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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
9 sham device (sham, no resistance) versus an ITD (increased inspiratory resistance) in 26 patients wi
11 nteraural mismatches in frequency tuning and ITD tuning during in vivo loose-patch (juxtacellular) re
16 (c) HAs altered the relationship between ITDs and ILDs, introducing large ITD-ILD conflicts in so
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
22 tance through an impedance threshold device (ITD) on orthostatic tolerance in patients with postural
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
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.
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
36 ate sounds, ie, interaural time differences (ITDs), interaural level differences (ILDs), and pinna sp
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
45 leukemia (AML), internal tandem duplication (ITD) of FLT3 at the juxtamembrane (JMD) and tyrosine kin
48 resence of FLT3-internal tandem duplication (ITD), and a < 4-log reduction in PB-MRD were significant
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
53 ion of somatic internal tandem duplications (ITDs) clustering in the C terminus of BCOR in 23 of 27 (
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,
59 aused distortions of high-frequency envelope ITDs and significantly reduced interaural coherence.
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
67 red gene expression profile in Npm1(cA);Flt3(ITD) , but not Npm1(cA/+);Nras(G12D/+) , progenitors com
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
75 in the FMS-like tyrosine kinase 3 gene (Flt3(ITD)) and the nucleophosmin gene (Npm1(c)) to induce AML
77 sk, then NPM1(MUT) cases with low-level FLT3(ITD) should not be considered as good risk without furth
96 Cox-model of predefined variables, age, FLT3-ITD and >1 course of chemotherapy to reach CR were risk
98 ed Hhex as a direct target of RUNX1 and FLT3-ITD stimulation and confirmed high HHEX expression in FL
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.
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
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
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
121 However, the molecular basis of how FLT3-ITD-driven ROS leads to the aggressive form of AML is no
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
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
135 activation of the PI3K/mTOR pathway in FLT3-ITD-dependent AML results in resistance to drugs targeti
138 cation of the FMS-like tyrosine kinase (FLT3-ITD) receptor is present in 20% of acute myeloid leukemi
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).
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
152 We hypothesize that this effect of FLT3-ITD might subvert immunosurveillance and promote leukemo
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
159 is and establishes a zebrafish model of FLT3-ITD(+) and FLT3-TKD(+) AML that may facilitate high-thro
161 esponsible for the early degradation of FLT3-ITD, which preceded the inhibition of mitogen-activated
165 d-risk cytogenetic abnormalities and/or FLT3-ITD (internal tandem duplication) mutation, or with seco
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
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
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
183 l genomic screening, we determined that FLT3-ITD is a biomarker of response to MTHFD2 suppression.
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
200 Smc3 haploinsufficiency cooperated with Flt3-ITD to induce acute leukemia in vivo, with potentiated S
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
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
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
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
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
234 aneous implantation might be capitalized for ITD processing with signal processing advances, which mo
237 h higher (>1,000 Hz) limit for low-frequency ITD sensitivity, suggesting the presence of a low-pass f
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
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 (
253 FLT3 and CBL and recurrent mutations in MYC-ITD, NRAS, KRAS and WT1 were frequent in pediatric AML.
255 ll firing rate at higher pulse rates, neural ITD JNDs were within the range of perceptual JNDs in hum
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
263 e shifts, which reduced the dynamic range of ITD and ILD response functions and the ability of neuron
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
270 dy, we compared the neural representation of ITDs in the inferior colliculus (IC) and primary auditor
272 inaural information was analyzed in terms of ITDs, ILDs, and interaural coherence, both for whole sti
274 of reported FLT3-ITDs when compared to other ITD detection algorithms, and discovered additional ITDs
276 FLT3 subtype was ITD (high) in 214 patients, ITD (low) in 341 patients, and TKD in 162 patients.
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
289 d-up tilt, the heart rate was lower with the ITD versus sham device (102+/-4 versus 109+/-4 beat/min,
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
295 Here, we assessed listeners' sensitivity to ITDs conveyed in pure tones and in the modulated envelop
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
300 reasing negative intrathoracic pressure with ITD breathing improves heart rate control in patients wi
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