ライフサイエンスコーパス: RLS

1 RLS also showed significant increases in tyrosine hydrox

2 RLS is a complex trait, for which genome-wide associatio

3 RLS is characterized by uncomfortable sensations in the

4 RLS measurements with a microfluidic dissection platform

5 RLS signal was therefore enhanced, and there is a linear

6 RLS tissue, compared with controls, showed a significant

7 RLS was assessed in 2002 using a set of standardized que

8 is shuttle, MAE1 and OAC1, largely abolishes RLS extension.

9 Forty-two patients were included; 14 had an RLS detected.

10 ely) compared with those who did not have an RLS identified.

11 lex sleep disorder and the development of an RLS animal model that closely recapitulates all disease

12 with long bone fractures, the presence of an RLS is associated with larger and more frequent microemb

13 The patients with an RLS showed higher counts and higher intensities of micro

14 tive correlations between ligand binding and RLS severity (international restless legs scale, IRLS) i

15 Both the CD and RLS intensities depend linearly on aggregate concentrati

16 uired for ssy5Delta-mediated NR increase and RLS extension.

17 ediated transport, rescued mitochondrial and RLS defects in nup116 mutants and increased longevity in

18 idiopathic generalized seizure and atypical RLS.

19 experiments, we determined that the average RLS of the yeast strains BY4741 and BY4742 is 25.9 buds

20 Because RLS symptoms peak at night when dopamine levels are lowe

21 , and there is a linear relationship between RLS increment and thrombin concentration in the range of

22 Doppler can be a useful tool to detect both RLS and the fat particles reaching the brain.

23 s, significantly more genes were detected by RLS compared to labeling by Cy3.

24 ssion profiles were obtained for labeling by RLS and fluorescence technologies.

25 effectively remove the hurdles presented by RLS analysis that have hindered S. cerevisiae aging stud

26 he GLFG domain of Nup116 displayed decreased RLSs, whereas longevity was increased in nup100-null mut

27 n conclusion, women with physician-diagnosed RLS had an increased risk of developing clinical depress

28 Physician-diagnosed RLS was collected via questionnaire.

29 Physician-diagnosed RLS was self-reported.

30 This study establishes RLS as a highly heritable trait, identifies a novel gene

31 y stage, we combined three GWAS datasets (EU-RLS GENE, INTERVAL, and 23andMe) with diagnosis data col

32 ) aggregates in aqueous HCl solution exhibit RLS when excited within the blue-shifted Soret band (H b

33 Here we report a novel approach to fabricate RLS crystal lines and 2D layers of unlimited dimensions

34 have emerged as the largest risk factors for RLS, suggesting that perturbations in this transcription

35 cloning and identification of the genes for RLS.

36 trait, identifies a novel genetic locus for RLS, and will facilitate further cloning and identificat

37 romosome 6 that confers substantial risk for RLS.

38 o discover and screen novel therapeutics for RLS.

39 to the possibility of a joint treatment for RLS targeting sensory and motor symptoms, as well as sle

40 role, a dopaminergic agonist widely used for RLS treatment.

41 st prior studies have used budding yeast for RLS studies.

42 Age, male gender, RLS, antidepressant treatment, and specific BTBD9, TOX3,

43 s were then treated with 80-nm-diameter gold RLS Particles coated with anti-biotin antibodies and ima

44 robial respiration, indicating that the high RLS is the result of lower particle fragmentation by zoo

45 iole, a dopamine agonist used to treat human RLS, reduced RLS-like movements.

46 uidic dissection platform produced identical RLS data at 2% (wt/vol) glucose.

47 gs documenting a dopaminergic abnormality in RLS brain tissue.

48 ve uncovered the iron-dopamine connection in RLS and the basic dopaminergic pathology related to the

49 a significant target for drugs effective in RLS, including dopamine agonists (pramipexole and ropini

50 for phenotypes similar to symptoms found in RLS patients.

51 e further evidence that BTBD9 is involved in RLS, and future studies of the Btbd9 mutant mice will he

52 a clear indication of dopamine pathology in RLS is revealed in this autopsy study.

53 s have implicated the dopaminergic system in RLS, while others have suggested that it is associated w

54 increase the availability of drug options in RLSs.

55 e virological monitoring suitable for use in RLSs is desperately needed.

56 is, age, male gender, antidepressant intake, RLS, and rs3923809, rs3104788, and rs2300478 SNPs were i

57 od of 12 weeks with use of the International RLS (IRLS) Study Group Rating Scale (on which the score

58 d questions recommended by the International RLS Study Group.

59 ng protonation of an Fe("0") intermediate (k(RLS) approximately 200 M(-1) s(-1)) that undergoes hydri

60 tly forms H(2) via a bimetallic mechanism (k(RLS) approximately 2000 M(-1) s(-1)).

