ライフサイエンスコーパス: drug exposure

1 ill likely influence responses to subsequent drug exposure.

2 of schizophrenia regardless of antipsychotic drug exposure.

3 sed during breastfeeding with minimal infant drug exposure.

4 nts and only 1/46 (2.2%) was detected during drug exposure.

5 pted chromosomal conformations shortly after drug exposure.

6 nces in susceptibility to propofol and track drug exposure.

7 drug concentrations and longer durations of drug exposure.

8 fect the occurrence of toxicities related to drug exposure.

9 ecules that persist for weeks after the last drug exposure.

10 eceptor availabilities determined before any drug exposure.

11 n six different murine tissues after chronic drug exposure.

12 acuity and stereoacuity were not affected by drug exposure.

13 bacterial subpopulation tolerates prolonged drug exposure.

14 gh local tissue levels with minimal systemic drug exposure.

15 ward unfavorable environmental conditions or drug exposure.

16 clinical features known to increase edoxaban drug exposure.

17 plasma HIV RNA in individuals with adequate drug exposure.

18 and neuroadaptations occurring from repeated drug exposure.

19 s during pregnancy can reduce antiretroviral drug exposure.

20 ood vessels to improve tumor oxygenation and drug exposure.

21 ment could circumvent the need for prolonged drug exposure.

22 onazole dose is required to achieve adequate drug exposure.

23 ociated with metabolic deficits and prenatal drug exposure.

24 particularly under conditions of suboptimal drug exposure.

25 or neuroadaptive changes following addictive drug exposure.

26 ciated with aging, early-life infection, and drug exposure.

27 cases and 472 controls with IBD matched for drug exposure.

28 deleterious effects of repeated dopaminergic drug exposure.

29 cancer cell lines to (18)F-FDG uptake after drug exposure.

30 entify ON cases occurring after onset of new drug exposure.

31 s myopathy associated with elevated systemic drug exposure.

32 match the physiological pharmacokinetics of drug exposure.

33 e influenced by the volitional nature of the drug exposure.

34 cy of in vivo antitumor activity on the free-drug exposure.

35 ivity, which is directly related to previous drug exposure.

36 nes via an alternative nuclear receptor upon drug exposure.

37 water consumption patterns and nitrosatable drug exposure.

38 ed apoptosis in melanoma following genotoxic drug exposure.

39 antidepressant-like responses 2 months after drug exposure.

40 ontext, suggesting a separate consequence of drug exposure.

41 ffer clinical benefit with the least risk of drug exposure.

42 s were observed between cells, regardless of drug exposure.

43 linical records notes were used to determine drug exposure.

44 iants by 143 or 148 variants under continued drug exposure.

45 behavioral abnormalities seen with repeated drug exposure.

46 eorganization of the mesolimbic system after drug exposure.

47 lity of the Fosb gene elicited by subsequent drug exposure.

48 ate-related information is affected by prior drug exposure.

49 combination to quantify changes in systemic drug exposure.

50 ity in individuals with a history of chronic drug exposure.

51 d in the brain of newborn pups 14 days after drug exposure.

52 ed and caused nuclear disorganization during drug exposure.

53 s assessed by measuring cell viability after drug exposure.

54 developed resistance in vivo upon continuous drug exposure.

55 rd blood, providing unambiguous assurance of drug exposure.

56 t treatment success is likely with increased drug exposure.

57 ulting from hypoxia/nutrient deprivation and drug exposure.

58 apse, even after relatively brief periods of drug exposure.

59 hile minimizing potential harms of long-term drug exposure.

60 nsults, particularly prior immunosuppressive drug exposure.

61 particular focus on the studies of maternal drug exposures.

62 3-AR agonists and thus have improved unbound drug exposures.

63 -based formulation for achieving efficacious drug exposures.

64 rance status, discharge disposition, and ICU drug exposures.

65 and by similar systemic fluorouracil (active drug) exposure.

