ライフサイエンスコーパス: time to treatment

1 prespecified groups (age, infarct location, time-to-treatment).

2 developed to assess factors associated with time to treatment.

3 al stage) were significantly associated with time to treatment.

4 erage time to iBNP draw also had the longest time to treatment.

5 tend clinic for treatment and did not reduce time to treatment.

6 ng may facilitate rapid detection and reduce time to treatment.

7 ocardial infarction is strongly dependent on time to treatment.

8 istering thrombolysis that facilitates rapid time to treatment.

9 ic characteristics, mechanism of injury, and time to treatment.

10 ide screening for HCV infection and expedite time to treatment.

11 ng at the hospital have been shown to reduce time to treatment.

12 and a delay between the finalized report and time to treatment.

13 e tests increased case finding, with a short time to treatment.

14 us medical therapy vs medical therapy alone; time to treatment.

15 ive patients starting therapy, and a shorter time to treatment.

16 in 50% of patients, which was independent of time to treatment.

17 oor attack recovery, no sensory attacks, and time-to-treatment.

18 adjusted for age, sex, baseline severity and time-to-treatment.

19 in rural areas also had significantly longer times to treatment.

20 atients transferred for PA had a longer mean time to treatment (187 vs. 120 min; p < 0.0001).

21 To simulate a clinically feasible time to treatment, 24 hours later rats were randomized t

22 tion (PCI) was associated with longer median times to treatment (3.0 h for TMPG 2/3 vs. 2.7 h for TMP

23 RMST]), but no differences were observed for time to treatment (83.2 days versus 83.5 days, P = 0.51,

24 significantly associated with an increase in time to treatment (86.5 +/- 50.2 days; P < .001).

25 significantly associated with an increase in time to treatment (86.5 50.2 days; P < .001).

26 ssociated with clinical trial enrollment and time to treatment among 1,358 AYA patients with cancer (

27 odels showed a nonlinear association between time to treatment and 12-month mortality with the lowest

28 the hospital is critical in reducing overall time to treatment and 2) in emergency medical care, rapi

29 l was used to assess the association between time to treatment and COVID-19 period.

30 Patients were divided by quartiles of time to treatment and iBNP levels, creating 16 categorie

31 ng blood cultures could potentially decrease time to treatment and improve outcomes, but it is unclea

32 significantly with disease severity (shorter time to treatment and overall survival).

33 ated administrative data were used to assess time to treatment and total health care costs.

34 identified overall stage, radiation therapy, time to treatment, and household income as the most infl

35 y outcomes included biomarker testing rates, time to treatment, and metastatic patterns.

36 ed patterns of clinical trial participation, time to treatment, and provider characteristics in a pop

37 Other experiences such as time to treatment, antibiotic synergy, and immune respon

38 gnose Chagas disease, thereby decreasing the time to treatment at a primary health care facility for

39 t method was used to evaluate differences in time to treatment between patients racialized as Black a

40 s infarction, anterior infarctions and later time to treatment (between 3 and 6 h) than adults.

41 he CD19-R cell fraction had a shorter median time to treatment compared with patients with <15.25% of

42 rombotic drugs, higher doses, and the longer time to treatment compared with the trials that used tPA

43 g ChAd63-MVA ME-TRAP demonstrated a delay in time to treatment, compared with unvaccinated controls.

44 hey used the Kaplan-Meier method to generate time-to-treatment curves and survival analysis to compar

45 The overall time-to-treatment curves revealed substantial difference

46 The relationships between time to treatment (days between PDR diagnosis and PRP) a

47 uspected lung cancer, because it reduces the time to treatment decision compared with conventional di

48 The median time to treatment decision was shorter with EBUS-TBNA (1

49 The primary endpoint was the time-to-treatment decision after completion of the diagn

50 The median time to treatment decreased from 44 d (interquartile ran

51 ials with changes in RT technique, dose, and time to treatment delivery was assessed using chi2 tests

52 Although time to treatment did not predict overall survival in a

53 tumor expression, was correlated with longer time to treatment discontinuation (> 4 months) in 25 pat

54 th White patients, Black patients had longer time to treatment discontinuation (2-year unadjusted rat

55 Kaplan-Meier analysis was used to estimate time to treatment discontinuation (TTD) and overall surv

56 Progression-free survival (PFS), time to treatment discontinuation (TTD), and time to nex

57 t of ICI therapy, overall survival (OS), and time to treatment discontinuation (TTD).

