ライフサイエンスコーパス: hrs

1 t HF in RA were calculated as hazard ratios (HRs).

2 between milestone ratios and hazard ratios (HRs).

3 ults are reported as adjusted hazard ratios (HRs).

4 models were used to estimate hazard ratios (HRs).

5 affected, until after prolonged exposure (96 hrs).

6 tients by using multivariable hazard ratios (HRs).

7 g behavioral/cognitive performance during 24 hrs.

8 mg/d from FFQs and 402 +/- 345 mg/d from 24-HRs.

9 ox proportional hazards regression to obtain HRs.

10 transiently transfected with ASYN-GFP for 72 hrs.

11 travenous boluses in the treatment of type 1 HRS.

12 travenous boluses in the treatment of type 1 HRS.

13 esized hydrothermally at 700 degrees C for 9 hrs.

14 had similar AUC, Brier score, and estimated HRs.

15 K-treated and untreated cells as early as 12 hrs.

16 acting injectable antipsychotic medications (HRs 0.65-0.80) were associated with the lowest rates of

17 r risks of myocardial infarction were shown [HRs: 0.75 (95% CI: 0.65, 0.86) and 0.73 (95% CI: 0.58, 0

18 /ml increments), 1.06; 95% CI, 1.03-1.09 and HRs(1 pg/ml increments), 1.03; 95% CI, 0.99-1.06, respec

19 l increments), 1.19; 95% CI, 1.08-1.32; IL6: HRs(1 pg/ml increments), 1.06; 95% CI, 1.03-1.09 and HRs

20 95% confidence interval (CI), 1.13-1.36 and HRs(1 pg/ml increments), 1.19; 95% CI, 1.08-1.32; IL6: H

21 y adjusted models: TNF-alpha: hazard ratios (HRs)(1 pg/ml increments), 1.24; 95% confidence interval

22 ent among recipients with iciHHV-6 (adjusted HRs, 1.7-3.1; P = .001-.040).

23 min vs placebo plus albumin in patients with HRS-1.

24 n men in the universal decolonisation group (HRs: 1.21 [95% CI 0.88-1.68] for screening or isolation,

25 han did participants in the lowest quartile [HRs: 1.80 (95% CI: 1.11, 2.91; P-trend 0.01) and 1.55 (9

26 l, and nonfatal incident CVD (hazard ratios [HRs] 1.47 [95% CI 1.13-1.91], 1.42 [1.01-1.99], and 1.46

27 astasis-free survival (DMFS) (Hazard Ratios [HRs] = 3.5, 3.1, and 3.8, respectively; P = 0.01, 0.009,

28 The adjusted HRs (95% CI) of fibrosis progression with statin cDDD 28

29 HRs (95% CIs) comparing the top and bottom quintiles of

30 Although the adjusted point estimates of HRs (95% CIs) for frail women scoring in the second, thi

31 acteristics, behaviors, and food groups, the HRs (95% CIs) for incident PAD increased across quintile

32 ed with patients harboring neither mutation, HRs (95% CIs) for PTC-specific mortality were 3.08 (0.87

33 us nephritis, and vasculitis associated with HRs (95% confidence intervals) for death of 1.57 (1.43 t

34 s had significantly increased hazard ratios (HRs [95% confidence interval]) for mortality: 1.04 (1.02

35 quartile [Q] 4, best scores), hazard ratios (HRs) (95% CI) were 1.12 (0.65-1.92) for Q3 (P = .68); 1.

36 competing risk, we estimated hazard ratios (HRs) (95% confidence intervals [CI]) for first kidney tr

37 Hazard ratios (HRs), 95% confidence intervals (CIs) and their interacti

38 ession was used to estimate country-specific HRs, 95% CIs, and P-interaction values, which were then

39 e adults in the Health and Retirement Study (HRS), a population-representative longitudinal study of

40 enal dysfunction (RD), hepatorenal syndrome (HRS), ACLF, and mortality.

