ライフサイエンスコーパス: ITD

1 ITD Assembler identified the highest percentage of repor

2 ITD Assembler is a very sensitive tool which can detect

3 ITD is a rare autosomal disorder that, if not treated pr

4 T3-ITDs to address this issue, including 114 ITDs with additional nucleotides of unknown origin locat

5 ection algorithms, and discovered additional ITDs in FLT3, KIT, CEBPA, WT1 and other genes.

6 ts without unfavorable cytogenetics or aFLT3-ITD mutation.

7 0.05 to 0.7) of mutant to wild-type alleles (ITD [high] and ITD [low], respectively).

8 mutant to wild-type alleles (ITD [high] and ITD [low], respectively).

9 TD rate of change across azimuth (ITDrc) and ITD variability over time (ITDv) were combined in a Fish

10 nteraural mismatches in frequency tuning and ITD tuning during in vivo loose-patch (juxtacellular) re

11 On average, ITD sensitivity was best for pulse rates near 80-160 pul

12 between frequency tuning mismatches and best ITDs.

13 The broad distributions of best ITDs within narrow frequency bands were not consistent w

14 (c) HAs altered the relationship between ITDs and ILDs, introducing large ITD-ILD conflicts in so

15 In birds, ITDs are mapped in an orderly array or place code, where

16 ground noise, degrading the fidelity of both ITD and ILD cues.

17 control operates in a similar manner on both ITD- and ILD-sensitive neurons, suggesting a shared mech

18 basis for this degradation, we characterized ITD tuning of single neurons in the inferior colliculus

19 Cortical ITD processing in children with simultaneous bilateral C

20 hypothyroidism due to I(-) transport defect (ITD).

21 tance through an impedance threshold device (ITD) on orthostatic tolerance in patients with postural

22 ICANCE STATEMENT Interaural time difference (ITD) is an important cue for sound localization, and the

23 Through study of interaural time difference (ITD) processing, the functional properties of neurons ca

24 stigated whether interaural time difference (ITD) statistics inherent in natural acoustic scenes are

25 to its own best interaural time difference (ITD), indicating the presence of an internal delay, a di

26 ght ears, called interaural time difference (ITD).

27 ng the two ears [interaural time difference (ITD)] to identify where the sound is coming from.

28 larly interaural time and level differences (ITD and ILD)-that correlate with sound-source locations.

29 ed of interaural time and level differences (ITD/ILD), which are the timing and intensity differences

30 amely interaural time and level differences (ITDs and ILDs), can be compromised by device processing.

31 Sensitivity to interaural time differences (ITDs) conveyed in the temporal fine structure of low-fre

32 Accurate use of interaural time differences (ITDs) for spatial hearing may require access to bilatera

33 Detection of interaural time differences (ITDs) is crucial for sound localization in most vertebra

34 sensitivity to interaural time differences (ITDs) is still poorer than normal.

35 ate sounds, ie, interaural time differences (ITDs), interaural level differences (ILDs), and pinna sp

36 nd direction: interaural timing differences (ITDs), interaural level differences (ILDs) and the direc

37 ironmental samples, intratypic differential (ITD) by PCR, and sequencing of the VP1 region to disting

38 rained listeners appear able to discriminate ITDs extremely well, even at modulation rates well beyon

39 ata thus suggest that axonal delays dominate ITD tuning.SIGNIFICANCE STATEMENT Neurons in the medial

40 AML) and a FLT3 internal tandem duplication (ITD) have poor outcomes to current treatment.

41 leukemia is the internal tandem duplication (ITD) in FLT3, the receptor for cytokine FLT3 ligand (FLT

42 a (AML) when an internal tandem duplication (ITD) in the fms-related tyrosine kinase 3 gene (FLT3) is

43 e identified an internal tandem duplication (ITD) in the switch II domain of NRAS from a patient with

44 receptor (FLT3) internal tandem duplication (ITD) is found in 30% of acute myeloid leukemia (AML) and

45 sized that FLT3/internal tandem duplication (ITD) leukemia cells exhibit mechanisms of intrinsic sign

46 domain (TKD) or internal tandem duplication (ITD) mutation with either a high ratio (>0.7) or a low r

47 containing FLT3 internal tandem duplication (ITD) mutations.