58 ients with >/=3 mutations also had a shorter time to treatment discontinuation and shorter overall su

59 Median time to treatment discontinuation as a result of any sym

60 Time to treatment discontinuation was analyzed and inclu

61 The time to treatment discontinuation was longer for patient

62 ffectiveness outcomes were overall survival, time to treatment discontinuation, and time to next trea

63 e association between buprenorphine dose and time to treatment discontinuation, controlling for poten

64 Neurocognitive improvement predicted longer time to treatment discontinuation, independently from sy

65 The primary outcome for this analysis was time to treatment discontinuation.

66 and spleen response remained associated with time to treatment discontinuation.

67 Effectiveness was described in terms of time-to-treatment discontinuation (TTD) and extended- to

68 In the experimental arm, median time-to-treatment-discontinuation was only 1.7 months.

69 d with the standard of care, and the average time to treatment discovery if these therapies had been

70 Examining the association of time to treatment (drug or placebo) with survival to hos

71 lized diagnostics can effectively reduce the time to treatment, especially in case of infectious dise

72 igher objective response rate (12% v 3%) and time to treatment failure (10 weeks v 8 weeks) for vinor

73 However, DES produced significantly longer time to treatment failure (26.4 v 9.7 months, P = .016)

74 The median time to treatment failure (9 months) and median survival

75 sceptibility was an independent predictor of time to treatment failure (adjusted hazards ratio [HR],

76 The time to treatment failure (defined by specific criteria

77 Time to treatment failure (disease progression, disease

78 prine with respect to the primary end point, time to treatment failure (hazard ratio, 0.44; 95% confi

79 erall survival (OS) (HR = 1.24, p = 0.47) or time to treatment failure (HR = 0.85, p = 0.44).

80 ve disease (HR, 1.05; 95% CI, 0.85 to 1.30), time to treatment failure (HR, 0.89; 95% CI, 0.72 to 1.1

81 ian, 4.5 v 9.2 months; HR, 1.78; P = .0001), time to treatment failure (median, 3.5 v 9.0 months; HR,

82 high levels of alkyltransferase had shorter time to treatment failure (P = 0.05) and death (P = 0.00

83 significant difference between the groups in time to treatment failure (relative risk of treatment fa

84 Currently, prediction of time to treatment failure (TTF) and overall survival (OS

85 ts to detect a 50% improvement in the median time to treatment failure (TTF) compared with that repor

86 primary end point was investigator-assessed time to treatment failure (TTF) defined as the interval

87 Median time to treatment failure (TTF) is 5.8, 6.0, and 8.0 mon

88 ta collection was not a trial objective, but time to treatment failure (TTF) was recorded in the firs

89 Time to treatment failure (TTF) was slightly longer for

90 erall survival (OS), response incidence, and time to treatment failure (TTF) were examined by race.

91 Response to tamoxifen and time to treatment failure (TTF) were not significantly a

92 to progression (TTP; primary end point) and time to treatment failure (TTF) were significantly longe

93 response rate (ORR), response duration (RD), time to treatment failure (TTF), clinical benefit rate (

94 Time to treatment failure (TTF), the primary parameter o

95 The primary end point-time to treatment failure (TTF), which included patients

96 ve response (OR), overall survival (OS), and time to treatment failure (TTF).

97 The primary end point of the study was time to treatment failure (TTF).

98 these therapies on overall survival (OS) and time to treatment failure (TTF).