66 o-fold to three fold gradient of mean trough drug exposure (16.0-48.5 ng/mL in 6780 patients with dat

67 t was rather associated with lower antiviral drug exposure (6.4 +/- 13 days vs 38.6 +/- 14 days, P <

68 conditions [e.g., premature birth, prenatal drug exposure], 64 toddlers with typical development, an

69 n by >10-fold, (ii) increase the duration of drug exposure above a critical therapeutic threshold, an

70 ing drug concentration-responses and optimal drug exposure achievement.

71 rameters results in inadequate antimicrobial drug exposure across all drug classes.

72 Reuptake is regulated by kinase pathways and drug exposure, allowing for fine-tuning of clearance in

73 Drug exposure also drives the emergence of resistance.

74 Clearly, repeated drug exposure alters a distributed network of neural cir

75 However, it is unknown how drug exposure alters the balance of long-range afferents

76 ith immune responses resulting in suboptimal drug exposure and a greater risk of relapse.

77 -drug interactions (DDIs) and alterations in drug exposure and accumulation in various tissues.

78 res, calculating intrapatient variability in drug exposure and applying electronic monitoring, and re

79 trol of drug release while reducing systemic drug exposure and associated toxicities.

80 children, as these may significantly impact drug exposure and clinical outcomes.

81 out evidence of benefit and with significant drug exposure and costs.

82 xposure, median latency period between first drug exposure and diagnosis, and proportion of cases res

83 ) with infants with similar non-cocaine poly drug exposure and drug-free controls.

84 zepin compounds that showed improved unbound drug exposure and effectively suppressed growth of tumor

85 toward epithelial tissue, thereby prolonging drug exposure and increasing drug permeation.

86 Reward modulates the saliency of a specific drug exposure and is essential for the transition to add

87 tions or environmental risk factors, such as drug exposure and neural injury, mental impairment is a

88 e risk and benefits associated with maternal drug exposure and of the risk factors associated with ad

89 ted through day 21, and associations between drug exposure and outcomes through day 42 were investiga

90 premise that there is a relationship between drug exposure and outcomes, and that considerable inter-

91 e unique properties that enhance intra-tumor drug exposure and reduce systemic toxicity of encapsulat

92 e-guided dosing results in adequate systemic drug exposure and significantly improves safety of fluor

93 these currently marketed drugs require high drug exposure and suffer from narrow therapeutic indices

94 cacy of TRAIL being proportional to systemic drug exposure and suggests that the previous clinical fa

95 ty extraction (AE) LC-MS to directly measure drug exposure and target engagement, two critical pharma

96 he level of platelet reactivity before study drug exposure and the initial degree of platelet inhibit

97 d the patient's (germline) genome influences drug exposure and the patient's sensitivity to toxicity.

98 eural-developmental consequences of prenatal drug exposure and thus open a new window for the advance

99 e two-drug regimens could decrease long-term drug exposure and toxicity with HIV-1 antiretroviral the

100 examine the relationship between miltefosine drug exposure and treatment failure in a cohort of Nepal

101 dopamine and norepinephrine signaling during drug exposure and withdrawal.

102 d after HFS-TB experiments predicted optimal drug exposures and doses, susceptibility breakpoints, an

103 We recorded antimicrobial drug exposures and interrogated the resistome at points

104 efficacy compared with L despite lower serum drug exposures and may remain the fluoroquinolone of cho

105 n allopurinol pregnancy registry to document drug exposures and outcomes.

106 myopathy (CCM) is associated with cumulative drug exposures and preexisting cardiovascular disorders.

107 ure-drug sensitivity test patterns, previous drug-exposures and are provided for 20-22 months.

108 tween NR1I2 polymorphisms, immunosuppressant drug exposure, and clinical outcomes in adult kidney tra

109 Outcomes were animal survival, quantified drug exposure, and distribution of cleaved caspase 3.

110 quent heavy lifting, night work, anti-cancer drug exposure, and overtime work were moderately associa

111 ity, intrinsic activity, receptor occupancy, drug exposure, and pharmacodynamic activity in relevant

112 platform for i.p. delivery, sustained multi-drug exposure, and potent antitumor efficacy in an ES-2-

113 ases of SCLE could be attributed to previous drug exposure, and smoking may be more closely associate

114 een performed in preclinical models, optimal drug exposures, and PK/PD parameters identified in these

115 barrier to facilitate central nervous system drug exposure are being developed.

