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 a significant concern for both ZIKV and DENV vacc

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

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

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

7 ADE results in increased intracellular de novo DV protei

8 ADE was detected in monocytes and a concurrent activatio

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

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

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

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

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

14 The function of NK cells against ADE was demonstrated using a depletion assay.

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

16 The results of the CTRW model and an ADE model are compared with the real breakthrough plots

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

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

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

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

21 de hypotheses about mechanisms of action and ADE etiology.

22 ADDM and ADE varied by diet (p < 0.001).

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

24 : 250 were randomly assigned between FLA and ADE; 356 to G-CSF versus no G-CSF; 362 to ATRA versus no

25 elationship among different flaviviruses and ADE.

26 ipheral blood mononuclear cells (PBMCs), and ADE and NK cell activation were simultaneously monitored

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

28 OAE-based ADE-specific ontologies, including ODNAE for drug-associ

29 Second, because ADE of disease cannot be reliably predicted after either

30 However, the molecular mechanism behind ADE is still elusive.

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

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

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

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

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

36 ing the potential for DENV immunity to cause ADE in vivo.

37 st congenital ZIKV infection without causing ADE.

38 ther neurons, including the dopaminergic CEP/ADEs.

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

40 ding dengue virus and SARS-CoV, and consider ADE in the context of the ongoing SARS-CoV-2 pandemic.

41 nt cell cytotoxicity (ADCC) in counteracting ADE.

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

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

44 ted-PBMCs or to purified monocytes decreased ADE.

45 Induction II consisted of low-dose ADE given alone or combined with sorafenib or vorinostat

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

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

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

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

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

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

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

53 d with a modified acoustic droplet ejection (ADE) system.

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

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

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

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

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

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

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

61 Apparent digestibility of energy (ADE) was calculated from ADDM and the GE of feces and di

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

63 itize humans to antibody-dependent enhanced (ADE) breakthrough infections?

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

65 IIB mediates antibody-dependent enhancement (ADE) activity by MW05.

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

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

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

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

70 Antibody (Ab)-dependent enhancement (ADE) is a hypothesized mechanism of increased disease se

71 Antibody-dependent enhancement (ADE) is a mechanism by which the pathogenesis of certain

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

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

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

75 sease via an antibody-dependent enhancement (ADE) mechanism.

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

77 there is no antibody-dependent enhancement (ADE) observed.

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

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

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

81 Antibody-dependent enhancement (ADE) of disease is a general concern for the development

82 that induce antibody-dependent enhancement (ADE) of heterologous flavivirus infection.

83 at can cause antibody-dependent enhancement (ADE) of infection.

84 Antibody-dependent enhancement (ADE) of viral entry has been a major concern for epidemi

85 s.IMPORTANCE Antibody-dependent enhancement (ADE) of viral entry has been observed for many viruses.

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

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

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

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

90 ocess termed antibody-dependent enhancement (ADE)(1,4,5).

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

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

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

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

95 o facilitate antibody-dependent enhancement (ADE).

96 infection by antibody-dependent enhancement (ADE).

97 utations and antibody-dependent enhancement (ADE).

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

99 ntibodies on antibody-dependent enhancement (ADE).

100 D-19 through antibody-dependent enhancement (ADE).

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

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

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

104 ced (through antibody-dependent enhancement [ADE]) or was suppressed by both DENV and ZIKV immunity.

105 ility using an advection diffusion equation (ADE).

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

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

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

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

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

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

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

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

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

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

116 events (AEs), or called adverse drug events (ADEs), are ranked one of the leading causes of mortality

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

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

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

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

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

122 oteins in plasma astrocyte-derived exosomes (ADEs) of subjects with sports-related TBI (sTBI) and TBI

123 ue we name averaged differential expression (ADE).

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

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

126 ctive antibodies may prime an individual for ADE on natural infection.

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

128 Here we identify a novel mechanism for ADE: a neutralizing antibody binds to the surface spike

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

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

131 On the other hand, ADE was not observed upon ZIKV infection in mice that we

132 cytarabine, daunorubicin, and etoposide (HD-ADE, n = 133) as induction I.

133 for Clo+AraC v 64.6% [56.2% to 74.2%] for HD-ADE, P = .1) did not differ significantly across the two

134 for Clo+AraC v 52.4% [44.0% to 62.4%] for HD-ADE, P = .94) and overall survival rate (74.8% [67.1% to

135 and 42 of 121 patients (35%) who received HD-ADE (odds ratio, 1.86; 95% CI, 1.03 to 3.41; P = .04).

