ライフサイエンスコーパス: ADR

1 ADR and advanced-ADR were 33.00% (95% CI: 29.52-36.54) a

2 ADR efflux is greater in COX-2-overexpressing cells, whe

3 ADR nephropathy only occurs among specific mouse inbred

4 ADR was the primary strategy in 30% (n=88/292), of which

5 ADR-associated major events occurred in 3.4% (n=10/292).

6 ADRs were evaluated following EAACI guidelines.

7 erimental groups: Control (C), C+ADR, Dose 1+ADR, and Dose 2+ADR.

8 Both 5HT-1A and alpha(1b) ADR mRNA were highly expressed throughout the DR, and th

9 c cells expressed either 5HT-1A or alpha(1b) ADR mRNA.

10 c neurons also expressed 5HT-1A or alpha(1b) ADR mRNA.

11 ely, 5HT-1A, alpha(1b) adrenergic (alpha(1b) ADR), and corticotropin-releasing factor type 1 (CRF-R1)

12 Although the function of the alpha(1D) ADR in the dentate gyrus is not known, these data provid

13 straint stress-induced increase in alpha(1d) ADR mRNA expression in the dentate gyrus.

14 se or restraint, and the effect on alpha(1d) ADR mRNA expression in the hippocampus was determined by

15 have previously demonstrated that alpha(1d) ADR mRNA expression in the rat hippocampus is modulated

16 tress on hippocampal expression of alpha(1d) ADR mRNA has not been determined.

17 esulted in a rapid upregulation of alpha(1d) ADR mRNA in the dentate gyrus, with expression peaking a

18 : Control (C), C+ADR, Dose 1+ADR, and Dose 2+ADR.

19 rine) infusion at 320 ng kg(-1) min(-1) (320 ADR), and (2) with vagal blockade (2 mg atropine), befor

20 A-aDO2 increased by 6 +/- 2 mmHg during 320 ADR and by 5 +/- 2 mmHg during ATR + 80 ADR, and the cha

21 During 320 ADR cardiac output (QT) and pulmonary artery systolic pr

22 A-aDO2 increased by 12 +/- 7 mmHg during 320 ADR, and by 9 +/- 6 mmHg during ATR + 80 ADR, and the ch

23 A total of 432 ADRs in 133 (69%) patients were recorded, 64% local and

24 2.0; 95% confidence interval [CI], 1.5-2.7), ADR (RR, 2.0; CI, 1.1-3.4), and relapse (RR, 1.3; CI, .9

25 against MCF-7 and multi-drug-resistant MCF-7/ADR breast cancer cell lines and in a tubulin assembly a

26 inst the MCF-7 and multidrug-resistant MCF-7/ADR breast cancer cell lines and in an in vitro tubulin

27 n MCF-7 breast cancer cells but not in MCF-7/ADR breast cancer cells.

28 7 and its doxorubicin-selected variant MCF-7/ADR by either C/EBPbeta or C/EBPbeta-LIP (a dominant-neg

29 lues of 50 and 580 pM in the MCF-7 and MCF-7/ADR cell lines, respectively.

30 oxicity against MCF-7/ADR cells, lower MCF-7/ADR cell viability and higher apoptotic cells.

31 affect cytotoxicity against MCF-7 and MCF-7/ADR cells compared to the parent compound.

32 uced or undetectable in T47D/C4:2W and MCF-7/ADR cells with lost expression of ERalpha.

33 h the increase of cytotoxicity against MCF-7/ADR cells, lower MCF-7/ADR cell viability and higher apo

34 then characterized and incubated with MCF-7/ADR human breast cancer cells and followed by US exposur

35 doxorubicin in the multidrug resistant MCF-7/ADR xenografted nude mice.

36 istant (MDR) breast cancer cell lines (MCF-7/ADR).

37 n in the ER-negative variant of MCF-7, MCF-7/ADR.

38 ficantly increased; however, during ATR + 80 ADR only QT was significantly increased, yet blood flow

39 e infusion at 80 ng kg(-1) min(-1) (ATR + 80 ADR).

