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1 pmental morphologic feature between FraX and Williams syndrome.
2 ndaries were more variable in the group with Williams syndrome.
3 on-deficit-hyperactivity disorder (ADHD) and Williams syndrome.
4 al and behavioral phenotype of patients with Williams syndrome.
5 s one of about 20 genes typically deleted in Williams syndrome.
6 commonly deleted in the congenital disorder, Williams syndrome.
7 phenotype of the usually sporadic condition Williams syndrome.
8 tu hybridization, useful in the diagnosis of Williams syndrome.
9 es relevant to autism spectrum disorders and Williams' syndrome.
10 mygdala coupling, both of which characterize Williams' syndrome.
11 keletal dynamics and is a candidate gene for Williams' syndrome.
12 n's syndrome (16%), Noonan's syndrome (15%), Williams' syndrome (12%), and 22q11.2 deletion syndrome
13 dings from two experiments with infants with Williams syndrome (a phenotype selected to bolster innat
14 actor family and are prime candidates in the Williams syndrome, a complex neurodevelopmental disorder
15 and deleted hemizygously in individuals with Williams syndrome, a dominant genetic condition characte
16 is deleted hemizygously in individuals with Williams Syndrome, an autosomal dominant genetic conditi
17 cortex (V1) in high-functioning adults with Williams syndrome and age- and IQ-matched control partic
18 al features of fragile X syndrome (FraX) and Williams syndrome and to review the putative neural and
19 e variation and key neural endophenotypes of Williams' syndrome and perhaps corticoamygdala regulatio
20 c valvular disease, such as that observed in Williams syndrome, and, as such, animal models involving
21 h the genetic variations leading to FraX and Williams syndrome are different, important similarities
23 a common symptom in patients with tinnitus, Williams syndrome, autism, and other neurologic diseases
25 f primary visual cortex is grossly normal in Williams syndrome, consistent with the notion that neura
26 ly flanking the interval commonly deleted in Williams syndrome have facilitated the identification of
27 ween these variants and neural signatures of Williams' syndrome in a normal population, using functio
28 lopmental correlates, occur in both FraX and Williams syndrome including aberrant frontostriatal path
29 e that should catalyze additional studies of Williams syndrome, including those that aim to character
31 by one of multiple genes that is deleted in Williams syndrome individuals, is the only currently kno
37 FZD9 (Frizzled9), a Wnt receptor related to Williams syndrome, is localized in the postsynaptic regi
38 nce that the absence of one or more genes in Williams syndrome leads to highly circumscribed patholog
40 ular machinery and processes across FraX and Williams syndrome occur as well - microRNAs involved in
42 of SVAS is quite variable, both in series of Williams syndrome patients and within SVAS kindreds, sug
43 zygous mice (the same frizzled 9 genotype as Williams syndrome patients) were intermediate between wi
45 ly 3.3 Mb of genomic sequence from the mouse Williams syndrome region, of which just over 1.4 Mb is f
46 ners given impoverished input, learners with Williams syndrome, specific language-impaired learners,
47 emizygous deletion in a patient with partial Williams syndrome suggests that loss of the LIM-Kinase1
52 VAS), and SVAS is also a frequent feature of Williams syndrome, where patients are hemizygous for ELN
55 Disorder (ASD), Prader-Willi Syndrome (PWS), Williams Syndrome (WS) and Fragile X syndrome (FXS).
56 l and ventral streams among individuals with Williams syndrome (WS) compared with two control groups
57 y 25 genes on chromosome 7q11.23 that causes Williams syndrome (WS) includes genes that regulate cyto
71 for human cognitive development, we studied Williams syndrome (WS), a developmental disorder that in
72 localized failure of cortical maturation in Williams syndrome (WS), a genetic condition associated w
75 tested reorientation in individuals who have Williams syndrome (WS), a genetic disorder that results
76 ties in the cerebral cortex of subjects with Williams syndrome (WS), a genetically based developmenta
78 etic determinants of cognition is offered by Williams syndrome (WS), a well-characterized hemideletio
80 characterized mainly by hyposociability, and Williams syndrome (WS), whose subjects exhibit hypersoci
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