ライフサイエンスコーパス: NRS

1 NRS is evaluated from preoperative risk assessment to it

2 SCORAD (kappa = 0.47), EASI (kappa = 0.37), NRS-itch (kappa = 0.49), POEM (kappa = 0.37), and DLQI (

3 EASI (-17.1/-9.8/-3.2), BSA (-46%/-15%/-4%), NRS-itch (-5/-2/0), POEM (-5/-2/0), and DLQI (-8/-6/-1)

4 , EASI (0.56 and 0.50), BSA (0.52 and 0.45), NRS-itch (0.60 and 0.53), POEM (0.50 and 0.48), and DLQI

5 as average pain intensity measured at day 7 (NRS, 0 to 10); secondary outcomes were analgesic consump

6 assay (EMSA) using whole-cell extracts and a NRS-containing DNA fragment detects a protein which spec

7 abolishes U11 binding (RG11) also abrogates NRS splicing inhibition, indicating that U11 is function

8 xy-4-nitroso-2,7-naphthalenedisulfonic acid (NRS) complexes on the quantification of the polyphenols

9 ously shown to abolish U11 snRNP binding and NRS function.

10 high correlation between the ItchyQuant and NRS (>0.92, P < 0.0001), demonstrating concurrent validi

11 st of symmetry to assess differences between NRS and non-NRS plaques, whereas we calculated receiver-

12 r of radiomic features are different between NRS and non-NRS plaques and exhibit excellent discrimina

13 eatures were significantly different between NRS and non-NRS plaques.

14 We investigated a link between NRS-mediated splicing inhibition and efficient polyadeny

15 icant difference in treatment effect between NRSs with PS analysis and RCTs.

16 ificantly higher oSCORAD, SCORAD, EASI, BSA, NRS-itch, POEM, and DLQI (P < .0001 for all).

17 embly process was sensitive to high salt but NRS complexes were salt stable once formed.

18 cohorts reported pain relief as assessed by NRS and SF-MPQ.

19 As compared to the CMAb NRS controls, delays in the mean time to lesion appearan

20 opy number per mug of rabbit DNA in the CMAb NRS group of 7.65 x 10(3) copies, while no T. pallidum D

21 nding that a large spliceosome-like complex (NRS-C) assembles on NRS RNA in nuclear extract, led to t

22 nsus C or G at any of these sites diminished NRS activity, whereas substitution of a single A generat

23 NRS, linked to a downstream intron and exon (NRS-Ad3'), was not capable of splicing in vitro.

24 One model to explain NRS splicing inhibition holds that the NRS interacts non

25 Fatigue dimensions, fatigue NRS score, interference of fatigue with daily life, symp

26 activity" and "reduced motivation," fatigue NRS, symptom burden, interference of fatigue with daily

27 Finally, NRS is proposed for treatment for postoperative acute re

28 o inhibit splicing in vivo are defective for NRS complex assembly in nuclear extract.

29 suggest that U1 is of primary importance for NRS splicing inhibition.

30 ating that U11 is functionally important for NRS activity and suggesting that the NRS is recognized a

31 All three of these U's are important for NRS-mediated splicing suppression.

32 e use of hand-held Raman instrumentation for NRS and EC-SERS, showing that Raman is a highly sensitiv

33 non-specific H complex, factors required for NRS complex assembly are limiting in nuclear extract.

34 acute rejection observed in allografts from NRS-treated recipients, the resulting rejection of the a

35 d to compare treatment effect estimates from NRSs with PS analysis and RCTs of surgery.

36 d read-through, indicating that a functional NRS is necessary for efficient RSV polyadenylation rathe

37 A higher NRS score was also significantly associated with the fol

38 dium (Tris; pH 8.0) with formation of Fe(II)/NRS complexes.

39 medicine were analysed by using both Fe(III)/NRS complexes and the Folin-Ciocalteu reagent.

40 We implement NRS to detect gentamicin, a commonly IV-administered ant

41 e minimum clinically important difference in NRS pain score of 1.3.

42 red the roles of several cellular factors in NRS-mediated polyadenylation.

43 The possible roles of hnRNP H in NRS function are discussed.

44 se data indicate a functional role for U1 in NRS-mediated splicing inhibition.

45 perimental intervention is more favorable in NRSs with PS analysis than RCTs.

46 e that efficient U11 binding to the isolated NRS involves at least two elements in addition to the U1

47 The baseline mean NRS pain score was 8.7 (SD, 1.3).

48 At 2 hours, the mean NRS pain score decreased by 4.3 (95% CI, 3.6 to 4.9) in

49 functional spliceosome formed on the mutant NRS-Ad3' RNA.