99 PI with respect to overall survival (OS) and time to treatment failure (TTF).

100 The principal end point of the study was time to treatment failure (TTF).

101 Time to treatment failure (TTF; defined as discontinuati

102 P; median, 12.2 v 8.5 months; P =.0019), and time to treatment failure (TTF; median, 11.6 v 6.2 month

103 Time to treatment failure analysis showed that 69% of pa

104 more frequent responses and a delay in both time to treatment failure and disease progression compar

105 Although there was a delay in time to treatment failure and disease progression in fav

106 Time to treatment failure and overall survival were asce

107 Results The 8-year time to treatment failure and progression-free survival

108 Secondary end points included time to treatment failure and safety.

109 Predictive variables for time to treatment failure and survival were visceral dis

110 We studied time to treatment failure and time to viral suppression

111 cost of resistance, and, in those cases, the time to treatment failure can be more than doubled.

112 However, the trend of the time to treatment failure curve does not indicate that c

113 Time to treatment failure did not differ between groups

114 ation compared with ADT resulted in a longer time to treatment failure during the 9-month follow-up p

115 Time to treatment failure for patients with CR was time

116 There were also no differences in time to treatment failure for patients with early-stage

117 The median observed time to treatment failure in the monotherapy group was 3

118 The median time to treatment failure in the placebo group was 119 d

119 The primary efficacy end point was the time to treatment failure occurring at or after week 6.

120 Time to treatment failure of CRs compared with PRs was s

121 ards regression model, the predictors of the time to treatment failure or death were a low hematocrit

122 tion between receptor discordance and either time to treatment failure or overall survival.

123 bamazepine, the standard drug treatment, for time to treatment failure outcomes and is therefore a co

124 with regard to response rate, survival, and time to treatment failure over single-agent cisplatin in

125 Outcomes were time to treatment failure overall, because of inadequate

126 ne without treatment change) at 48 weeks and time to treatment failure through 48 weeks (intention-to

127 3-not reached [NR]) months, while the median time to treatment failure time for those receiving early

128 with first-line therapy, adalimumab extended time to treatment failure to 24 weeks vs 13 weeks with p

129 The median time to treatment failure was 115 days for DaunoXome and

130 Median time to treatment failure was 16.7 months in patients al

131 Time to treatment failure was 17.4 months.

132 Median time to treatment failure was 2 months.

133 The median time to treatment failure was 24 weeks in the adalimumab

134 Median time to treatment failure was 27 months in patients rece

135 follow-up of 4.5 years, the estimated median time to treatment failure was 3.9 years for patients rec

136 The 40th percentile for time to treatment failure was 4.8 months in the placebo

137 The median time to treatment failure was 5.5 months.

138 Median time to treatment failure was 5.6 months; 38% of patient

139 val was 7.1, 4.9, and 6.8 months; and median time to treatment failure was 5.6, 4.3, and 6.7 months f

140 an follow-up of 11 months (IQR 6-18), median time to treatment failure was 6.7 months (95% CI 5.5-8.6

141 For responding patients, the median time to treatment failure was 7 months, with a median fo

142 months (95% CI, 6.0 to 15.0 months), median time to treatment failure was 7.6 months (95% CI, 6.2 to

143 tion of response was 11.2 months, the median time to treatment failure was 8.1 months, and the median

144 Median time to treatment failure was 8.4 weeks for NOL and 9.1

145 ponse rate was 48% (95% CI, 31%-66%), median time to treatment failure was 8.9 months (95% CI, 5.9-12

146 ial response rate was 38% (95% CI, 25%-52%), time to treatment failure was 9.7 months (95% CI, 6.0-13

147 The median time to treatment failure was 93.2 months (range, 3 to 9

148 Median time to treatment failure was also shorter in the high-M

149 Time to treatment failure was comparable in both treatme

150 Although time to treatment failure was longer in patients on gemc

151 Time to treatment failure was longer with bevacizumab th

152 Time to treatment failure was significantly improved in

153 Although median time to treatment failure was significantly longer in pa

154 Median time to treatment failure was significantly longer in th

155 sults were concordant with overall survival; time to treatment failure was significantly shorter in b

156 Time to treatment failure was significantly shorter in t

157 Time to treatment failure was similar for both groups, a

158 After a median follow-up of 10.6 years, the time to treatment failure was still significantly improv

159 icant factors in the multivariable model for time to treatment failure were treatment history (antiep

160 l survival, time to progressive disease, and time to treatment failure) in bladder cancer.

