ライフサイエンスコーパス: ARR

1 ARR and NNT for cardiovascular events were nonfatal 1.7%

2 ARR-1 activity also controlled immunity through ADF chem

3 ARRs at 10, 11 and 12 years were estimated based on pred

4 ARRs of major cardiovascular events by statin therapy ca

5 ARRs were independent of trimester.

6 n (HR, 0.69 [0.55-0.86], P=0.0012), and 4.0% ARR in patients with high genetic risk, irrespective of

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

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

9 A compared with 63.6% in Group O (P = 0.002; ARR = 25.0%, 95% CI = 9.7-40.4%; RRR = 68.9%).

10 ive of clinical risk (P(trend) for HR=0.017, ARR P(trend)=0.004).

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

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

13 % to -4.6%), ED utilization (71.6% vs 77.1%, ARR 95%CI: -8.5% to -2.4%), and rehospitalizations (47.4

14 Among 102 ARRs telephoned, contact was established with 95 (93%).

15 Thirty probands were enrolled, and 114 ARRs were identified.

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

18 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%-

19 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.

20 d with lower 3-year mortality (2.1% vs 3.2%, ARR 95%CI: -2.2% to -0.03%), complications (22.2% vs 27.

21 % to -5.2%), ED utilization (51.7% vs 57.2%, ARR 95%CI: -9.1% to -1.9%), and rehospitalizations (41.8

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 or reversal (OR(adj) 1.03, 95% CI 0.85-1.25; ARR(adj) -0.3%, 95% CI -2.4 to 1.5) nor extubation at a

24 of 21 694); OR(adj) 1.86, 95% CI 1.53-2.26; ARR(adj) -4.4%, 95% CI -5.5 to -3.2).

25 4%), and rehospitalizations (47.4% vs 52.3%, ARR 95%CI: -8.0% to -1.7%).

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

27 (HR, 0.87 [0.75-0.998], P=0.047) and a 1.4% ARR in patients with multiple clinical risk factors but

28 f reduction [ARR] 0.1%) in Lesotho to 76.4% (ARR 5.2%) in Malawi, and the pace of decline was faster

29 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

30 monitoring (OR(adj) 1.31, 95% CI 1.15-1.49; ARR(adj) -2.6%, 95% CI -3.9 to -1.4) and the administrat

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

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

33 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

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

35 At 6 months, 7 ARRs with pathogenic variants had undergone cancer surve

36 lower 3-year complications (20.1% vs 24.7%, ARR 95%CI: -7.6% to -1.7%), reinterventions (14.0% vs 21

37 to -2.6%), reinterventions (20.1% vs 27.7%, ARR 95%CI: -10.7% to -4.6%), ED utilization (71.6% vs 77

38 % to -0.03%), complications (22.2% vs 27.7%, ARR 95%CI: -8.5% to -2.6%), reinterventions (20.1% vs 27

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

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

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

42 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

43 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

44 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.

45 9%), and rehospitalizations (41.8% vs 45.8%, ARR 95%CI: -7.5% to -0.5%).

46 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.

47 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]).

48 .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

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

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

51 to -1.7%), reinterventions (14.0% vs 21.9%, ARR 95%CI: -10.7% to -5.2%), ED utilization (51.7% vs 57

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

53 -1.41); or ZDV-3TC-LPV-R (75 of 167 [44.9%]; ARR, 1.21; 95% CI, 1.01-1.45).

54 -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

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

56 6% vs 8.9%; OR, 0.60 [95% CI, 0.38 to 0.95]; ARR, 3.3 [95% CI, 0.4 to 6.3]).

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

58 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

59 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

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

61 he cytokinin response by facilitating type A ARR degradation.

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

63 lective autophagy receptors to target type-A ARR cargos for autophagic degradation, demonstrating mod

64 Type-A ARR proteins were degraded by autophagy in an AUTOPHAGY-

65 gic vesicles, have elevated levels of type-A ARR proteins, and are hyposensitive to cytokinin.

66 EXO70D family members interacted with type-A ARR proteins, likely in a phosphorylation-dependent mann

67 vity through autophagic regulation of type-A ARR proteins.

68 abidopsis type-A response regulators (type-A ARR) are negative regulators of cytokinin signaling that

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

70 Disruption of both type-A ARRs and EXO70D1,2,3 compromised survival in carbon-defi

71 ts exhibited compromised targeting of type-A ARRs to autophagic vesicles, have elevated levels of typ

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

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

74 partate in the receiver domain of the type-A ARRs.

75 to expected mean residual risk of 14.6% (A; ARR 2.6%) or 13.9% (B; ARR 3.2%).

