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 discrimination for the modulated high-frequency tone

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

5 ITD is encoded in the firing rate of neurons that detect

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

7 ts without unfavorable cytogenetics or aFLT3-ITD mutation.

8 0.05 to 0.7) of mutant to wild-type alleles (ITD [high] and ITD [low], respectively).

9 sham device (sham, no resistance) versus an ITD (increased inspiratory resistance) in 26 patients wi

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

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

12 Using a modeling approach, we assess ITD and ILD sensitivity of the neural filters to natural

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

14 The discovery of recurrent BCOR ITDs defines a major oncogenic event in this childhood s

15 between frequency tuning mismatches and best ITDs.

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

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

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

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

20 Cortical ITD processing in children with simultaneous bilateral C

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

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

23 The interaural time difference (ITD) is the primary cue to localize sound in horizontal

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

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

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

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

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

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

30 Interaural time differences (ITDs) are the dominant cue for the localization of low-f

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 ane, extracting interaural time differences (ITDs) from the stimulus fine structure and interaural le

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

35 ve (MSO) encode interaural time differences (ITDs) with sustained firing rates of >100 Hz.

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

37 lts of the ELISA intratypic differentiation (ITD) test.

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

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

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

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

44 containing FLT3 internal tandem duplication (ITD) mutations.

45 leukemia (AML), internal tandem duplication (ITD) of FLT3 at the juxtamembrane (JMD) and tyrosine kin

46 Internal tandem duplication (ITD) of fms-like tyrosine kinase 3 (FLT3) in acute myelo

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

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

49 st common type, internal tandem duplication (ITD), confers poor prognosis.

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

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

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

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

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

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

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

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

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

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

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

61 there was a significant interaction by FLT3 ITD mutation.

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

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

64 in NPM1(MUT) cases by the presence of a FLT3(ITD), but did not differ markedly according to FLT3(ITD)

65 cally important issue, we have analyzed FLT3(ITD) and NPM1(MUT) levels in 1609 younger adult cases of

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

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

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

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

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

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

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

73 s of FLT3 internal tandem duplications (FLT3(ITD)) do not have a worse prognosis if there is a concom

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 sk, then NPM1(MUT) cases with low-level FLT3(ITD) should not be considered as good risk without furth

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 ukemic cell purity by adjustment of the FLT3(ITD) level to the measured NPM1(MUT) level.

83 ut did not differ markedly according to FLT3(ITD) level.

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

85 FLT3-ITD AML patients treated with AC220 developed increased

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

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

88 FLT3-ITD molecules were detectable within autophagosomes afte

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

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

91 In a FLT3-ITD in vivo model, SYK is indispensable for myeloprolife

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

93 ulated via the ATM-DBC1-SIRT1 axis in a FLT3-ITD-dependent manner.

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

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

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

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

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

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

102 ring leukemic blasts in chemorefractory FLT3-ITD(+) AML, but leukemia progression invariably occurs.

103 ven by MLL-AF9 or AML1-ETO coexpressing FLT3-ITD, SIRT1 acts as a safeguard to counteract oncogene-in

104 JMD) and tyrosine kinase (TKD) domains (FLT3-ITD(+)) occurs in 30% of patients and is associated with

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

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

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

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

109 e kinase 3-internal tandem duplication (FLT3-ITD)(+)-cells protein, expression of SIRT1 is regulated

110 e kinase 3 internal tandem duplication (FLT3-ITD)-negative AML, BTK couples Toll-like receptor 9 (TLR

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

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

113 ole for SIRT1 inhibition in eradicating FLT3-ITD AML stem cells, potentially through a positive feedb

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

115 ear membrane in MV4-11 cells expressing FLT3-ITD.

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 2(phox) mediate the ROS production from FLT3-ITD that signal to the nucleus causing genomic instabili

119 l tandem duplications in the FLT3 gene (FLT3-ITD) and mutations in the NPM1, CEBPA, IDH2, ASXL1, and

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 ances SIRT1 protein expression in human FLT3-ITD AML LSCs and contributes to their maintenance.

123 ectively overexpressed in primary human FLT3-ITD AML LSCs.

124 Expressing human FLT3-ITD in zebrafish embryos resulted in expansion and clust

125 lopmental hematopoiesis and model human FLT3-ITD(+) and FLT3-TKD(+) AML.

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

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

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

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

130 activated SYK is predominantly found in FLT3-ITD positive AML and cooperates with FLT3-ITD to activat

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

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

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

134 TESC was highly expressed in FLT3-ITD(+) AML lines MOLM-13 and MV4-11, and its knockdown b

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

136 Increasing FLT3-ITD allelic ratio (P = .004) and IS in the tyrosine kina

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

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

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

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

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

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

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

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

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

146 rognostic classification combining NPM1/FLT3-ITD profile and classical risk factors were calculated.

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

148 that BTK RNAi inhibits proliferation of FLT3-ITD AML cells.

149 5 activation, and combined targeting of FLT3-ITD and BTK showed additive effects.

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

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

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

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

154 ibits the survival and proliferation of FLT3-ITD primary AML blasts and AML cell lines.

