ライフサイエンスコーパス: ARR

1 ARR has an apparent melting temperature of 41 degrees C,

2 ARR is a heterodimer of approximately 131 kDa, composed

3 ARR is expressed at the beginning of the exponential pha

4 ARR requires anaerobic conditions and molybdenum for act

5 ARR-1 activity also controlled immunity through ADF chem

6 ARR-1 is primarily expressed in the nervous system, incl

7 ARRs of major cardiovascular events by statin therapy ca

8 ARRs were independent of trimester.

9 ared with the placebo group (30.6% vs 60.0%; ARR with infliximab, 29.4%; 95% confidence interval: 18.

10 eased survival (OR, 1.81; 95% CI, 1.64-2.00; ARR 5.17%).

11 ival (OR, 1.15; 95% CI, 1.13-1.17; P < .001; ARR, 1.4%).

12 score matching (OR, 1.88; 95% CI, 1.74-2.03; ARR, 5.93%).

13 the organismal level, we studied arrestin-1 (ARR-1), which is the only GPCR adaptor protein in C. ele

14 ted sensitive; DRFS, 83% [95% CI, 68%-100%]; ARR, 26% [95% CI, 4%-48%]) subsets and was significant i

15 ted sensitive; DRFS, 97% [95% CI, 91%-100%]; ARR, 11% [95% CI, 0.1%-21%]) and ER-negative (26% predic

16 f reporting problems decreased from 6 to 12 (ARR 0.87, 95% CI: 0.83-0.90), 12 to 24 (ARR 0.94, 95% CI

17 s who initially received interferon beta-1a, ARR was lower after switching to fingolimod compared wit

18 2.5%-4.3%; 95% confidence interval for 3.2% ARR, -1.4% to 6.8%).

19 and mortality declined from 25.1% to 19.2% (ARR, 6.0%; 95% CI, 4.6%-7.3%; RRR, 23.7%; 95% CI, 19.7%-

20 ent mortality decreased from 25.1% to 22.2% (ARR, 3.0%; 95% CI, 1.6%-4.4%; RRR, 12%; 95% CI, 7.5%-16.

21 .23) in 1996 to 10.12% (9.58-10.69) in 2005 (ARR, 1.68; 95% CI, 1.55-1.81), or from 13.3 to 27.0 mill

22 12 (ARR 0.87, 95% CI: 0.83-0.90), 12 to 24 (ARR 0.94, 95% CI: 0.90-0.98), and 24 to 36 months (ARR 0

23 y on Rutgeerts scores >/=i2 (22.4% vs 51.3%; ARR with infliximab, 28.9%; 95% confidence interval: 18.

24 and NPV (ZDV-3TC-NVP) (647 of 1365 [47.4%]; ARR, 1.30; 95% CI, 1.20-1.41); or ZDV-3TC-LPV-R (75 of 1

25 tonavir (TDF-FTC-LPV-R) (112 of 231 [48.5%]; ARR, 1.31; 95% CI, 1.13-1.52); zidovudine, lamivudine, a

26 DVT (6 trials; RR, 0.29 [CI, 0.16 to 0.52]; ARR, 7.1%).

27 l PE (4 trials; OR, 0.13 [CI, 0.03 to 0.54]; ARR, 0.7%), and DVT (7 trials; RR, 0.37 [CI, 0.21 to 0.6

28 DVT (7 trials; RR, 0.37 [CI, 0.21 to 0.64]; ARR, 12.1%) with prolonged prophylaxis.

29 TC and nevirapine (NVP) (317 of 760 [41.7%]; ARR, 1.15; 95% CI, 1.04-1.27); TDF-FTC and lopinavir-rit

30 relative risk [RR], 0.48 [CI, 0.31 to 0.75]; ARR, 5.8%), symptomatic DVT (4 trials; OR, 0.36 [CI, 0.1

31 predicted benefit subgroup had a NNT of 76 (ARR = 0.013, 95% CI: -0.0001, 0.026; P = 0.053), and tho

32 lism (4 trials; RR, 0.38 [CI, 0.19 to 0.77]; ARR, 5.7%), nonfatal PE (4 trials; OR, 0.13 [CI, 0.03 to

33 and death by any cause (OR 0.69, 0.62-0.78; ARR 2.7%, 2.0-3.5; NNT 37, 29-52), implying that 145 sel

34 d mortality rate declined from 8.3% to 7.8% (ARR, 0.5%; 95% CI, 0.2%-0.9%; RRR, 6.3%; 95% CI, 3.8%-8.

