ライフサイエンスコーパス: hrs

1 essed as odds ratios (ORs) or hazard ratios (HRs).

2 .69 hrs, 95% confidence interval: 0.62, 0.76 hrs).

3 ipants from the Health and Retirement Study (HRS).

4 transfer tests with and without a delay of 3 hrs.

5 sin with noradrenaline in ACLF patients with HRS.

6 loride pump into a proton pump but cannot in HRs.

7 ts of WHO grade, age at diagnosis and sex as HRs.

8 RAGE (BAL and plasma) were elevated after 24-hrs.

9 Log (CFU/cm(2)) and produces results in 1-8 hrs.

10 a second plateau was established for 1 to 2 hrs.

11 ts for durations ranging between 1 min and 3 hrs.

12 a significant increase in LDH release at 24 hrs.

13 (CFUs) at 1 per 1000 CFUs in as little as 48 hrs.

14 S); we identified a histologic candidate for HRS.

15 fter three, four, and more than four cycles (HRs, 0.53, 0.41, and 0.21, respectively).

16 ver time (0- to 5-, 5- to 10-, and > 10-year HRs, 0.62, 0.47, and 1.35, respectively; treatment-by-ti

17 rent understanding of the pathophysiology of HRS-1 and existing challenges in its diagnosis and treat

18 ntly available to ascertain the diagnosis of HRS-1 and guide therapy are suboptimal.

19 ncluding those traditionally associated with HRS-1 and non-traditional factors, might contribute to t

20 From a clinical perspective, a diagnosis of HRS-1 guides utilization of vasoconstrictive therapy and

21 The pathogenesis of HRS-1 is largely viewed as a functional derangement that

22 nction has prompted the functional nature of HRS-1 to be re-examined.

23 Hepatorenal syndrome type 1 (HRS-1), which is a specific type of AKI that occurs in t

24 - 0.334; IL233 pre: 0.42 +/- 0.162; IL233 24 hrs: 1.34 +/- 0.43; IL233 1 week: 1.2 +/- 0.41; IL233 2

25 to senior controls but still had lower peak HRs (122+/-14 versus 156+/-15 beats per minute; P<0.001)

26 a high index score and high alcohol intake (HRs: 2.29 for all-cause and 1.78 for CVD mortality) were

27 reased risk of death and CRC (hazard ratios [HRs], 3.20 and 2.43, respectively; P < .001) and a lower

28 the lowest intakes (<=15th percentile), with HRs (95% CI; P-trend) of 0.54 (0.32, 0.90; P = 0.003) fo

29 For indoor nighttime LF WTN, the HRs (95% CIs) among persons [Formula: see text] of age e

30 HRs (95% CIs) for 30-day and 1-year all-cause mortality

31 l health index score and low alcohol intake, HRs (95% CIs) for all-cause mortality were 0.93 (0.89, 0

32 HRs (95% CIs) for all-cause mortality, all-cause readmis

33 ong persons [Formula: see text] of age, with HRs (95% CIs) for the highest exposure group ([Formula:

34 gurt consumption, the multivariable-adjusted HRs (95% CIs) of mortality were 0.89 (0.86, 0.93), 0.85

35 For CVD mortality, HRs (95% CIs) were 0.93 (0.86, 1.00; p = 0.058), 0.90 (0

36 For men, the corresponding HRs (95% CIs) were 0.99 (0.94, 1.03), 0.98 (0.91, 1.05),

37 risk of hospitalization and death: adjusted HRs (95% CIs) were 1.18 (1.18-1.19) and 1.25 (1.24-1.25)

38 HRs (95% CIs) were 1.22 (1.14, 1.31; p < 0.001), 1.24 (1

39 The multivariable-adjusted HRs (95% confidence intervals) for CVD across categories

40 cipants with a sleep timing SD <=30 min, the HRs (95% confidence intervals) for CVD were 1.16 (0.64 t

41 In UK Biobank, hazard ratios (HRs) (95% CI) for all-cause mortality in people with T2D

42 ary relative to the questionnaire (beta=0.28 hrs, 95% confidence interval: 0.22, 0.33 hrs), but sleep

43 re (7.07 hrs) by approximately 41 mins (0.69 hrs, 95% confidence interval: 0.62, 0.76 hrs).