161 The primary efficacy endpoint was time to treatment failure, a multicomponent endpoint enc

162 TTP, time to treatment failure, and median survival (17.2 mon

163 patients who achieved an objective response, time to treatment failure, and overall survival after tr

164 continuous partial remission for 2+ years), time to treatment failure, and overall survival were ass

165 Response rates, time to treatment failure, and overall survival were sim

166 re response rate, progression-free survival, time to treatment failure, and safety.

167 overall survival, progression-free survival, time to treatment failure, and safety.

168 complete response rates, response durations, time to treatment failure, and survival were the same in

169 igible patients were evaluated for response, time to treatment failure, and survival.

170 Primary outcomes were time to treatment failure, and time to 1-year remission,

171 Primary outcomes were time to treatment failure, and time to 12-months remissi

172 The primary end point was the time to treatment failure, defined according to a multic

173 The primary outcome was time to treatment failure, defined as a lack of predniso

174 The primary outcome was the time to treatment failure, defined as death; liver trans

175 The primary outcome was the time to treatment failure, defined by recurrence of uvei

176 For time to treatment failure, lamotrigine was significantly

177 d points included progression-free survival, time to treatment failure, objective response, and toxic

178 exception of toxicity, there is no response, time to treatment failure, or survival benefit for any o

179 ective tumor response, duration of response, time to treatment failure, or survival between the 13 pa

180 best overall response, duration of response, time to treatment failure, overall survival, and safety.

181 Main secondary end points were OS, time to treatment failure, quality of life, and safety.

182 tcomes: toxicity, progression-free survival, time to treatment failure, quality of life, and the pred

183 d for survival, time to disease progression, time to treatment failure, response, and quality-of-life

184 ditional end points included tumor response, time to treatment failure, survival, and quality of life

185 low-up of 34 months showed a superior 3-year time to treatment failure, the primary study end point,

186 l AP levels, no VM, and minimal fatigue; for time to treatment failure, they were low/normal AP level

187 For time to treatment failure, valproate was significantly b

188 For time to treatment failure, we identified several signifi

189 The primary efficacy end point was the time to treatment failure, which was defined as death, e

190 The primary outcome was the time to treatment failure.

191 The primary efficacy outcome was time to treatment failure.

192 vel of PDGF-BB was inversely correlated with time to treatment failure.

193 The primary end point of this trial was time to treatment failure.

194 predicts lower response rates and a shorter time to treatment failure.

195 reatment history alone was not predictive of time to treatment failure.

196 end points included tumor response rates and time to treatment failure.

197 t 6 months), time to clinical remission, and time to treatment failure.

198 The primary end point was time to treatment failure.

199 There were no significant differences in time to treatment failure.

200 sed adjustment of inhaled corticosteroids in time to treatment failure.

201 AIN OUTCOME MEASURE: The primary outcome was time to treatment failure.

202 herapy in the treatment of AGC with a better time-to treatment failure (TTF) compared to ECX, ECX arm

203 o [HR] 0.73 [95% CI 0.57-0.95], p=0.017) and time-to-treatment failure (median 13.7 months [95% CI 11

204 The primary criterion was time-to-treatment failure (TTF) of the first-line therap

205 including response rates and their duration; time-to-treatment failure (TTF) rates; retreatment resul

206 Time-to-treatment failure (TTF) to EGFR TKI in patients

207 res) vs. 9% (low scores), P = 0.024], longer time-to-treatment failure [hazard ratio (HR) = 0.52; 95%

208 At a median follow-up of 4 years, time-to-treatment failure has not been reached and overa

209 The primary outcome was time-to-treatment failure or death for IHHD patients com

210 free survival by independent central review, time-to-treatment failure, and overall survival.