35 DVT (4 trials; OR, 0.36 [CI, 0.16 to 0.81]; ARR, 1.5%), and proximal DVT (6 trials; RR, 0.29 [CI, 0.

36 t 5 to 8 years, 1.67 [95% CI, 1.57 to 1.81]; ARR at 18 to 20 years, 1.22 [95% CI, 1.08 to 1.37]).

37 .11]), stroke (RR, 0.73 [95% CI, 0.64-0.83]; ARR, 4.06 [95% CI, 2.53-5.40]), albuminuria (RR, 0.83 [9

38 ) than among those receiving only TIV (85%) (ARR, 0.93 [95% CI, .84-.997]).

39 cantly change (1996, 26.25% vs 2005, 26.85%; ARR, 0.95; 95% CI, 0.83-1.07), although the percentage o

40 g antipsychotic medications (5.46% vs 8.86%; ARR, 1.77; 95% CI, 1.31-2.38) increased and those underg

41 ng psychotherapy declined (31.50% vs 19.87%; ARR, 0.65; 95% CI, 0.56-0.72).

42 , albuminuria (RR, 0.83 [95% CI, 0.79-0.87]; ARR, 9.33 [95% CI, 7.13-11.37]), and retinopathy (RR, 0.

43 k of symptoms of depression (13.7% vs 49.9%; ARR, 0.28; 95% CI, 0.22 to 0.34; P < .001).

44 -1.41); or ZDV-3TC-LPV-R (75 of 167 [44.9%]; ARR, 1.21; 95% CI, 1.01-1.45).

45 -69), deaths by suicide (OR 0.75, 0.60-0.94; ARR 0.5%, 0.1-0.9; NNT 188, 108-725), and death by any c

46 score matching (OR, 1.73; 95% CI, 1.55-1.94; ARR, 4.69).

47 6% vs 8.9%; OR, 0.60 [95% CI, 0.38 to 0.95]; ARR, 3.3 [95% CI, 0.4 to 6.3]).

48 scular events (RR, 0.89 [95% CI, 0.83-0.95]; ARR, 3.90 [95% CI, 1.57-6.06]), coronary heart disease (

49 heart disease (RR, 0.88 [95% CI, 0.80-0.98]; ARR, 1.81 [95% CI, 0.35-3.11]), stroke (RR, 0.73 [95% CI

50 vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% CI, 0.3 to 8.3]) and a lower rate of pulmo

51 d retinopathy (RR, 0.87 [95% CI, 0.76-0.99]; ARR, 2.23 [95% CI, 0.15-4.04]).

52 he cytokinin response by facilitating type A ARR degradation.

53 suppressed by loss of function of the type A ARR family member ARR5.

54 f the receiver domain is required for type-A ARR function and suggest that negative regulation of cyt

55 mechanism by which cytokinin controls type-A ARR function.

56 tested the role of phosphorylation in type-A ARR function.

57 Disruption of eight of the 10 type-A ARR genes affects root development by altering the size

58 Alterations of PIN levels in the type-A ARR mutants result in changes in the distribution of aux

59 hermore, we show that a subset of the type-A ARR proteins are stabilized in response to cytokinin in

60 type B ARRs (response activators) and type A ARRs (negative-feedback regulators).

61 shed light on the mechanism by which type-A ARRs act to negatively regulate cytokinin signaling and

62 ulation of cytokinin signaling by the type-A ARRs most likely involves phosphorylation-dependent inte

63 te that cytokinin, acting through the type-A ARRs, alters the level of several PIN efflux carriers, a

64 okinin-regulated genes, including the type-A ARRs, although it does not impair the cytokinin inductio

65 One class of these, the type-A ARRs, are negative regulators of cytokinin signaling tha

66 o classes of response regulators, the type-A ARRs, which act as negative regulators of cytokinin resp

67 impair the cytokinin induction of the type-A ARRs.

68 likely to ever have committed a violent act (ARR = 0.86; 95% CI, 0.76-0.98).