44 onsecutive patients with ACLF diagnosed with HRS acute kidney injury (AKI) were randomized to albumin

45 l cohort study, we calculated hazard ratios (HRs) adjusted for likelihood of receiving clarithromycin

46 rk, estimating cause-specific hazard ratios (HRs) adjusted for potential confounding factors.

47 itrulline, glutamic acid and carnitine at 24 hrs after enrolment and significantly lower plasma gluta

48 m MR imaging time for carotid atheroma is 48 hrs after its administration.

49 e was also a marked increase in apoptosis 12 hrs after LPS treatment with caspase-3 levels being sign

50 ecovery (88.7 +/- 3.21%) in CD3 + T cells 19 hrs after muVS processing.

51 ior semicircular canal, 3 wks prior to, or 5 hrs after, noise exposure.

52 were hypovolemia-induced AKI (48%), 93 were HRS-AKI (29%), 39 were ATN (12%), and 35 were due to mis

53 tics, including AKI stage and sepsis-related HRS-AKI, were comparable between groups.

54 with improved survival in ACLF patients with HRS-AKI.

55 e data from the Health and Retirement Study (HRS) along with information on respondents' early educat

56 at other zfyve family members (FYCO1, WDFY3, Hrs) also distribute to nuclei of different cells in the

57 potential confounders were used to estimate HRs and 95% CIs for the association between fruit and ve

58 egression to estimate multivariable-adjusted HRs and 95% CIs for total invasive breast cancer risk an

59 d Cox proportional hazard models to estimate HRs and 95% CIs for whole grain and dietary fiber intake

60 rtional hazards models were used to estimate HRs and 95% CIs of cardiovascular disease (CVD), includi

61 the risk of metabolic syndrome we estimated HRs and 95% CIs using Cox proportional hazards models.

62 d Cox proportional hazard models to estimate HRs and 95% CIs.

63 HRs and 95% confidence intervals were used to measure th

64 Cox regression analysis was used to estimate HRs and corresponding 95% CIs.

65 enaline are routinely used in cirrhosis with HRS and have been found to be equally effective.

66 inated proteins and the prelysosomal markers HRS and LAMP1.

67 also contrasted methylation profiles of male HRs and LRs with a control rat strain that displays an i

68 HRs and PAFs showed more similarities than differences,

69 Associations are presented as HRs and PAFs with 95% CIs.

70 We used paired t tests to assess whether HRs and SEs from published AD differed on average from t

71 24-hours (24-hrs) and 1-Month (1-M) after exposure, echocardiography,

72 Hazard ratios (HRs) and 95% CIs for breast cancer were calculated using

73 dels to estimate multivariate hazard ratios (HRs) and 95% CIs for the associations between age at men

74 was used to estimate adjusted hazard ratios (HRs) and 95% CIs of the relationships between physical a

75 We estimated hazard ratios (HRs) and 95% CIs per SD increase in adiposity accounting

76 Hazard ratios (HRs) and 95% CIs were estimated controlling for over 140

77 Adjusted hazard ratios (HRs) and 95% CIs were estimated in each dataset and pool

78 Melanoma hazard ratios (HRs) and 95% CIs were estimated using Cox proportional h

79 Covariate-adjusted hazard ratios (HRs) and 95% CIs were estimated using Cox proportional h

80 ression was used to calculate hazard ratios (HRs) and 95% CIs.

81 models were used to estimate hazard ratios (HRs) and 95% CIs.

82 al hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CI) of overall cancer

83 atching were used to estimate hazard ratios (HRs) and 95% confidence intervals (CI).