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

156 previously reported that inhibition of FLT3-ITD signaling results in post-translational down-regulat

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

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

159 is and establishes a zebrafish model of FLT3-ITD(+) and FLT3-TKD(+) AML that may facilitate high-thro

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

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

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

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

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

165 d-risk cytogenetic abnormalities and/or FLT3-ITD (internal tandem duplication) mutation, or with seco

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

167 s age 55 to 65 years with NPM1-positive/FLT3-ITD-negative genotype had a significantly improved 2-yea

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 tions, FLT3-ITDs, and the NPM1-positive/FLT3-ITD-negative genotype.

173 rognostic significance of NPM1-positive/FLT3-ITD-negative status in older patients with AML.

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

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

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

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

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

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

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

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

182 be an attractive approach for targeting FLT3-ITD AML LSCs to improve treatment outcomes.

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

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

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

186 The FLT3-ITD mutation is frequently observed in acute myeloid leu

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

188 Here we place the FLT3-ITD upstream of BTK in AML and show that the BTK inhibit

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

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

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

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

193 transformation to AML and resistance to FLT3-ITD-targeted therapy.

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

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

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

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

198 valuation of ibrutinib in patients with FLT3-ITD mutated AML.

199 T3-ITD positive AML and cooperates with FLT3-ITD to activate MYC transcriptional programs.

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

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

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

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

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

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

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

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

208 gnostic significance of NPM1 mutations, FLT3-ITDs, and the NPM1-positive/FLT3-ITD-negative genotype.

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

210 atients with concomitant NUP98/NSD1 and FLT3/ITD had a worse outcome than those harboring NUP98/NSD1

211 riate analysis, the dual NUP98/NSD1 and FLT3/ITD remained an independent predictor of poor outcome, a

212 the interaction between NUP98/NSD1 and FLT3/ITD that determines the poor outcome of patients with NU

213 d a high overlap between NUP98/NSD1 and FLT3/ITD, raising the question as to whether the reported poo

214 nt levels of crenolanib to inhibit both FLT3/ITD and resistance-conferring FLT3/D835 mutants in vivo.

215 id leukemia (AML) patients coexpressing FLT3/ITD and cryptic translocation t(5;11)(q35;p15.5), known

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

217 Those with dual FLT3/ITD and NUP98/NSD1 (82% of NUP98/NSD1 patients) had a co

218 ainst FLT3 internal tandem duplication (FLT3/ITD) mutations.

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

220 otoxic to leukemic blasts isolated from FLT3/ITD-expressing AML patients, while displaying minimal to

221 Studies using human FLT3/ITD mutant leukemia cell lines revealed the half maximal

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

223 mber of point mutations selected for in FLT3/ITD alleles that confer resistance to other TKIs, includ

224 omplete remission rate of 27% vs 69% in FLT3/ITD without NUP98/NSD1 (P < .001).

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

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

227 ficance of NUP98/NSD1 in the context of FLT3/ITD AML.

228 NUP98/NSD1 was found in 15% of FLT3/ITD and 7% of cytogenetically normal (CN)-AML.

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

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

231 val and tumor burden of mice in several FLT3/ITD transplantation models is significantly improved by

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

233 of poor outcome, and NUP98/NSD1 without FLT3/ITD lost its prognostic significance.

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

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

236 eases the dynamic range of the rate code for ITDs.

237 h higher (>1,000 Hz) limit for low-frequency ITD sensitivity, suggesting the presence of a low-pass f

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

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

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

241 or the beneficial effect of allogeneic HSCT; ITD IS in TKD1 remained an unfavorable factor, whereas n

242 Identical ITD mutations are found in primary and relapsed tumour p

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

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

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

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

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

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

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

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

251 e auditory cortex ipsilateral to the leading ITD.

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

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

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

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

256 uditory pathways but does not support normal ITD sensitivity.

257 Novel ITDs were validated by analyzing the corresponding RNA s

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

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

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

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

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 n, there have been relatively few studies of ITD processing in auditory cortex.

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

266 C and A1 had a major impact on the coding of ITDs at the population level: while a labeled-line decod

267 While much is known about the processing of ITDs in the auditory brainstem and midbrain, there have

268 edances, consistent with their processing of ITDs in the temporal fine structure.

269 potential deficits in cortical processing of ITDs remain.

270 dy, we compared the neural representation of ITDs in the inferior colliculus (IC) and primary auditor

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

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

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

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

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

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

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

278 difference in the distribution of preferred ITDs in IC and A1 had a major impact on the coding of IT

279 In A1, however, we found that preferred ITDs were distributed evenly throughout the physiologica

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

281 robust under stimulus conditions that render ITD cues undetectable.

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

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

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

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

286 The ITD also improved stroke volume compared with the sham d

287 baseline hemodynamic parameters between the ITD and the sham devices.

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

289 d-up tilt, the heart rate was lower with the ITD versus sham device (102+/-4 versus 109+/-4 beat/min,

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

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

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

293 ies, with most cells responding maximally to ITDs that correspond to the contralateral edge of the ph

294 nd a high proportion of neurons sensitive to ITDs.

295 Here, we assessed listeners' sensitivity to ITDs conveyed in pure tones and in the modulated envelop

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

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

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

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

300 reasing negative intrathoracic pressure with ITD breathing improves heart rate control in patients wi