69 mary immunization with adenovirus 35 (Ad35) (ARR) vector expressing circumsporozoite protein.

70 strument, the instrumental-variable-adjusted ARR in mortality associated with early surgery was -11.2

71 subsequent inpatient psychiatric admission (ARR=0.81, 95% CI=0.71-0.93).

72 .16) but not with small for gestational age (ARR, 1.19), stillbirth (ARR, 1.11), or congenital malfor

73 I], 1.36-1.75) or small for gestational age (ARR, 1.30; 95% CI, 1.07-1.57) but not of congenital malf

74 , 0.35-1.57]) or short-acting beta-agonists (ARR, 0.95 [95% CI, 0.68-1.33]).

75 1.32; 95% CI, 1.06-1.63), drinking alcohol (ARR = 1.31; 95% CI, 1.09-1.58), smoking cigarettes (ARR

76 Furthermore, we found that although ARR-1 played a key role in the control of immunity by AF

77 ) and inversely related to African American (ARR, 0.86 [99% CI, 0.75-0.96]) and Hispanic (ARR, 0.86 [

78 c groups examined, except African Americans (ARR, 1.13; 95% CI, 0.89-1.44), who had comparatively low

79 re while driving of 1.04 per thousand and an ARR of 2.6, non-driving periods of 8 months are required

80 ng trial yielded a 10-year MRR of 90% and an ARR of 3 deaths per 10,000 women.

81 in a 1975 trial yielded an MRR of 90% and an ARR of 5 deaths per 10,000 women.

82 s-9) mutants did not flower but displayed an ARR response at the same time as Col-0.

83 About 30% had an ARR of >4% (median ARR, 3.2%; interquartile range, 2.5%-

84 and DRFS of 92% (95% CI, 85%-100%), with an ARR of 18% (95% CI, 6%-28%).

85 the mouse prostate under the control of an (ARR)2-Probasin promoter.

86 ogen, plasminogen activator inhibitor-1, and ARR were related to LV geometry (P<0.01).

87 BSE contained equimolar amounts of VRQ- and ARR-PrP, which contrasts with the excess (>95%) VRQ-PrP

88 r a range of risks of seizure recurrence and ARRs was calculated.

89 of children in the control group had anemia (ARR, 1.6 [95% CI, 0.86-2.9]).

90 inal detachment and beta-lactam antibiotics (ARR, 0.74 [95% CI, 0.35-1.57]) or short-acting beta-agon

91 the cytokinin response, mechanism of type-B ARR activation, and basis by which cytokinin regulates d

92 Three type-B ARR DNA-binding motifs, determined by use of protein-bin

93 d root meristem size correlating with type-B ARR expression levels.

94 n addition, our results indicate that type-B ARR expression profiles in the plant, along with posttra

95 kiss me deadly (KMD) family, targets type-B ARR proteins for degradation.

96 h elevated KMD expression destabilize type-B ARR proteins leading to cytokinin insensitivity.

97 se complex and directly interact with type-B ARR proteins.

98 sive genes that largely overlaps with type-B ARR targets.

99 abidopsis response regulators (ARRs): type B ARRs (response activators) and type A ARRs (negative-fee

100 X2 gene in vivo, which indicates that type B ARRs directly regulate genes that are repressed by cytok

101 ytokinin requires ARR1 and ARR12, two type B ARRs that mediate the primary transcriptional response t

102 vealed differing contributions of the type B ARRs to mutant phenotypes.

103 oss-of-function KMD mutants stabilize type-B ARRs and exhibit an enhanced cytokinin response.

104 there is functional overlap among the type-B ARRs and that they act as positive regulators of cytokin

105 To determine which type-B ARRs can functionally substitute for the subfamily 1 mem

106 ARR1 or ARR12, we expressed different type-B ARRs from the ARR1 promoter and assayed their ability to

107 Our results indicate that the type-B ARRs have diverged in function, such that some, but not

108 ight on the physiological role of the type-B ARRs in regulating the cytokinin response, mechanism of

109 proteins function in tandem with the type-B ARRs to mediate the initial cytokinin response.

110 lized response regulators (Type-A and Type-B ARRs).

111 well as a subset of other subfamily 1 type-B ARRs, restore the cytokinin sensitivity to arr1 arr12.