48 Although FLT3-internal tandem duplication (ITD) was an adverse risk factor for historical ATRA/chem

49 eliminate FLT3/internal tandem duplication (ITD)(+) LSCs.

50 resence of FLT3-internal tandem duplication (ITD), and a < 4-log reduction in PB-MRD were significant

51 referred to as internal tandem duplication (ITD), remains challenging due to inefficiencies in align

52 kinase 3 (FLT3)-internal tandem duplication (ITD), which mediate resistance to acute myeloid leukemia

53 ccur with FLT3 internal tandem duplications (ITD) or, less commonly, NRAS or KRAS mutations.

54 ion of somatic internal tandem duplications (ITDs) clustering in the C terminus of BCOR in 23 of 27 (

55 harboring FLT3 internal tandem duplications (ITDs) have poor outcomes, in particular AML with a high

56 Internal tandem duplications (ITDs) in the FLT3 receptor tyrosine kinase are common mu

57 ely activating internal tandem duplications (ITDs) of the FLT3 receptor tyrosine kinase.

58 s without FLT3-internal tandem duplications (ITDs; NPM1-positive/FLT3-ITD-negative genotype) are clas

59 those with FLT3 internal tandem duplications(ITDs) had significantly poorer outcome (hazard ratio [HR

60 We recorded IC neurons sensitive to either ITDs or ILDs in anesthetized guinea pig, before, during,

61 ion, and the optimal strategies for encoding ITD in neuronal populations are the subject of ongoing d

62 w-pass characteristics observed for envelope ITD processing is carrier-frequency dependent.

63 aused distortions of high-frequency envelope ITDs and significantly reduced interaural coherence.

64 dial portion had lower CO activity and fewer ITD-sensitive neurons.

65 Flt3(ITD) mice showed enhanced capacity to support T cell pro

66 Flt3(ITD) mutations and Tet2 loss cooperatively remodeled DNA

67 Cooperative interactions between Flt3(ITD) and Runx1 mutations are also blunted in fetal/neona

68 red gene expression profile in Npm1(cA);Flt3(ITD) , but not Npm1(cA/+);Nras(G12D/+) , progenitors com

69 However, Npm1(cA);Flt3(ITD) mutants displayed significantly higher peripheral l

70 und Npm1(cA/+);Nras(G12D/+) or Npm1(cA);Flt3(ITD) share a number of features: Hox gene overexpression

71 we show that Flt3(ITD) and cooperating Flt3(ITD)/Runx1 mutations cause hematopoietic stem cell deple

72 with Flt3 internal tandem duplication (Flt3(ITD)) leukaemic mutations to accelerate leukaemogenesis,

73 The FLT3 Internal Tandem Duplication (FLT3(ITD)) mutation is common in adult acute myeloid leukemia

74 cause they are not competent to express FLT3(ITD) target genes.

75 in the FMS-like tyrosine kinase 3 gene (Flt3(ITD)) and the nucleophosmin gene (Npm1(c)) to induce AML

76 intrinsic, and was further enhanced in Flt3(ITD/ITD) mice.

77 sitizes progenitors to the leukemogenic FLT3(ITD) mutation.

78 In adult progenitors, FLT3(ITD) simultaneously induces self-renewal and myeloid com

79 Multipotent Tet2(-/-);Flt3(ITD) progenitors (LSK CD48(+)CD150(-)) propagate disease

80 Here we show that Flt3(ITD) and cooperating Flt3(ITD)/Runx1 mutations cause hem

81 Pre-leukemic mice with the Flt3(ITD) knock-in allele manifested an expansion of classica

82 While FLT3(ITD) can activate STAT5 signal transduction prior to bir

83 FLT3-ITD AML patients treated with AC220 developed increased

84 FLT3-ITD directly impacts on RUNX1 activity, whereby up-regul

85 FLT3-ITD expressing cell lines have been shown to generate in

86 FLT3-ITD molecules were detectable within autophagosomes afte

87 FLT3-ITD N-regions have a G/C content (66.9%), dinucleotide c

88 FLT3-ITD(+) acute myeloid leukemia (AML) accounts for approxi

89 FLT3-ITD(+) AML drug resistance is attenuated by LCL-461, a m

90 the FLT3 gene is not mutated, exhibit a FLT3-ITD signature of gene expression.

