ライフサイエンスコーパス: CMD

1 CMD 50 D was activated by EDC/NHS for immobilization of

2 CMD is highly prevalent among at-risk individuals and is

3 CMD is one of the most important diseases of cassava and

4 CMD was estimated via quadriceps electromyogram.

5 CMD was highly prevalent both in men and women (51% and

6 CMD was measured using the General Health Questionnaire.

7 A total of 123 CMD patients were investigated using the traditional app

8 odontic movement in a mouse model carrying a CMD knock-in (KI) mutation (Phe377del) in the Ank gene.

9 The primary outcome was the presence of a CMD, as defined by the Revised Clinical Interview Schedu

10 ce of blocked group III/IV muscle afferents, CMD is less inhibited but O(2) transport compromised and

11 NGS, we performed mutation detection in all CMD genes of 26 samples and compared the results with Sa

12 no association between physical activity and CMD 10 years later.

13 l muscular dystrophy (CMD), Fukuyama CMD and CMD type 1C (MDC1C) are caused by mutations in the genes

14 Both CMD and CMD-b-PEG decreased the charge of alpha-lac below pH 5.5

15 e in moesin levels in the muscles of DMD and CMD mice.

16 and congenital muscular dystrophies (DMD and CMD, respectively) and dysferlinopathy, but not in the w

17 e and congenital muscle dystrophies (DMD and CMD, respectively), and dysferlinopathy.

18 nemia and reproductive tract infections) and CMD.

19 een alpha-lac and CMD-b-PEG or alpha-lac and CMD was determined following acidification by light scat

20 Formation of complexes between alpha-lac and CMD-b-PEG or alpha-lac and CMD was determined following

21 nd congenital muscular dystrophies (LGMD and CMD) are characterized by skeletal muscle weakness and d

22 ce rates increased with age for both MDS and CMD (P < .05) and were highest among whites and non-Hisp

23 nual age-adjusted incidence rates of MDS and CMD for 2001 through 2003 were 3.3 and 2.1 per 100,000,

24 S population, we evaluated trends in MDS and CMD incidence, estimated case numbers for the entire Uni

25 l relative 3-year survival rates for MDS and CMD were 45% and 80%, respectively, with males experienc

26 jected future precipitation, temperature and CMD at our study locations for four scenarios selected t

27 enarios projected increasing temperature and CMD in coming decades (e.g., from 4.5% to 29.5% higher C

28 ty, insulin resistance, type 2 diabetes, and CMDs.

29 is-/trans-gene regulation across tissues and CMDs.

30 In recent years, severe, atypical CMD symptoms have been observed occasionally on resistan

31 Both CMD and CMD-b-PEG decreased the charge of alpha-lac belo

32 Mutational analyses showed that both CMD-1 and HTH-4 are also necessary for activation of the

33 lbumin (alpha-lac) and carboxymethyldextran (CMD) in acidic solutions lead to phase-separated complex

34 molecules supported on carboxymethyldextran (CMD)-coated surfaces measured using surface plasmon reso

35 agnoses had variants in genes known to cause CMD (76%), and 11 of 59 (19%) had variants in genes asso

36 dystroglycan in mice is sufficient to cause CMD-like brain malformations, including disarray of cere

37 up of laminin alpha 2-chain-positive classic CMD likely is heterogeneous.

38 or breakthrough involves a type of "classic" CMD with abnormalities of the white matter on magnetic r

39 ng of the limb-girdle (LGMD) and congenital (CMD) muscular dystrophies have led to a new, genetically

40 from DMD, Ullrich CMD, and merosin-deficient CMD patients, all of which present high levels of fibros

41 large gradient in climatic moisture deficit (CMD) from warm and dry low elevation sites to relatively

42 Concerted metalation deprotonation (CMD) approach with appropriate proton shuttle precursor,

43 t with a concerted metalation deprotonation (CMD) pathway.