112 ators of cytokinin responses, and the type-B ARRs, which are transcription factors that play a positi

113 ssive (ARR=0.71, 95% CI=0.54-0.94), bipolar (ARR=0.70, 95% CI=0.51-0.94), and substance use (ARR=0.71

114 g pregnancy was not linked to preterm birth (ARR, 1.03; 95% CI, 0.84-1.27).

115 pregnancy was associated with preterm birth (ARR, 1.16) but not with small for gestational age (ARR,

116 ted with an increased risk of preterm birth (ARR, 1.54; 95% confidence interval [CI], 1.36-1.75) or s

117 41; 95% CI, 1.24-1.60), and marital breakup (ARR, 1.18; 95% CI, 1.13-1.23) in the 2 years after the s

118 ted to recent outpatient mental health care (ARR, 2.30 [99% CI, 2.11-2.50]) and treatment in a state

119 .31; 95% CI, 1.09-1.58), smoking cigarettes (ARR = 1.13; 95% CI, 1.01-1.27), and engaging in delinque

120 ) and those with paravalvular complications (ARR -17.3%, P<0.001), systemic embolization (ARR -12.9%,

121 In contrast, ARR-induced lower antibody responses, and protection was

122 ore likely to be hospitalized than controls (ARR at 5 to 8 years, 1.67 [95% CI, 1.57 to 1.81]; ARR at

123 cent use (0.3% of cases vs 0.2% of controls; ARR, 0.92 [95% CI, 0.45-1.87]) nor past use (6.6% of cas

124 past use (6.6% of cases vs 6.1% of controls; ARR, 1.03 [95% CI, 0.89-1.19]) was associated with a ret

125 {CI}, 1.10-1.25]) and self-harm by cutting (ARR, 1.18 [99% CI, 1.12-1.24]) and inversely related to

126 0 patient-days to 3.6 per 1000 patient-days (ARR, 1.7; 95% CI, 1.3-2.2).

127 CI, 1.01-1.27), and engaging in delinquency (ARR = 1.18; 95% CI, 1.03-1.36).

128 VC-bereaved counterparts to have depression (ARR, 1.30; 95% CI, 1.06-1.61), physical disorders (ARR,

129 ciated with an increased rate of depression (ARR, 2.14; 95% CI, 1.88-2.43), anxiety disorders (ARR, 1

130 s (ARR=0.70, 95%=0.57-0.87); and depressive (ARR=0.71, 95% CI=0.54-0.94), bipolar (ARR=0.70, 95% CI=0

131 on (ARR 0.51; 95% CI 0.36-0.71) or diabetes (ARR 0.65; 95% CI 0.44-0.95).

132 with veterans with no psychiatric diagnoses (ARR = 2.00; 95% confidence interval, 1.91-2.09) and comp

133 otherapy within 5 years of cancer diagnosis (ARR, 2.4; 95% CI, 1.6 to 3.7; P < .001) increased the ra

134 ts with no recent mental disorder diagnosis (ARR=0.57, 95% CI=0.41-0.79); any recent mental disorder

135 0.79); any recent mental disorder diagnosis (ARR=0.70, 95%=0.57-0.87); and depressive (ARR=0.71, 95%

136 2.14; 95% CI, 1.88-2.43), anxiety disorders (ARR, 1.41; 95% CI, 1.24-1.60), and marital breakup (ARR,

137 ed to recent diagnosis of anxiety disorders (ARR=1.56, 95% CI=1.30-1.86) or personality disorders (AR

138 95% CI=1.30-1.86) or personality disorders (ARR=1.67, 95% CI=1.19-2.34).

139 .30; 95% CI, 1.06-1.61), physical disorders (ARR, 1.32; 95% CI, 1.19-1.45), and low income (ARR, 1.34

140 ing tfl1-14 (terminal flower 1-14) displayed ARR at the same time as Col-0.

141 of co 1-2), and FRI (+) (FRIGIDA) displayed ARR before the transition to flowering occurred.

142 the sole arrestin in Caenorhabditis elegans (ARR-1).