41 Finally, we did not find any variation in HRs across breast carcinomas defined by their estrogen r

42 Pooling the study-specific Decipher HRs across the five studies resulted in an HR of 1.52 (9

43 They estimated hazard ratios (HRs) adjusted for confounders with 95% confidence interv

44 HRS adults with higher well-being polygenic scores exper

45 f the quality of evidence underlying AHA/ACC/HRS AF guidelines have improved over time.

46 e found that endogenous P2X7R increased at 3 hrs after ICH with peak at 24 hrs, then returned to norm

47 eak at 24 hrs, then returned to normal at 72 hrs after ICH.

48 nd transporters were decreased as early as 2 hrs after TBI until at least 24 hrs after TBI.

49 ion factors, Gli 1, Gli 2, Gli 3 at 2 and 24 hrs after TBI.

50 s early as 2 hrs after TBI until at least 24 hrs after TBI.

51 factor-regulated tyrosine kinase substrate (Hrs), an endosomal sorting complexes required for transp

52 RNA was extracted at 24 hrs and 48 hrs post exposure for RNA-seq.

53 ifferentially expressed for 3R4F smoke at 24 hrs and 48 hrs using a pFDR < 0.01 and a [fold change] >

54 nal hazards models were used to estimate T2D HRs and 95% CIs according to baseline and yearly updated

55 d Cox proportional hazard models to estimate HRs and 95% CIs for esophageal and gastric cancers and t

56 azards models were used to estimate adjusted HRs and 95% CIs for mortality associations with time spe

57 ency within families, were used to calculate HRs and 95% CIs of CRTs by ADII tertile.

58 onal hazards regression was used to estimate HRs and 95% CIs of diabetes risk.In 494,741 person-years

59 HRs and 95% CIs were obtained with the use of multivaria

60 Cox regression models were used to estimate HRs and 95% CIs.

61 ity score, and other medications to estimate HRs and 95% confidence intervals (CI) for cancer-specifi

62 n in the recalls, were calculated between 24-HRs and FFQs and between 24-HRs and TUPs.

63 h any cognitive outcomes (crude and adjusted HRs and ORs were approximately 1.0 for all continuous ex

64 Adjusted HRs and ORs were calculated with the use of Cox and logi

65 associates with the ESCRT-0 complex members HRS and STAM on endosomes.

66 Cox proportional hazards models to estimate HRs and their 95% CIs for time to incident hypertension.

67 ortional hazard models were used to estimate HRs and their 95% confidence intervals (CI).

68 was 0.46 (95% CI: 0.20, 0.93) and between 24-HRs and true intake was 0.61 (95% CI: 0.38, 1.00).The AH

69 lated between 24-HRs and FFQs and between 24-HRs and TUPs.

70 ere used to estimate adjusted hazard ratios (HRs) and 95% CIs after adjusting for maternal age, count

71 for time-to-event data, with hazard ratios (HRs) and 95% CIs derived from adjusted Cox models.

72 Hazard ratios (HRs) and 95% CIs estimated using multivariable Cox propo

73 Hazard ratios (HRs) and 95% CIs for colorectal cancer incidence and mor

74 on model was used to estimate hazard ratios (HRs) and 95% CIs for hypothyroidism.

75 gression was used to estimate hazard ratios (HRs) and 95% CIs for overall survival (OS) and CRC-speci

76 ere used to estimate adjusted hazard ratios (HRs) and 95% CIs of incident breast cancer, comparing lo

77 Hazard ratios (HRs) and 95% CIs were calculated using Cox proportional

78 Trial-level hazard ratios (HRs) and 95% CIs were pooled by fixed-effect and random-

79 was used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (95% CIs) for the asso

80 Multivariable hazard ratios (HRs) and 95% confidence intervals (95%CI) for developing

81 models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for cancer-speci

82 models were used to estimate hazards ratios (HRs) and 95% confidence intervals (CIs) for CVD events (

83 We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for TBI in a Cox

84 ression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for the associat

85 provided propensity-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for the relation

86 We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for the risk of

87 Hazard ratios (HRs) and 95% confidence intervals (CIs) of each end poin

88 d regression models estimated hazard ratios (HRs) and 95% confidence intervals (CIs), adjusted for co

89 al hazard models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs), adjusting for a

90 models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs), adjusting for s

91 We computed hazard ratios (HRs) and 95% confidence intervals (CIs), and assessed ni

92 gression to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs).