44 via the concerted metalation-deprotonation (CMD) mechanism in all types of reactions, the subsequent

45 ion by a concerted metalation-deprotonation (CMD) mechanism involves precoordination of the C-H bond

46 on via a concerted metalation-deprotonation (CMD) mechanism, and (5) reprotonation of the amide direc

47 cal of a concerted metalation-deprotonation (CMD) mechanism, were observed in the case of a bromopyro

48 p by the concerted metalation-deprotonation (CMD) pathway is important in further development of cros

49 upport a concerted metalation-deprotonation (CMD)-type ruthenation mode and shed light on the unusual

50 A) and "concerted metalation deprotonation" (CMD) concepts.

51 Noninvasive cardiac MRI MPRI can detect CMD defined by invasive CRT.

52 al in CMD, cardiac MRI may be able to detect CMD in this population.

53 ntified hundreds of cardiometabolic disease (CMD) risk loci.

54 ifferential risk of cardiometabolic disease (CMD), which can be predicted by epigenetic marks in prox

55 viruses (CMBs) cause cassava mosaic disease (CMD) across Africa and the Indian subcontinent.

56 ude diseases such as Cassava Mosaic Disease (CMD) and Cassava Bacterial Blight (CBB), drought, and ac

57 01, resistant to the cassava mosaic disease (CMD) and the cassava bacterial blight (CBB), and MECU72,

58 ral infections and cardiometabolic diseases (CMDs), controversy still lingers.

59 ood/beverage intake, common mental disorder (CMD) and depression and to examine the role of reverse c

60 local information on common mental disorder (CMD) and substance use by comparing data from the South

61 hysical activity and common mental disorder (CMD), defined as anxiety and depression, using data from

62 s) and chronic myeloproliferative disorders (CMDs) to population-based cancer registries in the Unite

63 age has two community medicine distributors (CMDs), who are the seed nodes and responsible for admini

64 trophic muscles of the murine models of DMD, CMD, and dysferlinopathy were the source of Cthrc1.

65 d cardiac muscles of mice, representing DMD, CMD, and dysferlinopathy.

66 the boundaries of this conserved Mga domain (CMD-1) spanning from residues 10 to 15 of the protein, w

67 on peripheral fatigue, central motor drive (CMD) and endurance capacity during high-intensity leg-cy

68 spasm or coronary microvascular dysfunction (CMD) due to microvascular spasm.

69 Coronary microvascular dysfunction (CMD) is a prevalent and prognostically important finding

70 ten have coronary microvascular dysfunction (CMD), diagnosed by invasive coronary reactivity testing

71 Craniometaphyseal dysplasia (CMD) is a rare genetic disorder encompassing hyperostosi

72 Craniometaphyseal dysplasia (CMD) is a rare genetic disorder with hyperostosis of cra

73 Craniometaphyseal dysplasia (CMD) is a rare skeletal disorder characterized by progre

74 inosis (CCAL2), craniometaphyseal dysplasia (CMD), mental retardation, deafness and ankylosis syndrom

75 The congenital muscular dystrophies (CMD) are a heterogeneous group of autosomal recessive di

76 hy types of congenital muscular dystrophies (CMDs) and ocular abnormalities termed muscle-eye-brain d

77 en in those congenital muscular dystrophies (CMDs) caused by mutations in genes involved in O-mannosy

78 The congenital muscular dystrophies (CMDs) comprise a heterogeneous group of heritable muscle

79 rs known as congenital muscular dystrophies (CMDs) with associated CNS abnormalities.

80 yndrome are congenital muscular dystrophies (CMDs) with associated developmental brain defects.

81 LGMD2I) and congenital muscular dystrophies (CMDs) with brain malformations and mental retardation.

82 Congenital muscular dystrophy (CMD) is a group of clinically and genetically heterogene

83 form of human congenital muscular dystrophy (CMD) is caused by mutations in the laminin-alpha2 gene.

84 Congenital muscular dystrophy (CMD) is characterized by severe muscle wasting, prematur

85 vere forms of congenital muscular dystrophy (CMD) such as Fukuyama type congenital muscular dystrophy

86 Two forms of congenital muscular dystrophy (CMD), Fukuyama CMD and CMD type 1C (MDC1C) are caused by

87 Both SEGS enhanced CMD symptoms in cassava (Manihot esculentaCrantz) when c

88 lia-associated chronic myeloid disorder (eos-CMD) characterized by the t(5;12)(q33;p13) cytogenetic a

89 ate the therapeutic value of imatinib in eos-CMD that is not associated with t(5;12)(q33;p13).

