ライフサイエンスコーパス: drug exposure

1 ward unfavorable environmental conditions or drug exposure.

2 clinical features known to increase edoxaban drug exposure.

3 plasma HIV RNA in individuals with adequate drug exposure.

4 and neuroadaptations occurring from repeated drug exposure.

5 s during pregnancy can reduce antiretroviral drug exposure.

6 ood vessels to improve tumor oxygenation and drug exposure.

7 onazole dose is required to achieve adequate drug exposure.

8 ociated with metabolic deficits and prenatal drug exposure.

9 particularly under conditions of suboptimal drug exposure.

10 or neuroadaptive changes following addictive drug exposure.

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

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

13 deleterious effects of repeated dopaminergic drug exposure.

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

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

16 s myopathy associated with elevated systemic drug exposure.

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

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

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

20 nes via an alternative nuclear receptor upon drug exposure.

21 water consumption patterns and nitrosatable drug exposure.

22 antidepressant-like responses 2 months after drug exposure.

23 ontext, suggesting a separate consequence of drug exposure.

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

25 linical records notes were used to determine drug exposure.

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

27 behavioral abnormalities seen with repeated drug exposure.

28 eorganization of the mesolimbic system after drug exposure.

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

30 bility of undetected schizophrenia predating drug exposure.

31 mood-related stimuli 24 h or 2 months after drug exposure.

32 incentive motivation is sensitized by prior drug exposure.

33 nce of drug-resistant clones after prolonged drug exposure.

34 onian syndromes and in some cases of illicit drug exposure.

35 nerally linking MRD eradication with greater drug exposure.

36 ill likely influence responses to subsequent drug exposure.

37 centrations of drug and a longer duration of drug exposure.

38 ued for at least 12 weeks to ensure adequate drug exposure.

39 g resistance-associated mutations before any drug exposure.

40 0.6 mg/kg were required to achieve adequate drug exposure.

41 cle function in mdx mice within 2-8 weeks of drug exposure.

42 of schizophrenia regardless of antipsychotic drug exposure.

43 sed during breastfeeding with minimal infant drug exposure.

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

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

46 pted chromosomal conformations shortly after drug exposure.

47 nces in susceptibility to propofol and track drug exposure.

48 drug concentrations and longer durations of drug exposure.

49 fect the occurrence of toxicities related to drug exposure.

50 eceptor availabilities determined before any drug exposure.

51 n six different murine tissues after chronic drug exposure.

52 acuity and stereoacuity were not affected by drug exposure.

53 nsults, particularly prior immunosuppressive drug exposure.

54 bacterial subpopulation tolerates prolonged drug exposure.

55 gh local tissue levels with minimal systemic drug exposure.

56 particular focus on the studies of maternal drug exposures.

57 3-AR agonists and thus have improved unbound drug exposures.

58 -based formulation for achieving efficacious drug exposures.

59 fectious anterior uveitis; evaluate systemic drug exposures.

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

61 ion Study, the authors examined nitrosatable drug exposure 1 month before and 1 month after conceptio

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

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

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

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

66 ous venovenous hemodialysis resulted in good drug exposure, achieved high peak concentrations to maxi

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

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

69 At higher drug exposures afforded by a new amorphous drug formulat

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

71 Drug exposure also drives the emergence of resistance.

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

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

74 responses to stress, it is unclear how such drug exposure alters the CRF modulation of excitatory sy

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

76 However, after adjusting for drug exposure and accounting for duration of therapy, on

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

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

79 ype was significantly associated with plasma drug exposure and clearance for efavirenz but not nevira

80 onor liver transplant (LDLT) patients on the drug exposure and clearance of tacrolimus is not known.

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

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

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 avioral adaptations associated with repeated drug exposure and highlight the utility of this approach

86 iogenic agents can be used to increase tumor drug exposure and improve therapeutic activity following

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

88 that accumulates in striatum after repeated drug exposure and mediates sensitized behavioral respons

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

90 nces, nootropic manipulations, teratological drug exposure and novelty seeking.

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

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

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

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

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

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

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

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

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

100 Structured treatment interruptions to reduce drug exposure and toxicity should not be used outside we

101 After adjusting for drug exposure and treatment duration, only decreases in

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

103 esistance to DAC could be rapidly induced by drug exposure and was related to a switch from heterozyg

104 elated: stress can promote drug-seeking, and drug exposure and withdrawal can increase activity in br

105 dopamine and norepinephrine signaling during drug exposure and withdrawal.