93 ls were used to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs).

94 s models were used to estimate hazard ratios(HRs) and 95% confidence intervals(CIs).

95 models were used to calculate hazard ratios (HRs) and C statistics to determine predictive and discri

96 We estimated hazard ratios (HRs) and corresponding 95% CIs per IQR (0.15) increase i

97 Adjusted hazard ratios (HRs) and risk differences (difference in incidence of de

98 Incidence rates, hazard ratios (HRs), and 95% confidence intervals (CIs) for time to fir

99 Baseline CysC is a biomarker of RD, HRS, and ACLF and an independent predictor of mortality

100 lity, it fails to predict development of RD, HRS, and ACLF.

101 intake and polyphenol intakes from FFQs, 24-HRs, and the biomarkers TUPs and plasma carotenoids were

102 ed to evaluate relationships (hazard ratios [HRs] and 95% CIs) between weight change and endometrial

103 puparium formation (APF, SOP selection), 40 hrs APF (neurogenesis), and adult antennae.

104 Hazard ratios (HRs) are reported for early (1 to 60 days) and late (61

105 e state (LRS) and the high resistance state (HRS), are sufficient to learn and recognize patterns.

106 her inflammatory targeting as observed at 72 hrs as compared to untreated cells.

107 In addition, HRs as high as 4 for CHD and death and 8 for HF were rec

108 iate regression analysis, the hazard ratios (HRs) associated with intermediate uveitis (HR, 2.21; 95%

109 x regression yielded adjusted hazard ratios (HRs) associating each disease outcome with self-reported

110 mega-herbivores, and data on digestion time (hrs), average daily movement (km h) and numbers of viabl

111 Rs between 0.68 and 0.75) and IHD mortality (HRs between 0.55 and 0.70).

112 significantly lower risks of CVD mortality (HRs between 0.68 and 0.75) and IHD mortality (HRs betwee

113 pyruvate (40 vs. 146 mumol L(-1) after 5:20 hrs between CMV and STIM; p < 0.0001), but not the lacta

114 moking and risk-time adjusted hazard ratios (HRs) between patients and controls were calculated.

115 factor-regulated tyrosine kinase substrate (HRS), but not to HRS knockdown, whereas CLRDelta9KR*RAMP

116 were independently associated with increased HRs, but compared with full-fat milk, HRs were lower in

117 Adjustment for PDR did not alter HRs by race/ethnicity, but differences between black per

118 egression analysis was performed to estimate HRs by using age as the time variable.

119 ology of cHL in which PD-L1(+) TAMs surround HRS cells and implicate CD4(+) T cells as a target of PD

120 ched for contacts with T cells, and PD-L1(+) HRS cells are enriched for contacts with CD4(+) T cells,

121 his striking feature suggests that malignant HRS cells escape immunosurveillance and interact with im

122 HRS cells expressing PD-1 ligands are thought to engage

123 s, which physically colocalize with PD-L1(+) HRS cells in a microenvironmental niche.

124 (TAMs), but the relationships among PD-L1(+) HRS cells, PD-L1(+) TAMs, and PD-1(+) T cells remain und

125 bute to robust PD-L1 and PD-L2 expression by HRS cells.

126 h rare malignant Hodgkin and Reed-Sternberg (HRS) cells are surrounded by an extensive but ineffectiv

127 ential for malignant Hodgkin Reed-Sternberg (HRS) cells to evade antitumor immunity in classical Hodg

128 and proliferation of Hodgkin/Reed-Sternberg (HRS) cells, the malignant cells of cHL.

129 y and evening MPAH were analyzed separately, HRs comparing extreme groups (5-7 MPAH versus 0-2 MPAH)

130 Adjusted HRs comparing neutrophil counts 6 to 7 versus 2 to 3 x 1

131 However, CHD HRs comparing these groups varied strongly with baseline

132 l period across all age and sex groups, with HRs consistently increasing with proximity to PD diagnos

133 her results were synthesised narratively and HRs could not be reported here.