116 the presence of sanctuary sites with little drug exposure are essential to this end.

117 nvironmental factors such as stress or prior drug exposure are known to play a role in the onset of t

118 DAbs) that cause acute thrombocytopenia upon drug exposure are nonreactive in the absence of the drug

119 inputs, such as sets of SNPs or a disease or drug exposure, are now being explored to probe the genet

120 namely, the effects of EE when applied after drug exposure, are often marginal and transient.

121 or 2 hours after dosing (C2) correlate with drug exposure (area under the curve [AUC]/dose) and outc

122 weeks of protracted abstinence from chronic drug exposure as compared with naive animals.

123 ct on many parameters that determine unbound drug exposure as well as drug potency.

124 h/ml of rifapentine drug exposure (as measured by AUC) was 0.11 CT/week (95%

125 of Tac Cmin, a surrogate marker for 24-hour drug exposure (AUC0-24), has been suggested.

126 osure - in contrast to withdrawal from acute drug exposure - but rather is manifested as exaggerated

127 ose pharmacokinetic study, DDCs enhanced the drug exposure by 7-fold and prolonged the plasma circula

128 rm use of these medications may affect fetal drug exposure by altering BCRP expression in human place

129 Our results demonstrate that prenatal drug exposure can influence a behavioural measure of vis

130 Thereby, estimates of unbound drug exposure can now be implemented at a much earlier s

131 where increasing population size or delaying drug exposure can promote population collapse.

132 Contextual cues associated with previous drug exposure can trigger drug craving and seeking, and

133 ination is potentially viable, providing the drug exposures can be carefully monitored.

134 To investigate whether drug exposure causes asymmetric effects on positive and

135 cortex (PFC) is one region in which chronic drug exposure changes expression and function of upstrea

136 macokinetic modelling generated estimates of drug exposure (Cmax and AUC) from individual-level post-

137 ver injury, and appear more sensitive to the drug exposure (Cmax) where more restrictive labeling occ

138 aily in patients on hemodialysis resulted in drug exposure comparable with that of the standard dose

139 g resulted in increased and protracted tumor drug exposure compared with CPT-11, leading to long-term

140 puts to the model are obtained under optimal drug exposure conditions in-vitro.

141 nctional D2 autoreceptors following repeated drug exposure could lead to aberrant DA activity in the

142 Optimal drug exposure (CSF detectable drugs and 95% inhibitory q

143 rategy, we integrated gene copy number data, drug exposure data and patient survival data to infer ge

144 ve spent extensive effort to standardize the drug exposure data, which enabled us to perform survival

145 In addition, GDISC provides the standardized drug exposure data, which is a valuable resource for dev

146 t "persisters" (DTPs), can survive cytotoxic drug exposure despite lacking resistance-conferring muta

147 Pharmacokinetic studies showed inconsistent drug exposures despite attempts to adjust dose and expos

148 Drug exposure did not increase the rate of congenital ma

149 elated to lifestyles and hygiene, surgeries, drug exposures, diet, microorganisms, and vaccinations.

150 etermine the duration and cumulative dose of drug exposure differ widely between studies.

151 tant breast cancer cells selected by chronic drug exposure displayed a relative increase in the level

152 el is highly accurate at identifying optimal drug exposures, doses, and dosing schedules for use in t

153 el is highly accurate at forecasting optimal drug exposures, doses, and dosing schedules for use in t

154 Drug exposure during critical periods of brain developme

155 Drug exposure during critical periods of development is

156 ges of melanoma progression and to adjust to drug exposure during treatment.

