ライフサイエンスコーパス: ADE

1 ADE analysis provides the potential to significantly alt

2 ADE cargo proteins may be useful for studies of mechanis

3 ADE is the increase in viral growth rate in the presence

4 ADE levels of beta-site amyloid precursor protein-cleavi

5 ADE of DENV serotype 2 (DENV-2) elevates mature IL-1beta

6 ADE patients experienced slightly more severe nonhematol

7 ADE results in increased intracellular de novo DV protei

8 ADE, butanedione monoxime, and NP were given for cardiop

9 ADEs complicated 2.43 per 100 admissions to the LDS Hosp

10 ve in protecting against DENV-1-4 and DENV-1 ADE infections, with 50% effective concentrations in the

11 tiple episodes were excluded, there were 190 ADEs, of which 60 were preventable.

12 During the study period, there were 247 ADEs among 207 admissions.

13 rs (5.7%), 115 potential ADEs (1.1%), and 26 ADEs (0.24%).

14 Of the 26 ADEs, 5 (19%) were preventable.

15 CI, 10.1-13.2) and 16.4 (95% CI, 13.0-19.9) ADE ED visits per 10,000 outpatient prescription visits,

16 , and both Syk and ERK1/2 inhibitors ablated ADE-induced IL-1beta secretion.

17 ibition with monoclonal antibodies abrogated ADE and associated downstream consequences.

18 HT]) and endothelium-independent (adenosine [ADE] or nitroprusside [NP]) vasodilators may be altered

19 ts attributable to an ADE were $2595 for all ADEs and $4685 for preventable ADEs.

20 te that the annual costs attributable to all ADEs and preventable ADEs for a 700-bed teaching hospita

21 outcomes included preventable or ameliorable ADEs, as well as potential ADEs.

22 An ADE is associated with a significantly prolonged length

23 conflicting symptoms (i.e., high pain and an ADE) are present.

24 risk of death among patients experiencing an ADE was 1.88 (95% confidence interval, 1.54-2.22; P<.001

25 than for errors that actually resulted in an ADE.

26 variables revealed that the occurrence of an ADE was associated with increased length of stay of 1.91

27 s cost of hospitalization attributable to an ADE was $2013 (P<.001).

28 a length of hospital stay attributable to an ADE was 1.74 days (P<.001).

29 estimated postevent costs attributable to an ADE were $2595 for all ADEs and $4685 for preventable AD

30 based on a pharmacophoric approach, with an ADE reference standard extracted from the SIDER database

31 and the increase in cost associated with an ADE was $3244 (P=.04).

32 additional length of stay associated with an ADE was 2.2 days (P=.04), and the increase in cost assoc

33 Cases were patients with an ADE, and the control for each case was the patient on th

34 ociated with a lower CR rate (P < .001), and ADE/ADEP, with a higher CR rate in younger patients (P =

35 r for DA versus ADE (84% v 86%; P = .14) and ADE versus FLAG-Ida (86% v 85%; P = .7), with more cours

36 de hypotheses about mechanisms of action and ADE etiology.

37 les for anterior visceral endoderm (AVE) and ADE.

38 l at 6 years was 40% (+/-4) for both DAT and ADE (P = .9).

39 In conclusion, DAT and ADE both achieve high remission rates and good long-term

40 : 250 were randomly assigned between FLA and ADE; 356 to G-CSF versus no G-CSF; 362 to ATRA versus no

41 elationship among different flaviviruses and ADE.

42 V capsid can mediate both neutralization and ADE may explain the failure of capsid-based vaccines.

43 Medication errors, potential ADEs, and ADEs were identified by clinical staff reports and revie

44 erestimate the degree of difficulty to avoid ADEs at the bedside.

45 , deaths in CR, relapse rate, or DFS between ADE and FLA, although survival at 4 years was worse with

46 lly expressed mRNA transcripts identified by ADE can be used for the detection of prostate cancer in

47 lly expressed mRNA transcripts identified by ADE were fewer in number, but were expressed in a greate

48 , but caspase-1 is suboptimally increased by ADE and can be significantly enhanced by a typical infla

49 rons (IFN-alpha/beta) that were modulated by ADE.

50 mediated, antibody-dependent enhancement (C'-ADE) of HIV-1IIIB and primary isolates was equally preva

51 lement-mediated Ab-dependent enhancement (C'-ADE) of SIVmac239/nef-open in vitro.

