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

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

4 ocardial infarction is strongly dependent on time to treatment.

5 istering thrombolysis that facilitates rapid time to treatment.

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

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

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

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

10 developed to assess factors associated with time to treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 Time to treatment discontinuation was analyzed and inclu

40 The time to treatment discontinuation was longer for patient

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

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

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

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

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

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

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

48 Time to treatment failure (disease progression, disease

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

68 Time to treatment failure (TTF; defined as discontinuati

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

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

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

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

73 Time to treatment failure and overall survival were asce

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

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

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

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

78 Time to treatment failure did not differ between groups

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

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

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

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

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

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

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

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

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

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

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

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

91 Time to treatment failure was 17.4 months.

92 Median time to treatment failure was 2 months.

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

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

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

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

97 The median time to treatment failure was 5.5 months.

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

99 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

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

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

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

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

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

105 Time to treatment failure was comparable in both treatme

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

107 Time to treatment failure was longer with bevacizumab th

108 Time to treatment failure was significantly improved in

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

110 Median time to treatment failure was significantly longer in th

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

112 Time to treatment failure was significantly shorter in t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 For time to treatment failure, lamotrigine was significantly

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

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

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

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

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

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

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

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

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

139 For time to treatment failure, valproate was significantly b

140 For time to treatment failure, we identified several signifi

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

142 The primary outcome was the time to treatment failure.

143 The primary efficacy outcome was time to treatment failure.

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

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

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

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

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

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

150 The primary end point was time to treatment failure.

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

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

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

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

155 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

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

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

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

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

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

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

162 4.3 and 4.7 months (log-rank P =.72), median times to treatment failure were 4.1 and 3.1 months (P =.

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

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

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

166 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

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

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

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

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

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

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

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

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

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

176 As time to treatment increased, the incidence of recurrent

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

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

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

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

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

182 9 vs 53%, p < 0.001), and they had a shorter time to treatment (mean 3.1 vs 3.3 h, p < 0.001).

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

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

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

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

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

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

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

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

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

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

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

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

195 Median time to treatment termination was significantly shorter

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

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

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

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

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

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

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

203 Time to treatment was compared between CIN and PTX group

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

205 Time to treatment was significantly longer in women (1.2

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

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

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

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

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

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

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

213 Time to treatment with thrombolytic therapy is a critica

214 Rapid time to treatment with thrombolytic therapy is associate

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

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

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