90 l men, median age = 46 years) and 2 with eos-CMD (both men, aged 45 and 58 years) were treated with i

91 3 weeks), 2 patients with HES and 1 with eos-CMD have achieved complete clinical remission and 1 addi

92 valence of vasomotor dysfunction (especially CMD) compared with male patients.

93 (59%) with a pathological ACH test, 33% for CMD and 26% for epicardial vasospasm.

94 Density functional calculations for CMD C-H activation at C6, C5, C8, and C2' sites imply th

95 insights into gene-regulatory mechanisms for CMD risk loci, facilitating their translation into oppor

96 is in homozygous Ank KI/KI mice, a model for CMD, showed that molars can be moved by orthodontic forc

97 ignificant with a female-male odds ratio for CMD and epicardial vasospasm of 4.2 (95% confidence inte

98 s independently associated with the risk for CMD were factors indicative of gender disadvantage, part

99 age cultures, peripheral blood cultures from CMD patients exhibited reduced osteoclastogenesis.

100 can lead to an improvement in recovery from CMD among patients attending public primary care facilit

101 Fukuyama CMD, muscle-eye-brain disease and Walker-Warburg syndrom

102 ongenital muscular dystrophy (CMD), Fukuyama CMD and CMD type 1C (MDC1C) are caused by mutations in t

103 ymethyl-dextran-block-poly(ethylene glycol) (CMD-b-PEG), the PEG block was hypothesized to reduce int

104 very sparse at the warmest and driest (high CMD) sites, particularly when combined with high topogra

105 ing decades (e.g., from 4.5% to 29.5% higher CMD by the 2080's compared to the 1971-2000 average), ev

106 obilize BSA, carboxymethyl dextran hydrogel (CMD) Au chip was used.

107 cation on gated computed tomography imaging, CMD was common in both sexes, despite normal stress perf

108 ugh initially similar, the percent change in CMD was 9 +/- 3% higher at end-exercise with fentanyl vs

109 ing the alpha2-chain of laminin 2 (LAMA2) in CMD patients.

110 oninvasive stress imaging is often normal in CMD, cardiac MRI may be able to detect CMD in this popul

111 ity was associated with a small reduction in CMD over 5 years.

112 l and functional brain abnormalities seen in CMD.

113 The onset of symptoms in CMD is within the first few months of life, whereas in L

114 Furthermore, their absence in CMDs suggests that hypoglycosylation of RPTPzeta/phospha

115 verages had a 23% increased odds of incident CMD after 5 years (95% CI: 1.02, 1.48) independent of he

116 Additionally, genetics influences CMDs, and this creates a confounding relationship among

117 ltaneous screening of mutations in all known CMD-associated genes would be a more effective diagnosti

118 rmed at pH values near pH 6, while alpha-lac/CMD complexes formed at pH 5.5.

119 Hydrodynamic radii of alpha-lac/CMD-b-PEG complexes was between 11 and 20 nm, which incr

120 separation, size, and structure of alpha-lac/CMD-b-PEG complexes were characterized by turbidimetry,

121 icrographs that were attributed to alpha-lac/CMD-b-PEG complexes.

122 Complexes of alpha-lac/CMD-b-PEG formed at pH values near pH 6, while alpha-lac

123 ck from group III/IV muscle afferents limits CMD but also minimizes locomotor muscle fatigue developm

124 CMD2 is a major CMD resistance locus that has been deployed in many cass

125 Neither CMD nor depression predicted intake changes.

126 c to CMD ratio, while the relative amount of CMD-b-PEG did not significantly influence either.

127 The clinical assessment of CMD in women must include exploration of violence and ge

128 Here, we investigated the effects of CMD-mutant ANK on mineralization and bone mass at a cell

129 glycol) (PEG) chain onto the reducing end of CMD, forming carboxymethyl-dextran-block-poly(ethylene g

130 gical symptoms may be somatic equivalents of CMD in women in Asian cultures.

