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1 napses are maintained for as long as 9 weeks postinduction.
2 m the packaging cells peaked on days 6 and 7 postinduction.
3 ients received two additional Isa-KRd cycles postinduction.
4 le mice were analyzed between 1 and 300 days postinduction.
5 orter, with an LOD <= 50.0 fM HgCl(2) 30 min postinduction.
6 ments, and measurable residual disease (MRD) postinduction.
7  residual disease (MRD) during induction and postinduction.
8 ge amounts (>10 microM) until after 24 hours postinduction.
9 ted that pili were expressed as early as 1 h postinduction.
10 tion of SP, with peak mRNA increase at 6-9 h postinduction.
11 tion factor 2 and NF-kappaB activity at 72 h postinduction.
12  HSV or Sendai virus, but not when added 4 h postinduction.
13 ocortisone, and cytarabine would improve the postinduction 5-year disease-free survival (DFS) compare
14                                              Postinduction, 51% (VTD) and 44% (VTDC) of patients achi
15                                   Absence of postinduction activity or blocking interactions between
16 wnstream promoter becomes detectable by 12 h postinduction and is the predominant transcript expresse
17 ary endpoint was complete response (CR) rate postinduction and post-autologous stem cell transplantat
18 th hypodiploid ALL came off protocol therapy postinduction and we retrospectively collected details o
19 antigenic focusing in LEW.1WR1 islets 5 days postinduction and were characterized by a substantial de
20 r segments were isolated after 7 and 21 days postinduction and were prepared for gross and radiograph
21 ain at diagnosis, we analyzed the diagnosis, postinduction, and first relapse samples, which showed a
22 mab maintenance (RM) with a response-adapted postinduction approach in patients with follicular lymph
23 to receive standard RM or a response-adapted postinduction approach on the basis of metabolic respons
24                                              Postinduction CA19-9 decline was associated with improve
25 regimen that provides prolonged, intensified postinduction chemotherapy relative to the CCG-modified
26 The trial took place in AIEOP centers during postinduction chemotherapy.
27 131 was designed to test the hypothesis that postinduction CNS prophylaxis with intrathecal triple th
28                                              Postinduction CNS prophylaxis with ITT did not improve 5
29                    The primary end point was postinduction combined rate of near-complete response (n
30 poside should be considered for inclusion in postinduction consolidative treatment programs aimed at
31  Interfant-06 trial with the addition of one postinduction course of blinatumomab (15 mug per square
32                                            A postinduction course of high-dose cytarabine can provide
33                                              Postinduction CR rates were 88% and 78%, respectively.
34                                            A postinduction CS > 2 identified a cohort of patients at
35                                          The postinduction CS maintained independent statistical sign
36 er induction was 2 in SIOPEN/HR-NBL1, with a postinduction CS of more than 2 being associated with an
37  cohort of patients (SIOPEN/HR-NBL1), with a postinduction CS of more than 2 being associated with an
38 -risk neuroblastoma trial, COG A3973, with a postinduction CS of more than 2 being associated with po
39               The prognostic significance of postinduction CSs has now been validated in an independe
40                                              Postinduction demyelination must be addressed for effect
41                                   The 5-year postinduction DFS and overall survival rates (+/- SE) of
42 imilar outcomes and subjects with persistent postinduction disease had inferior outcomes, regardless
43 ays after the induction dose and before each postinduction dose.
44  its protein level is rapidly reduced by 4 h postinduction during lytic reactivation.
45  CCR cycles of cisplatin had improved 5-year postinduction EFS (90.7% v 81.2%, P = .14).
46                                              Postinduction events included two relapses and one death
47  The IkappaBalpha N-NES is necessary for the postinduction export of nuclear NF-kappaB, which is a cr
48 ents with a mean (SD) of 9.1 (2.7) months of postinduction follow-up per event (median [IQR], 10 [8-1
49 lls, and the mRNA exhibited constitutive and postinduction half-lives like those of the alpha1-tubuli
50 s and those from the intermediate group with postinduction high minimal residual disease (>/=10(-4) c
51 utant was introduced into cells, the rate of postinduction IkappaBalpha-mediated export of NFkappaB f
52 of 77 patients and was not detected pre- and postinduction in 10 patients.
53                   Lethality occurred 4 weeks postinduction in one Cre/loxP line, while no apparent ph
54 d an increase in PKR expression through 96 h postinduction in the U1/106-4:27 clone, concomitant with
55 ronger) versus standard intensity regimen of postinduction intensification (PII) for children with ne
56                    Longer and more intensive postinduction intensification (PII) improved the outcome
57  induction were randomly assigned to receive postinduction IT MTX or ITT.
58                                              Postinduction IT therapy was given for a total of 21 to
59 uencies capable of maintaining CD4 counts at postinduction levels.
60 ard-risk and intermediate-risk patients with postinduction low minimal residual disease (<10(-4) cell
61                                              Postinduction marrow specimens at the end of induction (
62 ularly given the strong prognostic effect of postinduction measurable residual disease (MRD).
63                                              Postinduction, median nadir SAAs were similar ( 1.0 IU/m
64                                              Postinduction metaiodobenzylguanidine scans showed norma
65 ly worse EFS was observed in patients with a postinduction MIBG score of >/= 3 compared to those with
66  associated with longer RFS in patients with postinduction minimal residual disease (MRD) >/=10(-3) (
67                                              Postinduction molecular MRD reliably identifies those pa
68 of relapse was independently associated with postinduction MRD level >/=10(-4) and unfavorable geneti
69 of baseline molecular and clinical features, postinduction MRD status, and treatment intensity on the
70 .7%) and provided PFS benefit, regardless of postinduction MRD status, vs VTd alone.