157 relationship between Xpert CT trajectory and drug exposure during tuberculosis (TB) treatment to asse

158 igh sequence diversity of HCV and inadequate drug exposure during unsuccessful treatment may lead to

159 s study establishes the first evidence for a drug exposure-effect relationship for miltefosine in the

160 tion in central Abeta(X-40) levels at a free drug exposure equivalent to the whole cell IC(50) (100 n

161 y cocaine tolerance is reinstated by minimal drug exposure, even after recovery of DAT function over

162 The effects on plasma drug exposure following single-dose nevirapine may be gr

163 or multiple gram doses to ensure sufficient drug exposure for biological activity in patients.

164 riginal tumour and compatible with long-term drug exposure for drug efficacy and resistance studies.

165 ter-tolerated drug regimens, optimization of drug exposure for the component drugs, optimal managemen

166 There is scant evidence to support target drug exposures for optimal tuberculosis outcomes.

167 promotion (drug-predictive cues, stress, and drug exposure) for cocaine and alcohol.

168 to categorize participants into high and low drug exposure groups.

169 Compared with low drug exposure, high-exposure participants showed increas

170 dings highlight the necessity of considering drug exposure history when selecting control groups for

171 Here we show that drug exposure, hypoxia or nutrient starvation leads to a

172 Loss of response on repetitive drug exposure (i.e., tachyphylaxis) is a particular prob

173 However, upon continuous drug exposure IDTCs eventually transform into permanent

174 pharmacodynamics [PD]), is a given; however, drug exposure (ie, PK) can be influenced by adjusting th

175 l and analytical approaches to mimic in vivo drug exposure in an effort to provide insight into mecha

176 aluate the safety of in utero antiretroviral drug exposure in children not infected with human immuno

177 amined the relationship between nitrosatable drug exposure in conjunction with dietary nitrite intake

178 red monthly and ensure optimal and prolonged drug exposure in HIV target tissues.

179 ents, 30% higher doses are required to match drug exposure in HIV-negative patients.Conclusions: Weig

180 analysis of successful target coverage after drug exposure in human SSc, and conduct of biomarker-dri

181 Dose-related drug exposure in monkeys was established and renal trans

182 profound implications for the prediction of drug exposure in patients with compromised hepatic P450

183 In this Review, we discuss representation of drug exposure in pharmacoepidemiological investigations

184 ac cells in response to Blebbistatin and ATP drug exposure in real tme.

185 ects in infants with in utero antiretroviral drug exposure in the French Perinatal Cohort.

186 ze therapeutics and formulations to increase drug exposure in the gastrointestinal lumen, enterocytes

187 tered metformin pharmacokinetics and reduced drug exposure in the heart.

188 This study suggests that drug exposure in the large intestine is essential for ge

189 y applied to investigate liver damage due to drug exposure in toxicology.

190 t and assay in the same buffer to sequential drug exposure in treatment buffer, centrifugal separatio

191 long intracellular half-life of TFV and high drug exposure in vaginal tissues, we hypothesized that a

192 and measured ring-stage survival rates after drug exposure in vitro; these rates correlate with paras

193 ook subgroup analysis based on antiepileptic drug exposure in women with epilepsy.

194 District of Columbia, was queried for single drug exposures in individuals 12 years and older during

195 CFZ and MFX had higher drug exposures in lesions compared to plasma (median RPL

196 ic parameters of piperaquine result in lower drug exposures in small children after a standard mg per

197 , we identified 399 drugs used and 1,525,739 drug exposures in the first 28 postnatal days.

198 re we demonstrate that chronic antipsychotic drug exposure increases nuclear translocation of NF-kapp

199 Thus, paternal drug exposure induces a protective phenotype in offsprin

200 Drug exposure inducing epigenetic changes in neurons in

201 files were designed to precisely lead to the drug exposure intended by clinicians.

202 vivo response, specifically whether systemic drug exposure is crucial for in vivo efficacy.

203 When drug exposure is paired with a specific environment, con

204 schizophrenia in vivo and that antipsychotic drug exposure is unlikely to account for them.

