ライフサイエンスコーパス: postinduction

1 residual disease (MRD) during induction and postinduction.

2 ge amounts (>10 microM) until after 24 hours postinduction.

3 ted that pili were expressed as early as 1 h postinduction.

4 tion of SP, with peak mRNA increase at 6-9 h postinduction.

5 tion factor 2 and NF-kappaB activity at 72 h postinduction.

6 HSV or Sendai virus, but not when added 4 h postinduction.

7 m the packaging cells peaked on days 6 and 7 postinduction.

8 Postinduction, 51% (VTD) and 44% (VTDC) of patients achi

9 Absence of postinduction activity or blocking interactions between

10 wnstream promoter becomes detectable by 12 h postinduction and is the predominant transcript expresse

11 ary endpoint was complete response (CR) rate postinduction and post-autologous stem cell transplantat

12 antigenic focusing in LEW.1WR1 islets 5 days postinduction and were characterized by a substantial de

13 r segments were isolated after 7 and 21 days postinduction and were prepared for gross and radiograph

14 regimen that provides prolonged, intensified postinduction chemotherapy relative to the CCG-modified

15 The trial took place in AIEOP centers during postinduction chemotherapy.

16 The primary end point was postinduction combined rate of near-complete response (n

17 poside should be considered for inclusion in postinduction consolidative treatment programs aimed at

18 A postinduction course of high-dose cytarabine can provide

19 A postinduction CS > 2 identified a cohort of patients at

20 The postinduction CS maintained independent statistical sign

21 er induction was 2 in SIOPEN/HR-NBL1, with a postinduction CS of more than 2 being associated with an

22 cohort of patients (SIOPEN/HR-NBL1), with a postinduction CS of more than 2 being associated with an

23 -risk neuroblastoma trial, COG A3973, with a postinduction CS of more than 2 being associated with po

24 The prognostic significance of postinduction CSs has now been validated in an independe

25 Postinduction demyelination must be addressed for effect

26 Postinduction events included two relapses and one death

27 The IkappaBalpha N-NES is necessary for the postinduction export of nuclear NF-kappaB, which is a cr

28 lls, and the mRNA exhibited constitutive and postinduction half-lives like those of the alpha1-tubuli

29 s and those from the intermediate group with postinduction high minimal residual disease (>/=10(-4) c

30 utant was introduced into cells, the rate of postinduction IkappaBalpha-mediated export of NFkappaB f

31 of 77 patients and was not detected pre- and postinduction in 10 patients.

32 Lethality occurred 4 weeks postinduction in one Cre/loxP line, while no apparent ph

33 d an increase in PKR expression through 96 h postinduction in the U1/106-4:27 clone, concomitant with

34 ronger) versus standard intensity regimen of postinduction intensification (PII) for children with ne

35 Longer and more intensive postinduction intensification (PII) improved the outcome

36 uencies capable of maintaining CD4 counts at postinduction levels.

37 ard-risk and intermediate-risk patients with postinduction low minimal residual disease (<10(-4) cell

38 Postinduction marrow specimens at the end of induction (

39 Postinduction metaiodobenzylguanidine scans showed norma

40 ly worse EFS was observed in patients with a postinduction MIBG score of >/= 3 compared to those with

41 associated with longer RFS in patients with postinduction minimal residual disease (MRD) >/=10(-3) (

42 of relapse was independently associated with postinduction MRD level >/=10(-4) and unfavorable geneti

43 ed at 2 time points, diagnosis (n = 345) and postinduction (n = 330), before consolidation myeloablat

44 This study assessed the prognostic impact of postinduction NPM1-mutated ( NPM1m) minimal residual dis

45 Ten days postinduction of AIA, joint vascular reactivity was asse

46 ferences between B6.56R and B6.56R.TLR9(-/-) postinduction of cGVH disease.

47 ocytosis was initiated between 15 and 30 min postinduction of FSS, occurred via a clathrin- and dynam

48 cytochrome b were observed as early as day 2 postinduction of RNAi.

49 e, follow-up time, timing of MRD assessment (postinduction or consolidation), MRD detection method, p

50 by half, FHF rats were not warmed during the postinduction period and were allowed to gradually enter

51 sine during theta activity persists into the postinduction period in the basal dendrites of middle-ag

52 rade 3 or 4 toxicity during the induction or postinduction periods.

53 ss NF-kappaB DNA-binding activity during the postinduction phase, only IkappaBalpha allows the effici

54 of Nrf2 protein from the nucleus during the postinduction phase, therefore promoting restoration of

55 Although the rapidity of postinduction repression is explained partly by the fact

56 he newly synthesized IkappaBalpha induced by postinduction repression is recruited to TNF-alpha, IL-1

57 limp-1, is a DNA-binding protein involved in postinduction repression of interferon-beta gene transcr

58 uently, NF-kappaB activity was augmented and postinduction repression of NF-kappaB activity was impai

59 However, the rate of postinduction repression of NF-kappaB DNA binding is del

60 increased synthesis of IkappaBalpha leads to postinduction repression of nuclear NF-kappaB activity.

61 h corepressor complexes are required for the postinduction repression of the IFN-beta promoter.

62 Hence, postinduction repression of the Nrf2-mediated antioxidan

63 r results suggest the following mechanism of postinduction repression: upon recovery of cellular redo

64 iments suggest that IkappaB alpha works as a postinduction repressor of NF-kappaB independently of HM

65 appaB alpha can also act in the nucleus as a postinduction repressor of NF-kappaB/Rel proteins.

66 In this study, we identify Keap1 as a key postinduction repressor of Nrf2 and demonstrate that a n

67 etermined the prevalence and significance of postinduction residual disease (RD) by multidimensional

68 tion response, gene induction, and finally a postinduction response, culminating in the restoration o

69 ies demonstrating a similar association with postinduction response.

70 ement in appendage subtype determination and postinduction stage appendage development, however, has

71 -kappaB similarly to IkappaBalpha during the postinduction state.

72 Events occurred before postinduction surgery I in 18 (47%) of 38 patients with

73 At postinduction surgery I, patients with stage III or IV d

74 , safety, and long-term outcome of replacing postinduction surgery with additional chemoRT.

75 on chemotherapy benefit from early intensive postinduction therapy but do not benefit from a second i

76 eduction in mRNA level between diagnosis and postinduction therapy in BM or PB was not of additional

77 Patients with a negative postinduction therapy tumor site biopsy and cytology (a

78 al treatments during induction and augmented postinduction therapy with 18 Gy of cranial radiation.

79 These are increasingly being used to direct postinduction therapy, but they are also molecular targe

80 ant, and perhaps dominant, roles in planning postinduction therapy.

81 e cycles (n = 21) of high-dose cytarabine as postinduction therapy.

82 re associated with lower average rSo(2) from postinduction to 60 minutes post cardiopulmonary bypass

83 This postinduction transcription repression mechanism may be

84 llowing removal of TNF-alpha, there is rapid postinduction transcriptional repression common to both

85 y assigned therapies evaluated the impact of postinduction treatment intensification on outcome.

86 by subsequent weight status during intensive postinduction treatment phases.

87 omprehensive panel of drugs at 65 to 95 days postinduction were determined.

88 cytes in a stochastic manner as early as 6 h postinduction with 17beta-estradiol.

89 The MOG plus MBP disease can be treated postinduction with a combination of the MOG 41-60 peptid

90 y a precipitous increase between 12 and 24 h postinduction, with p18 protein finally accumulating to