ライフサイエンスコーパス: Gilbert

1 Gilbert damping increases approximately linearly with in

2 Gilbert et al. conclude that evidence from the Open Scie

3 Gilbert et al. presented DNA analysis of coprolites reco

4 Gilbert et al. report in a recent issue of Cell on the a

5 Gilbert Stork, professor emeritus at Columbia University

6 Gilbert syndrome (GS) is characterized by intermittent u

7 Gilbert syndrome is a common genetic disorder associated

8 Gilbert syndrome, a hyperbilirubinemic syndrome, has a p

9 Gilbert's syndrome is a common inherited disorder of bil

10 Gilbert-Diamond D, Emond JA, Baker ER, Korrick SA, Karag

11 In 1968, Gilbert and Pollak conjectured that for any P, Ls(P) >/=

12 syndrome, from 6 members of a family with 4 Gilbert members, and from 77 non-smoking, alcohol-free,

13 The linewidth is a Gilbert type at the saturated state, with damping of 0.0

14 More than 40 years ago, Gilbert Gottlieb and like-minded scholars argued for the

15 elopment of the chemical method of Maxam and Gilbert and the dideoxy method of Sanger, Nicklen and Co

16 e north arm (Gunnison Bay) to the south arm (Gilbert Bay) previously drove the perennial stratificati

17 on velocity gradients have been predicted by Gilbert and Jenkins.

18 rase 1 (UGT1A1) gene has been shown to cause Gilbert syndrome, a benign form of unconjugated bilirubi

19 curonosyltransferase-1A1 deficiency, causing Gilbert's syndrome, has been attributed to two extra (TA

20 curonosyltransferase-1A1 deficiency, causing Gilbert's syndrome, may be carried by the donor liver an

21 One confirmed Gilbert's patient, two recurrent jaundice patients (with

22 experimental study of temperature-dependent Gilbert damping in permalloy (Py) thin films of varying

23 vel controls on gene expression."In essence, Gilbert's conjecture, that DNA methylation is not one of

24 bin; the effects can be benign and frequent (Gilbert syndrome) or rare but severe, increasing the ris

25 211 (6%) patients had Gilbert's syndrome and 3168 (94%) did not have this cond

26 rwent a 24 h fasting test to see if they had Gilbert's syndrome, and all four positives had the 7/7 g

27 efore relapse was recorded (38 [18%] who had Gilbert's syndrome vs 461 [15%] who did not have Gilbert

28 00 after transplant (47 [22%] of 211 who had Gilbert's syndrome vs 617 [19%] of 3168 who did not have

29 ndrome vs 617 [19%] of 3168 who did not have Gilbert's syndrome), and for non-relapse mortality 499 (

30 ert's syndrome vs 461 [15%] who did not have Gilbert's syndrome).

31 Upon reactive pathway progression, as in Gilbert's Syndrome (GS; UGT1A1*28 polymorphism), aggrava

32 dition associated with jaundice in adults is Gilbert's syndrome, which is characterized by an allelic

33 ffusion model coupled to the Landau-Lifshitz-Gilbert equation numerically.

34 By solving stochastic Landau-Lifshitz-Gilbert equation of magnetization dynamics in the presen

35 s a broad consensus that the Landau-Lifshitz-Gilbert equation reliably describes the magnetization dy

36 ations based on a stochastic Landau-Lifshitz-Gilbert equation suggest that this rotation is driven so

37 s of iron oxide clusters and Landau-Lifshitz-Gilbert simulations confirmed our hypothesis, indicating

38 Using atomistic Landau-Lifshitz-Gilbert simulations we quantify the polarization changes

39 ferromagnet) governed by the Landau-Lifshitz-Gilbert-Slonczewski equation in the absence of magnetic

40 nAl-ferrite thin films with an unusually low Gilbert damping parameter (<3 x 10(-3) ), as well as str

41 roximately 10% of the population manifesting Gilbert's syndrome.

42 e of the difference between Sanger and Maxam-Gilbert indexing is examined for a number of duplexes of

43 1) promoter, as well as providing good Maxam-Gilbert sequence information.

44 fication and cleavage according to the Maxam-Gilbert sequencing protocol.

45 ive conditioning regimens, compared with non-Gilbert's syndrome patients.