91 yrosine kinase 3 gene (FLT3) is absent (FLT3-ITD(neg)) or present with a low allelic ratio (FLT3-ITD(

92 Moreover, activating FLT3-ITD signaling in crenolanib-resistant AML cells suppress

93 Constitutively active FLT3-ITD promotes the expansion of transformed progenitors, b

94 imized for cytotoxic activities against FLT3-ITD mutant cancer cells.

95 Cox-model of predefined variables, age, FLT3-ITD and >1 course of chemotherapy to reach CR were risk

96 tients with an MLL rearrangement and an FLT3-ITD.

97 we investigated the impact of RUNX1 and FLT3-ITD coexpression.

98 ed Hhex as a direct target of RUNX1 and FLT3-ITD stimulation and confirmed high HHEX expression in FL

99 bitory activities in FLT3-ITD-D835V and FLT3-ITD-F691L cells which were resistant to quizartinib.

100 CS2, was investigated using MLL-AF9 and Flt3-ITD/NPM1c driven mouse models of AML.

101 ly targets FLT3 D835 mutants as well as FLT3-ITD.

102 We show that AML samples bearing FLT3-ITD mutations are more sensitive to proteasome inhibitor

103 id ceramide generation is suppressed by FLT3-ITD signaling.

104 patients with a common mutation called FLT3-ITD.

105 y diagnosed AML and centrally confirmed FLT3-ITD were eligible: 284 patients were treated, including

106 ELN) recommendations defined 4 distinct FLT3-ITD genotypes based on the ITD AR and the NPM1 mutationa

107 ion of autophagy in vivo, downregulated FLT3-ITD protein expression and improved overall survival.

108 e kinase 3-internal tandem duplication (FLT3-ITD) at arginines 972 and 973 by protein arginine N-meth

109 FLT3 internal tandem duplication (FLT3-ITD) is an activating mutation found in 20-30% of patien

110 s the FLT3-internal tandem duplication (FLT3-ITD) mutation.

111 ation, the internal tandem duplication (FLT3-ITD) mutation.

112 ctory FLT3 internal tandem duplication (FLT3-ITD)-positive acute myeloid leukaemia have a poor progno

113 e kinase 3 internal tandem duplication (FLT3-ITD)-positive AML, BTK mediates FLT3-ITD-dependent Myc a

114 and FLT3 internal tandem duplications (FLT3-ITD).

115 We showed that 32D cells that express FLT3-ITD have a higher level of both oxidized DNA and DNA DSB

116 ty in internal tandem duplication FLT3 (FLT3-ITD) and JAK2V617F-mutated cells.

117 being developed as targeted therapy for FLT3-ITD(+) acute myeloid leukemia; however, their use is com

118 risk of relapse and death after HCT for FLT3-ITD-positive AML.

119 in the FMS-like tyrosine kinase 3 gene (FLT3-ITD) have a poor prognosis, frequently relapse, and die

120 ty is strongly correlated with a higher FLT3-ITD allelic burden.

121 However, the molecular basis of how FLT3-ITD-driven ROS leads to the aggressive form of AML is no

122 Functional studies in human FLT3-ITD+ cell lines showed that BMX is part of a compensator

123 ve the efficacy of kinase inhibitors in FLT3-ITD acute myeloid leukemia (AML).

124 F2, to improve the depth of response in FLT3-ITD AML.

125 n and confirmed high HHEX expression in FLT3-ITD AMLs.

