ライフサイエンスコーパス: Williams

1 Williams 82 individuals exhibited variation in the numbe

2 Williams 82, the soybean cultivar used to produce the re

3 Williams developed in his 1966 book Adaptation and Natur

4 Williams has suggested that the Earth's obliquity may ha

5 Williams syndrome (WMS) is a rare sporadic disorder that

6 Williams syndrome (WS) and 7q11.23 duplication syndrome

7 Williams syndrome (WS) is a complex developmental disord

8 Williams syndrome (WS) is a developmental disorder cause

9 Williams syndrome (WS) is a developmental disorder cause

10 Williams syndrome (WS) is a developmental disorder with

11 Williams syndrome (WS) is a developmental disorder with

12 Williams syndrome (WS) is a genetic condition characteri

13 Williams syndrome (WS) is a genetic disorder caused by a

14 Williams Syndrome (WS) is a neurodevelopment disorder as

15 Williams syndrome (WS) is a neurodevelopmental disorder

16 Williams syndrome (WS) is a neurogenetic-neurodevelopmen

17 Williams syndrome (WS) offers an exciting model for soci

18 Williams syndrome (WS), a genetic disorder caused by hem

19 Williams syndrome (WS), a genetic disorder resulting fro

20 Williams syndrome (WS), a rare disorder caused by a hemi

21 Williams syndrome (WS), caused by microdeletion of some

22 Williams syndrome is a complex developmental disorder th

23 Williams syndrome is also associated with specific neuro

24 Williams syndrome, caused by a hemizygous microdeletion

25 Williams' principle holds that, in order for an entity t

26 Williams-Beuren syndrome (also known as Williams syndrom

27 Williams-Beuren syndrome (WBS) is a developmental disord

28 Williams-Beuren syndrome (WBS) is a microdeletion disord

29 Williams-Beuren syndrome (WBS) is a neurodevelopmental d

30 Williams-Beuren syndrome (WBS), an autosomal dominant ge

31 Williams-Beuren syndrome (WBS), caused by a microdeletio

32 Williams-Beuren syndrome (WBS; OMIM 194050) is caused by

33 Williams-Beuren syndrome is a developmental multisystemi

34 Williams-Beuren syndrome is characterized by mild mental

35 n's syndrome (16%), Noonan's syndrome (15%), Williams' syndrome (12%), and 22q11.2 deletion syndrome

36 g module written by Goddard [1.], King [2.], Williams [3.], and Dean [4.] provides an overview of acc

37 .21 (48), 16p11.2 (autism, 34), and 7q11.23 (Williams-Beuren syndrome, 11).

38 used to perform in silico mapping on 80,700 Williams 82 BAC end sequences (BES).

39 sured with novel photoacoustic imaging and a Williams periodontal probe.

40 STSs) were anchored by PCR on a subset of a Williams 82 BstY I BAC library pooled into 208 pools in

41 uter-generated randomisation sequence with a Williams square design of size four to assign patients (

42 Gel-like dynamics with a Williams-Landel-Ferry temperature dependence then result

43 Application of activation, Williams-Landel-Ferry, and Rouse-Zimm models shows the m

44 dromes discussed include Angelman, Alagille, Williams, Langer-Giedeon, Prader-Willi, Smith-Magenis, M

45 Dodge LE, Ehrlich S, Meeker JD, Calafat AM, Williams PL, for the EARTH Study Team.

46 on-deficit-hyperactivity disorder (ADHD) and Williams syndrome.

47 t issue of Molecular Cell, Pidoux et al. and Williams et al. identify S. pombe Scm3 as the proximate

48 ssues of Neuron and Cell (Herrera et al. and Williams et al.).

49 viewpoints by Powers, Miller, and Cohen, and Williams and Dye, followed by a commentary by Fraser.

50 es relevant to autism spectrum disorders and Williams' syndrome.

