ライフサイエンスコーパス: Becker

1 Becker et al. reported that forest amphibians with terre

2 Becker muscular dystrophy (BMD) is a progressive X-linke

3 Becker muscular dystrophy is an X-linked disease due to

4 Becker muscular dystrophy is an X-linked disorder due to

5 Becker mutants lacking membrane proteins gE or gI replic

6 Becker syndrome, a recessive nondystrophic myotonia caus

7 and glycolytic ATP production in vivo in 14 Becker muscular dystrophy patients.

8 A Becker muscular dystrophy mutation reduces ankyrin bindi

9 Both DMD and Becker muscular dystrophy can result from out-of-frame p

10 In Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD), interventions reducing

11 er disease (GD) type III, Duchenne (DMD) and Becker muscular dystrophy (BMD), Parkinson disease (PD),

12 nclude Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD), X-linked dilated cardio

13 phies, Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD).

14 enerative muscle diseases Duchenne (DMD) and Becker muscular dystrophy result from mutations in the D

15 Duchenne and Becker muscular dystrophies (DBMD) are allelic disorders

16 These mutations result in the Duchenne and Becker muscular dystrophies (DMD and BMD).

17 rt failure is characteristic of Duchenne and Becker muscular dystrophies and X-linked dilated cardiom

18 ophin, the defective protein in Duchenne and Becker muscular dystrophies, and therapeutic utrophin de

19 g show promise as therapies for Duchenne and Becker muscular dystrophies.

20 were reported in patients with Duchenne and Becker muscular dystrophies; improved understanding of t

21 ted progress in gene therapy of Duchenne and Becker muscular dystrophy (DMD and BMD) skeletal muscle

22 dystrophin gene result in both Duchenne and Becker muscular dystrophy (DMD and BMD), as well as X-li

23 rophin gene are responsible for Duchenne and Becker muscular dystrophy (DMD/BMD).

24 Duchenne and Becker muscular dystrophy (the Xp21 dystrophies) are ass

25 A subset of patients with Duchenne and Becker muscular dystrophy similarly possess a nonsense m

26 trophin, the protein mutated in Duchenne and Becker muscular dystrophy.

27 mice with mdx mice, a model for Duchenne and Becker muscular dystrophy.

28 of predominant muscle weakness: Duchenne and Becker; Emery-Dreifuss; distal; facioscapulohumeral; ocu

29 Duchenne muscular dystrophy and Becker muscular dystrophy (BMD) are caused by mutations

30 codon mutations identified in Duchenne's and Becker's muscular dystrophy patients.

31 brillation (VF) articulated by Weisfeldt and Becker.

32 ne (DMD) or a typically milder form known as Becker (BMD).

33 th a mutation in the repeat in the S. aureus Becker chromosome and showed that the repeat affected CP

34 uous DNA fragment from Staphylococcus aureus Becker affecting type 8 capsule (CP8) biosynthesis was p

35 he brain was intermediate to that induced by Becker or Bartha.

36 ated with a less severe phenotype in certain Becker muscular dystrophy patients.

37 t and/or slow disease progression in certain Becker muscular dystrophy patients.

38 hy phenotype to that of the milder disorder, Becker muscular dystrophy, typically caused by in-frame

39 n humans [Duchenne muscular dystrophy (DMD), Becker muscular dystrophy, facioscapulohumeral muscular

40 patients, missense mutations can cause DMD, Becker muscular dystrophy, or X-linked cardiomyopathy.

41 n order to detect deletions causing Duchenne/Becker muscular dystrophy.

42 muscle protein dystrophin triggers Duchenne/Becker muscular dystrophy, but the structure-function re

43 ex mutants, including patients with Duchenne/Becker muscular dystrophy.

44 tin, MYO-029, in adult muscular dystrophies (Becker muscular dystrophy, facioscapulohumeral dystrophy

45 hting response) mouse is an animal model for Becker syndrome.

46 keletal muscle plasma membrane in many human Becker patients and in mouse models of dystrophinopathy.

47 nd of exercise being significantly higher in Becker muscular dystrophy patients.

48 later phases of exercise, skeletal muscle in Becker muscular dystrophy patients was less acidic than

49 cal mechanisms leading to muscle necrosis in Becker muscular dystrophy are still unknown.

50 d upon reframing, similar to observations in Becker muscular dystrophy.

51 functional, dystrophin protein as occurs in Becker muscular dystrophy (BMD).

52 ive results for non-DMD disorders, including Becker muscular dystrophy and forms of limb-girdle and c

53 In this issue, Becker et al. demonstrate that MCPyV DNA can be isolated

54 henne muscular dystrophy (DMD) or the milder Becker muscular dystrophy (BMD), largely depending on wh

55 in, similar to those expressed in the milder Becker muscular dystrophy (BMD).

56 Analysis of Becker-infected rats killed prior to virus-induced death

57 rate of proton efflux from muscle fibres of Becker muscular dystrophy patients was similar to that o

58 orphological changes in a novel pig model of Becker muscular dystrophy.