134 lation to 10 mg/m(3) of TiO2 nano-aerosol (6 hrs/day, 5 day/week, for 4 weeks).

135 For frequently examined prognostic factors, HRs derived by univariate and multivariate analysis were

136 study, the 95% confidence intervals for most HRs did not exclude 1.0.

137 ME with SND correlates with greater CT, more HRS, disruption of the ELM, and significant macular func

138 The HRs for 42-day and 1-year mortality in female patients w

139 ) in the pooled cohort, the ratio of nominal HRs for all-cause mortality was 0.61 (95% CI, 0.43-0.87)

140 1.56 (1.34 to 1.81), respectively, and with HRs for allograft failure excluding death as a cause of

141 ortional hazards models were used to compute HRs for breast cancer incidence associated with T2D rela

142 HRs for CVD mortality and IHD mortality for theoretical,

143 HRs for high-level candiduria were 1.14 (0.95-1.37) for

144 The HRs for intensity-weighted lifetime days of use of these

145 The adjusted HRs for living donor KT were 0.35 (95% CI, 0.24-0.51), 0

146 diabetic nephropathy associated with higher HRs for mortality [1.22 (1.12 to 1.34) and 2.57 (2.35 to

147 The HRs for mortality associated with cancer were 4.90 (95%

148 HRs for mortality in categories of coffee consumption we

149 For women (referent Q1 <155 cm), HRs for mortality were 1.00 (0.99-1.02), 1.05 (1.03-1.06

150 HRs for OS (the primary outcome measure) were pooled to

151 action and Synthesis: Data were pooled using HRs for OS of LCC vs RCC according to fixed or random-ef

152 Data were pooled using HRs for OS of LCC vs RCC according to fixed or random-ef

153 e prognostic: among nonsquamous patients, OS HRs for positive versus negative were ERCC1, 1.11 ( P =

154 ted adjusted RRs for inpatient mortality and HRs for postdischarge mortality for different anthropome

155 ory pattern score had multivariable adjusted HRs for premenopausal breast cancer of 1.35 for adolesce

156 r endocrine therapy exhibited slightly lower HRs for prostate cancer mortality with postdiagnosis sta

157 ata (IPD) meta-analysis was used to estimate HRs for results of particular importance.

158 In the new-onset RA cohort, the overall HRs for subsequent HF (any type), ischemic HF, and nonis

159 Estimated HRs for the primary end point for patients with an LGE e

160 ates versus none, the multivariable-adjusted HRs for the primary outcome were 1.32 (95% CI 1.16-1.50)

161 ted HR, 1.3; 95% CI, 1.1-1.5), with adjusted HRs for the subtypes of 1.2 (95% CI, 1.0-1.6) for essent

162 ed statistically significant PM2.5 mortality HRs for total and CVD mortality.

163 ls to estimate cause-specific hazard ratios (HRs) for 12 CVDs, adjusted for cardiovascular risk facto

164 lied to estimate the adjusted hazard ratios (HRs) for 3 health transitions (healthy to dead, healthy

165 hazards models, we estimated hazard ratios (HRs) for all NHL and common subtypes associated with a 1

166 ts model to calculate overall hazard ratios (HRs) for cardiovascular efficacy outcomes and odds ratio

167 Hazard ratios (HRs) for clinical outcomes were calculated for children

168 We estimated hazard ratios (HRs) for death by using Cox proportional hazards models,

169 We computed hazard ratios (HRs) for death, all-cause allograft failure, and allogra

170 Hazard ratios (HRs) for developing OAG with 95% CIs.

171 , to estimate subdistribution hazard ratios (HRs) for ESRD.

172 Hazard ratios (HRs) for incident parkinsonism per SD decrease in global

173 L/min per 1.73 m(2), adjusted hazard ratios (HRs) for incident study-specific peripheral artery disea

174 models were used to estimate hazard ratios (HRs) for outcomes related to AF type.