50 pears functionally significant since mutated NRS RNAs that fail to inhibit splicing in vivo are defec

51 ASLV and FP) were substituted for the native NRS purine region.

52 th NRS plaques and matched these with 30 non-NRS plaques with similar degree of calcification, lumina

53 c features are different between NRS and non-NRS plaques and exhibit excellent discriminatory value.

54 ry to assess differences between NRS and non-NRS plaques, whereas we calculated receiver-operating ch

55 significantly different between NRS and non-NRS plaques.

56 However, further mutational analyses of NRS sequences have identified a U1 binding site that ove

57 We observed a higher association of NRS scores between identical vs fraternal twins (r = 0.6

58 Timing and duration of NRS is also addressed.

59 However, identification of NRS is challenging because of its qualitative nature.

60 omic analysis improves the identification of NRS plaques.

61 Fe(III) to Fe(II) by [PA] in the presence of NRS in a buffered medium (Tris; pH 8.0) with formation o

62 We suggest that the removal of NRS-containing hnRNP proteins from pre-mRNA/mRNA is requ

63 Data supporting intraoperative use of NRS including preinduction continuous positive airway pr

64 We retrieved 70 reports of NRSs with PS analysis and 94 related RCTs evaluating 31

65 ndependent complex that rapidly assembled on NRS RNA.

66 pliceosome-like complex (NRS-C) assembles on NRS RNA in nuclear extract, led to the proposal that the

67 ee pain and stiffness (WOMAC), average pain (NRS), intermittent and constant knee pain (Intermittent

68 on the ItchyQuant, on a traditional 11-point NRS, and with verbal categorizations (no, mild, moderate

69 positive airway pressure and postextubation NRS for high-risk individuals and surgeries are examined

70 Prospective NRSs with suitable and careful PS analysis can be relied

71 rched MEDLINE via PubMed for all prospective NRSs with PS analysis evaluating a surgical procedure.

72 lement 1 or neural restrictive silencer (RE1/NRS).

73 mpared to levels of control groups receiving NRS.

74 RS) and a downstream 3'ss, which repositions NRS-bound SR proteins closer to the viral PAS.

75 A comparison of Ssa1p's NRSs to sequences of other Hsp70s and actin revealed tha

76 Surprisingly, the expectation that the same NRS mutants would be defective for splicing inhibition p

77 re C30, 0 to 100), and patient satisfaction (NRS, 0 to 10).

78 Two pCASL scans and numerical rating scale (NRS) estimates of ongoing pain were acquired in each of

79 llustrated self-report numeric rating scale (NRS) for itch severity.

80 uded changes in the Neurologic Rating Scale (NRS) score of 10 or greater (score range, 0-100), Multip

81 tory (THI) scores, and numeric rating scale (NRS) scores of tinnitus loudness and tinnitus perception

82 ed using an 11-point numerical rating scale (NRS), in which 0 indicates no pain and 10 indicates the

83 ed using the 0 to 10 numerical rating scale (NRS), primary biliary cholangitis-40 (PBC-40) itch domai

84 f was assessed using a numeric rating scale (NRS), the Short Form McGill Pain Questionnaire (SF-MPQ),

85 symptoms on a 0 to 10 numeric rating scale (NRS).

86 lking (assessed on a numerical rating scale [NRS]) and physical function (Western Ontario and McMaste

87 breathlessness (0-10 numerical rating scale [NRS]), measured twice a day (morning and evening).

88 pain intensity >/= 4 (numeric rating scale [NRS], 0 to 10) in the last 24 hours were eligible.

89 ), and the number of nonreversible segments (NRS).

90 existence of a negative regulatory sequence (NRS).

91 ause they bear a nuclear retention sequence (NRS) that is capable of overriding NESs.

92 eting antibody (dAb) or normal rabbit serum (NRS) 6 or 12 hours after intravitreal injection.

93 lling was observed when normal rabbit serum (NRS) or heat-inactivated complement was used.

94 rafts were treated with normal rabbit serum (NRS) or rabbit Mig antiserum (Mig AS) every other day fr

95 lizing MIP-2 pAb versus normal rabbit serum (NRS) resulted in reduced corneal PMN number and ocular d

96 disease, TIMP pAb- and normal rabbit serum (NRS)- (control) treated mice were examined macroscopical

97 monoclonal antibody in normal rabbit serum (NRS).