211 4.3 and 4.7 months (log-rank P =.72), median times to treatment failure were 4.1 and 3.1 months (P =.

212 Median times to treatment failure were also similar at 5, 4, an

213 Mean time to treatment for all patients was 27.8 +/- 41.4 day

214 Mean time to treatment for all patients was 27.8 41.4 days.

215 ificantly shorter report turnaround time and time to treatment for patients with cancer-associated iP

216 before initial systemic therapy, with median time to treatment for the observation group of 12 months

217 ced after accounting for differences in mean times to treatment for the hospitals in which patients w

218 o 0.5 days (IQR, 0.172-0.94 days) and median time to treatment from 73.5 to 3.0 days compared with in

219 The mean time to treatment from LKW was 543 minutes and from pres

220 The median time to treatment from stroke onset was 3.3 h (range 2.0

221 ial and ethnic disparities in achievement of time-to-treatment goals and mortality in STEMI is uncert

222 of symptoms to treatment (6.6% mortality for time to treatment >4 h vs. 3.3%; p < 0.001), even among

223 Delays in time to treatment >60 min associated with transferring p

224 e period of infectiousness due to decreasing time to treatment has a small effect on reducing transmi

225 Time to treatment in acute myocardial infarction (MI) ha

226 Time to treatment in men with CD4 cell counts of 250 cel

227 Thus, time to treatment in the current era of aggressive manag

228 The median time to treatment in the remaining 16 patients was 22 mo

229 cordingly, we sought to describe patterns of times to treatment in patients undergoing interhospital

230 ction-4 to compare in-hospital mortality and times to treatment in STEMI across different levels of h

231 As time to treatment increased, the incidence of recurrent

232 Inequities in time to treatment indicate the need to identify and redu

233 [aOR] 4.8 [95% CI: 1.8-12.8]; P = .002) and time to treatment initiation (adjusted hazard ratio [aHR

234 Among patients with negative first biopsies, time to treatment initiation did not differ significantl

235 ocket expenditures, medication adherence, or time to treatment initiation of oral drugs.

236 year and the total number of injections, the time to treatment initiation of the fellow eye, and BCVA

237 The time to treatment initiation or the length of time on tr

238 1) treatment course (eg, stage at diagnosis, time to treatment initiation), (2) surgical outcomes (eg

239 x, race/ethnicity, stage, site, tobacco use, time to treatment initiation, and insurance status, HIV

240 use, expenditures, medication adherence, or time to treatment initiation.

241 measured by proportion of days covered; and time to treatment initiation.

242 obability of TB treatment but did not reduce time to treatment initiation.

243 The secondary outcome was time to treatment initiation.

244 The primary outcomes were time-to-treatment initiation and sustained virologic res

245 s superior to standard treatment in terms of time-to-treatment initiation, and subsequently, more peo

246 nally used POC smear microscopy, can shorten time-to-treatment initiation, thus potentially curtailin

247 FujiLAM could improve time-to-treatment-initiation, especially in settings whe

248 ment curves and survival analysis to compare time-to-treatment intervals across the two surveys.

249 een the time to measurement of NP levels and time to treatment is not clear.

250 oke severity, sex, prestroke disability, and time to treatment (< or = 3 or > 3 hours after stroke on

251 Process of care (ie, time to treatment, lymph node dissection), as well as ou

252 Recent observations suggest that time to treatment may be less important for survival wit

253 Identification of inequities in time to treatment may have clinical, policy, and researc

254 9 vs 53%, p < 0.001), and they had a shorter time to treatment (mean 3.1 vs 3.3 h, p < 0.001).