175 We estimated hazard ratios (HRs) for overall survival (OS) and progression-free surv

176 s, we estimated IHD mortality hazard ratios (HRs) for PM2.5, trace constituents, and pollution source

177 Main outcome measures were hazard ratios (HRs) for post-surgery self-harm or hospitalization for d

178 ession models used to compute hazard ratios (HRs) for prostate cancer-specific mortality and all-caus

179 ssion was used to compute the hazard ratios (HRs) for recurrence.

180 ls were performed to estimate hazard ratios (HRs) for relative survival in CUP patients compared to t

181 Hazard ratios (HRs) for the diagnosis of nonaffective psychoses (Intern

182 riable Cox models to estimate hazard ratios (HRs) for the primary outcome (the time to first major ca

183 d race, were used to estimate hazard ratios (HRs) for the risk of cataract in radiologic technologist

184 models were used to estimate hazard ratios (HRs) for time to first fracture or time to first fall in

185 ne, the multivariate-adjusted hazard ratios (HRs) for type 2 diabetes for those with GSD were 1.09 (9

186 The hazard ratios [HRs] for these six factors ranged between 1.26 [95% conf

187 tegration categories above the lowest level (HRs from 0.58 to 0.52, P's < 0.01) and each of the highe

188 ssay (PLA) demonstrated the translocation of Hrs from the cytosol to the plasma membrane of infected

189 Data from the AHA/ACC/HRS guidelines on AF from 2001, 2006, 2011, and 2014 wer

190 ce base and changes over time in the AHA/ACC/HRS guidelines on AF with respect to the distribution of

191 Association (AHA), and Heart Rhythm Society (HRS) guidelines on the management of atrial fibrillation

192 s required for transport (ESCRT)-0 component Hrs [hepatocyte growth factor-regulated tyrosine kinase

193 SPOPL-dependent manner, and accumulates with HRS in cells lacking SPOPL.

194 FAs [HR: 0.66 (95% CI: 0.44, 0.98)], whereas HRs in cis MUFA quintiles were nonsignificant.

195 93]) complications (p < 0.001), with similar HRs in individuals with previously diagnosed and screen-

196 ll-cause) mortality between the diet groups: HRs in low meat eaters, fish eaters, and vegetarians com

197 Correlation among CT, RS, and HRS in patients with and without SND was determined.

198 Corresponding HRs in the postintervention period were close to null.

199 Thus, we propose a role for ubiquitin and HRS in the regulation of AM-induced degradation of CLR*R

200 the number of hyperreflective retinal spots (HRS) in the central 3000 mum; and the presence of SND an

201 Among community-dwelling decedents in the HRS, increasing obesity was associated with reduced hosp

202 tyrosine kinase substrate (HRS), but not to HRS knockdown, whereas CLRDelta9KR*RAMP2 degradation was

203 hen each one received the other treatment 24 hrs later.

204 icant associations with CD development risk (HRs not significant).

205 .4; 95% confidence interval [CI], 1.8-49.7), HRS (odds ratio, 4.2; 95% CI, 1.2-14.8), and ACLF (odds

206 ly significant, with unadjusted and adjusted HRs of 0.58 (p = 0.043) and 0.58 (p = 0.044), respective

207 nversely associated with CVD mortality, with HRs of 0.69 (95% CI: 0.54, 0.89) for >2-4 cups/d and 0.7

208 osis statin use was associated with adjusted HRs of 0.83 (95% CI, 0.77 to 0.89) for prostate cancer m

209 first infection-related hospitalization with HRs of 1.24 (95% CI, 1.08 to 1.42) and 1.06 (95% CI, 0.9

210 icipants with CVD at baseline (3.4%) had CHD HRs of 1.47 (95% CI: 1.12, 1.93) and 1.61 (95% CI: 1.02,

211 2-day and one-year mortality with respective HRs of 1.99 (95%CI, 1.03-3.84) and 1.84 (95%CI, 1.14-2.9

212 We estimated HRs of all-cause, CVD, and cancer mortality according to

213 The HRs of men with four risk practices comparing to those w

214 In addition, HRs of neovascular AMD after 2006 were calculated since

215 Similarly, adjusted HRs of progression to severe psoriasis were 0.44 (95% CI

216 Adjusted HRs of psoriasis were 0.52 (95% CI, 0.33-0.81) and 1.23

217 Adjusted HRs of psoriatic arthritis were 0.29 (95% CI, 0.12-0.71)

218 associated with incident HF: hazard ratios (HRs) of 0.99 per year (95% confidence interval [CI]: 0.9

219 core of 1 was associated with hazard ratios (HRs) of 1.26 (95% CI, 1.11-1.43) in women and 1.21 (95%

220 ears (PYs)], with an adjusted hazard ratios (HRs) of 1.69 [95% confidence interval (CI), 1.51-1.87].