98 Napkin-ring sign (NRS) is an independent prognostic imaging marker of majo

99 The nuclear receptor signaling (NRS) field has generated a substantial body of informati

100 ified age, ischemia (SDS), and infarct size (NRS) as independent predictors of CD.

101 In this subgroup only age and infarct size (NRS) were predictive of CD.

102 t according to the National Rosacea Society (NRS) grading system.

103 We show here, using specific NRS mutations to disrupt U11 binding and coexpression of

104 Normal Raman spectroscopy (NRS) provides a modestly sensitive, label-free, and comp

105 wn as non-equilibrium response spectroscopy (NRS) based on ion channel responses to rapidly fluctuati

106 ) within the negative regulator of splicing (NRS) and a downstream 3'ss, which repositions NRS-bound

107 racts on the negative regulator of splicing (NRS) element from Rous sarcoma virus.

108 A contains a negative regulator of splicing (NRS) element that aids in maintenance of unspliced RNA.

109 a cis-acting negative regulator of splicing (NRS) element that is implicated in viral polyadenylation

110 ll as in the negative regulator of splicing (NRS) element.

111 The negative regulator of splicing (NRS) from Rous sarcoma virus suppresses viral RNA splici

112 The negative regulator of splicing (NRS) is a long cis-acting RNA element in Rous sarcoma vi

113 virus (RSV) negative regulator of splicing (NRS) is an RNA element that represses splicing and promo

114 known as the negative regulator of splicing (NRS) that acts to inhibit viral RNA splicing.

115 equence, the negative regulator of splicing (NRS), is of interest because it blocks splicing but is n

116 element, the negative regulator of splicing (NRS), that binds SR proteins and U1/U11 snRNPs and funct

117 , termed the negative regulator of splicing (NRS), which serves to repress splicing of viral RNA but

118 t termed the negative regulator of splicing (NRS).

119 e called the negative regulator of splicing (NRS).

120 element that negatively regulates splicing (NRS).

121 n glycan from Geobacillus stearothermophilus NRS 2004/3a is mainly composed of repeating units of thr

122 Nonrandomized studies (NRSs) involving use of propensity score (PS) analysis to

123 utility of noninvasive respiratory support (NRS) in acute respiratory failure, it is likewise likely

124 The NRS acts as a pseudo 5' splice site (ss), and serine-arg

125 The NRS also efficiently binds U11 snRNP of the U12-dependen

126 The NRS binds components of the splicing machinery including

127 The NRS binds serine/arginine-rich (SR) proteins, hnRNP H an

128 The NRS binds U1 snRNA at a sequence that deviates from the

129 The NRS can also inhibit splicing of heterologous introns in

130 The NRS complex was not detected in reactions containing ATP

131 The NRS comprises approximately 78 amino acids and is largel

132 The NRS functions in either orientation, but only when locat

133 The NRS harbors a branch point-like/pyrimidine tract sequenc

134 The NRS is functionally divided into two parts termed NRS5'

135 The NRS score and rosacea subtype were assessed using the NR

136 The NRS scores improved significantly from a pretransplant m

137 The NRS specifically binds bacterially expressed SF2/ASF, wh

138 The NRS, linked to a downstream intron and exon (NRS-Ad3'),

139 ught to bridge the long distance between the NRS and poly(A) site.

140 Bound SR proteins may bridge between the NRS and the 3' LTR and aid in the recruitment of the 3'-

141 iral env 3' splice site sequence between the NRS and the LTR did not alter the level of polyadenylati

142 Here we show that U11 can bind the NRS as a mono-snRNP in vitro and that a G-rich element l

143 shown by UV cross-linking assays to bind the NRS preferentially.

144 nuclear ribonucleoproteins (snRNPs) bind the NRS, and a correlation was established between SF2/ASF a

145 nd how the low abundance U11 snRNP binds the NRS so well.

146 ng indicated that splicing inhibition by the NRS correlates most strongly with U1 snRNP.

147 for long-distance poly(A) stimulation by the NRS.

148 ro; however, if the transcript contained the NRS upstream of the LTR, polyadenylation was observed.

149 tions within the gag gene that encompass the NRS also lead to increased read-through past the viral p

150 yadenylation site, suggesting a role for the NRS in promoting polyadenylation.

151 y(A) site eliminated the requirement for the NRS-3' splice site interaction.

152 to levels approaching that observed for the NRS.

153 as assessed by minor class splicing from the NRS to a minor class 3'ss from the P120 gene.

154 et splicing does not normally occur from the NRS.

