ライフサイエンスコーパス: drug efficacy

1 seizures has changed minimally despite poor drug efficacy.

2 model ND diseases are discussed to evaluate drug efficacy.

3 rticles into the cytoplasm ultimately limits drug efficacy.

4 tory approval but may not accurately reflect drug efficacy.

5 lower disease risk factor levels and affect drug efficacy.

6 ory previously reported to result in reduced drug efficacy.

7 lly in fish and serve as a platform to study drug efficacy.

8 how that these models can effectively assess drug efficacy.

9 examining P. vivax liver stage infection and drug efficacy.

10 phenomenon that we suggest may contribute to drug efficacy.

11 omimetic systems to study cancer biology and drug efficacy.

12 g resistance that pose as major obstacles in drug efficacy.

13 test, suggesting an age-related decrease in drug efficacy.

14 overall survival benefit is needed to prove drug efficacy.

15 om gene overactivation and use it to predict drug efficacy.

16 f an in vivo human CF urine test to validate drug efficacy.

17 nvasive imaging of tumor pathophysiology and drug efficacy.

18 ection, and can be used to predict antiviral drug efficacy.

19 the bacterial drug tolerance and may enhance drug efficacy.

20 e often used to study cancer cell growth and drug efficacy.

21 ical mechanism contributes to antidepressant drug efficacy.

22 in some patients, without apparent change in drug efficacy.

23 ns could significantly enhance PI3K-targeted drug efficacy.

24 bitors and evaluate the apoptosis-associated drug efficacy.

25 ify the extent to which it inflates apparent drug efficacy.

26 function as a survival mechanism that limits drug efficacy.

27 phenotype was ameliorated in accordance with drug efficacy.

28 model systems for preclinical evaluation of drug efficacy.

29 e and well-controlled studies to demonstrate drug efficacy.

30 eatic tumor patients for early assessment of drug efficacy.

31 al model suited to evaluating antimetastatic drug efficacy.

32 e used as a surrogate marker of antiatheroma drug efficacy.

33 imes, decreasing drug dosages and increasing drug efficacy.

34 it cell-specific vulnerabilities for maximum drug efficacy.

35 for varied drug metabolism, which influences drug efficacy.

36 forth the possibility of improved antitumor drug efficacy.

37 as well as for the evaluation of antifungal drug efficacy.

38 n to disease outcome, and interpretations of drug efficacy.

39 ssessing disease progression, prognosis, and drug efficacy.

40 , treating autoimmune disease, and improving drug efficacy.

41 ns of the active forms of drugs, and thereby drug efficacy.

42 mistry and receptor conformation in defining drug efficacy.

43 intracellular delay and continuously varying drug efficacy.

44 armaceutical drugs correlate well with known drug efficacy.

45 seful model to predict subset assignment and drug efficacy.

46 xoid precursors for the purpose of improving drug efficacy.

47 to be only occasionally useful for studying drug efficacy.

48 nd these CRs may be the basis for changes in drug efficacy.

49 dentify complex causal mechanisms underlying drug efficacy.

50 bel claim affected physicians' beliefs about drug efficacy.

51 relevant in reducing standard antiepileptic drug efficacy.

52 strous cycle may underlie sex-differences in drug efficacy.

53 d targeted drug delivery, thereby increasing drug efficacy.

54 evelopment strategies, immune disorders, and drug efficacy.

55 gle-cell level are used as metrics to assess drug efficacy.

56 t the ITS force map can report anti-platelet drug efficacy.

57 owing accurate evaluation of antituberculous drug efficacy.

58 velopment, hampering predictions of clinical drug efficacy.

59 cts on host metabolism, which contributes to drug efficacy.

60 ce of inter-individual variability, impacted drug efficacy.

61 imicrobial in nature, they negatively affect drug efficacy.

62 nstrates how the model can be used to assess drug efficacy.

63 ermediate end point to assess renoprotective drug efficacy.

64 patients improve compliance and maximize the drug efficacy.

