ライフサイエンスコーパス: treatment failure

1 at 6 months (or prior, in the event of early treatment failure).

2 them to overdose, toxicity, underdosing, and treatment failure.

3 tment HPV testing are accurate predictors of treatment failure.

4 WHO criteria were used to define immunologic treatment failure.

5 throughout therapy and is able to anticipate treatment failure.

6 s were 30-day mortality and setting-specific treatment failure.

7 NA) may allow non-invasive identification of treatment failure.

8 dictor of human immunodeficiency virus (HIV) treatment failure.

9 atment-associated injury, a major reason for treatment failure.

10 mide approach but with differing patterns of treatment failure.

11 o identify vulnerable populations at risk of treatment failure.

12 hs), time to clinical remission, and time to treatment failure.

13 esistant tumorigenic cells that give rise to treatment failure.

14 c ethnicity remain independent predictors of treatment failure.

15 limb ischemia-related death were regarded as treatment failure.

16 and has been shown to increase the risk for treatment failure.

17 of pretreatment risk models to predict early treatment failure.

18 osbuvir and identify factors associated with treatment failure.

19 ngly than cells from patients with antiviral treatment failure.

20 alth outcomes, and reasons for high rates of treatment failure.

21 ptions and determine factors associated with treatment failure.

22 lation in blocking antibody-bound T cells at treatment failure.

23 a showed similar PFS and OS, with continuous treatment failure.

24 FO initiation were independent predictors of treatment failure.

25 positive and negative predictive values for treatment failure.

26 ratio of 8.444 (2.127-33.53; P = .0013) for treatment failure.

27 event adverse effects or unnecessary risk of treatment failure.

28 <25% of pretreatment value was considered a treatment failure.

29 ransfusion, emergency department visits, and treatment failure.

30 e of drug -resistant variants and subsequent treatment failure.

31 d probability of ocular TB was compared with treatment failure.

32 nerated during therapy are likely to lead to treatment failure.

33 c vessels, which may have contributed to the treatment failure.

34 ion for androgen-independent cells and rapid treatment failure.

35 emia (AL) either relapsed or at high-risk of treatment failure.

36 d choroidal involvement had a higher risk of treatment failure.

37 ency of recrudescent infection, resulting in treatment failure.

38 20225 of 28189 patients (71.7%) experienced treatment failure.

39 a and uncontrolled hyperglycaemia leading to treatment failure.

40 le patterns of change in alpha leading up to treatment failure.

41 ority of AQ-13, although there were no AQ-13 treatment failures.

42 ociation with dihydroartemisinin-piperaquine treatment failures.

43 g concentrations were investigated in the AL treatment failures.

44 ver, resistance to clarithromycin has led to treatment failures.

45 high rates of dihydroartemisinin-piperaquine treatment failures.

46 n balloon tamponade in the control of EVB in treatment failures.

47 TRMS patients have a high number of surgical treatment failures.

48 lyte maintenance solution, resulted in fewer treatment failures.

49 , of which 8.2% (95% CI, 2.5-9.6) were early treatment failures.

50 tner drugs, resulting in increasing rates of treatment failures.

51 iated with chronic infections and antibiotic treatment failure(1-3).

52 ment was not associated with a lower rate of treatment failure (3.4% for broad-spectrum antibiotics v

53 in BSID-3 motor or language scores, rates of treatment failure (35% and 24%, respectively; hazard rat

54 treatment had nearly 4 times higher odds of treatment failure (95% confidence interval, 1.22-13.07)

55 The primary efficacy endpoint was time to treatment failure, a multicomponent endpoint encompassin

56 t success) or stable or progressive disease (treatment failure)-according to prespecified criteria.

57 Most patients with treatment failure acquired resistance-associated substit

58 sociated with dihydroartemisinin-piperaquine treatment failure after adjusting for the presence of am

59 e has emerged as the most important cause of treatment failure after allogeneic hematopoietic stem ce

60 , frequency, and clinical characteristics of treatment failure after I-125 brachytherapy in patients

61 tric low-grade glioma (PLGG) who experienced treatment failure after initial treatment with chemother

62 Treatment failure after therapy of pulmonary tuberculosi

63 ngs indicate a high rate of symptomatic late treatment failures after 6-dose AL regime in nonimmune a

64 Although we did not demonstrate clinical treatment failures after ACT and the viability and trans

65 ange, sodium excretion, and incidence of AHF treatment failure also varied by EF group (interaction P

66 DSS that supports detection of immunological treatment failure among patients with HIV taking antiret

67 d treatment characteristics and (1) death or treatment failure and (2) loss to follow-up.