40 320 ADR, and by 9 +/- 6 mmHg during ATR + 80 ADR, and the change in calculated Q VA /QT was +2% in bo

41 320 ADR and by 5 +/- 2 mmHg during ATR + 80 ADR, and the change in calculated Q VA /QT was +2% in bo

42 to its intended pharmacologic target (type A ADR) or an unintended target (type B ADR).

43 in (P-gp and MRP1) and SN-38 (BCRP) in A2780/ADR (P-gp), H69AR (MRP1), and MDCK II BCRP (BCRP) cells.

44 provides a viable strategy to mitigate acute ADR induced cardiotoxicity.

45 Noradrenaline (NA) and adrenaline (ADR) effluxes were monitored from ex vivo adrenal medull

46 There were no differences in adrenaline (ADR) at rest or with heavy exercise, but the ArgArg grou

47 Adriamycin (ADR) is a commonly used chemotherapeutic agent that also

48 Adriamycin (ADR) is an anticancer agent that increases oxidative str

49 s against the DNA-damaging agent adriamycin (ADR) as a model for chemoresistance of SF/c-Met-overexpr

50 s such as ionizing radiation and adriamycin (ADR, a topoisomerase IIalpha inhibitor).

51 oteinuria, and renal fibrosis in adriamycin (ADR) nephropathy.

52 hemotherapeutic drugs, including Adriamycin (ADR).

53 odocyte number in the setting of Adriamycin (ADR)-induced nephropathy.

54 of MCF10A cells to cisplatin or adriamycin (ADR) induces recruitment of p14ARF into Rad6-p53 complex

55 Exposure of MCF10A cells to adriamycin (ADR) causes enhancement in the levels of RAD6B mRNA and

56 ucose (2-DG) in combination with Adriamycin (ADR) or paclitaxel in nude mouse xenograft models of hum

57 ADR and advanced-ADR were 33.00% (95% CI: 29.52-36.54) and 13.18% (95% CI

58 4, Wnt7a, Wnt7b, and Wnt10a expression after ADR accompanied these renoprotective effects of paricalc

59 s significantly improved cell survival after ADR treatment.

60 protection of DU-145 and MDCK cells against ADR (demonstrated using MTT (3-(4,5-dimethylthiazol-2-yl

61 anine kidney (MDCK) epithelial cells against ADR.

62 cIAP-2) contribute to the protection against ADR by HGF/SF.

63 NF-kappaB activity and SF protection against ADR, in a manner dependent upon its kinase and Src homol

64 ibutes to HGF/SF-mediated protection against ADR.

65 ADX-induced decrease in hippocampal alpha1d ADR mRNA, with the magnitude of effect depending on cort

66 r to determine whether expression of alpha1d ADR mRNA is influenced by circulating glucocorticoids, m

67 Levels of alpha1d ADR mRNA were profoundly decreased in hippocampal subfie

68 These data indicate that alpha1d ADR mRNA expression in the hippocampal formation is high

69 Although ADR is associated inversely with interval colorectal can

70 Although ADR is rare and declining in California, its costly cons

71 extends our knowledge on the interplay among ADRs and reveals their complexity in defense regulation.

72 he highest quintile ADR category (such as an ADR > 24.56%) decreased the adjusted hazard ratios for i

73 ly mild), and 78.9% and 48.1% experienced an ADR (mostly mild or moderate oral reactions).

74 METHODS AND Patients were selected if an ADR strategy was applied.

75 2-4.0), failure (3.7; 95% CI, 1.1-12.6), and ADR (10.0; 95% CI, 2.1-46.7) in arms with thrice weekly

76 mice were exposed to acute doses of ADR and ADR with mRQ.

77 on of actinomycin D abolishes both basal and ADR-induced RAD6B transcription indicating that ADR-indu

78 rk for enhancing the predictions of DDIs and ADR types by integrating drug-gene interactions (DGIs).

79 with both the glycolytic inhibitor 2-DG and ADR or paclitaxel results in a significant reduction in

80 NA depletion and recapitulated many MDDS and ADR injury phenotypes.

81 Nicotine (100 microM) evoked NA and ADR effluxes in control rats, and this response was abol

82 d to CIH, acute hypoxia evoked robust NA and ADR effluxes, whereas these responses were absent in con

83 nts were microbiologic failure, relapse, and ADR in patients on either DOT or SAT.