76 result in residual 30-year risk of 12.7% (A; ARR 4.4) or 9.9% (B; ARR 7.2%) and delaying by 20 years

77 The slope of the achieved ARR as a function of delay in treatment was also higher

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

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

80 Adjusted ARRs were 0.17 (95% CI 0.14-0.21) with ozanimod 1.0 mg,

81 Adjusted ARRs were 0.35 (0.28-0.44) for interferon beta-1a, 0.18

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

83 tial to promote early detection for affected ARRs and reduce cancer mortality and should be evaluated

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

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

86 , 0.35-1.57]) or short-acting beta-agonists (ARR, 0.95 [95% CI, 0.68-1.33]).

87 1.32; 95% CI, 1.06-1.63), drinking alcohol (ARR = 1.31; 95% CI, 1.09-1.58), smoking cigarettes (ARR

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

89 a kits resulted in high testing uptake among ARRs.

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

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

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

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

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

95 1; 15 648 individuals; 11 studies), anaemia (ARR 0.85, 0.77-0.92; p<0.0001; 15 026 individuals; 11 st

96 hout HIV (adjRR, 9.6; 95% CI, 6.9-13.3), and ARR was also associated with increased mortality, contro

97 , 1.27-1.78 for virologically suppressed and ARR, 1.38; 95% CI, 1.13-1.68 for viremic) among HIV-infe

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

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

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

101 ociated with more NCDs, especially with ART (ARR, 1.42; 95% CI, 1.22-1.66).

102 d the pace of decline was faster on average (ARR 3.2%) than that observed for infant (IMRs) (ARR 2.7%

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 ual risk of 14.6% (A; ARR 2.6%) or 13.9% (B; ARR 3.2%).

120 -year risk of 12.7% (A; ARR 4.4) or 9.9% (B; ARR 7.2%) and delaying by 20 years (treatment for 10 yea

121 isk reduction [ARR], 5.5%) or 6.5% (model B; ARR 10.6%).

122 Model-based ARR reductions in younger patients (<=12 years) were 91.

123 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

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

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

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

127 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

128 .31; 95% CI, 1.09-1.58), smoking cigarettes (ARR = 1.13; 95% CI, 1.01-1.27), and engaging in delinque

129 y the genetics team identified and contacted ARRs by telephone to disclose the familial pathogenic va

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

131 tizing personal beliefs relative to control (ARRs varied from 1.5-3.0, all p < 0.001).

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

133 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

134 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

135 0 patient-days to 3.6 per 1000 patient-days (ARR, 1.7; 95% CI, 1.3-2.2).

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

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

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

139 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

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

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

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

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

144 0.79); any recent mental disorder diagnosis (ARR=0.70, 95%=0.57-0.87); and depressive (ARR=0.71, 95%

145 2.14; 95% CI, 1.88-2.43), anxiety disorders (ARR, 1.41; 95% CI, 1.24-1.60), and marital breakup (ARR,

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

147 95% CI=1.30-1.86) or personality disorders (ARR=1.67, 95% CI=1.19-2.34).

148 .30; 95% CI, 1.06-1.61), physical disorders (ARR, 1.32; 95% CI, 1.19-1.45), and low income (ARR, 1.34

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

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

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

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

153 e for logistic regression; it over-estimated ARR attributable to intensive treatment (slope between p

154 ial data reveal that patients may experience ARRs not simply proportional to baseline cardiovascular

155 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

156 lysis performed to identify risk factors for ARR.

157 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

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

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

160 Heterozygous ARR/VRQ animals exhibit delayed incubation periods.

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

162 years; P = 0.047) and a significantly higher ARR (0.31 vs. 0.21; P = 0.025) than those without uveiti

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

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

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

166 However, ARRs were consistently lower under contemporary treatmen

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

168 Among 114 identified ARRs, 66 (58%) completed genetic testing.

169 3.2%) than that observed for infant (IMRs) (ARR 2.7%) and neonatal (NMRs) (ARR 2.0%) mortality rates

170 [95% confidence interval (CI) 0.60-1.65] in ARR, and a mean reduction of 0.85 (95% CI 0.36-1.34) in

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

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

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

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

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

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

177 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

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

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

180 82]; P = .02) and new bloodstream infection (ARR, 0.05 [95% CI, 0.00-0.09]; RR, 0.50 [95% CI, 0.25-0.

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

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

183 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%

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

185 1 studies), and subsequent clinical malaria (ARR 0.50, 0.39-0.60; p<0.0001; 1815 individuals; four st

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

187 07-1.57) but not of congenital malformation (ARR, 1.00; 95% CI, 0.83-1.20) or stillbirth (ARR, 1.45;

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

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

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

191 94, 95% CI: 0.90-0.98), and 24 to 36 months (ARR 0.95, 95% CI: 0.95-0.99).

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

193 The on-natalizumab ARR was 0.15, a 92.5% reduction from the year before ini

194 On-natalizumab ARRs were similar between patients who discontinued or r

195 200 cells/mm3 was associated with more NCDs (ARR, 1.43; 95% CI, 1.06-1.93).