126 c fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear bo

127 ed the myeloproliferative phenotypes in FLT3-ITD knock-in mice, and significantly prolonged the survi

128 Further, inhibition of miR-155 in FLT3-ITD(+) AML cell lines using CRISPR/Cas9, or primary FLT3

129 mitophagy in response to crenolanib in FLT3-ITD(+) AML cells expressing stable shRNA against endogen

130 R-155) is specifically overexpressed in FLT3-ITD(+) AML compared with FLT3 wild-type (FLT3-WT) AML an

131 owed excellent inhibitory activities in FLT3-ITD-D835V and FLT3-ITD-F691L cells which were resistant

132 activation of the PI3K/mTOR pathway in FLT3-ITD-dependent AML results in resistance to drugs targeti

133 JI6 effectively inhibited FLT3-ITD-containing MV4-11 cells and HCD-57 cells transformed

134 cation of the FMS-like tyrosine kinase (FLT3-ITD) receptor is present in 20% of acute myeloid leukemi

135 Mechanistically, FLT3-ITD targeting induced ceramide accumulation on the outer

136 n (FLT3-ITD)-positive AML, BTK mediates FLT3-ITD-dependent Myc and STAT5 activation, and combined tar

137 omposite complete remission <=6 months) FLT3-ITD acute myeloid leukaemia after standard therapy with

138 was recapitulated in an in vivo murine FLT3-ITD-positive (FLT3-ITD+) model of sorafenib resistance.

139 nsively treated patients with NPM1(mut)/FLT3-ITD(neg/low) AML who were prospectively enrolled in regi

140 Among 2,426 patients with NPM1(mut)/FLT3-ITD(neg/low) AML, 2,000 (82.4%) had a normal and 426 (17

141 In patients with NPM1(mut)/FLT3-ITD(neg/low) AML, adverse cytogenetics were associated w

142 ly associated with outcome in NPM1(mut)/FLT3-ITD(neg/low) AML.

143 inates over molecular risk in NPM1(mut)/FLT3-ITD(neg/low) AML.

144 M1(wt)/FLT3(wt), 66 +/- 3% in NPM1(mut)/FLT3-ITD, and 54 +/- 7% in NPM1(wt)/FLT3-ITD (P = .003).

145 Our findings show that mutated FLT3-ITD and JAK2 augment ROS production and HR, shifting the

146 Cells expressing mutated FLT3-ITD demonstrated a relative increase in mutation frequen

147 nd < 4-log reduction in PB-MRD, but not FLT3-ITD allelic ratio, remained of significant prognostic va

148 ostic and predictive impact of the NPM1/FLT3-ITD genotypes categorized according to the 2017 ELN risk

149 The 4 NPM1/FLT3-ITD genotypes differed significantly with regard to clin

150 y worse prognosis associated with NPM1c/FLT3-ITD vs NPM1/NRAS-G12D-mutant AML and functionally confir

151 5 activation, and combined targeting of FLT3-ITD and BTK showed additive effects.

152 s explain the less favorable outcome of FLT3-ITD APLs with ATRA-based regimens, and stress the key ro

153 ategies that modulate the expression of FLT3-ITD are also promising.

154 ibitor palbociclib induces apoptosis of FLT3-ITD leukemic cells.

155 We hypothesize that this effect of FLT3-ITD might subvert immunosurveillance and promote leukemo

156 We analyzed the effect of FLT3-ITD on dendritic cells (DCs), which express FLT3 and can

157 olecular or pharmacologic inhibition of FLT3-ITD reactivated ceramide synthesis, selectively inducing

158 d protein and to the down regulation of FLT3-ITD signature genes, thus linking two major prognostic i

159 ic lesions, including an association of FLT3-ITD with abundant progenitor-like cells.

160 ) AML and is critical for the growth of FLT3-ITD(+) AML cells in vitro.

161 NPM1 mutations in the absence of FLT3-ITD, mutated TP53, and biallelic CEBPA mutations were id

162 esponsible for the early degradation of FLT3-ITD, which preceded the inhibition of mitogen-activated

163 Treatment of FLT3-ITD- and JAK2V617F-mutant cells with the antioxidant N-a

164 r miR-155 influences the development of FLT3-ITD-induced myeloproliferative disease.

165 ses the cyto-protective role of BMSC on FLT3-ITD AML survival.