68 rget sites, which can predispose patients to treatment failure and adverse effects, respectively; how

69 rospective cohort, the primary outcomes were treatment failure and adverse events 14 days after diagn

70 tis was associated with higher rates of both treatment failure and all-cause hospital revisits.

71 ved stress-were independent risk factors for treatment failure and asthma exacerbations in the contex

72 he gyr mutation type on the time to death or treatment failure and compared this with in vitro FQ res

73 ich are potential biomarkers associated with treatment failure and death in children with tuberculosi

74 l tumor down-staging to LT, and criteria for treatment failure and exclusion from LT.

75 on of patients who experienced immunological treatment failure and had a documented clinical action.

76 elucidating an enigmatic cause of antibiotic treatment failure and highlighting the critical need for

77 s, although the majority rapidly progress to treatment failure and insulin therapy.

78 e incidence of acute rejections, infections, treatment failure and kidney function.

79 tory flow (PEF) are predictive of subsequent treatment failure and may be modified by controller ther

80 testing in predicting the hazard of death or treatment failure and may be superior.

81 istance to cisplatin is a principal cause of treatment failure and mortality of advanced bladder canc

82 are associated with a higher probability of treatment failure and mortality.

83 owever, plating may lead to a higher risk of treatment failure and non-operative complications.

84 with metastatic disease responsible for most treatment failure and patient death.

85 Results The 8-year time to treatment failure and progression-free survival rates we

86 ce and persistence are often associated with treatment failure and relapse, yet are poorly characteri

87 icantly predictive (P = .0009) of first-line treatment failure and symptomatic relapse and has the po

88 Treatment failure and symptomatic relapse are major conc

89 ory concentration corresponded with triazole treatment failure and that the efficacy of other classes

90 lead to persistent infections, resulting in treatment failure and the need for reintervention or ext

91 nduction; robust induction actually predicts treatment failure and viral persistence.

92 f CRISPR-based therapies to minimize risk of treatment failure and/or adverse outcomes.

93 ere lost to follow-up, 10 (4.7%) experienced treatment failure, and 9 (4.3%) died.

94 esting, ART initiation, ART discontinuation, treatment failure, and levels of condom use.

95 ed to identify baseline predictors of death, treatment failure, and loss to follow-up among children

96 vival by independent central review, time-to-treatment failure, and overall survival.

97 ciency virus (HIV) infection will experience treatment failure, and require second- or third-line ART

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

99 sults in more broad-spectrum antibiotic use, treatment failures, and adverse drug events.

100 hown to correlate with clinical outcomes and treatment failures, and this in turn has led to the crea

101 Although the reasons for treatment failure are multifactorial, intrinsic resistan

102 The mechanisms underlying treatment failure are well studied, but the processes go

103 een the front-line drug for several decades, treatment failures are common.

104 resistance among parasites, suggesting that treatment failure arises from LRV1-mediated effects on h

105 ustained direct bilirubin (DB) <2 mg/dL, and treatment failure as liver transplantation or death whil

106 6% v 93.4%, respectively P = .015) and fewer treatment failures as a result of toxicity (4.8% v 11.8%

107 sitive section margins and the occurrence of treatment failure associated with the marginal status, i

108 of liver metastases are predictors of local treatment failure at 1 y.

109 s during follow-up were not considered to be treatment failures) at day 63 and safety outcomes.

110 (HIVDR) plays a major role in pediatric HIV treatment failure because nonsuppressive maternal antire

111 When interpreting TOC results for possible treatment failure, both the occurrence of blips and a po

112 tin-resistant subpopulation similarly caused treatment failure but was misclassified as susceptible b

113 ble lung function (CVpef) is associated with treatment failure, but the pattern of change in self-sim

114 d plating had a 2.19 times increased risk of treatment failure, but this failed to reach significance

115 e primary outcome was the cumulative risk of treatment failure by day 28 by Kaplan-Meier analysis.

116 Treatment failure by day 28 was 61.1% (95% confidence in

117 The primary outcome was treatment failure by day 8, analyzed per protocol.

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

119 Although resistance is rare, treatment failure can occur in more than 20% of cases(3,

120 Twist has been shown to cause treatment failure, cancer progression, and cancer-relate

121 h threat, further complicated by unexplained treatment failures caused by bacteria that appear antibi

122 80) were associated with the lowest rates of treatment failure compared with the most widely used med

123 (15%) patients who received gatifloxacin had treatment failure, compared with 19 (16%) who received c