84 antly associated with failure of therapy and ADR in patients.

85 al efficacy [38.2%], inefficacy [26.5%], and ADRs [22.8%]).

86 discontinuation, followed by inefficacy and ADRs.

87 endoscopists (74.5%) increased their annual ADR category.

88 the whole data set to categorize the annual ADRs for each endoscopist.

89 st frequent serious cephalosporin-associated ADRs were Clostridium difficile infection within 90 days

90 Average ADRs increased significantly with screening experience (

91 (type A ADR) or an unintended target (type B ADR).

92 Immunologically mediated type B ADRs, such as drug hypersensitivity syndrome, drug react

93 at risk for immunologically mediated type B ADRs.

94 ose, reversed the oxidative damage caused by ADR, on both protein and lipid levels in all three organ

95 in glomeruli could be partially explained by ADR-mediated changes in GMC.

96 e inhibition of expression of these genes by ADR.

97 educed glomerulosclerotic lesions induced by ADR.

98 ave four experimental groups: Control (C), C+ADR, Dose 1+ADR, and Dose 2+ADR.

99 armacological, pharmacokinetic, and clinical ADR profiles of methylphenidate, aripiprazole, and rispe

100 The Controlled ADR (ie, combined CrossBoss-Stingray) subtype was applie

101 ined were microbiological sputum conversion, ADR, and relapse.

102 mple reports of thalidomide causing a deadly ADR when used against myeloma, a likely result of the di

103 elf-administered therapy (SAT) in decreasing ADR, microbiologic failure, and relapse in meta-analyses

104 ic administration of 2-deoxyglucose depleted ADR content in control rats, and CIH attenuated this res

105 0.2%-9.90%) vs 0.9% (95% CI, 0.4%-2.3%) for ADR, respectively.

106 r relapse .01 (95% CI, -.03 to .06), and for ADR 0.0 (95% CI, -0.01 to 0.01).

107 nonadherence is not a significant factor for ADR and that therapy failure only occurs after a large p

108 Incidence rates for ADRs causing hospital admission ranged from 0.4% to 10.3

109 erlying molecular mechanisms can emerge from ADR co-analysis.

110 se data suggest that COX-2 protects GMC from ADR-mediated apoptosis via transcriptional upregulation

111 Higher detectors had ADRs of 15% overall (men, 20%; women, 10%) and also dete

112 One strain was confirmed to have ADR, 2 were confirmed as causing exogenous reinfection,

113 n and control groups developed a hematologic ADR (7.4% vs 7.9%; relative risk, 0.93; 95% confidence i

114 ervention group (2.6%) developed hematologic ADRs compared with patients in the control group (22.9%)

115 there was a 10-fold reduction in hematologic ADRs among variant carriers who were identified and rece

116 outcomes were the occurrence of hematologic ADRs (leukocyte count < 3.0*10(9)/L or reduced platelet

117 the proportions of patients with hematologic ADRs during thiopurine treatment for IBD.

118 ly explained by an innovation effect (higher ADRs among incoming colonoscopists than among leaving co

119 ime incidence decreased with lower to higher ADRs (26.6; 95% CI, 20.0-34.3 for quintile 1 vs 12.5; 95

120 particularly interested in understanding how ADRs might be better detected, assessed and avoided.

121 Doxorubicin hydrochloride (ADR) is an anthracycline antibiotic used to treat variou

122 hree different types of immune response: (i) ADRs are required as "helper NB-LRRs" to transduce signa

123 ion during effector-triggered immunity; (ii) ADRs are required for basal defense against virulent pat

124 efense against virulent pathogens; and (iii) ADRs regulate microbial-associated molecular pattern-dep

125 of host genetics, microbes, and drugs in IM-ADR development; expand on the existing models of IM-ADR

126 lopment; expand on the existing models of IM-ADR pathogenesis to address multiple unexplained observa

127 cell-mediated and primary T cell-mediated IM-ADRs.