205 shown highly promising clinical results with drug exposure largely maintained over months after a sin

206 Preclinical data suggest that drug exposure levels are a key determinant of proposed d

207 To control channel states during drug exposure, lidocaine was applied with rapid-solution

208 y cancer trials, especially trials assessing drug exposure, makes much knowledge on the interaction o

209 and safety of therapy, optimizing individual drug exposure may improve these outcomes.

210 mpening cortical control over the NAc during drug exposure may lead to long-term changes in the abili

211 ion toward environmental challenges (stress, drug exposure, medication) in children affected by in ut

212 Reduced drug exposure might lessen the possibility of drug-relat

213 Before protracted drug exposure, most rats prefer natural rewards, such as

214 A high drug exposure NOEL on oral dosing in the rat suggested t

215 ve activity, increases brain and spinal cord drug exposure of intrathecally administered drugs in mic

216 tion, we investigated the effect of prenatal drug exposure on global motion perception, a behavioural

217 fter prolonged abstinence from noncontingent drug exposure or drug self-administration.

218 There was no evidence that prior drug exposure or duration of untreated psychosis correla

219 tance include prolonged or previous anti-CMV drug exposure or inadequate dosing, absorption, or bioav

220 commonly accompany aging, tinnitus, ototoxic drug exposure or noise damage.

221 rmalities are caused by the toxic effects of drug exposure, or the possibility that these may have pr

222 Slower plasma clearance and increased drug exposure over time of ALDC1 were observed compared

223 nd durable and greatly increased total tumor drug exposure over time.

224 n, little work has investigated how a single drug exposure paired with withdrawal influences catechol

225 Prenatal drug exposure, particularly prenatal cocaine exposure (P

226 survival analyses typically did not consider drug exposure, partly due to naming inconsistencies in t

227 ath, IC, and Candida colonization during the drug exposure period compared with infants given placebo

228 d Z-drug prescriptions were ascertained in a drug-exposure period 4-20 years before dementia diagnosi

229 individuals recruited for nonantiarrhythmic drug exposure phenotypes from October 5, 2012, to Septem

230 Further studies indicated that mismatched drug exposure profiles likely permitted induction of phe

231 Neuroinflammatory responses associated with drug exposure, proposed as one of the mechanisms contrib

232 Blood PHLDA3 mRNA expression correlated with drug exposure ( R(2) = 0.68; P < .001).

233 r phenotype that sustains them through early drug exposure, rare subclones acquire genetic changes th

234 l model that integrates temporal patterns of drug exposure, receptor occupancy, and signal transducti

235 Although drug exposure records are available in TCGA, existing su

236 aining medium spiny neurons (D2-MSNs) before drug exposure reduces the rewarding and psychomotor sens

237 he platform for drug assays employing cyclic drug exposure regimens.

238 Our results revealed common drug exposure-related connectivity disruptions within th

239 nts for these properties in order to predict drug exposure relative to solubility along the nephron.

240 exposure) and excess risk due to concomitant drug exposure (relative excess risk due to interaction [

241 nt is taking the medication correctly and if drug exposure remains stable.

242 ptic modifications in LHb neurons occur upon drug exposure remains, however, unknown.

243 In conclusion, substantially reduced drug exposure resulting from ADAs formation is associate

244 Drug exposure results in structural and functional chang

245 oximately 4 h) and safer (reducing hazardous drugs exposure risks) and to assess the oxaliplatin-spec

246 ncies in 331,414 women, those with antenatal drug exposure showed the greatest increased risks for al

247 afts (PDXs) established in mice and used for drug exposure studies.

248 al relationship between clonal evolution and drug exposure suggests that EPAG may promote expansion o

249 such as spatial-temporal synchronization of drug exposure, synergistic therapeutic effects and incre

250 nd, we found that, in vivo, a more prolonged drug exposure than anticipated was essential to derepres

251 es could achieve higher and/or longer plasma drug exposures than our previous lead and that one compo

252 ions are a serious unwanted manifestation of drug exposure that develops in a small percentage of the

253 However, over the course of drug exposure the control over drug seeking progressivel

254 Drug exposure (the area under the curve) was dose-depend

255 lag-censoring analysis (a measure of actual drug exposure), the relative hazard for fracture was 0.7

256 ed by 3 properties, namely the total days of drug exposure, the duration of the drug-free period afte

257 Over a median 24 months of study-drug exposure, the frequency of tubulopathy was 1.7% for

258 After long-term withdrawal of contingent drug exposure, the Pr was higher compared with i.p. inje

259 tion is complicated by multiple simultaneous drug exposures, the use of drugs with potent effects and

260 azid stress signature was induced by initial drug exposure, then disappeared after 4 days.