131 SELCoH sample prevalence estimates of CMD were nearly twice that of the APMS England sample es

132 Dental abnormalities are features of CMD that have been little discussed in the literature.

133 n gene (FKRP) is mutated in a severe form of CMD (MDC1C), characterized by the inability to walk, leg

134 in this autosomal recessive type 1A form of CMD results in neuromuscular dysfunction and, often, ear

135 the locus for the autosomal dominant form of CMD to an approximately 5-cM interval on chromosome 5p,

136 in the pathogenesis of the 'classic' form of CMD.

137 rter analyses demonstrated the importance of CMD-1 for activation of Pemm and autoactivation of Pmga

138 noninvasive identification and management of CMD patients.

139 of somatic gene therapy in a mouse model of CMD.

140 in-alpha2 deficiency in the murine models of CMD.

141 ty leisure-time activity had reduced odds of CMD 5 years later (below median vs. none: adjusted odds

142 hysically demanding jobs had reduced odds of CMD after 5 years, and there was no association between

143 FKRP may play a role in the pathogenesis of CMD and potentially explain why the allelic disorder LGM

144 erve <2.0 was used to define the presence of CMD.

145 information for estimating the prevalence of CMD and substance use is essential for surveillance and

146 The high prevalence of CMD in both sexes suggests that it may be a useful targe

147 The prevalence of CMD was 6.6% (95% confidence interval [CI], 5.7%-7.6%).

148 ents with a clinical phenotype suggestive of CMD, with muscle biopsy reserved as a second-tier invest

149 Among the group of CMDs with abnormalities of brain formation and mental re

150 is a pivotal molecule in the pathogenesis of CMDs.

151 her oral infections can increase the risk of CMDs independent of the aforementioned confounding facto

152 to changing pH, covalently immobilized onto CMD-coated supports.

153 The main outcome, CMD, was indicated by a score of 12 or above on the Revi

154 so presented, including the formation of pre-CMD intermediates and the analysis of bonding interactio

155 in childhood may have utility in predicting CMD risk.

156 an immunolabelling, unlinked to any reported CMD loci.

157 Serial Sanger sequencing of suspected CMD genes, while the current molecular diagnostic method

158 RI was performed in 118 women with suspected CMD who had undergone CRT and 21 asymptomatic reference

159 dysgalactiae subsp. dysgalactiae showed that CMD-1 and HTH-4 are critical for transcriptional activat

160 Here, we show that CMDs with tightly knit (clustered) friendship connection

161 The CMD pathway to the C-H bond cleavage for different class

162 Most of the CMD cases are caused by genetic mutations of laminin-alp

163 Successful validation and application of the CMD NGS panel to improve the diagnostic yield in a clini

164 boxylic groups, BSA was immobilized onto the CMD chip through covalent amide binding formation.

165 to quantify the various contributions to the CMD transition state (TS).

166 r accelerating the C-H deprotonation via the CMD mechanism; and (4) revealing the roles of the CsF ba

167 Thus, the CMDs are a model disorder group for development and vali

168 lycosylated in a mouse model of one of these CMDs, known as muscle-eye-brain disease, a disorder that

169 tion were both sensitive to the alpha-lac to CMD ratio, while the relative amount of CMD-b-PEG did no

170 which increased with increasing alpha-lac to CMD-b-PEG ratio and with decreasing pH.

171 pyrophosphate (PPi) transporter ANK leads to CMD-like features in an Ank(KI/KI) mouse model.

172 graphic and socioeconomic factors related to CMD and substance use across samples.

173 hat enhance symptoms and break resistance to CMD.

174 mon soil theory, the continuum of obesity to CMDs is the same pathology at different time points, and

175 With regard to CMDs, the major breakthrough involves a type of "classic

176 in muscle biopsy specimens from DMD, Ullrich CMD, and merosin-deficient CMD patients, all of which pr

177 The relative extent to which CMD affects both sexes is largely unknown.

178 Gene expression traits associated with CMD risk single-nucleotide polymorphism (SNPs) identifie

179 med dentofacial examination of patients with CMD and evaluated consequences of orthodontic movement i

180 ns for the dental treatment of patients with CMD are provided.

181 alometric analysis showed that patients with CMD tend to have a short anterior cranial base, short up

182 700 patients with MDS and 6300 patients with CMD were estimated for the entire United States in 2004.