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1                                              Becker et al. (2020) have highlighted three non-mutually
2                                              Becker et al. reported that forest amphibians with terre
3                                              Becker muscular dystrophy (BMD) is a progressive X-linke
4                                              Becker muscular dystrophy (BMD) is characterised by fibe
5                                              Becker muscular dystrophy is an X-linked disease due to
6                                              Becker muscular dystrophy is an X-linked disorder due to
7                                              Becker mutants lacking membrane proteins gE or gI replic
8                                              Becker syndrome, a recessive nondystrophic myotonia caus
9                                              Becker tumor regression grades 1a, 1b, 2, and 3 were obs
10  and glycolytic ATP production in vivo in 14 Becker muscular dystrophy patients.
11                                            A Becker muscular dystrophy mutation reduces ankyrin bindi
12                          Here, we describe a Becker-DeGroot-Marschak (BDM) auction-like mechanism tha
13 were averse to social risk as estimated in a Becker-DeGroot-Marschak auction-like procedure.
14 s may be applied to the more mildly affected Becker patients with lower dystrophin levels.
15                                 Both DMD and Becker muscular dystrophy can result from out-of-frame p
16 ity leads to dystrophinopathies like DMD and Becker muscular dystrophy, for which no cure is yet avai
17     In Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD), interventions reducing
18 er disease (GD) type III, Duchenne (DMD) and Becker muscular dystrophy (BMD), Parkinson disease (PD),
19 nclude Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD), X-linked dilated cardio
20 phies, Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD).
21 enerative muscle diseases Duchenne (DMD) and Becker muscular dystrophy result from mutations in the D
22                                 Duchenne and Becker muscular dystrophies (DBMD) are allelic disorders
23   These mutations result in the Duchenne and Becker muscular dystrophies (DMD and BMD).
24 rt failure is characteristic of Duchenne and Becker muscular dystrophies and X-linked dilated cardiom
25 ophin, the defective protein in Duchenne and Becker muscular dystrophies, and therapeutic utrophin de
26 g show promise as therapies for Duchenne and Becker muscular dystrophies.
27  were reported in patients with Duchenne and Becker muscular dystrophies; improved understanding of t
28 ted progress in gene therapy of Duchenne and Becker muscular dystrophy (DMD and BMD) skeletal muscle
29  dystrophin gene result in both Duchenne and Becker muscular dystrophy (DMD and BMD), as well as X-li
30 rophin gene are responsible for Duchenne and Becker muscular dystrophy (DMD/BMD).
31                                 Duchenne and Becker muscular dystrophy (the Xp21 dystrophies) are ass
32       A subset of patients with Duchenne and Becker muscular dystrophy similarly possess a nonsense m
33 trophin, the protein mutated in Duchenne and Becker muscular dystrophy.
34 mice with mdx mice, a model for Duchenne and Becker muscular dystrophy.
35 of predominant muscle weakness: Duchenne and Becker; Emery-Dreifuss; distal; facioscapulohumeral; ocu
36              Duchenne muscular dystrophy and Becker muscular dystrophy (BMD) are caused by mutations
37  prednisone in patients with Limb Girdle and Becker muscular dystrophy (LGMD and BMD, respectively).
38 D, Limb-girdle muscular dystrophy (LGMD) and Becker muscular dystrophy (BMD), strength-training impro
39 codon mutations identified in Duchenne's and Becker's muscular dystrophy patients.
40 brillation (VF) articulated by Weisfeldt and Becker.
41                     In their review article, Becker et al. (2020) have proposed a framework to explic
42 ne (DMD) or a typically milder form known as Becker (BMD).
43 r systematic review and critical assessment, Becker et al. (2020) identified common problems in exist
44 egatively impacts cell invasion of S. aureus Becker by promoting capsule and repressing FnbA.
45 th a mutation in the repeat in the S. aureus Becker chromosome and showed that the repeat affected CP
46 uous DNA fragment from Staphylococcus aureus Becker affecting type 8 capsule (CP8) biosynthesis was p
47 he brain was intermediate to that induced by Becker or Bartha.
48 ated with a less severe phenotype in certain Becker muscular dystrophy patients.
49 t and/or slow disease progression in certain Becker muscular dystrophy patients.
50 true subjective value in individual choices [Becker-DeGroot-Marschak (BDM) mechanism].
51  patients with recessive myotonia congenita (Becker disease) experience debilitating bouts of transie
52 hy phenotype to that of the milder disorder, Becker muscular dystrophy, typically caused by in-frame
53 n humans [Duchenne muscular dystrophy (DMD), Becker muscular dystrophy, facioscapulohumeral muscular
54  patients, missense mutations can cause DMD, Becker muscular dystrophy, or X-linked cardiomyopathy.