196 te, ART usage was associated with more NCDs (ARR, 1.50; 95% CI, 1.27-1.78 for virologically suppresse

197 nfant (IMRs) (ARR 2.7%) and neonatal (NMRs) (ARR 2.0%) mortality rates.

198 atment (slope between predicted and observed ARR of 0.73 [95% CI, 0.30-1.14] versus 1.06 [95% CI, 0.7

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

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

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

202 Persons with HIV had greater risk of ARR than persons without HIV (adjRR, 9.6; 95% CI, 6.9-13

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

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

205 Surveys of ARRs at the time of genetic testing and 6 months later d

206 A meta-analysis on ARR was conducted in 200 patients from 4 studies and on

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

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

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

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

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

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

213 Predicted ARRs using logistic regression were generally proportion

214 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

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

216 icantly reduced the annualised relapse rate (ARR) and rate of new/newly enlarged T2 (n/neT2) lesions

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

218 rimary endpoint was annualised relapse rate (ARR) during the treatment period and was assessed in the

219 eatment outcomes as Annualized Relapse Rate (ARR) or Expanded Disability Status Scale (EDSS) before a

220 rimary endpoint was annualised relapse rate (ARR) over 24 months.

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

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

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

224 Annualised relapse rates (ARRs) and disability progression/improvement were analys

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

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

227 h individual referrals (adjusted rate ratio [ARR] 0.45, 95% CI 0.43-0.46; P < 0.001) or those referre

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

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

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

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

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

233 .63 to -4.10; P < .001; adjusted risk ratio [ARR], 0.21; 95% CI, 0.15 to 0.29; P < .001).

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

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

236 differences (ARDs) and adjusted risk ratios (ARRs) with 95% confidence intervals (CIs) were also calc

237 f mental illness type (adjusted risk ratios [ARRs] varied from 1.7-3.1, all p < 0.001).

238 ment-naive subpopulation, fingolimod reduced ARR and n/neT2 lesions by 85.8% and 53.4%, respectively

239 es with a rapid pace of mortality reduction (ARR >= 3.2%) across ages would be more likely to achieve

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

241 (adj)) and adjusted absolute risk reduction (ARR(adj)).

242 Group O [P < 0.001; absolute risk reduction (ARR) = 35.7%, 95% confidence interval (CI) = 19.1-52.4%;

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

244 The absolute risk reduction (ARR) in cardiovascular events from therapy is generally

245 95% CI, 0.78-0.96); absolute risk reduction (ARR) in events per 1000 patient-years (3.16; 95% CI, 0.9

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

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

248 azard reduction and absolute risk reduction (ARR).

249 eclined from 3.3% (annual rate of reduction [ARR] 0.1%) in Lesotho to 76.4% (ARR 5.2%) in Malawi, and

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

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

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

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

254 d ratio [HR], 1.02; absolute risk reduction [ARR], -0.2%, P=0.86).

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

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

257 .14-1.17; P < .001; absolute risk reduction [ARR], 1.5%).

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

259 to 11.6% (model A; absolute risk reduction [ARR], 5.5%) or 6.5% (model B; ARR 10.6%).

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

261 Absolute risk reductions (ARRs) and numbers needed to treat (NNTs) were estimated.

262 s not the developmental event that regulates ARR competence.

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

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

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

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

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

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

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

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

271 ng and possible acquired rifampin-resistant (ARR) TB.

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

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

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

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

276 on models estimated adjusted relative risks (ARRs) and 95% confidence intervals (CIs) for the number

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

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

279 reased P falciparum prevalence (adjusted RR [ARR] 0.46, 95% CI 0.40-0.53; p<0.0001; 15 648 individual

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

281 5 years, SVR was associated with significant ARRs for liver mortality, all-cause mortality, SLM, and

282 0.001) or those referred from other sources (ARR 0.51, 95% CI 0.50-0.53; P < 0.001).

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

284 ; 95% CI: 2.31, 9.19) but not of stillbirth (ARR: 2.71; 95% CI: 0.88, 8.36) than women in the adequat

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

286 8 [95% CI, .52-.89]; P = .005) and students (ARR, 0.45 [95% CI, .21-.98]; P = .044), and highest with

287 disaster compared to those without support (ARR = 0.70; 95% CI: 0.56-0.88).

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

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

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

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

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

293 ere highly associated with protection in the ARR cohort.

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

295 Twelve ARRs were excluded (lived outside of the United States,

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

297 =0.70, 95% CI=0.51-0.94), and substance use (ARR=0.71, 95% CI=0.53-0.96) disorder diagnoses.

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

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

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

301 .72; 95% CI 0.58-0.88) or bicycling to work (ARR 0.66; 95% CI 0.55-0.77) were significantly less like

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