143 ARR -17.3%, P<0.001), systemic embolization (ARR -12.9%, P=0.002), S aureus NVE (ARR -20.1%, P<0.001)

144 From baseline to the end of the study (EOS), ARR in patients on continuous-fingolimod 0.5 mg was sign

145 oxygen therapy group for new shock episode (ARR, 0.068 [95% CI, 0.020-0.120]; RR, 0.35 [95% CI, 0.16

146 CI, 0.16-0.75]; P = .006) or liver failure (ARR, 0.046 [95% CI, 0.008-0.088]; RR, 0.29 [95% CI, 0.10

147 For ARR to be functional, the two subunits must be expressed

148 lysis performed to identify risk factors for ARR.

149 of a heterologous overexpression system for ARR will facilitate future structural and/or functional

150 and 2.1 (95% CI, .9-5.2; P=.3), whereas for ARR, the RRs were 21.1 (95% CI, 2.6-184; P<.001) and 8.2

151 ion in downstream signaling molecules (e.g., ARR-1, AKT-1, and SGK-1) and effectors (e.g., CCA-1 and

152 tained in 33 patients (92%), all of whom had ARRs in the normal range (P < .01).

153 Heterozygous ARR/VRQ animals exhibit delayed incubation periods.

154 rotein (PrP(res)) from brain of heterozygous ARR/VRQ scrapie-infected sheep was compared with that of

155 NT and ACCORD-BP who had lower versus higher ARRs in CVD events/deaths with intensive BP treatment, a

156 ARR, 0.86 [99% CI, 0.75-0.96]) and Hispanic (ARR, 0.86 [99% CI, 0.75-0.99]) race/ethnicity.

157 epressant treatment increased for Hispanics (ARR, 1.75; 95% CI, 1.60-1.90), it remained comparatively

158 CI, 1.08-1.89]; P = .013) and homelessness (ARR, 1.72 [95% CI, 1.25-2.39]; P = .001).

159 89]) and recent psychiatric hospitalization (ARR, 0.74 [99% CI, 0.67-0.81]).

160 However, ARR-1 partially controlled longevity through ADF neurons

161 However, ARRs were consistently lower under contemporary treatmen

162 nificantly less likely to have hypertension (ARR 0.51; 95% CI 0.36-0.71) or diabetes (ARR 0.65; 95% C

163 on a large community-based sample identified ARR as a key correlate of concentric and eccentric LV hy

164 ous fingolimod showed persistent benefits in ARR (0.5 mg fingolimod [n=356], 0.12 [95% CI 0.08-0.17]

165 There is a wide distribution in ARR that may complement informed decision making.

166 Therefore, the wide distribution in ARR was a consequence of the underlying distribution in

167 tein, via a C-terminal PDZ binding domain in ARR-1.

168 ally treated with IFN had a 50% reduction in ARR (0.40 vs 0.20), reduced MRI activity and a lower rat

169 ts, 26 (87%) exhibited a marked reduction in ARR over 5 years (mean [SD] pretreatment vs posttreatmen

170 ceptibility is reduced to near resistance in ARR/ARR animals while it is strongly enhanced in VRQ/VRQ

171 ; P = .044), and highest with incarceration (ARR, 1.43 [95% CI, 1.08-1.89]; P = .013) and homelessnes

172 R, 1.32; 95% CI, 1.19-1.45), and low income (ARR, 1.34; 95% CI, 1.18-1.51) before their offspring's d

173 Ten-year individualized ARR on major cardiovascular events by statin therapy wer

174 tions in PrP(res) material from BSE-infected ARR/VRQ sheep.

175 82]; P = .02) and new bloodstream infection (ARR, 0.05 [95% CI, 0.00-0.09]; RR, 0.50 [95% CI, 0.25-0.

176 r of rosette leaves is necessary to initiate ARR competence under short-day conditions.

177 lopmental event is the switch that initiates ARR competence in mature plants.

178 Interestingly, ARR-1 and MPZ-1 are found in a complex with the phosphat

179 ted RR (ARR: 2.29; 95% CI: 1.62, 3.24], LBW (ARR: 2.06; 95% CI: 1.03, 4.11), and PTB (ARR: 4.61; 95%

180 inked to high (VRQ/VRQ and ARQ/VRQ) and low (ARR/VRQ and AHQ/VRQ) lymphoreticular system involvement

181 ron beta-1a to fingolimod, we recorded lower ARRs (0.18 [95% CI 0.14-0.22] for 0.5 mg; 0.20 [0.16-0.2

182 rth (ARR, 1.11), or congenital malformation (ARR, 0.90).