51 h the genetic variations leading to FraX and Williams syndrome are different, important similarities

52 lopmental correlates, occur in both FraX and Williams syndrome including aberrant frontostriatal path

53 ular machinery and processes across FraX and Williams syndrome occur as well - microRNAs involved in

54 pmental morphologic feature between FraX and Williams syndrome.

55 al features of fragile X syndrome (FraX) and Williams syndrome and to review the putative neural and

56 Haroush and Williams trained pairs of monkeys to play in a prisoner'

57 characterized mainly by hyposociability, and Williams syndrome (WS), whose subjects exhibit hypersoci

58 Suwannee River humic acid (SRHA) and Williams Lake hydrophobic acid (WLHPoA) substantially en

59 e, Miller-Dieker lissencephaly syndrome, and Williams-Beuren syndrome--in which the deleted region en

60 sphere geometry was introduced by Vallee and Williams with the concept of entasis, which is frequentl

61 xample of Williams-Beuren syndrome (WBS) and Williams-Beuren region duplication syndrome to illustrat

62 y deleted regions of Prader-Willi, Angelman, Williams, Smith-Magenis, and DiGeorge/velocardiofacial s

63 SoyBase also contains the well-annotated 'Williams 82' genomic sequence and associated data mining

64 zygous mice (the same frizzled 9 genotype as Williams syndrome patients) were intermediate between wi

65 However, as Williams and Baum suggest in their Perspective, the disc

66 Williams-Beuren syndrome (also known as Williams syndrome) is caused by a deletion of a 1.55- to

67 condition or in syndromic conditions such as Williams-Beuren syndrome.

68 y exhibited gene content differences between Williams 82 individuals.

69 Genomic structural variation between Williams and Kingwa was maintained between the Williams

70 isite Langmuir model, augmented with a Bragg-Williams model for lateral interactions, to calculate ad

71 Combined with the Bragg-Williams/Langmuir model and taking into account the expe

72 etic determinants of cognition is offered by Williams syndrome (WS), a well-characterized hemideletio

73 traditional extra-binomial model proposed by Williams and can analyse both rare and common variants w

74 As proposed by Williams, we overcome the problem of susceptibility to o

75 As demonstrated earlier by Shilov, Cambie, Williams, Fahey, and others, alkenes can undergo a conce

76 q11.23, where the reciprocal deletion causes Williams-Beuren syndrome, characterized by a highly soci

77 y 25 genes on chromosome 7q11.23 that causes Williams syndrome (WS) includes genes that regulate cyto

78 7q11, the reciprocal of the deletion causing Williams-Beuren syndrome.

79 mygdala coupling, both of which characterize Williams' syndrome.

80 is normalization do not follow the classical Williams-Landel-Ferry (WLF) equation developed for long-

81 phenotype of the usually sporadic condition Williams syndrome.

82 troduction of PSS1 into the soybean cultivar Williams 82, the transgenic plants exhibited enhanced re

83 sciptome of seed development in the cultivar Williams, the reference cultivar for the first soybean g

84 BAC clones spanning this region in cultivar "Williams 82" [rps2, Rmd (adult onset), rj2].

85 rogen fixation with soybean (Glycine max cv. Williams 82).

86 Duplication (dup7q11.23) and deletion (Williams syndrome) of chromosomal region 7q11.23 cause n

87 ral, and gene content variation of different Williams 82 individuals.

88 iniscent of the human microdeletion disorder Williams-Beuren syndrome (WBS); craniofacial imaging rev

89 The neurodevelopmental disorder Williams-Beuren syndrome (WBS), is caused by a microdele

90 commonly deleted in the congenital disorder, Williams syndrome.

91 keletal dynamics and is a candidate gene for Williams' syndrome.

92 ngle genes have been identified, whereas for Williams and Langer-Giedion syndromes, more than one gen

93 e flavoenzyme described by S. Liao and H. G. Williams-Ashman, thus establishing their genetic identit

94 j4 genotypes, including the reference genome Williams 82.