55 l myopathy/muscular dystrophies and Duchenne/Becker muscular dystrophy) delivered a ~59% 'solved' and
56 n order to detect deletions causing Duchenne/Becker muscular dystrophy.
57  muscle protein dystrophin triggers Duchenne/Becker muscular dystrophy, but the structure-function re
58 ex mutants, including patients with Duchenne/Becker muscular dystrophy.
59 tin, MYO-029, in adult muscular dystrophies (Becker muscular dystrophy, facioscapulohumeral dystrophy
60                      In the well-established Becker-DeGroot-Marschak (BDM) auction-like mechanism, pa
61 hting response) mouse is an animal model for Becker syndrome.
62 way for meaningful targeted therapeutics for Becker MD and for certain patients with Duchenne MD.
63 keletal muscle plasma membrane in many human Becker patients and in mouse models of dystrophinopathy.
64 nd of exercise being significantly higher in Becker muscular dystrophy patients.
65 later phases of exercise, skeletal muscle in Becker muscular dystrophy patients was less acidic than
66 cal mechanisms leading to muscle necrosis in Becker muscular dystrophy are still unknown.
67 d upon reframing, similar to observations in Becker muscular dystrophy.
68  functional, dystrophin protein as occurs in Becker muscular dystrophy (BMD).
69 ive results for non-DMD disorders, including Becker muscular dystrophy and forms of limb-girdle and c
70 als related to dystrophinopathies, including Becker muscular dystrophy (BMD).
71                               In this issue, Becker et al. demonstrate that MCPyV DNA can be isolated
72                  In the 81 patients with MD, Becker was the most common type (42%-52%).
73  thiophosphinate in stereospecific Michaelis-Becker, Hirao, or Pudovik reactions.
74 he Michaelis-Arbuzov reaction, the Michaelis-Becker reaction, the Pudovik reaction, the Hirao couplin
75 relates with the clinical severity of milder Becker muscular dystrophy and DMD patients.
76  Duchenne muscular dystrophy (DMD) or milder Becker muscular dystrophy (BMD).
77 henne muscular dystrophy (DMD) or the milder Becker muscular dystrophy (BMD), largely depending on wh
78 in, similar to those expressed in the milder Becker muscular dystrophy (BMD).
79 ttransplant survival of Becker MD versus non-Becker MD (P=0.12; hazard ratio [95% CI], 2.17 [0.79-6.0
80                                  Analysis of Becker-infected rats killed prior to virus-induced death
81  rate of proton efflux from muscle fibres of Becker muscular dystrophy patients was similar to that o
82                    First, a modified form of Becker-Doring nucleation kinetic equations is used to es
83 orphological changes in a novel pig model of Becker muscular dystrophy.
84 th genetic and pharmacologic mouse models of Becker disease to identify the mechanism underlying tran
85 V in the genetic and pharmacologic models of Becker disease.
86 rial ATP production was similar in muscle of Becker muscular dystrophy patients and controls.
87 e was observed in posttransplant survival of Becker MD versus non-Becker MD (P=0.12; hazard ratio [95
88    Mutations in this locus cause Duchenne or Becker muscular dystrophies in human patients and are th
89 ns in about 65% of patients with Duchenne or Becker muscular dystrophy (DMD or BMD).
90  clinical trial of patients with Duchenne or Becker muscular dystrophy whose LVEF was preserved and M
91 could benefit many patients with Duchenne or Becker muscular dystrophy, regardless of genotype, and c
92 for development as a therapy for Duchenne or Becker muscular dystrophy.
93 utations associated with Duchenne (L54R), or Becker muscular dystrophy (L172H).
94 etrograde or anterograde transport after PRV Becker was injected into the vitreous body of the eye.
95 ISPR/Cas9-mediated gene replacement: (i) PRV Becker defective for UL13 expression (PRV UL13), (ii) PR
96                            The wild-type PRV Becker strain spreads efficiently to postsynaptic neuron
97       By 60 to 67 h after infection, all PRV-Becker-infected animals were dead.
98       Mice infected with virulent (e.g., PRV-Becker, PRV-Kaplan, or PRV-NIA3) strains self-mutilate t
99 ntrast, rats infected with PRV-Bartha or PRV-Becker gE mutants survived to at least 96 h and exhibite
100 nfected or infected with either purified PRV-Becker or HSV-1(F).
101 , and three gE mutants isogenic with the PRV-Becker strain.