183 07-1.57) but not of congenital malformation (ARR, 1.00; 95% CI, 0.83-1.20) or stillbirth (ARR, 1.45;

184 The mean ARR was lower with 40 mg ponesimod versus placebo, with

185 About 30% had an ARR of >4% (median ARR, 3.2%; interquartile range, 2.5%-4.3%; 95% confidenc

186 in 33 (92%) patients, with a starting median ARR of 8583 pmol/L per microg/(L . h) that normalized to

187 94, 95% CI: 0.90-0.98), and 24 to 36 months (ARR 0.95, 95% CI: 0.95-0.99).

188 These patients sustained less morbidity (ARR 19%, 95% CI 3-34; p=0.016), including less infectiou

189 ization (ARR -12.9%, P=0.002), S aureus NVE (ARR -20.1%, P<0.001), and stroke (ARR -13%, P=0.02) but

190 The association of ARR and the floral transition was examined using floweri

191 Comparison of ARR, potassium, and blood pressure levels before and aft

192 ment success was defined as normalization of ARR at the latest assessment.

193 tuberculosis regimen are at a higher risk of ARR, compared with HIV-uninfected patients, in the prese

194 T reduces but does not eliminate the risk of ARR.

195 in vivo approach to investigate the role of ARR-1, the sole arrestin ortholog in C. elegans, on long

196 We studied the impact of HIV and HAART on ARR among patients taking thrice-weekly antituberculosis

197 s assigned to EVAR compared with 25% for OR (ARR = 4.4% 95% CI: -11% to +20%).

198 -2 signaling, whereas animals overexpressing ARR-1 have decreased longevity.

199 tation is enhanced in animals overexpressing ARR-1.

200 nd control groups (49 [53%] of 92 patients) (ARR -7%, 95% CI -22 to 7; p=0.30).

201 r, and four to five [4Fe-4S] are present per ARR.

202 patient-days in the postimmunization period (ARR, 2.1; 95% CI, 1.9-2.5), and intubation increased fro

203 2-1.24]) and inversely related to poisoning (ARR, 0.84 [99% CI, 0.80-0.89]) and recent psychiatric ho

204 increased from 24- to 36-months postinjury (ARR 1.06, 95% CI: 1.01, 1.12).

205 ars (mean [SD] pretreatment vs posttreatment ARR, 2.4 [1.5] vs 0.3 [1.0]).

206 BW (ARR: 2.06; 95% CI: 1.03, 4.11), and PTB (ARR: 4.61; 95% CI: 2.31, 9.19) but not of stillbirth (AR

207 with psychiatric disorders other than PTSD (ARR = 1.51; 95% confidence interval, 1.43-1.59; p < .001

208 To purify ARR, a heterologous expression system was developed in E

209 were the annualised confirmed relapse rate (ARR) and time to first confirmed relapse.

210 Outcomes included annualised relapse rate (ARR), confirmed disability progression and MRI measures.

211 Annualized relapse rate (ARR), disability (Expanded Disability Status Scale score

212 cacy endpoints were annualised relapse rate (ARR), disability progression, and MRI outcomes.

213 the hospital and the adjusted relative rate (ARR) of hospitalizations in survivors compared with cont

214 Adjusted relative rates (ARRs) were generated by generalized estimating equation

215 tion, CT images, aldosterone-to-renin ratio (ARR), serum potassium level, and blood pressure control

216 m (aldosterone and renin modeled as a ratio [ARR]) and echocardiography at a routine examination.

217 , abdominopelvic tumor (adjusted rate ratio [ARR], 3.6; 95% CI, 1.9 to 6.8; P < .001) and abdominal/p

218 ostimmunization period (adjusted rate ratio [ARR], 3.7; 95% CI, 3.2-4.4).

219 es vs 0.6% of controls; adjusted rate ratio [ARR], 4.50 [95% CI, 3.56-5.70]).

220 nalysis, those walking (adjusted risk ratio [ARR] 0.72; 95% CI 0.58-0.88) or bicycling to work (ARR 0

221 ined from any drug use (adjusted risk ratio [ARR] = 1.32; 95% CI, 1.06-1.63), drinking alcohol (ARR =

222 .63 to -4.10; P < .001; adjusted risk ratio [ARR], 0.21; 95% CI, 0.15 to 0.29; P < .001).