65 nity and drug residence time toward improved drug efficacy.

66 ant parameters for the prediction of in vivo drug-efficacy.

67 tease inhibitors are simulated using various drug efficacies.

68 primarily responsible for the differences in drug efficacies.

69 anding of the effects of gene alterations on drug efficacies.

70 type CEPs were defined for immunosuppressive drug efficacy (7 items) and for toxicity (15 items).

71 Anthelmintic drug efficacy (ADE) is generally estimated as a populati

72 nation with ivermectin would ensure improved drug efficacies against trichuriasis and strongyloidiasi

73 will greatly expand the ability to evaluate drug efficacy against gram-positive bacteria in living a

74 Studies of drug efficacy against IA and Aspergillus virulence rely

75 gh-throughput in vivo model for the study of drug efficacy against IA and Aspergillus virulence.

76 experiments are frequently used to determine drug efficacy against the survival and proliferation of

77 ssay has been optimized for determination of drug efficacy against two potentially pathogenic species

78 encing the great variation in toxicities and drug efficacy among individual patients.

79 HCV clinical trials, but large variation in drug efficacy among the various HCV genotypes has been d

80 ants who received at least one dose of study drug; efficacy analyses were by intention to treat.

81 ents who received at least one dose of study drug; efficacy analyses were done in all patients who re

82 macology approach to infer the combinatorial drug efficacies and synergy mechanisms through drug func

83 orm could provide both an early indicator of drug efficacy and a potential molecular stratifier for h

84 off-target sites, can translate to improved drug efficacy and a widened therapeutic window.

85 zation and internalization that depends upon drug efficacy and affinity.

86 were detected and potentially contribute to drug efficacy and cardiotoxicity.

87 accurate, time-dependent, live monitoring of drug efficacy and clearance in live tumors.

88 w that fa metrics may bias our assessment of drug efficacy and combination effectiveness.

89 us would be extremely valuable for assessing drug efficacy and could provide new pathophysiological i

90 clear condensates, providing new insights to drug efficacy and creating the opportunity for enhanced

91 otentially broad implications for bispecific drug efficacy and design.

92 s of determining the molecular substrates of drug efficacy and drug-induced adverse events.

93 one with cimetidine and vitamin E to enhance drug efficacy and frequent intramuscular administrations

94 randomized clinical trials can characterize drug efficacy and generate transcriptional, functional,

95 DR) is challenging due to the uncertainty of drug efficacy and heterogeneity of cancer patients.

96 anti-drug Abs (ADA) that may interfere with drug efficacy and impact patient safety.

97 metabolizing enzymes, resulting in decreased drug efficacy and increased resistance.

98 rst, combination drug regimens showed higher drug efficacy and less patient variation than single dru

99 nefits, allowing more accurate assessment of drug efficacy and more informed benefit-vs-risk decision

100 s, and is robust across several estimates of drug efficacy and of treatment cost.

101 the stability, and ultimately to ensure the drug efficacy and patient safety.

102 4-mediated drug metabolism, thereby reducing drug efficacy and potentially requiring dose adjustments

103 We incorporated published data on drug efficacy and probability of HIT-related thromboembo

104 cells and as a means of evaluating targeted drug efficacy and resistance in cancer cells.

105 compatible with long-term drug exposure for drug efficacy and resistance studies.

106 erstanding of mechanisms of antitrypanosomal drug efficacy and resistance will aid the rational desig

107 might pursue a more personalized approach to drug efficacy and risk.

108 , clinical trials should be designed to test drug efficacy and safety according to sex, age, reproduc

109 In the field of cardiac drug efficacy and safety assessment, information on drug

110 ibody (ADA) responses are a concern for both drug efficacy and safety, and high drug concentrations i

111 tical research: drug discovery and delivery, drug efficacy and safety, pharmacoepidemiology and drug

112 ein higher order structures needed to ensure drug efficacy and safety.

113 tionized drug delivery in terms of improving drug efficacy and safety.