71 ed at 2 time points, diagnosis (n = 345) and postinduction (n = 330), before consolidation myeloablat
72 This study assessed the prognostic impact of postinduction NPM1-mutated ( NPM1m) minimal residual dis
73                                     Ten days postinduction of AIA, joint vascular reactivity was asse
74 and secondary lymphoid organs after 3 months postinduction of autoimmune uveitis.
75                                              Postinduction of carcinogenicity, mutations further prop
76 ferences between B6.56R and B6.56R.TLR9(-/-) postinduction of cGVH disease.
77 ocytosis was initiated between 15 and 30 min postinduction of FSS, occurred via a clathrin- and dynam
78 cytochrome b were observed as early as day 2 postinduction of RNAi.
79 e, follow-up time, timing of MRD assessment (postinduction or consolidation), MRD detection method, p
80 nduced phenotypic and functional alterations postinduction (p.i.) of sepsis.
81 by half, FHF rats were not warmed during the postinduction period and were allowed to gradually enter
82 east 1 month of long-term follow-up during a postinduction period beginning 12 months after taper ini
83 yses, adjusted incidence rate ratios for the postinduction period compared with the pretaper period w
84 sine during theta activity persists into the postinduction period in the basal dendrites of middle-ag
85 Outcome counts were assessed in pretaper and postinduction periods (from 12 to 24 months after taper
86 rade 3 or 4 toxicity during the induction or postinduction periods.
87 ss NF-kappaB DNA-binding activity during the postinduction phase, only IkappaBalpha allows the effici
88  of Nrf2 protein from the nucleus during the postinduction phase, therefore promoting restoration of
89 d disease-free survival during induction and postinduction phases of therapy among children and adole
90 xperienced mucositis during the induction or postinduction phases of treatment, respectively.
91 ed with a second anti-TNF agent had a higher postinduction remission rate (p = 0.002), and drug survi
92                     Although the rapidity of postinduction repression is explained partly by the fact
93 he newly synthesized IkappaBalpha induced by postinduction repression is recruited to TNF-alpha, IL-1
94 limp-1, is a DNA-binding protein involved in postinduction repression of interferon-beta gene transcr
95 uently, NF-kappaB activity was augmented and postinduction repression of NF-kappaB activity was impai
96                         However, the rate of postinduction repression of NF-kappaB DNA binding is del
97 increased synthesis of IkappaBalpha leads to postinduction repression of nuclear NF-kappaB activity.
98 h corepressor complexes are required for the postinduction repression of the IFN-beta promoter.
99                                       Hence, postinduction repression of the Nrf2-mediated antioxidan
100 r results suggest the following mechanism of postinduction repression: upon recovery of cellular redo
101 iments suggest that IkappaB alpha works as a postinduction repressor of NF-kappaB independently of HM
102 appaB alpha can also act in the nucleus as a postinduction repressor of NF-kappaB/Rel proteins.
103    In this study, we identify Keap1 as a key postinduction repressor of Nrf2 and demonstrate that a n
104 etermined the prevalence and significance of postinduction residual disease (RD) by multidimensional
105 tion response, gene induction, and finally a postinduction response, culminating in the restoration o
106 ies demonstrating a similar association with postinduction response.
107 cluding key factors used in preinduction and postinduction risk stratification.
108 ement in appendage subtype determination and postinduction stage appendage development, however, has
109 -kappaB similarly to IkappaBalpha during the postinduction state.
110                       Events occurred before postinduction surgery I in 18 (47%) of 38 patients with
111                                           At postinduction surgery I, patients with stage III or IV d
112 , safety, and long-term outcome of replacing postinduction surgery with additional chemoRT.
113     The experimental arm used three types of postinduction therapies: for complete metabolic response
114 on chemotherapy benefit from early intensive postinduction therapy but do not benefit from a second i
115 operative predictor for early recurrence was postinduction therapy carbohydrate antigen (CA) 19-9>=10
116 eduction in mRNA level between diagnosis and postinduction therapy in BM or PB was not of additional
117 up (COG) AALL0331 tested whether intensified postinduction therapy that improves survival in children
118                     Patients with a negative postinduction therapy tumor site biopsy and cytology (a
119 al treatments during induction and augmented postinduction therapy with 18 Gy of cranial radiation.
120  These are increasingly being used to direct postinduction therapy, but they are also molecular targe
121 ant, and perhaps dominant, roles in planning postinduction therapy.
122 e cycles (n = 21) of high-dose cytarabine as postinduction therapy.
123 re associated with lower average rSo(2) from postinduction to 60 minutes post cardiopulmonary bypass
124                                         This postinduction transcription repression mechanism may be
125 llowing removal of TNF-alpha, there is rapid postinduction transcriptional repression common to both
126 row to assess MRD in paired samples obtained postinduction, transplant, consolidation and after 24 cy
127 y assigned therapies evaluated the impact of postinduction treatment intensification on outcome.
128 d lncScores were correlated with initial and postinduction treatment outcomes using Cox proportional
129 by subsequent weight status during intensive postinduction treatment phases.
130 omprehensive panel of drugs at 65 to 95 days postinduction were determined.
131 cytes in a stochastic manner as early as 6 h postinduction with 17beta-estradiol.
132      The MOG plus MBP disease can be treated postinduction with a combination of the MOG 41-60 peptid
133 y a precipitous increase between 12 and 24 h postinduction, with p18 protein finally accumulating to

 
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