223 e emergency department (adjusted risk ratio [ARR]=0.66, 95% CI=0.55-0.79) and directly related to rec

224 sk for an accident (the accident risk ratio; ARR).

225 Rates and adjusted risk ratios (ARRs) of discharge to the community, mental health asses

226 strain ANA-3 arsenate respiratory reductase (ARR), the key enzyme involved in this metabolism.

227 subgroup had no significant risk reduction (ARR = 0.006, 95% CI: -0.007, 0.018; P = 0.71).

228 and for OR was 47% [absolute risk reduction (ARR) = 5.4%; 95% confidence interval (CI): -13% to +23%]

229 95% CI, 0.78-0.96); absolute risk reduction (ARR) in events per 1000 patient-years (3.16; 95% CI, 0.9

230 primary outcome was absolute risk reduction (ARR) in morbidity (defined by Clavien-Dindo grade II or

231 al (CI), 1.81-2.10; absolute risk reduction (ARR), 6.37%].

232 azard reduction and absolute risk reduction (ARR).

233 ment sensitive and absolute risk reduction ([ARR], difference in DRFS between 2 predicted groups) at

234 for survivor bias (absolute risk reduction [ARR] -5.9%, P<0.001).

235 m (0.84, 0.77-0.91; absolute risk reduction [ARR] 2.6%, 1.5-3.7; numbers needed to treat [NNT] 39, 95

236 death over 5 years (absolute risk reduction [ARR] = 0.042, 95% CI: 0.018, 0.066; P = 0.001), those in

237 CI, 1.31 to 2.00]; absolute risk reduction [ARR] in events per 100 infants, -12.0 [95% CI, -17.3 to

238 nt (12.9% vs 20.0%; absolute risk reduction [ARR] with infliximab, 7.1%; 95% confidence interval: -1.

239 ing their ICU stay (absolute risk reduction [ARR], 0.086 [95% CI, 0.017-0.150]; relative risk [RR], 0

240 CI, 0.04 to 0.47]; absolute risk reduction [ARR], 0.8%), asymptomatic deep venous thrombosis (DVT) (

241 .14-1.17; P < .001; absolute risk reduction [ARR], 1.5%).

242 from 5.8% to 4.2% (absolute risk reduction [ARR], 1.6%; 95% CI, 1.4%-1.9%; relative risk reduction [

243 ovide estimates of absolute risk reductions (ARR) and numbers needed to treat (NNT) for 5-HT(3) antag

244 ict individualized absolute risk reductions (ARR) of cardiovascular events.

245 s not the developmental event that regulates ARR competence.

246 nsive type-A Arabidopsis response regulator (ARR) genes increases in buds following CK supply, and th

247 of Arabidopsis thaliana Response Regulator (ARR) proteins containing a receiver domain with a conser

248 The type B Arabidopsis Response Regulators (ARRs) of Arabidopsis thaliana are transcription factors

249 the type-B ARABIDOPSIS RESPONSE REGULATORs (ARRs) that mediate the cytokinin primary response, makin

250 n of type-A Arabidopsis response regulators (ARRs), which are negative regulators of cytokinin signal

251 n of type-B Arabidopsis response regulators (ARRs).

252 otransfer proteins, and response regulators (ARRs).

253 classes of Arabidopsis response regulators (ARRs): type B ARRs (response activators) and type A ARRs

254 regulators (ARABIDOPSIS RESPONSE REGULATORS [ARRs]) form three subfamilies based on phylogenic analys

255 Age-related resistance (ARR) is a plant defense response characterized by enhanc

256 factors for acquired rifampicin resistance (ARR) in human immunodeficiency virus (HIV)/tuberculosis

257 antly higher than that for scrapie-resistant ARR/ARR sheep which were kept in the same farm environme

258 significantly higher adjusted relative risk (ARR) for diagnosis with any of the autoimmune disorders

259 activities item; the adjusted relative risk (ARR) of reporting problems decreased from 6 to 12 (ARR 0

260 had iron deficiency (adjusted relative risk [ARR], 0.90 [95% confidence interval [CI], 0.74-1.1]); in

261 nts (39.6% vs 28.9%; adjusted relative risk [ARR], 1.40; 95% CI, 1.36-1.44).