95 tropy) in the somatic environment, as George Williams called for in 1957, and how they make the dispo

96 the oft-quoted evolutionary theorist George Williams, "It is remarkable that after a seemingly mirac

97 nd the least reduction in the placebo group (Williams test = 4.97, P < .01).

98 invariably deleted in the haploinsufficiency Williams-Beuren Syndrome.

99 tested reorientation in individuals who have Williams syndrome (WS), a genetic disorder that results

100 consisted of 5 learning tasks: detour, Hebb-Williams, radial maze, olfactory foraging, and fear cond

101 periments used 2 versions of a modified Hebb-Williams maze to test the role of the dorsal hippocampus

102 elf had significant positive effects on Hebb-Williams maze learning.

103 This study indicates that Hebb-Williams maze performance deficits after unilateral ento

104 adult, male Sprague-Dawley rats in the Hebb-Williams maze were examined at 6 months after unilateral

105 omposite ]) were compared by using Hotelling-Williams test.

106 t contains the Xenopus ortholog of the human Williams syndrome transcription factor (WSTF).

107 , we isolated a Xenopus homolog of the human Williams-Beuren syndrome critical region 11 (XWBSCR11),

108 on structure of the PHD motif from the human Williams-Beuren syndrome transcription factor (WSTF) pro

109 In Williams syndrome (WS), a deletion of approximately 1.5

110 Thus, in contrast to the conclusions in Williams et al., this could indeed be a "Rosetta stone"

111 ly flanking the interval commonly deleted in Williams syndrome have facilitated the identification of

112 by one of multiple genes that is deleted in Williams syndrome individuals, is the only currently kno

113 s one of about 20 genes typically deleted in Williams syndrome.

114 t the 7q11.23 region hemizygously deleted in Williams-Beuren syndrome (WBS), a complex multisystemic

115 b region on chromosome 7 which is deleted in Williams-Beuren syndrome (WBS).

116 SCR11), one of the genes commonly deleted in Williams-Beuren syndrome patients.

117 ome 7q11.23 that is hemizgygously deleted in Williams-Beuren syndrome, a multisystemic developmental

118 nce that the absence of one or more genes in Williams syndrome leads to highly circumscribed patholog

119 findings show that genetic heterogeneity in Williams 82 primarily originated from the differential s

120 localized failure of cortical maturation in Williams syndrome (WS), a genetic condition associated w

121 f primary visual cortex is grossly normal in Williams syndrome, consistent with the notion that neura

122 c valvular disease, such as that observed in Williams syndrome, and, as such, animal models involving

123 on of peripheral pulmonary stenosis (PPS) in Williams syndrome (WS) is limited.

124 Genetic/syndromic diagnoses included Williams syndrome (n=23), non-Williams familial arteriop

125 ed complex stability according to the Irving-Williams series (Mn(II) < Fe(II) < Ni(II) < Co(II) < Cu(

126 II) in vitro, thus diverging from the Irving-Williams series without requiring auxiliary factors such

127 For instance, as described in the Irving-Williams series, Cu(2+) and Zn(2+) typically form more s

128 l ion affinity trend suggested by the Irving-Williams series, demonstrating that this trend operates

129 Consistent with the Irving-Williams series, MncA only binds Mn(2+) after folding in

130 Co > Fe > Mg > Mn > Zn, following the Irving-Williams stability order.

131 isconsin, Madison, with Bob Alberty and Jack Williams, then at Oxford University with A.G. ("Sandy")

132 epsilon(omega, T), and a general Kohlrausch-Williams-Watts (KWW) form for time-domain relaxation.

133 onential functions as well as the Kohlrausch-Williams-Watts (KWW) stretched exponential model.

134 ng spectrum are analyzed with the Kohlrausch-Williams-Watts formalism, the exponent beta decreases wi

135 arameter was calculated using the Kohlrausch-Williams-Watts function and found to be 0.39.

136 al but were well described by the Kohlrausch-Williams-Watts model, from which a characteristic rate c

137 mbination was quantified with the Kohlrausch-Williams-Watts model.