166 These findings complement our FLT3-ITD data, suggesting illegitimate TdT activity contribut

167 in an in vivo murine FLT3-ITD-positive (FLT3-ITD+) model of sorafenib resistance.

168 n multivariable analysis, NPM1-positive/FLT3-ITD-negative genotype remained independently associated

169 NPM1-positive/FLT3-ITD-negative genotype remains a relatively favorable pro

170 L age 55 to 65 years with NPM1-positive/FLT3-ITD-negative genotype treated in SWOG trials had a signi

171 andem duplications (ITDs; NPM1-positive/FLT3-ITD-negative genotype) are classified as better risk; ho

172 ased HR activity in G0 arrested primary FLT3-ITD NK-AML in contrast to wild-type FLT3 NK-AML.

173 , was significantly elevated in primary FLT3-ITD normal karyotype acute myeloid leukemia (NK-AML) com

174 with our observations in mice, primary FLT3-ITD(+) AML clinical samples have significantly higher mi

175 ell lines using CRISPR/Cas9, or primary FLT3-ITD(+) AML samples using locked nucleic acid antisense i

176 Results indicate that miR-155 promotes FLT3-ITD-induced myeloid expansion in the bone marrow, spleen

177 broblast growth factor 2 (FGF2) protect FLT3-ITD+ MOLM14 cells from AC220, providing time for subsequ

178 /MLL rearrangements, t(15;17)/PML-RARA, FLT3-ITD, and/or NPM1 mutations.

179 )) or present with a low allelic ratio (FLT3-ITD(low)).

180 However, miR-155's role in regulating FLT3-ITD-mediated disease in vivo remains unclear.

181 l genomic screening, we determined that FLT3-ITD is a biomarker of response to MTHFD2 suppression.

182 odels, we unexpectedly demonstrate that FLT3-ITD severely blunts ATRA response.

183 Parental cell lines carry the FLT3-ITD (tandem duplication) mutation and are highly respons

184 y highlights the value of targeting the FLT3-ITD driver mutation with a highly potent and selective F

185 Thus, the FLT3-ITD mutation directly affects DC development, indirectly

186 f older patients (50-60 years) with the FLT3-ITD or NPM1 mutation.

187 prevented AML cell death in response to FLT3-ITD inhibition by crenolanib, which was restored by wild

188 refore, selecting patients according to FLT3-ITD mutations could be a new way to detect a significant

189 thal mitophagy induction in response to FLT3-ITD targeting was mediated by dynamin-related protein 1

190 mide-dependent mitophagy in response to FLT3-ITD targeting.

191 Patients with FLT3-ITD (24%),DNMT3A(24%), and NPM1(26%) mutant AML all bene

192 done in 318 of 549 trial patients with FLT3-ITD AML.

193 cells and HCD-57 cells transformed with FLT3-ITD and D835 mutants.

194 Co-occurrence of mutant NPM1 with FLT3-ITD carries a significantly worse prognosis than NPM1-RA

195 AML patient samples with FLT3-ITD express high levels of RUNX1, a transcription factor

196 Smc3 haploinsufficiency cooperated with Flt3-ITD to induce acute leukemia in vivo, with potentiated S

197 nd phosphorylated RUNX1 cooperates with FLT3-ITD to induce AML.

198 could replace RUNX1 in cooperating with FLT3-ITD to induce AML.

199 nced HSC self-renewal or cooperate with Flt3-ITD to induce myeloid transformation.

200 a reveal that miR-155 collaborates with FLT3-ITD to promote myeloid cell expansion in vivo and that t

201 loblast-like cell line transfected with FLT3-ITD, have a higher protein level of p22(phox) and p22(ph

202 In the subset of patients with FLT3-ITD, only age, white blood cell count, and < 4-log reduc

203 : DRKS00000591), 83 adult patients with FLT3-ITD-positive AML in complete hematologic remission after

204 ut)/FLT3-ITD, and 54 +/- 7% in NPM1(wt)/FLT3-ITD (P = .003).

205 e sequence and molecular anatomy of 300 FLT3-ITDs to address this issue, including 114 ITDs with addi

206 FLT3-internal tandem duplications (FLT3-ITDs) are prognostic driver mutations found in acute mye

207 high TdT show an increased incidence of FLT3-ITDs (M0; P = .0017).