52 ther neurons, including the dopaminergic CEP/ADEs.

53 The most common ADEs (urticaria, dyspnea, vomiting, pruritus, facial ede

54 Our results, while confirming ADE in vitro, suggest that pre-existing DENV immunity do

55 courses were not different from that with DA/ADE with consolidation.

56 and etoposide 100 mg/m(2) daily for 3 days (ADE), or daunorubicin 40 mg/m(2) and etoposide 60 mg/m(2

57 fication and generated enriched sets of drug-ADE signals.

58 ides, a pharmacovigilance resource with drug-ADE associations extracted from the FDA Adverse Event Re

59 Maturation of pro-IL-1beta during ADE requires caspase-1 and NLRP3, but caspase-1 is subop

60 r rats and in an alcohol deprivation effect (ADE) model in long-term alcohol drinking Wistar rats, tw

61 Anthelmintic drug efficacy (ADE) is generally estimated as a population average effe

62 nt transporter exhibits anomalous DA efflux (ADE) and lacks capacity for amphetamine (AMPH)-stimulate

63 (hDAT A559V) results in anomalous DA efflux (ADE) similar to that caused by amphetamine-like psychost

64 idic EMSA card by acoustic droplet ejection (ADE), which reduces EMSA variability compared to sample

65 Strategies to eliminate ADE were explored by altering the antibody Fc structures

66 ly specify the anterior definitive endoderm (ADE) and prechordal plate (PCP) progenitors.

67 hypoblast and anterior definitive endoderm (ADE) in patterning the overlying ectoderm, whereas data

68 including the anterior definitive endoderm (ADE), anterior mesendoderm (AME) and anterior neural rid

69 uently, in the anterior definitive endoderm (ADE), anterior neuroectoderm (ANE), anterior mesendoderm

70 es (VDEs) and adiabatic detachment energies (ADEs) are obtained.

71 pharmacophoric similarity models to enhance ADE recognition in Offsides, a pharmacovigilance resourc

72 otypes of DENV, antibody-dependent enhanced (ADE) infection, and ex vivo and in vivo DENV infections.

73 e process of antibody-dependent enhancement (ADE) as a primary risk factor.

74 presence of Antibody Dependent Enhancement (ADE) heterogeneity can increase the persistence of multi

75 mechanism of antibody-dependent enhancement (ADE) in a variety of Fc receptor-bearing cells in vitro.

76 s induced by antibody-dependent enhancement (ADE) in multiserotype disease models.

77 Antibody-dependent enhancement (ADE) is implicated in severe, usually secondary, dengue

78 nfections is antibody-dependent enhancement (ADE) leading to increased replication in Fc receptor-bea

79 The proposed antibody-dependent enhancement (ADE) mechanism for severe dengue virus (DENV) disease su

80 through the antibody-dependent enhancement (ADE) mechanism.

81 Antibody-dependent enhancement (ADE) of dengue virus (DENV) infection is believed to con

82 Ab-dependent enhancement (ADE) of dengue virus (DENV) infection is mediated throug

83 and prevents antibody-dependent enhancement (ADE) of disease in mice.

84 n vitro that antibody-dependent enhancement (ADE) of ZIKV infection can occur.

85 ble to drive antibody-dependent enhancement (ADE) of ZIKV infection.

86 , as well as antibody-dependent enhancement (ADE) of ZIKV infection.

87 Moreover, antibody-dependent enhancement (ADE) was not observed against any serotype at a 1:10 ser

88 Antibody-dependent enhancement (ADE), a phenomenon in which viral replication is increas

89 Antibody-dependent enhancement (ADE), a process best described in vitro, is epidemiologi

90 ociated with antibody-dependent enhancement (ADE), and it was recently suggested that previous exposu

91 he effect of antibody-dependent enhancement (ADE).

92 ntibodies on antibody-dependent enhancement (ADE).

93 non known as antibody-dependent enhancement (ADE).

94 tor-mediated antibody-dependent enhancement (ADE).

95 ferred to as antibody-dependent enhancement (ADE).

96 infection by antibody-dependent enhancement (ADE).

97 ttributed to antibody-dependent enhancement (ADE); however, because only a fraction of infections occ

98 nees such as Antibody-Dependent Enhancement (ADE, a phenomenon involved in pathogenesis of DENV, and

99 e temporal auxiliary differential equations (ADEs) with a high degree of efficiency.