61 med a meta-analysis of replicative lifespan (RLS) data published in more than 40 different papers.

62 The replicative lifespan (RLS) of a cell-defined as the number of cell divisions b

63 stem in which mother cells maintain a normal RLS--a median of 36 generations in the diploid MEP strai

64 ed the linkage result and defined this novel RLS disease locus to a critical interval.

65 of the depolarization ratio (rho(v)(90)) of RLS for a given aggregate geometry.

66 using refined approaches to ascertainment of RLS and depression are warranted.

67 cause iatrogenic worsening (augmentation) of RLS with long-term treatment.

68 he anatomic and genetic etiological bases of RLS are diverse.

69 -of-concept including key characteristics of RLS crystals is demonstrated using the example of Sb2S3

70 h Study, taking into account the duration of RLS symptoms.

71 es did not take into account the duration of RLS symptoms.

72 IS1 loss of function to the etiopathology of RLS, highlight how combined sequencing and systematic fu

73 A higher frequency of RLS symptoms was also associated with an increased risk

74 he risk increased with a higher frequency of RLS symptoms.

75 a population over time becomes a function of RLS, and it displays features of a survival curve such a

76 Implications of RLS growth on biomineralization and spherulitic crystal

77 constitute a main pathogenetic mechanism of RLS symptoms.

78 refore be the first genotypic mouse model of RLS.

79 led to new understanding of the morbidity of RLS and the many conditions associated with RLS, which h

80 Although the pathophysiology of RLS is unknown, dopaminergic neurotransmission and defic

81 opioids contribute to the pathophysiology of RLS remain unknown.

82 e role for opioids in the pathophysiology of RLS with respect to sensory and motor symptoms.

83 its potential role in the pathophysiology of RLS.

84 light on its role in the pathophysiology of RLS.

85 The presence of RLS at baseline was also associated with higher scores o

86 by SIR2 and FOB1, two opposing regulators of RLS in yeast.

87 cal examinations to evaluate the relation of RLS and microembolic signals to the development of fat e

88 s, as being associated with a higher risk of RLS.

89 red following standard criteria; symptoms of RLS were also assessed.

90 The use of RLS Particles is particularly attractive for detection a

91 These results suggest that RLS or RLS-associated conditions may contribute to the origin o

92 logical symptoms; all of them had a positive RLS (P=<0.001).

93 tor availability in 15 patients with primary RLS and 12 age-matched healthy volunteers using PET and

94 ned at autopsy from individuals with primary RLS and a neurologically normal control group.

95 t disruption of these circuit nodes produces RLS-like movements.

96 ine agonist used to treat human RLS, reduced RLS-like movements.

97 netic or environmental factors that regulate RLS.

98 external globus pallidus (GPe) in regulating RLS-like movements, in particular pallidocortical projec

99 ere is significant variation in the reported RLS data, which appears to be mainly due to the low numb

100 The remineralization length scale (RLS, the vertical distance over which organic particle f

101 ) solutions show resonance light scattering (RLS) at wavelengths within both the H and J aggregate ab

102 e application of resonance light scattering (RLS) particles for high-sensitivity detection of DNA hyb

103 of intensity in resonance light scattering (RLS) spectra.

104 sor was based on resonance light scattering (RLS) using magnetic nanoparticles (MNPs) as the RLS prob

105 and by enhanced resonance light scattering (RLS).

106 Both drugs were effective on sensory RLS symptoms.

107 oviral therapy in resource-limited settings (RLSs) are delayed until patients experience immunologica

108 therapy (ART) in resource-limited settings (RLSs) is monitored clinically and immunologically, accor

109 An intracardiac right-to-left shunt (RLS) could allow larger fat particles to reach the syste

110 ge analysis identified one novel significant RLS-susceptibility locus on chromosome 9p24-22 with a mu

111 Such rotating lattice single (RLS) crystals are found, but only as spherulitic grains

112 (ssy5Delta) increases replicative life span (RLS) by approximately 50%.

113 Using the replicative life span (RLS) of Saccharomyces cerevisiae as a model, we find tha

114 The replicative life span (RLS) of Saccharomyces cerevisiae has been established as

115 including control of replicative life span (RLS), prevention of collision between replication and tr

116 recombination and the replicative life span (RLS).

117 on and controlled the replicative life span (RLS).

118 The rate-limiting step (RLS) in the catalytic cycle is not the oxidative additio

119 endent rostral rhombic-lip migratory stream (RLS) that generates some neurons of the parabrachial, la

120 nitrogen-fixing Rhizobium legume symbiosis (RLS)(8) or by reverse genetic analyses of differentially

121 Restless leg syndrome (RLS) is a sensorimotor disorder.

122 eizures, and atypical restless leg syndrome (RLS).