261 CANCE STATEMENT Over the course of addictive drug exposure, there is a transition in the control over

262 ics and effectiveness, and to improve tissue drug exposure through modulation of the cervicovaginal,

263 cer in a time-to-event analysis constraining drug exposure to 1 year before first cancer diagnosis an

264 techniques allow the response of a tumor to drug exposure to be more thoroughlyinvestigated.

265 dence has also indicated the possibility for drug exposure to even impact subsequent generations.

266 rgan transplant-specific thresholds of prior drug exposure to guide rational ganR-CMV testing in SOT

267 may be a balance between providing adequate drug exposure to inhibit human immunodeficiency virus (H

268 op an anti-Wolbachia chemotherapy by linking drug exposure to pharmacological effect.

269 er, recent data suggest that chronic (hours) drug exposure to phosphoinositide 3-kinase inhibitors us

270 Drug exposure to the posterior retina was 523,910 times

271 iotic concentrations while limiting systemic drug exposure to tolerable levels.

272 itro synergism and the challenge of matching drug exposures to obtain a synergistic outcome in vivo.

273 In contrast to platinum drugs, exposure to this organo-osmium compound does not

274 to perform PK/PD studies including humanlike drug exposures, to identify bactericidal and sterilizing

275 To assess causality from drug exposure, true predrug baseline imaging and neuroco

276 ast cancer, Z-endoxifen provides substantial drug exposure unaffected by CYP2D6 metabolism, acceptabl

277 lines and primary CML cells following acute drug exposure using intracellular fluorescence-activated

278 monitor cell stress and death dynamics upon drug exposure using simple electronic devices and, possi

279 ansplantation since infant immunosuppressive drug exposure via breastmilk is extremely low.

280 tive risk (incidence rate ratio [IRR] during drug exposure vs nonexposure) and excess risk due to con

281 ne, determining the consequences of repeated drug exposure warrants further study.

282 The median duration of study-drug exposure was 21.2 months in the cinacalcet group, v

283 At 36 months, prenatal antiepileptic drug exposure was associated with adverse development re

284 Drug exposure was determined based on prescriptions of n

285 Second, the lack of an isotope effect on drug exposure was evaluated in a monkey study by i.v. do

286 Avoralstat was well tolerated, and drug exposure was sufficient to meet target levels for i

287 egression with time-dependent covariates for drug exposures was employed to evaluate the association

288 ty in response to opioid and psychostimulant drug exposure; we further discuss how the understanding

289 tissue samples, and drug release and plasma drug exposure were higher for the original-dose than for

290 Cox regression models in which time-varying drug exposures were lagged by 1 year.

291 for the need to consider the history of past drug exposure when designing strategies to mitigate resi

292 icant increase (approximately 15% to 20%) in drug exposure when taken with food.

293 aptic mechanisms following acute and chronic drug exposure, which are part of brain-wide adaptations

294 t cancer S-phase entries would coincide with drug exposure, which is required for S-phase-dependent D

295 t is currently impossible to predict whether drug exposure will result in a health benefit, hypersens

296 he association of epilepsy and antiepileptic drug exposure with pregnancy outcomes needs to be quanti

297 no timeline was found for the association of drug exposure with the incidence in development of myelo

298 s evaluated, the method detected 19 distinct drug exposures with statistically significant, large rel

299 An oseltamivir dose of 3.0 mg/kg produced drug exposures within the target range in subjects 0-8 m

300 months of age, a dose of 3.5 mg/kg produced drug exposures within the target range.