ライフサイエンスコーパス: RLS

1 RLS 1) was an independent risk factor for fewer days ali

2 RLS alone explained 5% (tetralogy of Fallot repair) to 2

3 RLS also showed significant increases in tyrosine hydrox

4 RLS are clinically relevant modifiers of uveitis activit

5 RLS extension was SIR2-dependent in KN99alpha, but not i

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

7 RLS is characterized by uncomfortable sensations in the

8 RLS is considered to be a complex condition in which pre

9 RLS is poorly recognized by physicians and it is accordi

10 RLS measurements with a microfluidic dissection platform

11 RLS occurs alone or with comorbidities, for example, iro

12 RLS participants were 52.7 +/- 12.0 years old, 61.9% wer

13 RLS severity was assessed by International RLS Study Gro

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

15 RLS tissue, compared with controls, showed a significant

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

17 RLS was associated with higher rates of TOLS (78.3% vs 7

18 venipuncture at 19:00, 20:30, and 22:00; 37 RLS and 36 controls had lumbar puncture at 21:30.

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

20 nces in the distribution of ACC grades among RLS were observed, with a peak in prepuberty and early p

21 An RLS autopsy study reveals decreases in endogenous opioid

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

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

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

25 ntify the role of Mn in the regulation of an RLS genetic risk factor BTBD9, characterize the function

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

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

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

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

30 minated the relationship between rDNA CN and RLS.

31 ated increases in mitochondrial function and RLS extension.

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

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

34 61.9% were women, 21.4% had painful RLS, and RLS severity was 24.8 +/- 9.0.

35 etic associations with insomnia symptoms and RLS against the outcomes of risk of major depressive dis

36 idiopathic generalized seizure and atypical RLS.

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

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

39 studies have reported an association between RLS, cardiovascular disease, and hypertension although t

40 tatistically significant interaction between RLS and sex (P = .044), with a perimenopausal peak retai

41 significant common variant overlaps between RLS and neuroticism (r(g) = 0.40, se = 0.08, p value = 5

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

43 nes the epidemiological relationship between RLS, cardiovascular disease and hypertension, potential

44 tized potential causal relationships between RLS and relevant comorbidities and risk factors for foll

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

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

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

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

49 ed by polysomnography and by the 3-D-camera (RLS: r = 0.654; p = 0.004).

50 However, they cause RLS-like symptoms and periodic limb movements when injec

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

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

53 Physician-diagnosed RLS was collected via questionnaire.

54 Physician-diagnosed RLS was self-reported.

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

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

57 rative echocardiography and clinical events: RLS 1 (trivial or no residual lesions), RLS 2 (minor res

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

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

60 re might be an environmental risk factor for RLS.

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

62 cloning and identification of the genes for RLS.

63 high-complexity technologies impractical for RLS.

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

65 Outcomes for RLS 1 versus 2 did not differ consistently.

66 romosome 6 that confers substantial risk for RLS.

67 o discover and screen novel therapeutics for RLS.

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

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

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

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

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

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

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

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

76 changes closest to those seen in idiopathic RLS.

77 In RLS patients 72.8% of leg movements confirmed by polysom

78 gs documenting a dopaminergic abnormality in RLS brain tissue.

79 striatal zinc paralleling similar changes in RLS.

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

81 ncreased and CSF beta-endorphin decreased in RLS patients with painful symptoms.

82 hat neuronal intracellular iron depletion in RLS also manifests as NDEV abnormalities in other iron r

83 for HIV-2 is feasible and can be deployed in RLS with limited infrastructure.

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

85 ng hormone (alpha-MSH) and beta-endorphin in RLS patients and controls.

86 that increased NDEV ferritin occurs even in RLS accompanied by systemic ID and that neuronal intrace

87 for phenotypes similar to symptoms found in RLS patients.

88 in serum ferritin that are normally found in RLS.

89 Plasma POMC was significantly greater in RLS than controls (17.0 +/- 11.5 vs 12.7 +/- 6.1fmol/ml,

90 CSF alpha-MSH was higher in RLS than controls (34.2 +/- 40.9 vs 20.3 +/- 11.0pg/ml,

91 ondrial function, and undergo an increase in RLS as they adapt to the loss of mtDNA.