208 ssing" microhomology in the majority of FLT3-ITDs through occult microhomology: specifically, by prim

209 Understanding the origin of FLT3-ITDs would advance our understanding of the genesis of A

210 to prime such slippage in one-third of FLT3-ITDs.

211 for the lymphoid enzyme TdT in priming FLT3-ITDs.

212 fied the highest percentage of reported FLT3-ITDs when compared to other ITD detection algorithms, an

213 ortantly, the drug combination depletes FLT3/ITD(+) LSCs in a genetic mouse model of AML, and prolong

214 l of this drug combination to eliminate FLT3/ITD(+) LSCs and reduce the rate of relapse in AML patien

215 tly inhibited survival of primary human FLT3/ITD(+) AML cells compared to FLT3/ITD(neg) cells and spa

216 y, preferentially inducing apoptosis in FLT3/ITD(+) cell lines and patient samples.

217 ing within hours following treatment of FLT3/ITD AML cells with selective inhibitors of FLT3.

218 demonstrate decreased clonogenicity of FLT3/ITD(+) cells upon treatment with ATRA and TKI.

219 Furthermore, engraftment of primary FLT3/ITD(+) patient samples is reduced in mice following trea

220 nts with AML without high allelic ratio FLT3/ITD treated in the Children's Oncology Group trial AAML1

221 human FLT3/ITD(+) AML cells compared to FLT3/ITD(neg) cells and spared normal umbilical cord blood ce

222 aneous implantation might be capitalized for ITD processing with signal processing advances, which mo

223 ITD statistics underlie the neural code for ITD and thus influence spatial perception.

224 sts that, at downstream stages, the code for ITD may not be qualitatively different across species.

225 lights the need to more effectively look for ITD's in other cancers and Mendelian diseases.

226 L) developed into the critical structure for ITD detection.

227 of the round windows differed markedly from ITD tuning in the same cells.

228 RUNX1, CEBPalpha), signaling molecules (FTL3-ITD, RAS) and the nuclear protein NPM1).

229 procedure with isooctane partitioning and GC-ITD, were at the average level of 2 mg kg(-1).

230 ractions detected via gas chromatography (GC/ITD) using electron ionization (EI) were: carbonyl sulfi

231 The degradation in ITD sensitivity at low pulse rates was caused by strong,

232 nues to support the notion of differences in ITD representation across species and brain regions, the

233 neural just-noticeable differences (JNDs) in ITD were computed using signal detection theory.

234 hows a parallel between human performance in ITD discrimination and neural responses in the auditory

235 ural ITD sensitivity to human performance in ITD discrimination, neural just-noticeable differences (

236 pts and proteins are markedly upregulated in ITD-positive tumours.

237 be of particular importance when informative ITD cues are unavailable.

238 In this paper we introduce ITD Assembler, a novel approach that rapidly evaluates a

239 ve firing rates of two broadly and inversely ITD-tuned channels.

240 he first crystal structures of NRAS and KRAS ITD at 1.65-1.75 angstrom resolution, respectively, prov

241 hip between ITDs and ILDs, introducing large ITD-ILD conflicts in some cases.

242 e auditory cortex ipsilateral to the leading ITD.

243 t auditory cortex in both groups but limited ITD processing in children with bilateral CIs.

244 Therefore, we measured ITD-dependent responses in the NL of anesthetized Americ

245 FLT3 and CBL and recurrent mutations in MYC-ITD, NRAS, KRAS and WT1 were frequent in pediatric AML.

246 We hypothesized that natural ITD statistics underlie the neural code for ITD and thus

247 The natural ITD rate of change across azimuth (ITDrc) and ITD variab

248 l perception showed correlation with natural ITD statistics, supporting our hypothesis.

249 To compare neural ITD sensitivity to human performance in ITD discriminati

250 ll firing rate at higher pulse rates, neural ITD JNDs were within the range of perceptual JNDs in hum

251 uditory pathways but does not support normal ITD sensitivity.