124 The association of LRV1 with clinical drug treatment failure could serve to guide more-effective tr

125 This escalation was based on meeting treatment failure criteria, which differed between group

126 The primary outcome was a composite of treatment failure defined by any of the following occurr

127 Treatment failure (defined as an organ-space infection)

128 Risk of rehospitalization and treatment failure (defined as psychiatric rehospitalizat

129 comes were BSID-3 motor and language scores, treatment failure (defined as treatment-related death or

130 The primary outcome was treatment failure (defined in the trial protocol as a si

131 The primary end point was the time to treatment failure, defined according to a multicomponent

132 Treatment failure, defined as a persistence or recurrenc

133 The primary outcome was a composite of treatment failure, defined as the occurrence of at least

134 The primary outcome was treatment failure, defined as: initial failure of aneury

135 ent class model did not successfully predict treatment failure, despite taking all variables into acc

136 Treatment failure developed in 102 of the 801 patients (

137 Treatment failure does not correlate well with resistanc

138 s should be optimized to efficiently prevent treatment failure due to HCV resistance.

139 oups in the number of patients classified as treatment failure during the double blind phase assessed

140 There were 248 treatment-failure events in the combination group as com

141 ive invasive breast cancer (IBC) at risk for treatment failure following trastuzumab and chemotherapy

142 o chemotherapy is the fundamental reason for treatment failure for many cancer patients.

143 s the single most important driver of cancer treatment failure for modern targeted therapies, and the

144 The primary end point was treatment failure free survival (TFFS).

145 d to study the risk of rehospitalization and treatment failure from July 1, 2006, to December 31, 201

146 cting self-similarity of PEF, in relation to treatment failure from the run-in period of open-label i

147 dentified a 3-month and a 6-month cohort of "treatment failures" from both CATT and DRCR.net studies.

148 All patients with treatment failure had therapeutic plasma CQ concentratio

149 All patients with treatment failure had uneventful outcome after retreatme

150 Increasing rates of treatment failure have resulted in an urgent need for ne

151 reatment of uncomplicated malaria in Sweden, treatment failures have been reported in adults.

152 kely than those in the placebo group to have treatment failure (hazard ratio, 0.50; 95% confidence in

153 9% (low scores), P = 0.024], longer time-to-treatment failure [hazard ratio (HR) = 0.52; 95% confide

154 The co-primary endpoints were treatment failure (histological progression of cancer fr

155 the Gag P2/NC CS could increase the risk of treatment failure if there is increased use of PIs-based

156 faced significantly higher risk of death or treatment failure if they had severe disease or were und

157 rformance of a test of cure (TOC) to monitor treatment failure, if this is indicated.

158 a was similar between those with and without treatment failure in all three groups during the run-in

159 s), due to the small number of patients with treatment failure in approval studies.

160 re often employed after discharge to prevent treatment failure in children with complicated appendici

161 is highly susceptible to severe disease and treatment failure in Clostridium difficile infection (CD

162 nsitization to Api m 10 as a risk factor for treatment failure in HBV immunotherapy.

163 ce in vitro, and the factors responsible for treatment failure in patients are not well understood.

164 omenon may be a major contributing factor in treatment failure in patients with atopic dermatitis, ye

165 95 may be a useful imaging metric to predict treatment failure in patients with locally advanced cerv

166 Treatment failure in solid tumors occurs due to the surv

167 ve early recognition and management of local treatment failure in such patients.

168 Twelve infants (2.8%) had treatment failure in the amoxicillin arm and 25 (5.9%) i

169 run-in phase but was higher among those with treatment failure in the F and F + S groups during the t

170 The CVpef was higher in those with treatment failure in the F and F + S groups in the run-i

171 thromycin resistance may bring the threat of treatment failure in the United States with the current

172 Treatment failure in those with the high-risk ITPKC geno

173 ents (27%) in the adalimumab group versus 18 treatment failures in 30 patients (60%) in the placebo g

174 We observed 16 treatment failures in 60 patients (27%) in the adalimuma

175 oach could help find ways to slow or prevent treatment failures in cancer and infectious diseases.

176 ty in animal models and humans and with drug treatment failures in humans.

177 and human disease, and associated with drug-treatment failures in Leishmania braziliensis and Leishm

178 Factors predicting treatment failure included being treated in the Centers

179 Treatment failure included local recurrence alone in 75

180 rd ratio, 0.323; P </= .001) of experiencing treatment failure, independent of conventional karyotype

181 gions with earlier replacement with ACT when treatment failure is detected.Clinical Trials Registrati

182 Among the mechanisms of treatment failure is multidrug resistance (MDR) mediated

183 n of change in self-similarity leading up to treatment failure is variable across individuals.

184 To compare treatment failure leading to hospital readmission in chi

185 administered dilute apple juice experienced treatment failure less often than those given electrolyt

186 t consistent across trials, particularly for treatment failure (local, regional, and distant).