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

93 on-derived extracellular vesicles (NDEVs) in RLS, suggesting a mechanism for depleting intracellular

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

95 Receptor blocker studies in RLS patients suggest that the therapeutic efficacy of op

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

97 raction explained over 70% of variability in RLS among a series of wild-type strains.

98 orate residual DSPN after initiating cART in RLSs.

99 increase the availability of drug options in RLSs.

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

101 and 4, and Mendelian randomization indicated RLS as a causal risk factor for diabetes.

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

103 RLS severity was assessed by International RLS Study Group Severity Scale.

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

105 d questions recommended by the International RLS Study Group.

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

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

108 Deletion of SIS2 gene led to the largest RLS increase observed.

109 nts: RLS 1 (trivial or no residual lesions), RLS 2 (minor residual lesions), or RLS 3 (reintervention

110 ction (CR) prolongs Cn replicative lifespan (RLS) and mimics low-glucose environments in which Cn res

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

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

113 chromosomal array and replicative lifespan (RLS).

114 mtDNA is a decrease in replicative lifespan (RLS).

115 measurements of yeast replicative lifespan (RLS); however, comparative quantification of lifespan ac

116 shared pathophysiological mechanisms linking RLS and PLMs to cerebrovascular pathology, highlighting

117 t in painful RLS, intermediate in nonpainful RLS, and highest in controls (8.0 +/- 3.4 vs 10.8 +/- 3.

118 diate, and lowest in painful RLS, nonpainful RLS, and controls (p = 0.007).

119 nificantly higher in painful than nonpainful RLS or controls (48.2 +/- 24.8 vs 32.1 +/- 14.8 vs 32.6

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

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

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

123 Clear advantages of RLS over LLS have rarely been demonstrated, and the asso

124 and genome-wide association meta-analysis of RLS cases (n = 9,851) and controls (n = 38,957) in 3 pop

125 understanding of the genetic architecture of RLS, and highlights the contributions of common variants

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

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

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

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

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

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

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

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

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

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

136 Implications of RLS growth on biomineralization and spherulitic crystal

137 tive review details the current knowledge of RLS, a still underdiagnosed and poorly recognized disord

138 constitute a main pathogenetic mechanism of RLS symptoms.

139 mu-opioid receptor knock-out mouse model of RLS show circadian motor changes akin to RLS and, althou

140 refore be the first genotypic mouse model of RLS.

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

142 The pathophysiology of RLS and periodic leg movement is still poorly understood

143 The genetic basis and pathophysiology of RLS are incompletely understood.

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

145 opioids contribute to the pathophysiology of RLS remain unknown.

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

147 its potential role in the pathophysiology of RLS.

148 light on its role in the pathophysiology of RLS.

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

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

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

152 ights on the potential clinical relevance of RLS in cerebrovascular risk assessment and management.

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

154 an precipitate or exacerbate the symptoms of RLS and PLMs.

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

156 nd perhaps Met-enkephalin in the thalamus of RLS patients.

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

158 lesions), RLS 2 (minor residual lesions), or RLS 3 (reintervention for or major residual lesions befo

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

160 While both produce excellent outcomes, RLS might facilitate slightly higher TOLS rates than LLS

161 ars old, 61.9% were women, 21.4% had painful RLS, and RLS severity was 24.8 +/- 9.0.

162 CSF beta-EDP was lowest in painful RLS, intermediate in nonpainful RLS, and highest in cont

163 highest, intermediate, and lowest in painful RLS, nonpainful RLS, and controls (p = 0.007).

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

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

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

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

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

169 netic or environmental factors that regulate RLS.

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

171 prepuberty and puberty than in the remaining RLS (P = .012).

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

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

174 scopy as well as resonance light scattering (RLS) and time-resolved measurements, and where possible,

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

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

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

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

179 and by enhanced resonance light scattering (RLS).

180 ution, line edge roughness, and sensitivity (RLS) trade-off has fundamentally limited the lithographi

181 Both drugs were effective on sensory RLS symptoms.

182 tment of HIV-2 in resource-limited settings (RLS) is complicated by the limited availability of HIV-2

183 ood) that work in resource-limited settings (RLS).