59 rial ATP production was similar in muscle of Becker muscular dystrophy patients and controls.

60 Mutations in this locus cause Duchenne or Becker muscular dystrophies in human patients and are th

61 ns in about 65% of patients with Duchenne or Becker muscular dystrophy (DMD or BMD).

62 clinical trial of patients with Duchenne or Becker muscular dystrophy whose LVEF was preserved and M

63 for development as a therapy for Duchenne or Becker muscular dystrophy.

64 etrograde or anterograde transport after PRV Becker was injected into the vitreous body of the eye.

65 The wild-type PRV Becker strain spreads efficiently to postsynaptic neuron

66 By 60 to 67 h after infection, all PRV-Becker-infected animals were dead.

67 Mice infected with virulent (e.g., PRV-Becker, PRV-Kaplan, or PRV-NIA3) strains self-mutilate t

68 ntrast, rats infected with PRV-Bartha or PRV-Becker gE mutants survived to at least 96 h and exhibite

69 nfected or infected with either purified PRV-Becker or HSV-1(F).

70 , and three gE mutants isogenic with the PRV-Becker strain.

71 strains in this circuitry: the wild-type PRV-Becker strain, the attenuated PRV-Bartha vaccine strain,

72 The clone, pBecker1, was colinear with PRV-Becker genomic DNA, lacking detectable rearrangements, d

73 A recombinant Becker strain, PRV634, which expresses the Bartha Us3 pr

74 strated improvement by at least 1 Rutherford-Becker category in 88.7% of patients.

75 oup showed an improvement of >/=1 Rutherford-Becker class (P=0.31).

76 ts with peripheral artery disease Rutherford-Becker class 2 to 5 who had a de novo lesion in the popl

77 amputation rates, and changes in Rutherford-Becker class after treatment of focal infrapopliteal les

78 terquartile range) improvement in Rutherford-Becker class was -2 (-3 to -1) in the SES group and -1 (

79 scularization rate and changes in Rutherford-Becker class.

80 revascularization, and changes in Rutherford-Becker class.

81 ne muscular dystrophy (DMD) into less severe Becker muscular dystrophy (BMD) by altering pre-mRNA spl

82 ap gene expression not only in type 8 strain Becker but also in strains representing the four agr gro

83 8) genes, a plasmid library of type 8 strain Becker was screened with a labelled DNA fragment contain

84 CP8 strains such as strain Becker produce a small amount of capsule on their surfac

85 entification of CYL5614, derived from strain Becker, with a mutation that affects the expression of t

86 iptional and translational fusions in strain Becker and its agr, sarA, and agr-sarA isogenic mutants

87 es required for the CP8 production in strain Becker are transcribed as a single large transcript by a

88 native promoter of the cap8 operon in strain Becker with the strong constitutive promoter of the cap1

89 sponding region from the CP1-negative strain Becker.

90 in the gG locus of the wild-type PRV strain Becker had no effect on the ability of virus infection t

91 the virulent pseudorabies virus (PRV) strain Becker into late-stage chicken embryos, the virus spread

92 ity shift assay, we demonstrated that strain Becker produced at least one protein capable of specific

93 The wild-type PRV strain, Becker, replicated in the eye and then spread to the bra

94 To test the hypothesis that Becker infection induced an inflammatory response in the

95 Our analysis revealed that Becker virions contain the Us3 protein, whereas Bartha v

96 The Becker-deGroot-Marschak auction, which assesses subjecti

97 hat the severe pathology elicited during the Becker infection is due not to immunopathology but to da

98 t Bartha strain, PRV632, which expresses the Becker Us3 protein.

99 ived from a 20.5-kb contiguous region of the Becker chromosome.

100 ct the chicken embryo CNS from damage due to Becker infection.

101 isruption of the reading frame often lead to Becker muscular dystrophy, but a genotype/phenotype corr

102 posttranslational modifications relative to Becker VP22.

103 ed by the Us3 gene relative to the wild-type Becker strain.

104 explore the mechanism by which the virulent Becker strain mediates pathology in the chicken embryo c

105 Whereas Becker packaged VP22 into virions, Bartha had a severe d

106 s situation presents a striking analogy with Becker muscular dystrophy, where in-frame deletions in t

107 me pseudoexon mutations (one associated with Becker muscular dystrophy and one with DMD), mutation-in

108 Thirteen men with Becker muscular dystrophy, 10 female carriers and 23 con

109 Patients with Becker muscular dystrophy (BMD) and Duchenne muscular dy

110 s preserved in calf muscles of patients with Becker muscular dystrophy (BMD, n = 14) and limb-girdle

111 Materials and Methods Eight patients with Becker muscular dystrophy and eight matched control subj

112 d the clinical phenotype of 17 patients with Becker muscular dystrophy harbouring in-frame deletions

113 sociated protein expression in patients with Becker muscular dystrophy with deletions relevant for on

114 ping the patients by deletion, patients with Becker muscular dystrophy with deletions with an end-poi

115 individuals versus symptomatic patients with Becker muscular dystrophy.