187 ] score </=7 at weeks 10 and 12), and 24 had treatment failure (<30% decrease from baseline in HAM-D

188 .73 [95% CI 0.57-0.95], p=0.017) and time-to-treatment failure (median 13.7 months [95% CI 11.9-15.0]

189 wever, high-risk HPV post-treatment predicts treatment failure more accurately than margin status.

190 tment sex differences contribute to clinical treatment failure more commonly experienced by the forme

191 uded and classified as responder (n = 79) or treatment failure (n = 36) on the basis of absence or pr

192 groups for hemoglobin level, ferritin level, treatment failure, need for transfusion, or emergency de

193 Treatment failure occurred in 14 of 144 patients (9.7%).

194 Treatment failure occurred in 22 patients (16%) in the s

195 Treatment failure occurred in 61 (55%) of 111 patients i

196 Treatment failure occurred in 71 of 278 infants (25.5%)

197 Most imiquimod treatment failures occurred in year 1.

198 No treatment failures occurred.

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

200 ated significantly with an increased risk of treatment failure (odds ratio, 3.99; P = .04).

201 ated with an adjusted hazard ratio (aHR) for treatment failure of 20.4 (95% CI 9.1-45.5, p<0.0001).

202 is proposed as a major mechanism underlying treatment failure of these molecule-targeted agents.

203 in the intervention group had immunological treatment failure, of whom 332 (30%) and 727 (54%), resp

204 as the most frequent reason for periodontal treatment failure on a community basis.

205 bination strategies that maximize time until treatment failure on hypothetical patients, using parame

206 enrollment was associated with tuberculosis treatment failure or death (aOR, 3.3; 95% CI, 1.2-9.3).

207 come was time to bacteriologically confirmed treatment failure or disease recurrence, or death (all-c

208 cin would reduce bacteriologically confirmed treatment failure or disease recurrence, or death, by en

209 us 71 (18%) who received placebo experienced treatment failure or disease recurrence, or died (absolu

210 11 patients had treatment failure or recurrent disease during post-treat

211 Primary outcomes were treatment failure or reintubation within 7 days of extub

212 er immunosuppressive therapy correlated with treatment failure or relapse in AA patients.

213 ing for resistant strains is advisable after treatment failure or relapse.

214 Patients continued the trial regimen until treatment failure or until 18 months had elapsed.

215 (64%) assigned to placebo were classified as treatment failures (p=0.0974).

216 nables identification of patients at risk of treatment failure, permitting treatment alternatives suc

217 tandard dosing, evolution of resistance with treatment failure (radiographic progression) occurs at a

218 e data safety monitoring board due to higher treatment failure rate and the occurrence of 2 deaths in

219 A low treatment failure rate occurred in patients with TB uvei

220 Treatment failure rate was defined as the percentage of

221 Treatment failure rate was observed in 9 of 39 eyes (23.

222 s with lower income had higher rates of both treatment failures (rate ratio, 1.6; 95% CI, 1.1-2.3; P

223 th increasing dihydroartemisinin-piperaquine treatment failure rates (r=0.89 [95% CI 0.77-0.95], p<0.

224 etrospective, open cohort study to determine treatment failure rates and associated risk factors.

225 Kaplan-Meier methods were used to determine treatment failure rates and Cox proportional hazards mod

226 nt or better fever clearance times and lower treatment failure rates in comparison to all other antim

227 mmunologic treatment failure with cumulative treatment failure rates increasing to 50.5% at month 60

228 able tuberculosis and unfavourable outcomes (treatment failure, relapse, default, or death despite tr

229 ction, stroke, hemoglobin A1c (HbA1C) level, treatment failure (rescue treatment or lack of efficacy)

230 taining combination therapy did not decrease treatment failures (risk ratio, 1.13; 95% CI, 0.92 to 1.

231 umefantrine group, two participants had late treatment failures (same markers as original isolates).

232 ion, but this still leaves a large number of treatment failures secondary to the emergence of resista

233 The secondary outcomes were risk factors for treatment failure, serious adverse events, and side effe

234 ing of M. tuberculosis from 34 patients with treatment failure showed that most strains persisted gen

235 es between virologically suppressed (VS) and treatment failure (TF) patients with respect to clinical

236 tion and was associated with a lower rate of treatment failure than placebo among children and adoles

237 The broad spectrum showed a lower rate of treatment failure than the standard therapy (18% vs. 51%

238 nput for our model predicted higher rates of treatment failure than were obtained when adherence was

239 f 34 months showed a superior 3-year time to treatment failure, the primary study end point, with R-C

240 clinical improvement and/or of lower risk of treatment failure this effect on mortality cannot be ret

241 At a treatment failure threshold of >1,000 copies/ml, the sen

242 (TIPS 32% vs. endoscopy 26%; P = 0.418) and treatment failure (TIPS 38% vs. endoscopy 34%; P = 0.685

243 ly associated with outcomes of remission and treatment failure to CBT and antidepressant medication a

244 lly identifies the outcomes of remission and treatment failure to these interventions.