84 Unadjusted and adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) are presented in

85 The hazard ratios (HRs) and 95% confidence intervals (CIs) for developing d

86 We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) for incident AMI

87 timate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for NAFLD in ass

88 Hazard ratios (HRs) and 95% confidence intervals (CIs) for outcomes wer

89 gression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for risk associa

90 Cox regression yielded hazard ratios (HRs) and 95% confidence intervals (CIs) for risk of card

91 onal hazard models calculated hazard ratios (HRs) and 95% confidence intervals (CIs) for survival, an

92 Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated

93 Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated

94 med for studies that reported hazard ratios (HRs) and 95% confidence intervals (CIs).

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

96 s were performed to calculate hazard ratios (HRs) and 95% credible intervals (CrIs)/CIs.

97 models were used to estimate hazard ratios (HRs) and adjust for confounding.

98 of anion pumps, the archaeal halorhodopsins (HRs) and bacterial chloride-pumping rhodopsins, have bee

99 regression models to estimate hazard ratios (HRs) and corresponding 95% CIs for the association betwe

100 s of death were assessed with hazard ratios (HRs) and Cox proportional hazards modeling.

101 Hazard ratios (HRs) and receiver operating characteristic curve analyse

102 ssion was used to compute the hazard ratios (HRs) and respective 95% confidence intervals (CIs) while

103 We extracted or estimated hazard ratios (HRs) and standard errors (SEs) for survival from trial r

104 50+ from the US Health and Retirement Study (HRS) and, 10,388 from the English Longitudinal Study of

105 We describe the prevalence, hazard ratios (HRs), and population-attributable fractions (PAFs) for c

106 rkers specific to this vesicle type, CD9 and HRS, and the trophoblast proteins placental alkaline pho

107 l hazard models to calculate cohort-specific HRs, and used fixed-effects models to calculate the pool

108 Hyperreflective foci and HRS are markers of cellular activity associated with vis

109 al model, we demonstrate the capabilities of HRS as a complementary chiroptical method, ideally suite

110 Hazard ratios (HRs) assessing the association between markers and HBeAg

111 mpared with never using soy supplements, the HRs associated with current use of soy supplements were

112 proportional hazards models, hazard ratios (HRs) associated with postdiagnosis obesity (BMI >= 30 kg

113 k groups compared with low-risk groups, with HRs at 10 years in the high-risk group ranging from 1.67

114 ble by generating time-dependent Cox models; HRs at an ELF threshold of 10.51 were 1.94 (95% CI 1.10-

115 were used to estimate multivariable-adjusted HRs between lifetime ovulatory cycles (LOC) and its comp

116 .28 hrs, 95% confidence interval: 0.22, 0.33 hrs), but sleep apnea was not significantly associated w

117 ase inhibitors were associated with elevated HRs, but with CIs including the null value, for myocardi

118 longer than that of the questionnaire (7.07 hrs) by approximately 41 mins (0.69 hrs, 95% confidence

119 Hepatorenal syndrome (HRS) carries a high short-term mortality in patients wit

120 e, respectively, are greater within a 75 mum HRS cell niche relative to areas outside this region (CT

121 immunologically privileged niche surrounding HRS cells and raise the possibility that patients with c

122 grammed cell death-1 ligand (PD-L1)-positive HRS cells and tumor-associated macrophages (TAMs), which

123 In addition, T cells touching HRS cells are more frequently positive for CTLA-4 than f

124 We further found that HRS cells, and a subset of TAMs, are positive for the CT

125 ter-derived B cells (Hodgkin Reed-Sternberg [HRS] cells) embedded within a robust but ineffective inf

126 onths showed higher event rates, but similar HRs compared with those at the 3-year analysis.

127 States in the north had higher HRs compared with those of the central-south, except for

128 d models were used to compute hazard ratios (HRs) comparing the mortality of individuals at the 80th

129 reement show that for individual trials, the HRs could deviate substantially.

130 f the AD was large, individual meta-analysis HRs could still differ from their IPD equivalents by a r

131 visual vs olfactory) sensed before 1 h and 3 hrs delays.

132 On average, trial HRs derived from published AD were slightly more in favo

133 rs' (n = 519) HBGA status and hazard ratios (HRs) derived for all-cause diarrhea and specific enterop

134 We used hazard ratios (HRs) derived from Cox proportional hazard models for tim

135 d models were fit to estimate hazard ratios (HRs) describing the relationship between IgA thresholds

136 sed to calculate the adjusted hazard ratios (HRs), focusing on heavy alcohol use and neutrophil funct

137 0.001) was found on carotid MR imaging at 48 hrs following the ferumoxytol infusion.