102 strains in this circuitry: the wild-type PRV-Becker strain, the attenuated PRV-Bartha vaccine strain,
103   The clone, pBecker1, was colinear with PRV-Becker genomic DNA, lacking detectable rearrangements, d
104                                A recombinant Becker strain, PRV634, which expresses the Bartha Us3 pr
105 strated improvement by at least 1 Rutherford-Becker category in 88.7% of patients.
106 oup showed an improvement of >/=1 Rutherford-Becker class (P=0.31).
107 ts with peripheral artery disease Rutherford-Becker class 2 to 5 who had a de novo lesion in the popl
108 ement from baseline to 2 years in Rutherford-Becker category (row mean scores difference, 1.7; P = .1
109  amputation rates, and changes in Rutherford-Becker class after treatment of focal infrapopliteal les
110  amputation rates, and changes in Rutherford-Becker class at 1 year.
111 terquartile range) improvement in Rutherford-Becker class was -2 (-3 to -1) in the SES group and -1 (
112 3% (n=12; P=0.308), the median in Rutherford-Becker class was 2 (0.25-5) versus 5 (0.25-5; P=0.329),
113 scularization rate and changes in Rutherford-Becker class.
114 revascularization, and changes in Rutherford-Becker class.
115 ne muscular dystrophy (DMD) into less severe Becker muscular dystrophy (BMD) by altering pre-mRNA spl
116 ap gene expression not only in type 8 strain Becker but also in strains representing the four agr gro
117 8) genes, a plasmid library of type 8 strain Becker was screened with a labelled DNA fragment contain
118                   CP8 strains such as strain Becker produce a small amount of capsule on their surfac
119 entification of CYL5614, derived from strain Becker, with a mutation that affects the expression of t
120 iptional and translational fusions in strain Becker and its agr, sarA, and agr-sarA isogenic mutants
121 es required for the CP8 production in strain Becker are transcribed as a single large transcript by a
122 native promoter of the cap8 operon in strain Becker with the strong constitutive promoter of the cap1
123 sponding region from the CP1-negative strain Becker.
124  in the gG locus of the wild-type PRV strain Becker had no effect on the ability of virus infection t
125 the virulent pseudorabies virus (PRV) strain Becker into late-stage chicken embryos, the virus spread
126                         We found that strain Becker possessed one fibronectin-binding protein, FnbA,
127 ity shift assay, we demonstrated that strain Becker produced at least one protein capable of specific
128                    The wild-type PRV strain, Becker, replicated in the eye and then spread to the bra
129                  To test the hypothesis that Becker infection induced an inflammatory response in the
130                   Our analysis revealed that Becker virions contain the Us3 protein, whereas Bartha v
131                                          The Becker-deGroot-Marschak auction, which assesses subjecti
132 hat the severe pathology elicited during the Becker infection is due not to immunopathology but to da
133 t Bartha strain, PRV632, which expresses the Becker Us3 protein.
134 ived from a 20.5-kb contiguous region of the Becker chromosome.
135 ct the chicken embryo CNS from damage due to Becker infection.
136 isruption of the reading frame often lead to Becker muscular dystrophy, but a genotype/phenotype corr
137  posttranslational modifications relative to Becker VP22.
138 ed by the Us3 gene relative to the wild-type Becker strain.
139     We offered a 12-month subscription using Becker-DeGroot-Marschak auctions with real money payment
140  explore the mechanism by which the virulent Becker strain mediates pathology in the chicken embryo c
141 tructed four new PRV mutants in the virulent Becker strain using CRISPR/Cas9-mediated gene replacemen
142                                      Whereas Becker packaged VP22 into virions, Bartha had a severe d
143 s situation presents a striking analogy with Becker muscular dystrophy, where in-frame deletions in t
144 me pseudoexon mutations (one associated with Becker muscular dystrophy and one with DMD), mutation-in
145                            Thirteen men with Becker muscular dystrophy, 10 female carriers and 23 con
146 r volume fraction in study participants with Becker muscular dystrophy.
147 ved skeletal muscle cells from patients with Becker MD and mdx mice subjected to exon skipping exhibi
148                                Patients with Becker muscular dystrophy (BMD) and Duchenne muscular dy
149 s preserved in calf muscles of patients with Becker muscular dystrophy (BMD, n = 14) and limb-girdle
150    Materials and Methods Eight patients with Becker muscular dystrophy and eight matched control subj
151 d the clinical phenotype of 17 patients with Becker muscular dystrophy harbouring in-frame deletions
152 sociated protein expression in patients with Becker muscular dystrophy with deletions relevant for on
153 ping the patients by deletion, patients with Becker muscular dystrophy with deletions with an end-poi
154 individuals versus symptomatic patients with Becker muscular dystrophy.
155                 D., Lehrmann, E., Zhang, Y., Becker, K.

 
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