114 reening, and function in cellular assays for drug efficacy and safety.

115 Additionally, it has been used to evaluate drug efficacy and selectivity, and to identify new targe

116 ndividual variations in the microbiome shape drug efficacy and side effect profiles.

117 nd understanding susceptibility to diseases, drug efficacy and side effects for different populations

118 howed robust and pervasive correlations with drug efficacy and side effects in both CATIE and STAR*D.

119 says for comprehensive prediction of in vivo drug efficacy and side effects represent an actual bottl

120 her disappointing results, with low, if any, drug efficacy and significant side effects.

121 eptor binding affinity is not a guarantee of drug efficacy and that other factors, including pharmaco

122 Therapeutic drug efficacy and tolerability of memantine have been at

123 ing effective antitumor drugs, and balancing drug efficacy and toxicity are discussed.

124 Short-term drug efficacy and toxicity data have previously been pre

125 lization of human-on-a-chip for testing both drug efficacy and toxicity in a single system.

126 ng major diseases and the molecular basis of drug efficacy and toxicity is a fundamental problem in m

127 ma proteins is of fundamental importance for drug efficacy and toxicity studies.

128 The relative strengths of drug efficacy and toxicity that vary in human population

129 of the human gastrointestinal microbiome on drug efficacy and toxicity, there is often an incomplete

130 ronidase inhibition, which may improve human drug efficacy and toxicity.

131 s) and off-target(s), providing evidence for drug efficacy and toxicity.

132 y genetic contributors to human variation in drug efficacy and toxicity.

133 and contribute to individual differences in drug efficacy and toxicity.

134 kers for disease diagnosis and for assessing drug efficacy and toxicity.

135 consequences for interpersonal variation in drug efficacy and toxicity.

136 om blood to the retina and thereby influence drug efficacy and toxicity.

137 interpret the growing compendium of data on drug efficacy and toxicology in patient populations.

138 analysis and offers a more direct measure of drug efficacy and treatment response, potentially provid

139 identify clinically meaningful predictors of drug efficacy and/or side-effect burden.

140 herefore be a novel determinant of antiviral drug efficacy, and could serve as a target for future an

141 ssment of immune response, immunosuppressive drug efficacy, and graft function as discussed on day 1

142 (ciprofloxacin, cefixime, and amoxycillin), drug efficacy, and IC(50).

143 for a number of protein substrates, monitor drug efficacy, and identify disease biomarkers in an ani

144 rance was therefore an unreliable measure of drug efficacy, and instead that human immunity is the pr

145 Results were sensitive to drug price, drug efficacy, and quality of life after successful trea

146 ll be deployed in future studies of disease, drug efficacy, and toxicity to discover and identify bio

147 ate the role played by virulence attributes, drug efficacy, and vaccine candidates.

148 st commonly used in studies of antipsychotic drug efficacy, antidepressant drug response, and drug-in

149 roBNP changes in response to therapy predict drug efficacy are needed.

150 cological optimization had limited impact on drug efficacy as the compounds retained IC(50) values at

151 e genome with disease risk, progression, and drug efficacy, as well as for admixture mapping.

152 mental tool in cancer research, diagnostics, drug efficacy assessment, and therapeutics owing to its

153 is (RA) would be useful for RA diagnosis and drug efficacy assessment.

154 The B+C approach had more drug efficacy at lower frequencies, underscoring potenti

155 come effects on healthy tissue and increases drug efficacy at the target site.

156 , which in turn will contribute to increased drug efficacy, avoidance of adverse effects, or repositi

157 bes Project Rephetio to systematically model drug efficacy based on 755 existing treatments.

158 arasite clearance) is an indirect measure of drug efficacy because of the persistence of unviable par

159 s H2009.1 targeted liposomes fail to improve drug efficacy because the liposome drug platform prevent

160 As testing for drug efficacy before providing treatment to malaria pati

161 lineate the genomic basis for differences in drug efficacy between black and white heart failure coho

162 activity, were also of potential concern in drug efficacy between the follow-on and innovator produc

163 500 cm(-1) band did not correlate well with drug efficacy but could indicate death initiation.