138 The adjusted HRs for 1-year mortality increased significantly with de

139 The corresponding HRs for 12-month [Formula: see text] exposure was 0.96 (

140 d MI were 16.1%, 19.2%, and 19.0%, and their HRs for 2-year mortality were 8.58 (95% CI, 5.63-13.09;

141 BMI and SMI were associated with early PD1 [HRs for 9-wk BMI: 1.54 (95% CI: 1.33, 1.76); 9-wk SMI: 1

142 HRs for a doubling of micronutrient intake differed only

143 HRs for all-cause mortality were 0.86 (95% confidence in

144 (AUC(inf) 1698 +/- 352 vs. 53.3 +/- 7.9 ID/g*hrs for alphaICAM and 1023 +/- 507 vs. 114 +/- 37 ID/g*h

145 phaICAM and 1023 +/- 507 vs. 114 +/- 37 ID/g*hrs for alphaPECAM mAb vs scFv).

146 isk quartile with the other three quartiles, HRs for bone attenuation, muscle attenuation, V/S fat ra

147 HRs for current use were 1.36 (95% CI: 0.95, 1.93) and 0

148 HRs for heart failure or cardiomyopathy and venous throm

149 The HRs for higher-dose edoxaban versus warfarin for SSEE we

150 e (AUC(inf) 141 +/- 3.2 vs 12.4 +/- 4.2 ID/g*hrs for ICAM and 188 +/- 90 vs 34.7 +/- 19.9 ID/g*hrs fo

151 The estimated HRs for incident T2D in the multimetabolite score (model

152 fter adjusting for confounders, the adjusted HRs for ION in the second- and third-level groups were 1

153 For fish consumption, HRs for late AMD in quartile 4 versus 1 were 0.69 (0.58-

154 er, HR 1.10 (95% CI 1.09-1.12), with highest HRs for liver (3.31), pancreas (2.19) and uterine cancer

155 EXSCEL-observed HRs for MACE and ACM remained robust after right censori

156 The corresponding HRs for mortality within 30 days, 90 days, 1 year, and 5

157 HRs for NDCMP were similar to those from UK Biobank for

158 HRs for other efficacy end points were similar to those

159 or ICAM and 188 +/- 90 vs 34.7 +/- 19.9 ID/g*hrs for PECAM), despite having similar blood PK, indicat

160 nal regression models were used to calculate HRs for T2D associated with changes in dairy product con

161 In NHANES 1999-2006, adjusted HRs for the 80th vs. 20th percentile of blood cadmium we

162 hazards regression was used to estimate the HRs for the association between the flavonoid intakes an

163 HRs for the combination of a high index score and high a

164 HRs for type-specific CVDs and <5.0-mg daily dose use we

165 HO was associated with higher hazard ratios (HRs) for all types of CVD; however, almost 40% of those

166 Multivariable hazard ratios (HRs) for all-cause and cardiovascular disease (CVD) mort

167 Hazard ratios (HRs) for all-cause, cardiovascular disease, and cancer m

168 ression was used to calculate hazard ratios (HRs) for any MACE, MALE, and MALE including lower extrem

169 We applied per-day hazard ratios (HRs) for cancer progression that we generated from obser

170 ional hazard models estimated hazard ratios (HRs) for chronic health conditions and 95% CIs.

171 riable analysis, the adjusted hazard ratios (HRs) for dementia per 1-SD (10-point) AHEI increment wer

172 d model was used to calculate hazard ratios (HRs) for different patient factors.