155 aseline than the double-blind placebo in the NRS (-23%, 95% CI -45 to -1; p=0.037), PBC-40 itch domai

156 One of two critical sequences located in the NRS 3' region resembles a minor class 5' splice site and

157 The largest difference in decline in the NRS pain score from baseline to 2 hours was between the

158 However, a double-point mutation in the NRS pseudo-5' splice site sequence converted it into a f

159 Improvements in the NRS scores of tinnitus perception correlated positively

160 Assembly of the NRS complex appears functionally significant since mutat

161 The probable relationship of the NRS complex to spliceosomal complexes is discussed.

162 To test whether disruption of the NRS or of the MA protein was responsible for inducing sh

163 Thus, we propose that disruption of the NRS sequence promotes readthrough transcription and spli

164 SR proteins that bind to the 5' half of the NRS, confirming an earlier proposal that this region is

165 ng RSV polyadenylation in the context of the NRS-3' splice site complex, which is thought to bridge t

166 the authentic 5' splice site upstream of the NRS.

167 inically important difference was 1.3 on the NRS.

168 he ItchyQuant easier to use (45.8%) than the NRS (20.8%) or had no preference (33.3%), P = 0.008.

169 ts (47.2%) preferred the ItchyQuant than the NRS (23.6%) or had no preference (29.2%), P = 0.0015.

170 These results show that the NRS can interact with a 3' splice site and suggest that

171 plain NRS splicing inhibition holds that the NRS interacts nonproductively with and sequesters U2-dep

172 In this study, we provide evidence that the NRS interacts with an adenovirus 3' splice site.

173 ant for NRS activity and suggesting that the NRS is recognized as a minor-class 5' splice site (5' ss

174 uclear extract, led to the proposal that the NRS is recognized as a minor-class 5' splice site.

175 We conclude that the NRS promotes polyadenylation in vitro and can do so with

176 s harboring compensatory mutations, that the NRS U11 site is functional when paired with a minor-clas

177 on stimulatory activity maps directly to the NRS and is most likely dependent upon SR proteins and U1

178 he binding sites of U1 and U11 snRNPs to the NRS did not affect polyadenylation, whereas hnRNP H stro

179 ce, was also required for U11 binding to the NRS in vivo as assessed by minor class splicing from the

180 ports the notion that SF2/ASF binding to the NRS is relevant, but other SR proteins may substitute if

181 NP protein, hPrp8, did not cross-link to the NRS pseudo-5' splice site, suggesting that the tri-snRNP

182 pproximately half of the contribution to the NRS score could be accounted for by genetics and the oth

183 e region in facilitated snRNP binding to the NRS via SF2/ASF.

184 f U2 snRNP also decreased U11 binding to the NRS.

185 gion is involved in recruiting snRNPs to the NRS.

186 ear ribonucleoprotein (snRNP) binding to the NRS.

187 om HeLa cells cross-link specifically to the NRS.

188 H and SR proteins compete for binding to the NRS.

189 and rosacea subtype were assessed using the NRS grading system and physical examination by board-cer

190 In vitro, the NRS acted as a potent, orientation-dependent enhancer of

191 In vitro, the NRS alone activated a model RSV polyadenylation substrat

192 adenylation in proviral clones only when the NRS-3' splice site complex could form.

193 We propose a model in which the NRS serves to enhance polyadenylation of RSV unspliced R

194 fails to block splicing when paired with the NRS 3' region supports the notion that SF2/ASF binding t

195 As with the NRS, the Env enhancer also stimulated use of the viral P

196 ition of SR protein binding sites within the NRS and Env enhancer, is required for long-range polyade

197 erated a preferred 5' splice site within the NRS.

198 and presentation of public data relevant to NRS.

199 sier to use when compared with a traditional NRS.

200 , if not better than, that for the wild-type NRS.

201 emonstrate two individual cases where we use NRS and electrochemical SERS (EC-SERS) to detect IV ther

202 Using NRS-specific deletions and mutations, we show here that

203 n of corneal tissues from TIMP-1 pAb- versus NRS-treated mice confirmed that TIMP-1 pAb treatment res

204 , expert readers identified 30 patients with NRS plaques and matched these with 30 non-NRS plaques wi

205 latency lymphomas, we generated viruses with NRS point mutations that maintained the wild-type Gag am

206 dition, U11 snRNP was present only in the WT NRS-Ad3' complex.

207 parin to these complexes destabilized the WT NRS-Ad3' complex; it was incapable of forming a B comple

208 The wild-type (WT) NRS-Ad3' transcript assembled an approximately 50S splic