252 Novel ITDs were validated by analyzing the corresponding RNA s

253 enging due to inefficiencies in alignment of ITD-containing reads to the reference genome.

254 Transcriptome analysis of ITD-positive CCSKs reveals enrichment for PRC2-regulated

255 The neural coding of ITD and its similarity across species have been strongly

256 n of ITD-sensitive neurons and the degree of ITD sensitivity decreased monotonically with increasing

257 ith temporal windowing, both the fraction of ITD-sensitive neurons and the degree of ITD sensitivity

258 We show that alligators form maps of ITD very similar to birds, suggesting that their common

259 or external time differences, formed maps of ITD.

260 esults are consistent with classic models of ITD coding and can explain the ITD tuning distribution o

261 Thus, the presence of ITD maps in the brainstem may reflect a local optimum in

262 bservations suggest integrated processing of ITD and ILD.

263 e shifts, which reduced the dynamic range of ITD and ILD response functions and the ability of neuron

264 Such topographical representation of ITD, however, is not evident in mammals.

265 However, nontopographic representations of ITD cannot be excluded due to different anatomical and e

266 is that optimal computational strategies of ITD detection depend mainly on head size and available f

267 his study provides a better understanding of ITD processing with bilateral CIs and shows a parallel b

268 potential deficits in cortical processing of ITDs remain.

269 To characterize the representation of ITDs relative to the frequency and hodological organizat

270 inaural information was analyzed in terms of ITDs, ILDs, and interaural coherence, both for whole sti

271 iciently large to have a potential impact on ITD tuning.

272 of reported FLT3-ITDs when compared to other ITD detection algorithms, and discovered additional ITDs

273 In particular, ITD sensitivity of most CI users degrades with increasin

274 FLT3 subtype was ITD (high) in 214 patients, ITD (low) in 341 patients, and TKD in 162 patients.

275 Evidence of polymorphic ITDs in 54 genes were also found.

276 Instead, the preferred ITD of neurons in the mammalian brainstem often lies out

277 were strongly ITD tuned, and their preferred ITDs correlated with the position in NL.

278 lying on sound localization to capture prey, ITDs within the physiological range determined by the he

279 mechanism for sustained activity of the RAS ITD protein.

280 is revealed increased interaction of the RAS ITD with Raf proto-oncogene Ser/Thr kinase (RAF), leadin

281 rast, children with CIs demonstrated reduced ITD-related changes in both auditory cortices.

282 robust under stimulus conditions that render ITD cues undetectable.

283 However, recent studies reveal ITD responses in the owl's forebrain and midbrain premot

284 zed responses by temporal windowing revealed ITD sensitivity in these neurons.

285 imately 73% of IC neurons showed significant ITD sensitivity in their overall firing rates.

286 similar results to each other in simulating ITD and ILD coding.

287 d potentials, or neurophonics, were strongly ITD tuned, and their preferred ITDs correlated with the

288 We tested ITD Assembler on The Cancer Genome Atlas AML dataset as

289 The ITD prevented interaction with neurofibromin 1 (NF1)-GTP

290 sic models of ITD coding and can explain the ITD tuning distribution observed in the mammalian brains

291 d 4 distinct FLT3-ITD genotypes based on the ITD AR and the NPM1 mutational status.

292 We hypothesized that the ITD would result in a greater negative intrathoracic pre

293 y to interaural differences in sound timing (ITD) and level (ILD).

294 aring, interaural differences in the timing (ITD) and level (ILD) of impinging sounds carry critical

295 istening conditions, cortical sensitivity to ITD and ILD takes the form of broad contralaterally domi

296 nd a high proportion of neurons sensitive to ITDs.

297 The upper limit of sensitivity to ITDs conveyed in the envelope of high-frequency modulate

298 tigate, sensitivity to parametrically varied ITD or ILD cues was measured using fMRI during spatial a

299 ity evoked by bilateral stimuli with varying ITDs (0, +/-0.4, +/-1 ms) was recorded using multichanne

300 The FLT3 subtype was ITD (high) in 214 patients, ITD (low) in 341 patients, a