138 ancing Translational Science, the Loughridge Williams Foundation, and the Betsy and Jonathan Blattmac

139 dissected seedlings of soybean (Glycine max 'Williams 82'), we show that genes involved in photosynth

140 Using G. max ([Williams 82/PI 518671]) as a reference, a G --> T(2,822)

141 al, but differ from the susceptible G. max ([Williams 82/PI 518671]) by the presence of several singl

142 548402]) allele in the susceptible G. max ([Williams 82/PI 518671]) genotype suppressed H. glycines

143 8402]) allele, but differs from the G. max ([Williams 82/PI 518671]) ortholog.

144 Overexpression of Gm-SYP38 rescues G. max [Williams 82/PI 518671], genetically rhg1 (-/-), by suppr

145 copy of a duplicated gene flanking the 2-Mb Williams-Beuren syndrome (WBS) common deletion at 7q11.2

146 With this in mind, Williams and co-workers developed a model that quantifie

147 ly 3.3 Mb of genomic sequence from the mouse Williams syndrome region, of which just over 1.4 Mb is f

148 noses included Williams syndrome (n=23), non-Williams familial arteriopathy (n=12), and Alagille synd

149 may help identify molecular determinants of Williams-Beuren syndrome.

150 tu hybridization, useful in the diagnosis of Williams syndrome.

151 A diagnosis of Williams-Beuren syndrome was made based on the microdele

152 e variation and key neural endophenotypes of Williams' syndrome and perhaps corticoamygdala regulatio

153 A new study uses the example of Williams-Beuren syndrome (WBS) and Williams-Beuren regio

154 VAS), and SVAS is also a frequent feature of Williams syndrome, where patients are hemizygous for ELN

155 s 82 genome sequence consists of a mosaic of Williams and Kingwa haplotypes.

156 ation of a girl with a clinical phenotype of Williams-Beuren syndrome, associated with unilateral ant

157 d faster than that for the infrared probe of Williams et al., which measures the average helix conten

158 1.23 near the telomeric duplicated region of Williams-Beuren syndrome, a developmental disorder affec

159 of SVAS is quite variable, both in series of Williams syndrome patients and within SVAS kindreds, sug

160 ween these variants and neural signatures of Williams' syndrome in a normal population, using functio

161 e that should catalyze additional studies of Williams syndrome, including those that aim to character

162 tested), a prevalence comparable to that of Williams, Angelman and Prader-Willi syndromes.

163 RECENT FINDINGS: Research on Williams syndrome is taken as a model, used to demonstra

164 onor parent Kingwa into the recurrent parent Williams.

165 ns identical to those of C. diphtheriae Park-Williams No. 8 (tox type 1).

166 emizygous deletion in a patient with partial Williams syndrome suggests that loss of the LIM-Kinase1

167 hared and symmetrically opposite phenotypes--Williams-Beuren syndrome and 7q-microduplication syndrom

168 Previously, Williams et al. showed that the binding of this antibody

169 Disorder (ASD), Prader-Willi Syndrome (PWS), Williams Syndrome (WS) and Fragile X syndrome (FXS).

170 yrin framework (UNLPF-10) consisting of rare Williams beta-tetrakaidecahedral cages was constructed u

171 ions of genomic heterogeneity, the reference Williams 82 genome sequence consists of a mosaic of Will

172 in', 'Eilon', 'Gruesa', 'Silver', 'Ricasa', 'Williams' and 'Zelig') was studied by gas chromatography

173 Rickey Williams provides a report on office economics that incl

174 DT-laced coating marketed in 1946 by Sherwin-Williams Research Laboratories.

175 Since Williams syndrome is associated with severe visuospatial

176 for human cognitive development, we studied Williams syndrome (WS), a developmental disorder that in

177 In a recent study, Williams and colleagues report that plant Guard receptor

178 article ends with a quotation from Tennessee Williams that reflects the theater, which has given me s

179 The Williams Syndrome Transcription Factor (WSTF), the produ

180 The Williams' nonbonded parameters combined with partial cha

181 lliams and Kingwa was maintained between the Williams 82 individuals within the regions of heterogene

182 commonly deleted in patients affected by the Williams-Beuren syndrome, which is a complex neurodevelo

183 are associated with a cognitive defect, the Williams-Beuren cognitive profile.