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

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

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

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

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

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

142 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.

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

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

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

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

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

148 Cprotein levels in ADEs were from 12- to 35-fold higher than the correspond

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

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

151 Blocking IFN-gamma expression also increased ADE.

152 NK cell-depleted PBMCs had increased ADE as compared to whole PBMCs.

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

154 nse does not cross-react with DENV or induce ADE of DENV infection.

155 therefore showed a lower potential to induce ADE in vitro Our data demonstrated a higher efficacy of

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

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

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

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

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

161 ion FcgammaRIIa-ITIM significantly inhibited ADE.

162 Here, we describe key ADE mechanisms and discuss mitigation strategies for SAR

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

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

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

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

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

168 %-13.4%) of all adult psychiatric medication ADE ED visits and in 21.0% (95% CI, 16.3%-25.7%) of visi

169 % CI, 68,641-109,548) psychiatric medication ADE ED visits annually, with 19.3% (95% CI, 16.3%-22.2%)

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

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

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

173 method achieved an F1-score of 85.1% on n2c2-ADE sub-dataset.

174 as first occurrence of severe morbidity (new ADE, selected serious infections, serious non-ADE, immun

175 DE, selected serious infections, serious non-ADE, immune reconstitution inflammatory syndrome, or dea

176 CD81 exosome marker-normalized ADE levels of classical pathway C4b, alternative pathway

177 establish the primate model for analysis of ADE.

178 l, biological, or pathological attributes of ADE disease exemplified by dengue viruses (DENV).

179 titers, suggesting a signaling component of ADE.

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

181 onsiderable variability in the definition of ADE.

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

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

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

185 In contrast, significant elevations of ADE levels of C4b, factor D, Bb, MBL, C3b and C5b-9 term

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

187 ariation among individual-level estimates of ADE.

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

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

190 ls would offer benefits to the evaluation of ADE.

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

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

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

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

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

196 by ADCC Abs and can control the magnitude of ADE.

197 he putative FcgammaR-dependent mechanisms of ADE overlap with the role of these receptors in mediatin

198 In vitro modelling of ADE has attributed enhanced pathogenesis to Fcgamma rece

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

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

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

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

203 and animal models do not predict the risk of ADE of disease, in part because protective and potential

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

205 the virion, thereby eliminating the risk of ADE.

206 review observations relevant to the risks of ADE of disease, and their potential implications for SAR

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

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

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

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

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

212 -1 RNA, CD4+ cell recovery or development of ADEs.

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

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

215 Plasma levels of ADEs were decreased after acute sTBI and returned to nor

216 and drug-treated disease) on the outcomes of ADEs.

217 ODAE provides a general representation of ADEs given different conditions and can be used for quer

218 With more ontological studies of ADEs, it is also critical to develop a general purpose o

219 mantic and logic representation and study of ADEs of more drugs in the future.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

234 -based clinical pharmacists 94% of potential ADEs.

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

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

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

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

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

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

241 ot neutralize infection but potently promote ADE.

242 to neutralize the virus and instead promoted ADE.

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

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

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

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

247 a general purpose ontology for representing ADEs for various types of drugs.

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

249 e of the counteractive ADCC Abs, in the same ADE-serum, capable of strongly promoting NK cell activat

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

251 1beta provides an informative model to study ADE-induced cytokines.

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

253 died cell types except immature DC supported ADE.

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

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

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

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

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

259 The ADE model is shown to be insufficient, whereas a coupled

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

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

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

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

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

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

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

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

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

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

270 However, these ADE-specific ontologies do not consider the effects of o

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

272 ntiviral protection and pathogenesis through ADE.

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

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

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

276 s but only subneutralize another, leading to ADE of the latter viruses.

277 ration of fecal fat was inversely related to ADE (r = -0.729, p < 0.001).

278 ealed human clinical safety risks related to ADE, resulting in failed vaccine trials.

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

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

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

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

283 The study suggests that under ADE conditions, NK cells can be activated by ADCC Abs an

284 similar FcgammaRIIa levels, did not undergo ADE.

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

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

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

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

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

290 While ADE infection rates were remarkably consistent in monocy

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

292 s, determinants and outcomes associated with ADE.

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

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

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

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

297 presence of enhancement serum together with ADE-affected monocytes and soluble factors, suggesting t

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

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.