245 Currently, prediction of time to treatment failure (TTF) and overall survival (OS) in man

246 n the treatment of AGC with a better time-to treatment failure (TTF) compared to ECX, ECX arm (ECX fo

247 Median time to treatment failure was 16.7 months in patients allocated

248 The median time to treatment failure was 24 weeks in the adalimumab group a

249 The 40th percentile for time to treatment failure was 4.8 months in the placebo group an

250 7.1, 4.9, and 6.8 months; and median time to treatment failure was 5.6, 4.3, and 6.7 months for each

251 Treatment failure was a multicomponent outcome that was

252 Local treatment failure was a relatively infrequent event afte

253 Treatment failure was associated with the emergence of S

254 ssociated with the marginal status, in which treatment failure was defined as occurrence of residual

255 e primary outcome was failure-free survival (treatment failure was defined as radiologic, clinical, o

256 tes of 72%-78% for remission and 75%-89% for treatment failure was demonstrated.

257 Treatment failure was due to nonresponse (n = 2), posttr

258 Treatment failure was followed by a change in antibiotic

259 d of clinicians taking appropriate action on treatment failure was higher with CDSS alerts than with

260 er bound of the 95% CI for the difference in treatment failure was less than 5.0.

261 Time to treatment failure was longer with bevacizumab than with

262 Immunologic treatment failure was moderate to substantial among trea

263 INTERPRETATION: The primary endpoint of treatment failure was not significantly lower in the BII

264 Treatment failure was observed in all cases where isolat

265 ut positive resection margins and subsequent treatment failure was pooled using procedures for meta-a

266 In the matched analysis, the rate of treatment failure was significantly higher for the intra

267 Time to treatment failure was significantly improved in the adal

268 survival (PFS) per nodule (including initial treatment failures) was assessed by using the Kaplan-Mei

269 fy miRNA biomarkers that are associated with treatment failure, we performed a comprehensive sequence

270 rstand the nature of factors contributing to treatment failure, we performed a retrospective cohort s

271 Patterns of treatment failure were categorized as local/regional or

272 Treatment response and treatment failure were paralleled by concordant changes

273 9 isolates in patients discharged home after treatment failure were resistant to eight or more drugs.

274 Independent baseline predictors of death or treatment failure were the presence of severe disease (a

275 Five late treatment failures were detected after AL and one slow r

276 All treatment failures were due to viral relapse (41%).

277 Treatment failures were largely (31 [48%] patients) dist

278 Surgical treatment failures were observed in 34 of 135 patients u

279 However, treatment failures were still common and the rate of pro

280 Treatment failures were uncommon (3.8%, 4.4%, and 1.9% i

281 CI, 0.6 to 3.2 days), but no differences in treatment failure when objective clinical criteria were

282 We observed a hazard of death and treatment failure with "intermediate-level" gyr mutation

283 eukaemia based on local site assessment, and treatment failure with a hypomethylating drug in the pas

284 associated with remission to medication and treatment failure with CBT.

285 Overall, 30.4% had immunologic treatment failure with cumulative treatment failure rate

286 hether these genetic variants are markers of treatment failure with dihydroartemisinin-piperaquine.

287 an individual's probability of remission or treatment failure with first-line treatment options for

288 risk patients with CLL after they experience treatment failure with ibrutinib therapy.

289 y was associated with remission with CBT and treatment failure with medication, whereas negative summ

290 a third-generation EGFR TKI, after previous treatment failure with one or more other EGFR TKIs.

291 There were 139 (6.6%) treatment failures with 1 death.

292 We also present data of early treatment failures with an oral artemisinin combination

293 Recent treatment failures with dihydroartemisinin-piperaquine,

294 tion of previous drug classes, in which more treatment failures with resistant strains occurred and T

295 Babesiosis treatment failures with standard therapy have been repor

296 Gag cleavage sites (CS) are associated with treatment failure, with limited knowledge among non-B su

297 The primary outcome was treatment failure within 7 days of enrolment and the pri

298 Treatment failure within 7 days of enrolment was reporte

299 The primary outcome was treatment failure within 72 hours after randomization.

300 (20 vs 32) or met prespecified criteria for treatment failure (zero vs two).