255 ian, 0.66 hour vs 24.68 hours, P < .001) and time to treatment (median, 0.98 hour vs 28.05 hours, P <

256 TMPG 0/1) remained associated with increased time to treatment (odds ratio 1.14 per hour of delay; p

257 Both the time to treatment of the first MOGAD attack (late vs ear

258 In addition, the impact of time to treatment on clinical outcomes has not been demo

259 0.001), and poor VFMD outcome (adjusting for time to treatment: OR, 6.81; 95% CI, 1.85-28.98; P = 0.0

260 of individuals with recent-onset psychosis, time-to-treatment outcomes differed by ethnoracial group

261 an interaction between treatment effect and time to treatment (p = 0.048).

262 Effects of trial design, such as time to treatment, patient age, and use of adjuvant ther

263 onse (median, 15.5 v 26.2 months; P = .001), time to treatment progression (TTP; median, 4.5 v 9.2 mo

264 pendent data sets of patients with CLL using time to treatment, progression-free survival, and overal

265 , including different primary end points and time to treatment, publication bias, neglected quality c

266 Within the time-to-treatment quartiles, mortality increased with in

267 Mean ED time increased with increased time-to-treatment quartiles.

268 nitiation (range 51%-73% by 6 mo) and median time to treatment (range 15-36 d, n = 1,450), and only 5

269 The median time to treatment response was 11 weeks (range=2-13).

270 t-in-time measure of treatment response, and time to treatment response.

271 ceived a diagnosis after prolonged workup or time to treatment, resulted in patient harm.

272 em for patients in shock continued to reduce time to treatment, resulting in a continued decrease in

273 c acid on death due to bleeding according to time to treatment, severity of haemorrhage as assessed b

274 Median time to treatment termination was significantly shorter

275 The main outcomes were accessibility (time to treatment, travel distance, and multi-institutio

276 CD38 status (HR = 10.8, P = .006) predicted time to treatment (TTT) among MBL patients.

277 IGHD), and IGH joining (IGHJ) gene usage and time to treatment (TTT).

278 he relationship of 25(OH)D serum levels with time-to-treatment (TTT) and overall survival (OS) in new

279 We assessed the association with time to treatment using time-dependent Cox regression sh

280 ine for all patients was 14.4+/-2.6, and the time to treatment was 2.9+/-0.8 hours.

281 The median time to treatment was 39 days (IQR, 27-52 days) for the

282 was 12, median age was 72 years, and median time to treatment was 5.2 hours.

283 al portion of the racial/ethnic disparity in time to treatment was accounted for by the specific hosp

284 Time to treatment was compared between CIN and PTX group

285 Time to treatment was shorter (1.7 vs. 3.3 years, P<0.01

286 Time to treatment was significantly longer in women (1.2

287 he presence of baseline Q waves, rather than time to treatment, was significantly associated with adv

288 tage of patients who initiated treatment and time to treatment were weighted to account for the sampl

289 , including household income, residence, and time to treatment, were associated with survival outcome

290 tinued drug development in this space delays time to treatment with chemotherapy, and hopefully contr

291 is known about the relationship between the time to treatment with direct coronary angioplasty and c

292 The time to treatment with direct PTCA, as with thrombolytic

293 We re-examined the effect of time to treatment with intravenous rt-PA (alteplase) on

294 cs, time to thrombolytic administration, and time to treatment with poloxamer 188 or placebo.

295 udies have confirmed the benefit of reducing time to treatment with thrombolysis (between onset of pa

296 Time to treatment with thrombolytic therapy is a critica

297 Rapid time to treatment with thrombolytic therapy is associate

298 eplase, the net outcome is predicted both by time to treatment (with faster time increasing the propo

299 nce-based thrombolysis resulted in decreased time to treatment without an increase in adverse events.

300 gative groups, and for a previously reported time-to-treatment x treatment interaction (p = 0.03).