100 Antimicrobial de-escalation (ADE) is a strategy to reduce the spectrum of antimicrobi

101 of cytarabine, daunorubicin, and etoposide (ADE) with or without PSC-833 (P), a modulator of p-glyco

102 ne arabinoside, daunorubicin, and etoposide (ADE).

103 abine given with daunorubicin and etoposide (ADE; induction 1).

104 d cytarabine (DA) with or without etoposide (ADE; n = 1983) or ADE versus fludarabine, cytarabine, gr

105 ession (to either a new AIDS-defining event [ADE] or death).

106 nic visit to death and AIDS-defining events (ADE), adjusted for baseline characteristics with and wit

107 recovery and rates of AIDS defining events (ADEs) within the first year of cART using linear mixed e

108 Adverse drug events (ADEs) are a significant and costly cause of injury durin

109 Adverse drug events (ADEs) are the most common type of iatrogenic injury occu

110 Adverse drug events (ADEs) constitute one of the leading causes of post-thera

111 icularly susceptible to adverse drug events (ADEs) due to their rapidly changing and unstable physiol

112 ventable or ameliorable adverse drug events (ADEs), as well as medication discrepancies or nonadheren

113 ex differences exist in Adverse Drug Events (ADEs).

114 Adverse drugs events (ADEs) detection constitutes a considerable concern in pa

115 Mature DC exhibited ADE, whereas immature DC, expressing higher levels of DC

116 uantification in astrocyte-derived exosomes (ADEs) and NDEs, enriched separately from plasmas of pati

117 ue we name averaged differential expression (ADE).

118 tional DE, acoustic differential extraction (ADE) analysis was developed on a microfluidic device.

119 sponse, and death were 46%, 34%, and 20% for ADE, versus 39%, 17%, and 44% for ADEP (P =.008).

120 CR was 42% (+/-4) for DAT and 43% (+/-4) for ADE (P = .8); relapse rate at 6 years was 50% (+/-4) for

121 22%, and 8% for DAT and 74%, 21%, and 5% for ADE.

122 rs was 50% (+/-4) for DAT and 49% (+/-5) for ADE (P = .6); survival at 6 years was 40% (+/-4) for bot

123 ous enough to provide a strong mechanism for ADE identification.

124 es it a promising target for data mining for ADE identification and intervention.

125 Our results support the need for ADE to explain the complexity of the epidemiological dat

126 clinical situations with increased risk for ADE-related injury.

127 ths of stay and costs of hospitalization for ADEs are substantial.

128 sification provides a way of determining how ADE-preventing technologies in the intensive care unit c

129 To reevaluate the role of the hypoblast/ADE (lower layer) in patterning the chick ectoderm, we u

130 hout tissue replacement), that the hypoblast/ADE (lower layer) is required and sufficient for pattern

131 at mortality enhancement must be dominant if ADE really is responsible for the immunological distance

132 is important to develop methods that improve ADE signal detection in pharmacovigilance databases.

133 pharmacovigilance data in Offsides improved ADE identification and generated enriched sets of drug-A

134 were DNR 90 mg/m(2) and ETOP 100 mg/m(2) in ADE, and DNR and ETOP each 40 mg/m(2) in ADEP.

135 oxicity was not seen with high doses of D in ADE.

136 aRIIb) isoforms, but their relative roles in ADE are not well understood.

137 Identifying those sex differences in ADEs could reduce the experience of ADEs for patients an

138 ed States, 307 drugs have sex differences in ADEs.

139 levels also were a mean of 7-fold higher in ADEs than in NDEs from cultured rat type-specific neural

140 ly higher and of GDNF significantly lower in ADEs of patients with AD than in those of controls, but

141 of the Abeta42 peptide-generating system in ADEs may sustain levels in neurons.

142 as sera from non-HSK patients did not induce ADE, and that anti-gD antibody in sera of HSK patients c

143 d higher anti-gK antibody titers and induced ADE in vitro compared with non-HSK or seronegative sera.

144 titers and HSV-1 IgG, that HSK sera induced ADE whereas sera from non-HSK patients did not induce AD

145 antibody-dependent enhancement of infection (ADE)-induced disease.