221 Hazard ratios (HRs) of all-cause mortality and 95% confidence intervals

222 Hazard ratios (HRs) of breast cancer were estimated using Cox proportio

223 ing confounders, we estimated hazard ratios (HRs) of death and of AIDS-defining illness or death, ris

224 models were used to estimate hazard ratios (HRs) of distant metastasis.

225 th late donor identification, hazard ratios (HRs) of events were adjusted on the time-dependent treat

226 cumulative probabilities and hazard ratios (HRs) of interval CRC, defined as a CRC diagnosis 6 to 59

227 For each trial, we extracted hazard ratios (HRs) of the effects of docetaxel or bisphosphonates on s

228 ge-adjusted and multivariable hazard ratios [HRs] of pregnancy for overall survival for all exposure

229 lls also led to greater overlap of Rme-8 and Hrs on endosomes.

230 .03), mean CT (P = .009), and mean number of HRS (P = .0001) were all higher in SND+ vs SND- eyes.

231 ne data, duration of surgery (02:29 vs 02:47 hrs, P = 0.17) and mean hospital stay (10 +/- 7.1 vs 8 +

232 ime point (2.6 vs. 0.9 mmol L(-1) after 5:20 hrs; p < 0.001).

233 RNA was extracted at 24 hrs and 48 hrs post exposure for RNA-seq.

234 correlation was found between the number of HRS, presence of SND, CT, and RS within 12 degrees in SN

235 Overexpression, but not knockdown of HRS, promoted hyperubiquitination of CLR under basal con

236 ociations for all 9 anthropometric measures (HRs ranging from 1.08 [95% confidence interval (CI): 1.0

237 erinatal events and increased OCD risk, with HRs ranging from 1.11 (95% CI, 1.07-1.15) for 1 event to

238 Hrs recruits ROCK1 to the membrane, which is required fo

239 Hrs requires mTORC1 activity to maintain its protein exp

240 HRS reversal was achieved in 23 of 97 (23.7%) patients r

241 and evaluated the differences by a ratio of HRs (rHRs): the HR for PFS to that for OS.

242 The HRs showed progressively decreased rates of mortality in

243 hazard ratios per population SD difference (HRs) showed highly statistically significant, positive a

244 of the cells with albumin (40 mug/ml) for 72 hrs significantly increased the protein levels of HIF-1a

245 STAM proteins and the role of the STAM Vps27/Hrs/STAM domain.

246 ed Cox regression to estimate hazard ratios (HRs), stratifying by birthdate to control for age, year,

247 ; men diagnosed during adolescence had lower HRs than survivors of childhood cancer (HR, 0.56 v 0.70)

248 [HR]) was significantly lower; men had lower HRs than women (HR, 0.65 v 0.79).

249 increased at 3 hrs after ICH with peak at 24 hrs, then returned to normal at 72 hrs after ICH.

250 pocampus after pilocarpine-induced SE from 4 hrs to 35 days.

251 ollected by the Health and Retirement Study (HRS) to perform the first genome-wide association study

252 We used Cox regression (hazard ratios [HRs]) to compare survival, adjusting for age, sex, SES,

253 ly expressed for 3R4F smoke at 24 hrs and 48 hrs using a pFDR < 0.01 and a [fold change] > 2 threshol

254 We pooled sex-specific HRs using random-effects meta-analysis.Over 24-30 y of f

255 by pooling the study-specific hazard ratios (HRs) using random-effects modeling.