164 is not necessarily an indication of greater drug efficacy but rather an expected consequence of the

165 hat the viral decay rate depends not just on drug efficacy, but also on several viral infection param

166 folate transporter, RFC expression may alter drug efficacies by affecting cellular tetrahydrofolate (

167 to escort LAmB to APCs in vivo, enhanced the drug efficacy by 83% and drug APC targeting by 10-fold a

168 ored the possibility of using CLI to monitor drug efficacy by comparisons against PET.

169 n can help prevent adverse events or improve drug efficacy by enabling the physician to optimize dosa

170 nteractions of new drugs with DNA before the drug efficacy can be assessed in more expensive testing

171 Patients were monitored for drug efficacy, clinical benefit, and safety of DD.

172 In addition, drug efficacy correlated with the presence of G6 in the

173 ce over a wide range of treatment coverages, drug efficacies, costs of resistance, and mixing pattern

174 G(1) cell cycle arrest, and cell death, with drug efficacy dependent on the levels of phosphorylated

175 en, we were unable to detect any evidence of drug efficacy despite demonstration of target engagement

176 le under a wide variety of assumptions about drug efficacy, drug cost, and rates of cardiac and cereb

177 y system research for comprehensive study of drug efficacy, drug penetration, receptor targeting, and

178 ppropriate biomarkers that aide in assessing drug efficacy during clinical trials independent of clin

179 recently introduced the notion of a critical drug efficacy, epsilon(c), such that if overall drug eff

180 g efficacy, epsilon(c), such that if overall drug efficacy, epsilon(tot), is higher than the critical

181 athematical model that includes the critical-drug efficacy (epsilonc; the efficacy required for a dru

182 n between knockout phenotype and anticipated drug efficacy, establishing an important marker for supe

183 failure (recrudescence) and to adjust final drug efficacy estimates.

184 aintenance of plasma drug concentrations and drug efficacy for almost 3 weeks after a single dose.

185 appear to be clinically useful for comparing drug efficacy for the prevention of P. vivax infection r

186 hope it not only will support translation of drug efficacy from animal models to clinical trials but

187 ometry (qSCMS) methods to fully characterize drug efficacy from individual cells within cell populati

188 We investigated the possibility of assessing drug efficacy from measurements of plasma HIV-1 concentr

189 rate, so that it is not possible to extract drug efficacy from viral decay rate alone.

190 Anticancer drug efficacy has been tested on circulating tumor cells

191 ies involving the observation of MB-enhanced drug efficacy have been conducted on 2D monolayer cell c

192 recognized pharmacogenomic associations with drug efficacy have been further validated (e.g. with clo

193 gonist, have been discovered, but studies of drug efficacy have been hampered by the lack of a model

194 association between reporting CVD events and drug efficacy (hazard ratio: 0.68 vs. 0.67; p = 0.22).

195 y, epsilon(tot), is higher than the critical drug efficacy (i.e., epsilon(tot) > epsilon(c)) then vir

196 ination of IC50 values allowed us to compare drug efficacy in 2D and 3D culture models and moreover,

197 these animal models, additional evidence for drug efficacy in a human context might improve our chanc

198 al conditions cannot accurately reflect true drug efficacy in a patient, as a tumor is often under lo

199 are contemporary information on antimalarial-drug efficacy in all endemic regions so that decisions o

200 rial nucleotide metabolism genes that affect drug efficacy in C. elegans.

201 would be helpful in assessing antiarrhythmic drug efficacy in children, because their results may dif

202 Real-time monitoring of drug efficacy in glioblastoma multiforme (GBM) is a majo

203 rs may have very limited value in predicting drug efficacy in human disease.

204 of preclinical tests that accurately predict drug efficacy in humans.

205 ing noninvasive monitoring of c-Myc-targeted drug efficacy in intact cells and living mice.