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

185 N prevalence in 7 resource-limited settings (RLSs) for combination antiretroviral therapy (cART)-naiv

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

187 Severe RLS symptoms can negatively impact sleep, mood, and qual

188 Forty-two untreated moderate-to-severe RLS patients and 44 matched controls underwent venipunct

189 disease in patients with moderate-to-severe RLS.

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

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

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

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

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

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

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

197 recombination and the replicative life span (RLS).

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

199 profiles and the Regularized Least Squares (RLS) classifier.

200 vity varies across reproductive life stages (RLS) according to sex.

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

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

203 In the subgroups, RLS tended to have higher TOLS rates, compared with LLS,

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

205 Insomnia and restless leg syndrome (RLS) are associated with increased risk for suicidal beh

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

207 ve been implicated in restless leg syndrome (RLS) pathogenesis.

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

209 Restless legs syndrome (RLS) affects up to 10% of older adults.

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

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

212 Restless legs syndrome (RLS) and periodic limb movements (PLMs) are increasingly

213 ensory discomfort of restless legs syndrome (RLS) and properties of melanocortin hormones, including

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

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

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

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

218 Restless legs syndrome (RLS) is a common neurological disorder, but the etiology

219 Restless legs syndrome (RLS) is a common sensorimotor disorder characterized by

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

221 Restless legs syndrome (RLS) is a frequent sleep-related sensorimotor disorder d

222 Restless legs syndrome (RLS) is a neurological condition that causes uncomfortab

223 Restless legs syndrome (RLS) is responsive to opioid, dopaminergic and iron-base

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

225 ng (19 patients with restless legs syndrome (RLS), 21 patients with obstructive sleep apnea (OSA), an

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

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

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

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

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

231 athogenetic model of restless legs syndrome (RLS).

232 ents with idiopathic restless legs syndrome (RLS).

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

234 METHODS, INTERVENTION, OR TESTING: RLS (prepuberal, early puberty, late puberty, reproducti

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

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

237 The RLS (Residual Lesion Score) study explored the impact of

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

239 The RLS was assigned based on post-operative echocardiograph

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

241 e kissing and recombination and enhanced the RLS.

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

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

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

245 Here we microfluidically measure the RLS of 307 yeast strains, each deleted for a single gene

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

247 activated dopaminergic system as part of the RLS pathology.

248 putamen that correlated with severity of the RLS.

249 ltimately enable researchers to overcome the RLS trade-off.

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

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

252 us should provide an elegant solution to the RLS barrier.

253 basic dopaminergic pathology related to the RLS symptoms.

254 Importantly, the RLSs of reported lifespan-enhancing mutations were signi

255 hough MATalpha and MATa cells extended their RLS in response to CR, they engaged different pathways.

256 of RLS show circadian motor changes akin to RLS and, although both models show sensory changes, the

257 altered melanocortin system may be causal to RLS as well.

258 Genetically proxied liability to RLS did not significantly influence the risk of any of t

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

260 ogenous opioid deficiency is pathogenetic to RLS and that an altered melanocortin system may be causa

261 cription factor might be causally related to RLS susceptibility.

262 onlinear interactions are likely relevant to RLS risk prediction.

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

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

265 he 10.075 included patients, 1.507 underwent RLS and 8.568 LLS.

266 tudy, the outcomes of patients who underwent RLS and LLS for all indications between 2009 and 2021 in

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

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

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

270 we studied 71 women with ID anemia, 36 with RLS, and 35 without RLS.

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

272 l novel genetic risk factors associated with RLS susceptibility.

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

274 number (rDNA CN) positively correlated with RLS and this interaction explained over 70% of variabili

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

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

277 ociation studies in 116,647 individuals with RLS (cases) and 1,546,466 controls of European ancestry.

278 s of rare MEIS1 variants in individuals with RLS.

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

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

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

282 Patients with RLS often display periodic leg movements during sleep or

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

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

285 ess are found in 60% to 80% of patients with RLS.

286 Subjects with RLS again showed higher NDEV ferritin and also decreased

287 s with sleep disorders, including those with RLS.

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

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

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

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

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

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

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

295 with ID anemia, 36 with RLS, and 35 without RLS.

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

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

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

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