46 We assessed the association of Gilbert's syndrome with overall mortality and non-relaps

47 The genetic basis of Gilbert's syndrome is ill-defined.

48 he (TA)7 allele was considered diagnostic of Gilbert's syndrome.

49 However, the effect of Gilbert's syndrome on the disposition of some drugs can

50 The effect of Gilbert's syndrome on the risk of overall mortality and

51 ether or not they had laboratory evidence of Gilbert's syndrome.

52 xistence of a mild and a more severe form of Gilbert's syndrome, depending on whether the gene defect

53 applied to a cohort from PGP, predictions of Gilbert syndrome, Graves' disease, non-Hodgkin lymphoma,

54 ) peaks can be modeled by isotherms based on Gilbert-Jenkins theory, providing a robust approach to e

55 ues acting against the equilibrium-restoring Gilbert damping of the magnetization dynamics.

56 nucleophilic addition-elimination, Seyferth-Gilbert homologation, transphosphorylation, and a 1,3-di

57 n the 40 years since Harvard medical student Gilbert Omenn first described a rare, inherited disorder

58 from 12 patients with confirmed or suspected Gilbert's syndrome, from 6 members of a family with 4 Gi

59 recurrent jaundice patients (with suspected Gilbert's syndrome), and nine clinically diagnosed cases

60 east milk jaundice, and the realization that Gilbert's syndrome may play a greater role in neonatal j

61 The Gilbert damping is found to be almost independent of the

62 The Gilbert damping of ferromagnetic materials is arguably t

63 The Gilbert Ridge and Tokelau Seamounts are the only seamoun

64 umanized UGT1 mice that expressed either the Gilbert's UGT1A1*28 allele [Tg(UGT1(A1*28))Ugt1(-/-) mic

65 a single-mode damped sinusoid to extract the Gilbert damping parameter.

66 The pathway of ATP hydrolysis follows the Gilbert-Johnson pathway determined previously for a simi

67 0Ar/39Ar ages indicate that the bends in the Gilbert Ridge and Tokelau seamount trail were formed muc

68 n indinavir-treated HIV patients lacking the Gilbert's polymorphism versus 1.45 mg/dl in those who we

69 ortant insight to the physical origin of the Gilbert damping in ultrathin magnetic films.

70 Understanding the physical origin of the Gilbert damping is highly relevant to developing future

71 We first show how the increase of the Gilbert damping, caused by the inclusion rare-earth dopa

72 opment, a finding that is independent of the Gilbert's UGT1A1*28 promoter polymorphism.

73 nside the poly(A) tail, at the same time the Gilbert group at Harvard was sequencing the 5' end.

74 ndence, two independent contributions to the Gilbert damping are identified, namely bulk damping and

75 While the Gilbert damping constant can reach 10(-4) to 10(-5) in s

76 Segregation of the 7/7 genotype with the Gilbert phenotype was also demonstrated in the family wi

77 n HIV-infected patients with and without the Gilbert's polymorphism.

78 ia in liver transplant recipients was due to Gilbert's syndrome acquired through the liver allograft.

79 e diffusion-free limit previously subject to Gilbert-Jenkins theory.

80 In 1985 Walter Gilbert challenged members of the DNA methylation commun

81 Since the work of William Gilbert in 1600, it has been widely believed that the Ea

82 homozygous for the mutation associated with Gilbert syndrome and heterozygous for a second mutation

83 A1 promoter variant sequence associated with Gilbert's syndrome, and the fourth was a heterozygote.

84 Patients with Gilbert syndrome have low levels of a normal form of uri

85 Patients with Gilbert's syndrome should receive busulfan-containing my

86 Patients with Gilbert's syndrome were defined as having laboratory val

87 nt were significantly worse in patients with Gilbert's syndrome who received busulfan-containing myel

88 that contained busulfan (n=1131), those with Gilbert's syndrome (n=60) were at a significantly increa

89 melphalan conditioning regimens, those with Gilbert's syndrome had similar outcomes to those without

90 with low UGT1A1 activity, such as those with Gilbert's syndrome, may be at an increased risk for irin

91 ality by day 200 compared with those without Gilbert's syndrome (n=1071; hazard ratio [HR] 2.30, 95%

92 ndrome had similar outcomes to those without Gilbert's syndrome (overall mortality at day 200 HR 0.90