173 , and the association between hazard ratios (HRs) for disease-free survival and overall survival usin

174 ed Cox regression to estimate hazard ratios (HRs) for future inflammatory bowel disease in IgA nephro

175 Baseline hazard ratios (HRs) for graft failure (HR, 4.69; P = 0.009) and death (

176 Hazard ratios (HRs) for HS in patients with IE compared with the matche

177 sed Cox regression to compute hazard ratios (HRs) for incident CRC, and for CRC mortality, taking tum

178 ds model was used to estimate hazard ratios (HRs) for incident CVD according to SD of sleep duration

179 roups, compared with placebo, hazard ratios (HRs) for incident THR/TKR during follow-up were 0.60 (95

180 models and estimated adjusted hazard ratios (HRs) for incident tuberculosis with mixed-effects Poisso

181 o estimate crude and adjusted hazard ratios (HRs) for ION development with respect to the different l

182 riable), was used to estimate hazard ratios (HRs) for lung cancer incidence by sex, tobacco smoking,

183 cts model to estimate overall hazard ratios (HRs) for MACE, its components, death from any cause, hos

184 iable Cox regression provided hazard ratios (HRs) for mortality in participants who did and did not h

185 The main estimated hazard ratios (HRs) for OS and PFS were 0.76 (0.71-0.82) and 0.81 (0.73

186 r widely-accepted predictors, hazard ratios (HRs) for overall (OS) and progression free (PFS) surviva

187 Hazard ratios (HRs) for progression in aMedi tertile 3 versus 1 were 0.

188 t for parents' BMI to compute hazard ratios (HRs) for risk of mortality per standard deviation (SD) h

189 gression was used to estimate hazard ratios (HRs) for severe liver disease at 5, 10, and a maximum fo

190 d Cox regression to calculate hazard ratios (HRs) for small bowel adenocarcinoma, adenomas, and carci

191 tive node stage migration and hazard ratios (HRs) for survival with more ELNs were fitted using a LOW

192 Hazard ratios (HRs) for the effects of radiotherapy timing on event-fre

193 gression was used to estimate hazard ratios (HRs) for the primary outcome, ASD, before and after adju

194 used Kaplan-Meier curves and hazard ratios (HRs) for time to first recurrence, which was a pre-plann

195 On average, meta-analysis HRs from published AD slightly tended to favour the rese

196 In this study we found that HRs from published AD were most likely to agree with tho

197 We estimated hazard ratios (HRs) from stratified Cox regression comparing risk of ma

198 d and multivariable adjusted subdistribution HRs in 2014 versus 1998 were 0.4 (CI, 0.25-0.55) and 0.4

199 ycatch from a total of 403 trawl sets (1,273 hrs) in the Gulf of Papua.

200 We restricted our sample to age-eligible HRS Life History Mail Survey respondents who provided da

201 l experiences collected in the 2015 and 2017 HRS Life History Mail Survey to examine whether school c

202 HRF and HRS may serve as structural end points in clinical trial

203 ated with longer LOS [smaller hazard ratios (HRs) mean longer LOS; ARS 1-2: adjusted HR 0.94, 95% con

204 Hazard ratios (HRs), mortality rates, and 95% CIs were estimated using

205 Approximately 2 hrs of "quasi-continuous" measurements were recorded for

206 -specific survival and overall survival with HRs of 0.65 (p = 0.02) and 0.71 (p < 0.01), respectively

207 mortality benefits over vertebroplasty, with HRs of 0.77 (95% CI: 0.77, 0.78; P < .001) and 0.87 (95%

208 (HR 0.77, 95% CI 0.68-0.87; p<0.0001), with HRs of 0.89 (0.78-1.01; p=0.066) for sustained decline i

209 ition, dose-response analyses gave estimated HRs of 0.97 (95% CI: 0.95, 0.99) for intake of total who

210 imilar results for all-cause mortality, with HRs of 1.50 (1.14-1.98) for high-income countries, 1.80

211 les, higher hospital volume did not decrease HRs of 30-day re-intervention (adjusted HR = 1.14, 95% C

212 The HRs of EAC were stable comparing the surgery group with

213 lar mortality in the 2 external cohorts (eg, HRs of IDH by the 2017 ACC/AHA definition were 1.17 [95%

214 The overall SIRs and HRs of the combined outcome laryngeal or pharyngeal squa

215 was associated with adjusted hazard ratios (HRs) of 0.95 (95% CI, 0.89 to 1.01) for prostate cancer-

216 hospital discharge rate, with hazard ratios (HRs) of 1.03 (95% confidence interval [CI], 0.47-2.25) a

217 ung residence time (AUC(inf) 253 +/- 18 ID/g*hrs) of all TM modalities.