256 riven more so by lower rates of waitlisting (HRs vs IgAN, ranged from 0.49 for DN to 0.92 for membran

257 The total polyphenol intake from 24-HRs was correlated with FFQs in crude (r = 0.51, P < 0.0

258 For the key secondary end point, the HRs were 0.73 (0.59-0.91; P=0.0040) for those with PAD a

259 For the key secondary endpoint, the HRs were 0.82 (0.72-0.93; p=0.0021) for those with diabe

260 th the increase accounted for by ER- cancer: HRs were 1.02 (95% CI, 0.80-1.31) for ER+ and 1.43 (95%

261 <37 weeks) and very preterm (<32 weeks), the HRs were 1.22 (95% CI, 0.96-1.54) and 2.01 (95% CI, 1.47

262 Compared with never drinkers, the HRs were 1.25 for ever drinkers, 1.24 for current drinke

263 Corresponding HRs were 15.5 (11.0-21.8) for exacerbations, 2.8 (2.4-3.

264 HRs were adjusted for age, smoking status, and education

265 ort of patients with RA of any duration, the HRs were between 1.71 and 1.88 for the different HF subt

266 reased HRs, but compared with full-fat milk, HRs were lower in consumers of medium- and low-fat milk.

267 The HRs were obtained by comparing the risk in the cohort of

268 HRs were similar across different categories of maternal

269 ial and socioeconomic risk factors and their HRs were similar between the three countries.

270 HRs were similar for IHD mortality.

271 mone receptor-negative disease, although the HRs were substantially smaller.

272 imary composite endpoint, the hazard ratios (HRs) were 0.83 (95% CI 0.75-0.93; p=0.0008) for patients

273 Hazard ratios (HRs) were adjusted for marital status, immigration statu

274 Hazard ratios (HRs) were adjusted for predictors of multiple-type infec

275 Hazard ratios (HRs) were calculated comparing quartiles 2 through 4 to

276 Hazard ratios (HRs) were calculated from time of exposure to the occurr

277 for potential treatment bias, hazard ratios (HRs) were calculated using Cox regression and were teste

278 Hazard ratios (HRs) were estimated by country (Cox survival model) and

279 Hazard ratios (HRs) were estimated by Cox proportional hazard model and

280 lated, and crude and adjusted hazard ratios (HRs) were estimated by Cox regression models and present

281 -specific mortality rates and hazard ratios (HRs) were estimated from a retrospective cohort within 4

282 Hazard ratios (HRs) were estimated from Cox models stratified by matche

283 Hazard ratios (HRs) were estimated from Cox models, and survival curves

284 Hazard ratios (HRs) were estimated with multivariable adjusted Cox prop

285 Hazard ratios (HRs) were estimated with the Cox proportional hazards mo

286 In this analysis, all HRs with 95% CIs were pooled to obtain prognostic inform

287 gression models were constructed to estimate HRs with 95% CIs, with adjustment for potential confound

288 each trial, we extracted the hazard ratios (HRs) with 95% CIs for both outcomes and evaluated the di

289 regression modeling generated hazard ratios (HRs) with 95% CIs identifying factors associated with pa

290 e rates of cerebral palsy and hazard ratios (HRs) with 95% CIs, adjusted for maternal age, country of

291 Hazard ratios (HRs) with 95% confidence intervals (CIs) associated with

292 Hazard ratios (HRs) with 95% confidence intervals (CIs) for developing

293 Hazard ratios (HRs) with 95% confidence intervals (CIs) for each outcom

294 ds regression models provided hazard ratios (HRs) with 95% confidence intervals (CIs) of disease-spec

295 ine propensity score-adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) of outcomes in

296 random-effects models to pool hazard ratios (HRs) with 95% confidence intervals (CIs) of the followin

297 Hazard ratios (HRs) with 95% confidence intervals (CIs) of visiting an

298 used to extract the adjusted hazard ratios (HRs) with adjustments for baseline age, sex, body mass i

299 ber of deaths/recurrences and hazard ratios (HRs), with 95% confidence intervals (CI), for the time-d

300 Silencing Hrs without decreasing mTORC1 activity is sufficient to