206 points are available to delineate antifungal drug efficacy in non-Aspergillus invasive mold infection

207 Although comparisons of drug efficacy in nonrandomized studies should be viewed

208 inical determination of drug sensitivity and drug efficacy in nucleotide triphosphatases.

209 uency assessments are unreliable, studies of drug efficacy in panic disorder have generally used redu

210 ween Jan 1, 1960, and Jan 5, 2018, assessing drug efficacy in patients with uncomplicated P falciparu

211 inhibition could work in concert to enhance drug efficacy in response to food restriction.

212 and dopamine receptor 2 genes may influence drug efficacy in schizophrenia.

213 employed to generate mathematical models for drug efficacy in terms of measurable physical values.

214 ths were found to be the key factors for the drug efficacy in the 3D tumor model, governed by the Cu(

215 Optimization of drug efficacy in the brain requires understanding of the

216 toward predicting therapeutic mechanisms of drug efficacy in the setting of CPVT and then using thes

217 The implications of these results for drug efficacy in the treatment of individual patients wi

218 iduals have prevented us from achieving high drug efficacy in treating many complex diseases, includi

219 ry parameter because it can reliably predict drug efficacy in vivo.

220 Drug efficacy is a major target of beta1-AR voltage-depe

221 or Metastatic Prostate Cancer: Evaluation of Drug Efficacy is a randomized controlled trial using a m

222 al disease (MRD) as a marker of antileukemic drug efficacy is being used to assess risk status and, i

223 ic death rate of infected cells when overall drug efficacy is close to 1.

224 ing molecular biomarkers that predict cancer drug efficacy is crucial for the advancement of precisio

225 effects and real-time in situ monitoring of drug efficacy is highly desirable for personalized medic

226 Early assessment of antiretroviral drug efficacy is important for prevention of the emergen

227 These findings indicate that drug efficacy is increased when the subcellular site of

228 terestingly, our analysis uncovered that the drug efficacy is inferred from tissue intensity levels.

229 lines of evidence suggest that antipsychotic drug efficacy is mediated by dopamine type 2 (D(2)) rece

230 integration with other factors relevant for drug efficacy is poorly understood.

231 required to prevent a false conclusion about drug efficacy is presented.

232 nued high efficacy of praziquantel; however, drug efficacy is rarely monitored using appropriate stat

233 Similar to clinical observations, drug efficacy is variable across donors, even within the

234 The large change in drug efficacy linked to DNAJA1 suggests a personalized m

235 Antipsychotic drug efficacy may have decreased over recent decades.

236 rystal structure provides understanding of a drug efficacy mechanism related to the induction and sta

237 Anticancer drug efficacy might be leveraged by strategies to target

238 Although drug efficacy might not correlate with specificity, it w

239 D and 3D multiwell-multielectrode device for drug efficacy monitoring based on direct real-time imped

240 combinations using easily obtainable single drug efficacy, no detailed mechanistic understanding of

241 ave shown that it is possible to extract the drug efficacy of antivirals from the viral decay rate of

242 is study, to improve the tumor targeting and drug efficacy of the poorly water-soluble drug, doxorubi

243 and minimizes side effects while maximizing drug efficacy, offers a potential new approach for treat

244 ved in bone colonization and to rapidly test drug efficacies on bone micrometastases.

245 ble of real-time and continuous screening of drug efficacy on (cancer) cell subpopulations without th

246 hes with the aim of predicting the impact of drug efficacy on disease progression and the persistence

247 Therefore, trials that assess drug efficacy on exacerbations are done late in clinical

248 oward enabling the personalized screening of drug efficacy on individual patients' samples that poten

249 Enhanced drug efficacy on positively supercoiled DNA is due prima

250 etic mouse model may be useful in evaluating drug efficacy on schizophrenia vulnerability.