146 nduce Ab-dependent enhancement of infection (ADE).

147 In the context of influenza, ADE has been used to explain several preclinical and cli

148 ion FcgammaRIIa-ITIM significantly inhibited ADE.

149 eral blood mononuclear cells and in a lethal ADE-infection mouse model.

150 Although the number of patients was limited, ADE patients whose pretreatment cells exhibited PSC-833-

151 ychiatric medications are implicated in many ADEs treated in US EDs.

152 2)R provides support for hDAT A559V-mediated ADE.

153 us particles into immune complexes, mediated ADE, and neutralized virus infectivity in vitro.

154 %-13.4%) of all adult psychiatric medication ADE ED visits and in 21.0% (95% CI, 16.3%-25.7%) of visi

155 % CI, 68,641-109,548) psychiatric medication ADE ED visits annually, with 19.3% (95% CI, 16.3%-22.2%)

156 medication use and of psychiatric medication ADE ED visits per 10,000 outpatient visits at which psyc

157 In our models, ADE induces the onset of oscillations without external f

158 produced 22,785 reports of mild or moderate ADEs, 2,639 reports of serious but nonfatal ADEs, and 92

159 We developed a multi-ADE predictor implementing 3D drug similarity based on a

160 ADEs, 2,639 reports of serious but nonfatal ADEs, and 920 reports of death.

161 Reports of serious, nonfatal ADEs are uncommon relative to the use of contrast media.

162 a were associated with 512 serious, nonfatal ADEs reported in 1978-1986; 1,068 were reported in 1987-

163 CM were associated with 17 serious, nonfatal ADEs reported in 1978-1986; 609 were reported in 1987-19

164 sociated with 235 reported serious, nonfatal ADEs; intrathecal ionic [corrected] contrast media were

165 establish the primate model for analysis of ADE.

166 titers, suggesting a signaling component of ADE.

167 Induction 2 consisted of ADE with or without gemtuzumab ozogamicin (GO anti-CD33

168 onsiderable variability in the definition of ADE.

169 Because the determinants of ADE are markers of clinical improvement and/or of lower

170 s were designed to investigate the effect of ADE on antimicrobial resistance.

171 The pooled effect of ADE on mortality is protective (relative risk, 0.68; 95%

172 National estimates of ADE ED visits resulting from therapeutic psychiatric med

173 ariation among individual-level estimates of ADE.

174 structured longitudinal data on estimates of ADE; (ii) permit robust inference on the association of

175 drug safety, applicable to the evaluation of ADE signals selected through pharmacovigilance data mini

176 ls would offer benefits to the evaluation of ADE.

177 The most striking in vivo example of ADE in humans is dengue hemorrhagic fever, a disease in

178 e results, together with earlier findings of ADE of DENV-2 infection by a polyclonal serum, establish

179 We examine the epidemiological impact of ADE on the prevalence and persistence of viral serotypes

180 dynamic behavior created by the interplay of ADE and CI using mathematical models.

181 e advantage provided by increasing levels of ADE, because greater levels of enhancement induce large

182 he current ZIKV outbreak, the possibility of ADE is especially concerning and may pose unique challen

183 We propose a redefinition of ADE in the context of complex immunological flavivirus i

184 The repression of ADE genes in adenine-replete cells involves down-regulat

185 moglobin contributed to their higher risk of ADE and death.

186 vector, thus averting the potential risk of ADE associated with structural protein-based ZIKV vaccin

187 The risk of ADE was higher among women in both models, but not stati

188 animal models to further confirm the role of ADE in the development of congenital and neurological co

189 ral kinetics modeling, we assess the role of ADE in the treatment of influenza with a bNAb.

190 No signs of ADE were observed in vivo in patients with acute ZIKV in

191 hogen persistence during the deep troughs of ADE-induced large amplitude oscillations of virus replic

192 The substantial costs of ADEs to hospitals justify investment in efforts to preve

193 pression, immune recovery and development of ADEs were comparable between foreign-born and US-born pa

194 -1 RNA, CD4+ cell recovery or development of ADEs.

195 Unfortunately, the onset and effects of ADEs are often underreported complicating timely interve

196 ences in ADEs could reduce the experience of ADEs for patients and could be conducive to the developm

197 these costs and data about the incidence of ADEs, we estimate that the annual costs attributable to

198 uthors observed no decrease in the number of ADEs reported since the introduction of LOCM but did not

199 patient injury secondary to a broad range of ADEs.