218 odels were used to assess the hazard ratios (HRs) of breast cancer in relation to SoC.

219 cidence was assessed by using hazard ratios (HRs) of Cox regression.

220 Hazard ratios (HRs) of CVD < 1 year after initiation of BEP treatment w

221 hazard regression to estimate hazard ratios (HRs) of death for SRH, controlling for pathology, biomet

222 valent dose-related risks and hazard ratios (HRs) of first all-cause and type-specific cardiovascular

223 ed Cox regression to estimate hazard ratios (HRs) of IS for persons with vs without a history of left

224 sed to calculate the adjusted hazard ratios (HRs) of mortality with their 95% confidence intervals (C

225 ed the multivariable-adjusted hazard ratios (HRs) of sitting for each sitting-MVPA combination group

226 gression was used to estimate hazard ratios (HRs) of the primary outcome and 95% CIs.

227 elation of treatment effects (hazard ratios [HRs]) on both EFS and OS (trial level).

228 showed no meaningful changes in MACE or ACM HRs or P values, although simulations of substantially g

229 DA was associated strongly with more HRF and HRS (P < 0.0001).

230 No difference was seen in the relative HRs (p=0.17).

231 0.41; IL233 2 week: 0.47 +/- 0.37; IL233 24 hrs + PC61: 3.5 +/- 0.74) and fibrosis in all treatment

232 Hazard ratios (HRs) per 1-SD higher log CES-D or PHQ-2 adjusted for age

233 Hazard ratios (HRs) per 5 BMI-units, calculated using proportional haza

234 tors, but these factors had little impact on HRs (Poor SRH: HR 1.99; CI: 1.72, 2.31).

235 as performed before and at 24, 48, 72 and 96 hrs post ferumoxytol infusion.

236 24-hrs post-exposure, there was a significant reduction in

237 orly through the hindbrain between 18 and 48 hrs postfertilization, alongside the r4-derived FBMNs.

238 ted from subjects' plasma at fasting and 3.5 hrs postprandial to a test meal high in saturated fat.

239 the heatwave definition used, hazard ratios (HRs) ranged from 1.10 (95% CI: 1.01, 1.20) to 1.92 (1.39

240 th that of controls; adjusted hazard ratios (HRs) ranged from 1.72 (95% CI 1.57-1.89) in patients aft

241 mors with low Beclin 1 expression, endosomal HRS recruitment was diminished and receptor function was

242 Their hyper-Rayleigh scattering (HRS) responses in solution were accordingly assessed, us

243 levels as compared with the first quartile (HRs, second quartile: 1.19 [1.00-1.42]; third quartile:

244 the chloride-binding mode is more similar to HRs than chloride-pumping rhodopsins, but the overall st

245 uspension event by estimating hazard ratios (HRs) that compared mortality and graft survival between

246 egression methods to estimate hazard ratios (HRs) that compared posttransplantation mortality in diff

247 athological subgroups analysed, with similar HRs to that for the broader intended-use population.

248 We used Cox proportional hazard ratios (HRs) to estimate the association between HR-pQCT bone in

249 ly of EGFR ubiquitylation but dependent upon Hrs/Tsg101 that are required for the formation of intral

250 asures of growth kinetics in as little as 30 hrs under a wide variety of environmental conditions.

251 lung healthy subpopulation with even higher HRs up to 2.76 (95% CI 1.52-4.93).

252 nal-hazards models and pooled hazard ratios (HRs) using random-effects meta-analyses.