106 potentiation was achieved by similar overall drug exposure and without altering systemic toxicities.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 .7 microg/mL in normal brain, with the total drug exposure, as indicated by the tissue/plasma area un

127 in 90% confidence interval limits for total drug exposure (AUC(0-t) ) and peak concentration (Cmax)

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

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

130 s were significantly decreased after 24 h of drug exposure both in vitro and in vivo.

131 mission that is not detectable minutes after drug exposure but is fully expressed within 3 h.

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

133 They may increase with drug exposure, but probably do so only in individuals in

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

135 uced influx measured over the first 5 min of drug exposure by 81%.

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

137 or attribution of liver injury to a selected drug exposure by individual experts can be aided by care

138 Although previous drug exposure can enhance behavioral and neurochemical r

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

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

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

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

143 The identical procedures were used except drug exposure ceased on the cocaine-paired side during t

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

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

146 deferasirox had significantly lower systemic drug exposure compared with control patients (P < .00001

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

148 in vivo biomarker modulation and plasma free drug exposures consistent with dual FLT3 and Aurora kina

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

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

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

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

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

154 Tumor growth inhibition was dose and drug exposure dependent.

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

156 ations support the hypothesis that long-term drug exposure differentially alters A(2A)/D(2) receptor

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

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

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

160 Drug exposure during critical periods of brain developme

161 Drug exposure during critical periods of development is

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

163 is newborn was born to a mother who had many drug exposures during pregnancy.

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

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

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

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

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

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

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

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

172 Dysregulation of these systems by chronic drug exposure has been hypothesized to play a role in th

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

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

175 lex interactions among psychiatric symptoms, drug exposure history, and addiction vulnerability.

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

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

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

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

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

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

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

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

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

185 it increase the toxicity of chemotherapeutic drug exposure in mice.

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

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

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

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

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

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

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

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

194 ellular response to irradiation or cytotoxic drug exposure in vitro and clinical outcome.

195 ellular response to irradiation or cytotoxic drug exposure in vitro.

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

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

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

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

200 es within the population during intermittent drug exposure, including the emergence of multiple resis

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

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

203 Drug exposure inducing epigenetic changes in neurons in

204 Since foetal antiepileptic drug exposure is associated with lower verbal than non-v

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

206 y period after transplantation when adequate drug exposure is essential to prevent rejection.

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

208 striatal neurons after chronic dopaminergic drug exposure, is suspected to mediate these adaptive ch

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

210 related side effect in PS2-deficient mice at drug exposure levels resulting in a substantial decrease

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

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

213 We hypothesize that foetal drug exposure may alter normal cerebral lateralization.

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

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

216 Mdm2-mediated down-regulation of TopoII; on drug exposure, MDM2 bound to TopoII and resulted in decr

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

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

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

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

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

222 reased reliance on glucose, the influence of drug exposure on glucose homeostasis, myocardial glucose

223 male prairie voles to examine the effects of drug exposure on pair bonding and related neural circuit

224 dose-related effects of foetal antiepileptic drug exposure on verbal and non-verbal cognitive measure

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

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

227 of cocaine, varies depending on the stage of drug exposure or withdrawal and the cell population invo

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

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

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

231 Prenatal drug exposure, particularly prenatal cocaine exposure (P

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

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

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

235 Chronic drug exposure produced myeloma cell lines that were tole

236 ries of drug addiction propose that repeated drug exposure produces a long-lasting homeostatic dysreg

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

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

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

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

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

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

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

244 e neuroadaptations that occur with long-term drug exposure remain poorly understood.

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

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

247 characterized by delayed presentation after drug exposure, responsiveness to conventional ITP therap

248 ion, which is necessary to estimate systemic drug exposure resulting from this novel clinical approac

249 Drug exposure results in structural and functional chang

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

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

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

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

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

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

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

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

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

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

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

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

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

263 correlate gene expression changes caused by drug exposure to chronic toxicity are required.

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

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

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

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

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

269 n which homeostatic adaptations triggered by drug exposure to produce drug tolerance become counter-a

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

271 Single drug exposures to methiothepin or scopolamine did not no

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

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

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

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

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

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

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

282 Drug exposure was determined based on prescriptions of n

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

284 Increased cumulative drug exposure was related to regression of CIMT with nia

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

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

287 dds ratios for anencephaly with nitrosatable drug exposure were reduced among women who also took dai

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

289 ation of ERK2, CREB, and mTOR 2 months after drug exposure when compared with VEH-treated rats.

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

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

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

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

294 ing it possible to estimate the steady-state drug exposure with a single trough-level measurement.

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

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

297 nuated or exaggerated depending on stress or drug exposure, with cortisol levels generally expected t

298 ion occurred rapidly within several hours of drug exposure, with O(2)(-) and H(2)O(2) accumulation ma

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.