200 ssociated with a substantially lower rate of ADEs caused by prescribing errors.

201 Reports of ADEs submitted were reviewed for use of iodinated contra

202 The global ROC curve for the Offsides ADE candidates ranked with the 3D similarity score showe

203 se preferences weakened the effect of opioid ADE understanding on decisions to withhold opioids when

204 with or without etoposide (ADE; n = 1983) or ADE versus fludarabine, cytarabine, granulocyte colony-s

205 under direct infection (without antibody) or ADE conditions (with antibody).

206 rm groups, L-ARG did not alter basal flow or ADE, ACh, 5-HT, or NP responses, whereas L-NAME and AVP

207 rate ratio, 0.92 [95% CI, 0.77 to 1.10]) or ADEs (unadjusted incidence rate ratio, 1.09 [CI, 0.86 to

208 The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (9

209 k by CYT 17 O2' on the scissile phosphorous (ADE 1.1 P), and is therefore consistent with the experim

210 previous adult hospital study, the potential ADE rate was 3 times higher.

211 616 medication errors (5.7%), 115 potential ADEs (1.1%), and 26 ADEs (0.24%).

212 s of target potential ADEs and all potential ADEs decreased by 74% and 63%, respectively.

213 curred in 258 patients (30.3%) and potential ADEs in 253 patients (29.7%).

214 all rates of dispensing errors and potential ADEs substantially decreased after implementing bar code

215 le or ameliorable ADEs, as well as potential ADEs.

216 Medication errors, potential ADEs, and ADEs were identified by clinical staff reports

217 vention group tended to have fewer potential ADEs (unadjusted incidence rate ratio, 0.80 [CI, 0.61 to

218 hough this decrease was larger for potential ADEs than for errors that actually resulted in an ADE.

219 th high potential for future harm (potential ADEs).

220 Most potential ADEs occurred at the stage of drug ordering (79%) and in

221 3.88 (P=.37), while nonintercepted potential ADEs declined 84% from 5.99 to 0.98 per 1000 patient-day

222 tive reduction in the incidence of potential ADEs (P < 0.001).

223 The rate of potential ADEs was significantly higher in neonates in the neonata

224 -based clinical pharmacists 94% of potential ADEs.

225 (by 2.4-fold) incidence of target potential ADEs (P = 0.014).

226 Overall, the rates of target potential ADEs and all potential ADEs decreased by 74% and 63%, re

227 as designed to address, and target potential ADEs, defined as target dispensing errors that can harm

228 ted, IgG1 RNNIg during infection may prevent ADE of DENV disease.

229 While the preventable ADE rate was similar to that of a previous adult hospita

230 Preventable ADEs declined 17% from 4.69 to 3.88 (P=.37), while nonin

231 Preventable ADEs were identified by review of medical records of the

232 sts attributable to all ADEs and preventable ADEs for a 700-bed teaching hospital are $5.6 million an

233 For preventable ADEs, the increases were 4.6 days in length of stay (P=.

234 $2595 for all ADEs and $4685 for preventable ADEs.

235 therapy, probable route of infection, prior ADE, absolute CD4, and %CD4 was performed; prior ART (P<

236 ot neutralize infection but potently promote ADE.

237 to neutralize the virus and instead promoted ADE.

238 ion (CR), compared with 82% of 140 receiving ADE/ADEP (P = .04).

239 ith an ITAM (FcgammaRIIb-ITAM) reconstituted ADE capacity to levels of the wild type activating count

240 Efforts to reduce ADEs should include adults of all ages but might priorit

241 fectiveness of many technologies in reducing ADEs, we will review the technologies currently availabl

242 media were associated with 14 such reported ADEs.

243 re classified as to whether they represented ADEs.

244 28), and 2779 (95% CI, 1764-3794) respective ADE ED visits annually.

245 ly, we employ our method to discover several ADEs which, though present in medical literature and Twi

246 Thirty-seven drug-specific ADEs were targeted.

247 1beta provides an informative model to study ADE-induced cytokines.

248 NV mAbs and primary human monocytes to study ADE-induced IL-1beta and other cytokines.

249 died cell types except immature DC supported ADE.