184 ts, some of which may be responsible for the Williams syndrome phenotype.

185 actor family and are prime candidates in the Williams syndrome, a complex neurodevelopmental disorder

186 rizzled gene, FZD3, now renamed FZD9, in the Williams-Beuren syndrome (WBS) deletion region at chromo

187 niofacial and cognitive abnormalities in the Williams-Beuren syndrome.

188 These include the Williams-Landel-Ferry model, the activation model, and t

189 eoselectively is a Lewis acid variant of the Williams' three-component coupling.

190 we determined the expression profile of the Williams-Beuren syndrome critical region-deleted genes a

191 ISWI, and WCRF180, a protein related to the Williams syndrome transcription factor.

192 ygous microdeletion distally adjacent to the Williams-Beuren syndrome region on chromosome 7q11.23.

193 of the primate-specific inversion within the Williams-Beuren syndrome critical region.

194 a common symptom in patients with tinnitus, Williams syndrome, autism, and other neurologic diseases

195 ply with increasing temperature according to Williams-Landel-Ferry (WLF) behavior.

196 at haploinsufficiency in BEN is causative to Williams-Beuren syndrome, these results may further lead

197 pment and suggest how it could contribute to Williams-Beuren syndrome.

198 a patient with deletion of elastin owing to Williams-Beuren syndrome.

199 FZD9 (Frizzled9), a Wnt receptor related to Williams syndrome, is localized in the postsynaptic regi

200 7q11.23, usually associated with the typical Williams-Beuren syndrome.

201 Unlike Williams syndrome, we found no chromosomal inversions fl

202 the yellow seeds produced by the unmodified Williams 82 parental cultivar.

203 The Vaughn Williams classification divides antiarrhythmic agents in

204 region on 1q21.1 and duplication at the WBS (Williams-Beuren syndrome) region at 7q11.23.

205 cortex (V1) in high-functioning adults with Williams syndrome and age- and IQ-matched control partic

206 cardiovascular complications associated with Williams-Beuren syndrome and isolated supravalvular aort

207 ntribute to certain deficits associated with Williams-Beuren syndrome.

208 ogy of intellectually disabled children with Williams (WS) syndrome and its relationship to the behav

209 nd voice hoarsening in a baby diagnosed with Williams-Beuren syndrome that was born premature and req

210 The association of the Limk1 gene with Williams Syndrome indicates that proteins of this family

211 ndaries were more variable in the group with Williams syndrome.

212 l and ventral streams among individuals with Williams syndrome (WS) compared with two control groups

213 Individuals with Williams syndrome are hemizygous for the elastin gene, o

214 and deleted hemizygously in individuals with Williams syndrome, a dominant genetic condition characte

215 is deleted hemizygously in individuals with Williams Syndrome, an autosomal dominant genetic conditi

216 nation between controls and individuals with Williams, Smith-Magenis, 22q11 deletion, or Noonan syndr

217 dings from two experiments with infants with Williams syndrome (a phenotype selected to bolster innat

218 ners given impoverished input, learners with Williams syndrome, specific language-impaired learners,

219 al and behavioral phenotype of patients with Williams syndrome.

220 rtic stenosis (SVAS), and five patients with Williams-Beuren syndrome (WBS).

221 or both proteins are deleted in persons with Williams-Beuren syndrome, who often manifest muscle weak

222 ties in the cerebral cortex of subjects with Williams syndrome (WS), a genetically based developmenta

223 ) Ogston, and finally back at Wisconsin with Williams and Lou Gosting.

224 one variant H2A.X is phosphorylated by WSTF (Williams-Beuren syndrome transcription factor), a compon

225 a new regulatory mechanism mediated by WSTF (Williams-Beuren syndrome transcription factor, also know