innat
18 actor family and are prime candidates in the Williams syndrome, a complex neurodevelopmental disorder
19 nd 9 years of age, as well as 46 adults with Williams syndrome, a developmental disorder with known i
20 and deleted hemizygously in individuals with Williams syndrome, a dominant genetic condition characte
21 o develop than scene categorization, and (2) Williams syndrome adults are impaired in visually guided
22 cumscribed set of genes that are affected in Williams syndrome, along with the well-characterized neu
23 is deleted hemizygously in individuals with Williams Syndrome, an autosomal dominant genetic conditi
24 cortex (V1) in high-functioning adults with Williams syndrome and age- and IQ-matched control partic
25 ed for effects of the LIMK1 gene, deleted in Williams syndrome and important for neuronal maturation
26 al features of fragile X syndrome (FraX) and Williams syndrome and to review the putative neural and
27 e variation and key neural endophenotypes of Williams' syndrome and perhaps corticoamygdala regulatio
28 factors (TFs) among the 28 genes deleted in Williams syndrome, and prior mouse models of each TF sho
29 c valvular disease, such as that observed in Williams syndrome, and, as such, animal models involving
30 h the genetic variations leading to FraX and Williams syndrome are different, important similarities
32 a common symptom in patients with tinnitus, Williams syndrome, autism, and other neurologic diseases
33 edback improved learning in individuals with Williams syndrome but not in typically developing contro
35 e menopause, Down syndrome, Turner syndrome, Williams syndrome, chronic fatigue syndrome, IgA nephrop
36 rsonality that typify Williams syndrome, the Williams syndrome cohort exhibited opposite patterns of
37 = 510) were performed: (i) 20 children with Williams syndrome compared to 20 age- and sex-matched ty
38 f primary visual cortex is grossly normal in Williams syndrome, consistent with the notion that neura
39 ly flanking the interval commonly deleted in Williams syndrome have facilitated the identification of
40 ween these variants and neural signatures of Williams' syndrome in a normal population, using functio
41 functional connectivity in individuals with Williams syndrome, in whom LIMK1 is hemideleted, with ty
42 lopmental correlates, occur in both FraX and Williams syndrome including aberrant frontostriatal path
43 e that should catalyze additional studies of Williams syndrome, including those that aim to character
45 by one of multiple genes that is deleted in Williams syndrome individuals, is the only currently kno
52 FZD9 (Frizzled9), a Wnt receptor related to Williams syndrome, is localized in the postsynaptic regi
53 nce that the absence of one or more genes in Williams syndrome leads to highly circumscribed patholog
55 ular machinery and processes across FraX and Williams syndrome occur as well - microRNAs involved in
57 of SVAS is quite variable, both in series of Williams syndrome patients and within SVAS kindreds, sug
58 zygous mice (the same frizzled 9 genotype as Williams syndrome patients) were intermediate between wi
60 be structurally and functionally altered in Williams syndrome, providing a target for investigating
61 ly 3.3 Mb of genomic sequence from the mouse Williams syndrome region, of which just over 1.4 Mb is f
62 eported SCIN reduction, such as Tourette and Williams syndromes.SIGNIFICANCE STATEMENT Selecting the
63 ners given impoverished input, learners with Williams syndrome, specific language-impaired learners,
64 emizygous deletion in a patient with partial Williams syndrome suggests that loss of the LIM-Kinase1
65 ment and hypersocial personality that typify Williams syndrome, the Williams syndrome cohort exhibite
66 vity were calculated comparing children with Williams syndrome to matched typically developing childr
72 nectivity patterns similar to those found in Williams syndrome were associated with sequence variatio
73 VAS), and SVAS is also a frequent feature of Williams syndrome, where patients are hemizygous for ELN
76 Disorder (ASD), Prader-Willi Syndrome (PWS), Williams Syndrome (WS) and Fragile X syndrome (FXS).
77 l and ventral streams among individuals with Williams syndrome (WS) compared with two control groups
79 man deletions make the positive sociality of Williams syndrome (WS) ideal for determining transcripti
80 y 25 genes on chromosome 7q11.23 that causes Williams syndrome (WS) includes genes that regulate cyto
99 for human cognitive development, we studied Williams syndrome (WS), a developmental disorder that in
100 localized failure of cortical maturation in Williams syndrome (WS), a genetic condition associated w
103 tested reorientation in individuals who have Williams syndrome (WS), a genetic disorder that results
104 ties in the cerebral cortex of subjects with Williams syndrome (WS), a genetically based developmenta
107 etic determinants of cognition is offered by Williams syndrome (WS), a well-characterized hemideletio
110 vestigated laterality in a genetic disorder, Williams Syndrome (WS), caused by ~ 27 deleted genes on
111 tic syndromes such as Down syndrome (DS) and Williams syndrome (WS), difficulties with executive func
112 characterized mainly by hyposociability, and Williams syndrome (WS), whose subjects exhibit hypersoci
114 (DS; N = 557; Mage = 16.52; 233 female) and Williams syndrome (WS, N = 247; Mage = 18.43; 113 female