250 cocirculating dengue serotypes, we find that ADE may provide a competitive advantage to those serotyp

251 We show that ADE is inversely correlated with surface expression of D

252 Our data suggest that ADE effects are cell type specific, are influenced by ho

253 Theory has suggested that ADE may be responsible for the large immunological dista

254 The ADE method relies on acoustic trapping of sperm cells in

255 The ADE response in HSK sera was attributed to anti-gK antib

256 s in the distal tip of the conceptus and the ADE fails to form, whereas the node and notochord form n

257 as L-NAME and AVP reduced basal flow and the ADE response, abolished ACh and 5-HT responses, and incr

258 ion of the most similar drug that causes the ADE under study, which could provide hypotheses about me

259 drinking weeks, which was selective for the ADE as the SDE was unaffected.

260 disease-free survival was 1.34 years in the ADE arm and 1.09 years in the ADEP arm (P = .74, log-ran

261 edian overall survival was 1.86 years in the ADE arm and 1.69 years in the ADEP arm (P = .82).

262 nd etoposide 100 mg/m(2)/d for 3 days in the ADE group.

263 enine-regulated step in transcription of the ADE genes.

264 this paper, we derive approximations of the ADE parameter needed to induce oscillations and analyze

265 Here we report for the first time the ADE phenomenon in primary human dendritic cells (DC), ea

266 precursors that selectively give rise to the ADE and PCP mesoderm.

267 nd female fractions can be obtained with the ADE microdevice from mock sexual assault samples in 14 m

268 re were several potentially life-threatening ADEs involving intravenous dopamine and intravenous hepa

269 d after randomization of 120 patients (61 to ADE and 59 to ADEP) because of excessive early mortality

270 le of anti-gD- and gK-specific antibodies to ADE was investigated.

271 e allocated to DAT and 928 (143 children) to ADE.

272 emonstrating that there is no correlation to ADE when ZIKV infection occurs in the presence of pre-ex

273 of DV infection and their susceptibility to ADE will aid our understanding of complex disease and co

274 ation, leaving dengue viruses susceptible to ADE by antibody to prM, a finding that has implications

275 Errors leading to ADEs are often due to restricted availability of informa

276 ities to prevent patient injury secondary to ADEs at a rate of 64 per 1000 admissions.

277 ed that the application of our 3D multi-type ADE predictor to the pharmacovigilance data in Offsides

278 y influence Ab-mediated DENV infection under ADE conditions both at the level of cellular infection a

279 similar FcgammaRIIa levels, did not undergo ADE.

280 All cells undergoing ADE secreted proinflammatory cytokines (interleukin-6 [I

281 l remission rates were similar for DA versus ADE (84% v 86%; P = .14) and ADE versus FLAG-Ida (86% v

282 aunorubicin, cytarabine, thioguanine) versus ADE (daunorubicin, cytarabine, etoposide) regimens in th

283 ng of safe actions that will treat pain when ADE symptoms are present.

284 anding on decisions to withhold opioids when ADEs (i.e., nausea/vomiting or oversedation) were presen

285 dengue hemorrhagic fever, a disease in which ADE is thought to increase the severity of clinical mani

286 While ADE infection rates were remarkably consistent in monocy

287 sion (CR) rate was 81% with DAT and 83% with ADE (P = .3).

288 ant disease were 11% with DAT versus 9% with ADE (P = .07).

289 ity scores were consistently associated with ADE (P= .04 to <.001).

290 s, determinants and outcomes associated with ADE.

291 in CR during consolidation chemotherapy with ADE (9%) than with DAT (6%) (P = .06).

292 of DNR and ETOP given in ADEP compared with ADE.

293 n the association of measurable factors with ADE; and (iii) enable estimation of variation among indi

294 new therapeutic targets for interfering with ADE-induced cytokine expression during severe dengue.

295 dian disease-free survival was 5 months with ADE and 14 months with ADEP (P =.07).

296 44 patients achieved complete remission with ADE, compared with 29 (44%) of 66 patients treated with

297 e points of failure commonly associated with ADEs (i.e., the five "Rights": right patient; right drug

298 Cases were defined as patients with ADEs that occurred during hospitalization; controls were

299 aunorubicin (D), and etoposide (E), without (ADE) or with (ADEP) PSC-833 (P).

300 abine were evaluated with (ADEP) or without (ADE) a fixed dose of PSC-833.