253 We obtained hazard ratios (HRs) using restricted cubic splines based on Cox proport

254 the 27 Gy group, and 21 in the 26 Gy group); HRs versus 40 Gy in 15 fractions were 0.86 (95% CI 0.51

255 Reversal of HRS was also better with terlipressin (40% vs. 16.7%; P

256 diary-reported overall sleep duration (7.76 hrs) was longer than that of the questionnaire (7.07 hrs

257 Meta-analysis of hazard ratios (HRs) was performed for mortality risk, and pooled odds r

258 and HRF plus smaller hyperreflective specks (HRS); we identified a histologic candidate for HRS.

259 The HRs were 0.81 (0.71-0.92) for patients with a history of

260 with the lowest, the multivariable-adjusted HRs were 0.81 for total stroke (95% CI: 0.54, 1.23; P-tr

261 HRs were 0.88 (95% CI 0.81-0.96; p=0.003) for death from

262 6-3.64) (adjusted) and at a threshold of 9.8 HRs were 1.85 (95% CI 1.09-3.15) (unadjusted) and 1.80 (

263 Molecule-specific HRs were 1.86 (CI, 1.11 to 3.10) for dapagliflozin, 2.52

264 Our HRs were adjusted for age, baseline educational level, m

265 HRs were adjusted for age, sex, educational level, marit

266 riate, whereas in the pharmacogenomic study, HRs were adjusted for age, sex, history of myocardial in

267 HRs were adjusted for important confounders and immortal

268 HRs were also favourable for cardiovascular death alone

269 HRs were compared among calendar periods.

270 In OCT scans, HRF and HRS were counted manually.

271 In 101 eyes of 101 patients, HRF and HRS were identified in 25 and 95 eyes, respectively, wit

272 HRs were increased for patients with ulcerative colitis

273 HRs were independent of sex and age.

274 ficantly associated with mortality; however, HRs were largest for concordant conditions.

275 agnitude and statistical significance of the HRs were not materially changed after adjustment for add

276 al weight as reference, for CD the following HRs were observed: BMI < 18.5, 1.35; 95% CI, 1.12-1.62,

277 Pooled HRs were similar across subgroups.

278 Corresponding HRs were small bowel adenocarcinoma 3.05 (95% confidence

279 Reported hazard ratios (HRs) were based on interquartile range increases of 5.3,

280 Hazard ratios (HRs) were calculated using Cox regression analysis.

281 Hazard ratios (HRs) were calculated using the Cox proportional hazard m

282 Adjusted hazard rate ratios (HRs) were computed using Cox regression models.

283 Hazard ratios (HRs) were estimated by multivariable Cox regression mode

284 Hazard ratios (HRs) were estimated in each propensity score-matched coh

285 es and multivariable adjusted hazard ratios (HRs) were used to assess outcomes including hospitalizat

286 yte growth factor tyrosine kinase substrate (HRS), which was necessary for sorting surface receptors

287 The HRs with 95% CIs comparing the highest with lowest COex

288 HRs with 95% CIs for a CHD event, in relation to intake

289 HRs with 95% CIs for yogurt (nonfrozen or frozen) and ot

290 Cox models estimated hazard ratios (HRs) with 95% CIs according to a mental health index (lo

291 nsoring weighting to estimate hazard ratios (HRs) with 95% CIs comparing new users of aromatase inhib

292 odels estimated site-specific hazard ratios (HRs) with 95% CIs of DKA comparing receipt of SGLT-2 inh

293 We estimated hazard ratios (HRs) with 95% CIs using Cox proportional-hazards regress

294 Hazard ratios (HRs) with 95% CIs were pooled across trials, and efficac

295 hazards regression, providing hazard ratios (HRs) with 95% CIs, compared EAC risk in GERD patients wi

296 isk estimates are reported as hazard ratios (HRs) with 95% CIs.

297 regression models to estimate hazard ratios (HRs) with 95% CIs.

298 regression providing adjusted hazard ratios (HRs) with 95% confidence intervals (95% CIs).

299 gression was used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) adjusted for ul

300 iable Cox regression provided hazard ratios (HRs) with 95% confidence intervals (CIs) for risk of the

301 Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) were used to de

302 The results were presented as hazard ratios (HRs) with 95% confidence intervals (CIs).

303 HRs, with corresponding 95% CIs, were estimated using Co