262 e who did not (14%) (adjusted relative risk [ARR], 3.26; 95% confidence interval [CI], 2.72-3.81).

263 sion, we calculated adjusted relative risks (ARRs) for adverse outcomes of pregnancy according to end

264 up had a higher risk of anemia [adjusted RR (ARR: 2.29; 95% CI: 1.62, 3.24], LBW (ARR: 2.06; 95% CI:

265 with tuberculosis (TB) disease (adjusted RR [ARR], 0.68 [95% CI, .52-.89]; P = .005) and students (AR

266 d coverage of mental health clinic services (ARR, 1.13 [99% CI, 1.05-1.22]) and inversely related to

267 5 years, SVR was associated with significant ARRs for liver mortality, all-cause mortality, SLM, and

268 for gestational age (ARR, 1.19), stillbirth (ARR, 1.11), or congenital malformation (ARR, 0.90).

269 ; 95% CI: 2.31, 9.19) but not of stillbirth (ARR: 2.71; 95% CI: 0.88, 8.36) than women in the adequat

270 ARR, 1.00; 95% CI, 0.83-1.20) or stillbirth (ARR, 1.45; 95% CI, 0.87-2.40).

271 ureus NVE (ARR -20.1%, P<0.001), and stroke (ARR -13%, P=0.02) but not those with valve perforation o

272 8 [95% CI, .52-.89]; P = .005) and students (ARR, 0.45 [95% CI, .21-.98]; P = .044), and highest with

273 tients with a higher propensity for surgery (ARR -10.9% for quintiles 4 and 5, P=0.002) and those wit

274 reased subsequent mortality among survivors (ARR, 1.8; 95% CI, 1.1 to 2.9; P = .016), adjusting for t

275 These results demonstrate that ARR-1 functions to regulate chemosensory signaling, enab

276 The results indicate that ARR-1 is required for GPCR signaling in ASH, ASI, AQR, P

277 Here, we report that ARR-1 functions to positively regulate DAF-2 signaling i

278 Genetic and biochemical analysis reveal that ARR-1 functions to regulate DAF-2 signaling via direct i

279 r, we detected a strong interaction, in that ARRs were considerably higher for individuals with nonmi

280 phism effect is quite different although the ARR allotype remains the least susceptible.

281 study suggests that SVP is required for the ARR response and that the floral transition is not the d

282 ere highly associated with protection in the ARR cohort.

283 , the NF-kappaB pathway was activated in the ARR(2)PB-myc-PAI (Hi-myc) mouse prostate by cross-breedi

284 Our results suggest that the ARR-1-MPZ-1-DAF-18 complex functions to regulate DAF-2 s

285 transfer proteins, but is independent of the ARRs.

286 TIV and 67% among those receiving only TIV (ARR, 0.76 [95% CI, .65-.88]), 52% among those who receiv

287 endocytosis, whereas C-terminally truncated ARR-1 does not.

288 n vitro studies demonstrating that wild-type ARR-1 binds proteins of the endocytic machinery and prom

289 B-type ARRs bind to the promotors of HEMA1 and LHCB6 genes, ind

290 =0.70, 95% CI=0.51-0.94), and substance use (ARR=0.71, 95% CI=0.53-0.96) disorder diagnoses.

291 p-32 (short vegetative phase), and Ws-2 were ARR-defective, whereas early-flowering tfl1-14 (terminal

292 e transition to flowering is associated with ARR competence, suggesting that this developmental event

293 grown Col-0 but this was not associated with ARR competence.

294 .72; 95% CI 0.58-0.88) or bicycling to work (ARR 0.66; 95% CI 0.55-0.77) were significantly less like

295 We also report assessment of WT1 ARR methylation in developmental and tumour tissues, inc

296 at the WT1 antisense regulatory region (WT1 ARR).

297 Here, we report characterization of the WT1 ARR differentially methylated region and show that it co

298 failure of methylation spreading at the WT1 ARR early in renal development, followed by imprint eras

299 Predicted 10-year ARR by statin therapy was <2% for 13% of the patients.

300 er patient age (21-31 years vs 45-64 years) (ARR, 1.18 [99% confidence interval {CI}, 1.10-1.25]) and