123 association between restless legs syndrome (RLS) and coronary heart disease (CHD).

124 association between restless legs syndrome (RLS) and depression has involved cross-sectional data.

125 ieve symptoms of the restless legs syndrome (RLS) but have the potential to cause iatrogenic worsenin

126 Restless legs syndrome (RLS) is a CNS disorder involving abnormal limb sensation

127 Restless legs syndrome (RLS) is a common neurologic condition characterized by n

128 Restless legs syndrome (RLS) is a common neurological disorder that affects 5%-1

129 Although restless legs syndrome (RLS) is a disorder recognized in the medical literature

130 study, we found that restless legs syndrome (RLS) was associated with erectile dysfunction (ED).

131 Restless legs syndrome (RLS), also known as Willis-Ekbom disease, is a sensory-m

132 Restless Legs Syndrome (RLS), first chronicled by Willis in 1672 and described i

133 d in the etiology of Restless Legs Syndrome (RLS), which is more prevalent in females as compared wit

134 n the development of restless legs syndrome (RLS)-like movements during sleep.

135 nd motor symptoms in restless legs syndrome (RLS).

136 ents with idiopathic restless legs syndrome (RLS).

137 athogenetic model of restless legs syndrome (RLS).

138 higher proportion of restless legs syndrome (RLS; p < 0.001), had a higher body mass index (p = 0.001

139 all types of relative pairs, indicating that RLS is a highly heritable trait in this ascertained coho

140 These results suggest that RLS or RLS-associated conditions may contribute to the o

141 The RLS result is consistent with a model for the aggregates

142 ) using magnetic nanoparticles (MNPs) as the RLS probe.

143 e kissing and recombination and enhanced the RLS.

144 netic perturbations and drugs can extend the RLS via an aging-independent mechanism.

145 iron insufficiency similar to that from the RLS autopsy data.

146 These results are used to interpret the RLS depolarization ratios of four aggregates: tetrakis(4

147 evity despite the inherent difficulty of the RLS assay, which requires separation of mother and daugh

148 activated dopaminergic system as part of the RLS pathology.

149 putamen that correlated with severity of the RLS.

150 r findings suggest that, the more severe the RLS, the greater the release of endogenous opioids withi

151 Furthermore, we found that the RLS measured at 2% (wt/vol) glucose in CR experiments is

152 basic dopaminergic pathology related to the RLS symptoms.

153 nheritance, validated the 9p24-22 linkage to RLS in two families (two-point LOD score of 3.77; multip

154 cription factor might be causally related to RLS susceptibility.

155 ice model several characteristics similar to RLS and would therefore be the first genotypic mouse mod

156 ss in understanding, diagnosing and treating RLS, it remains an underdiagnosed and undertreated condi

157 tely 1150 positive genes were detected using RLS compared to approximately 110 positive genes detecte

158 ucted a prospective study to examine whether RLS was associated with a higher risk of developing ED b

159 Therefore, we prospectively examined whether RLS was associated with an increased risk of CHD in wome

160 onsisting of 453 subjects (134 affected with RLS).

161 RLS and the many conditions associated with RLS, which have also supported new approaches to treatme

162 Combinations of other sleep disorders with RLS further increased the risk of ED.

163 died patients with femur shaft fracture with RLS evaluation, daily transcranial Doppler with embolus

164 s of rare MEIS1 variants in individuals with RLS.

165 loss-of-function alleles in individuals with RLS.

166 In conclusion, men with RLS had a higher risk of ED, and the magnitude of the ri

167 Men with RLS were more likely to develop ED (relative risk = 1.38

168 gnal counts and intensities in patients with RLS was strongly predictive of the occurrence of neurolo

169 d efficacy and augmentation in patients with RLS who were treated with pregabalin as compared with pl

170 r, 0.07) for GDS-15 score between women with RLS and those without RLS (P < 0.0001).

171 Women with RLS at baseline had a marginally higher risk of developi

172 Women with RLS at baseline were more likely to develop clinical dep

173 nfidence interval, 1.09-2.73) for women with RLS for >/=3 years (P trend=0.03).

174 ariable-adjusted hazard ratios of women with RLS for >/=3 years were 1.80 (95% confidence interval, 1

175 nfidence interval, 0.44-2.19) for women with RLS for <3 years and 1.72 (95% confidence interval, 1.09

176 We observed that women with RLS for at least 3 years had an elevated risk of CHD.

177 ore between women with RLS and those without RLS (P < 0.0001).

178 (CI): 1.1, 2.1; P = 0.02) than those without RLS.

179 .04) for fatal CHD relative to women without RLS.

180 rval, 0.97-2.18) compared with women without RLS.