251 This technique showcases heterogeneity of drug efficacy on the single-cell level.

252 loss of free virus (P = .039) and decreased drug efficacy (P = .048), suggesting functional relevanc

253 (k(tau)), a biologically-meaningful kinetic drug efficacy parameter, by fitting time course data usi

254 We confirmed KinCon-based drug efficacy predictions for BRAF mutations other than

255 ant strains is widened for a higher level of drug efficacy provided that the treatment is not potent

256 two-stage phase II trial, accepting a target drug efficacy rate of 20% and a rejection error of 5%.

257 sharp band at 1000 cm(-1), gave the correct drug efficacy ratio as determined by the commonly used X

258 iffness to in vivo tumor growth kinetics and drug efficacy remains elusive.

259 s did not significantly inflate estimates of drug efficacy, reporting biases led to significant incre

260 es for cell phenotypic behaviors involved in drug efficacy responses.

261 improved drug delivery methods that increase drug efficacy, safety and patient compliance.

262 ical research and clinical trials to improve drug efficacy, safety and repurposing.

263 e results demonstrate that our network-based drug efficacy screening approach can reliably prioritize

264 ug discovery and provide novel platforms for drug efficacy screens.

265 luation of specific therapeutic targets, and drug efficacy.SIGNIFICANCE STATEMENT Understanding norma

266 n animals, CRD has been employed to evaluate drug efficacy, strain, sex or genetic differences and ch

267 Drug efficacy strongly depends on the presence of the dr

268 Current drug efficacy studies focus on reducing leukemia cell bu

269 the study of chronic biofilm infections and drug efficacy studies in vivo.

270 hough the World Health Organization clinical drug efficacy studies protocol does not permit classific

271 se devices in the drug discovery process and drug efficacy studies.

272 rther, we define and characterize a critical drug efficacy, such that for efficacies above the critic

273 trate the usefulness of our model/method for drug efficacy testing, we examined the effect of CTLA4-I

274 cer diagnosis, therapeutic applications, and drug efficacy tests.

275 circuit, are taken into account in deciding drug efficacy, thereby mapping each malfunction to an ap

276 tal study or broaden the generalizability of drug efficacy through a preplanned meta-analysis.

277 tter and more precise assessment of in vitro drug efficacy through the development of computational a

278 y with rate control and anticoagulation, but drug efficacy to control rate remains uncertain.

279 ct and real-time measurements of bevacizumab drug efficacy to the VEGF-VEGFR angiogenic switch in liv

280 sformative potential for in vitro testing of drug efficacy towards prediction of in vivo outcomes and

281 o disease sites significantly contributes to drug efficacy, toxicity and clearance.

282 of differences in incidence rates as well as drug efficacy, toxicity, and costs, the role of differen

283 ribe a systematic study of nitroheterocyclic drug efficacy using highly sensitive bioluminescence ima

284 to explore the possibility of extracting NAI drug efficacy using only the observed viral titer decay

285 Differences in drug efficacy using pooled binary endpoint hazard ratios

286 pan-cancer cell lines, accurately predicted drug efficacy using the driver genes and their seeded ge

287 Drug efficacy was assessed on a modified intention-to-tr

288 Decreased drug efficacy was due primarily to a drop in baseline (i

289 Drug efficacy was evaluated by retinal histologic analys

290 Drug efficacy was evaluated over 2 wk using (18)F-FDG sm

291 Drug efficacy was evaluated with magnetic resonance imag

292 However, drug efficacy was greatest in subjects with low Spd:Spm

293 ing seemed to reduce predicted toxicity, and drug efficacy was maintained.

294 urs of the boys' afternoon dose, testing for drug efficacy was performed by using objective measures

295 Drug efficacy was tested by measuring muscle strength ma

296 , even with the simplification of a constant drug efficacy, we show that the viral decay rate depends

297 oteins provides a new approach for improving drug efficacy while mitigating side effects.

298 Correct folding of a mAb is critical for drug efficacy, while misfolding can impact safety by eli

299 Measurement of antiplatelet drug efficacy with a point-of-care device and alternativ

300 netics are an important predictor of in vivo drug efficacy, yet the relationship between ligand struc