128 In ADR nephrotoxicity, a pathologic change in glomeruli cou

129 Compared with no increase in ADR, reaching or maintaining the highest quintile ADR ca

130 rease in RAD6 protein expression observed in ADR-treated cells is dependent upon transcription and de

131 The differences in ADRs were due to variation in performance of the endosco

132 Differences in ADRs were not explained by patient characteristics, inci

133 We observed a strong increase in ADRs from 2003 through 2012 in Germany.

134 Incident ADR was estimated to have ranged from 0.3% (95% confiden

135 The colonoscopy quality indicators including ADR were calculated, and patient factors associated with

136 An increased ADR was associated with an adjusted hazard ratio for int

137 An increased ADR was defined as an increase by at least 1 quintile ca

138 r Screening Program, we associated increased ADR with a reduced risk of interval colorectal cancer an

139 re used to evaluate the effects of increased ADR on the risk of interval colorectal cancer and death.

140 l cancer death, the effects of an increasing ADR have not been shown.

141 We investigated whether increasing ADRs from individual endoscopists is associated with red

142 esistant mouse strain to adriamycin-induced (ADR-induced) focal segmental glomerulosclerosis (FSGS).

143 e is extensive literature which investigates ADRs in children.

144 We successfully predict previously known ADRs for drugs prescribed to cutaneous diseases, and are

145 pharmacokinetics; and iv) DDIs without known ADRs.

146 d that induced COX-2 expression would lessen ADR nephrotoxicity.

147 avy exercise, but the ArgArg group had lower ADR with light exercise (P = 0.04).

148 itaxel-resistant Pgp-expressing tumor, Mam17/ADR.

149 d poly(ADP-ribose) polymerase (PARP) in MCF7/ADR cells, probably via activation of caspase-6, -7, and

150 ell cycle arrest in the G(2)/M phase in MCF7/ADR cells.

151 bserved after sangivamycin treatment of MCF7/ADR cells but not MCF7/WT cells.

152 ondria-mediated apoptotic cell death of MCF7/ADR cells via activation of JNK in a protein kinase Cdel

153 Transfection of MCF7/ADR cells with PKCdelta small interfering RNAs or PKCdel

154 Pretreatment of MCF7/ADR cells with SP600125, a specific inhibitor of JNK, or

155 Several features of T cell-mediated ADRs are strikingly similar to those displayed by patien

156 sing and searching predictive small-molecule/ADR connections.

157 Overall and monthly ADRs were compared using multivariable logistic regressi

158 Most ADRs are caused by drugs that form reactive species that

159 human ovarian adenocarcinoma cell line, NCI-ADR/Res (NAR), over expressing the targeted gene and pre

160 ion of the P-glycoprotein-overexpressing NCI-ADR-RES and Messa/Dx5MDR cell lines.

161 noma), MCF7 (human breast carcinoma) and NCI/ADR-Res (doxorubicin resistant and P-glycoprotein [Pgp]

162 6, IL-1F8, and IL-1F9 in both Jurkat and NCI/ADR-RES cells.

163 Pgp-mediated drug-resistant cells (i.e. NCI/ADR) and MRP1-mediated resistant cells (i.e. MCF-7/VP).

164 In NCI/ADR-RES cells, the three IL-1 homologs activated the MAP

165 ely, knockdown of endogenous testisin in NCI/ADR-Res ovarian tumor cells reduces PAR-2 N-terminal pro

166 = 0.0159 muM), ovarian cancer cell line NCI/ADR-RES (GI(5)(0) = 0.0169 muM), and renal cancer cell l

167 MCF-7, and an ovarian cancer cell line, NCI/ADR-RES, and by using genomic DNA as starting material.

168 In a mammary epithelial cell line, NCI/ADR-RES, which naturally expresses IL-1Rrp2, all three c

169 pressing multi-drug-resistant cell lines NCI/ADR-RES and Messa/Dx5.

170 tion was no different in the presence of NCI/ADR-Res cells expressing Pgp compared to MCF7 cells.

171 d A2780PAR) but not cisplatin-resistant (NCI/ADR-RES and A2780CP20) ovarian cancer cells.

172 ehavior of clones of multidrug-resistant NCI/ADR-RES breast carcinoma cells stably transfected with h

173 efficacy in nude mice bearing resistant NCI/ADR-RES tumors versus all control groups.

174 bine, vinblastine, and paclitaxel in the NCI/ADR-RES and Messa/Dx5 cell lines, which overexpress P-gl

175 A cytotoxicity assay with NCI/ADR-RES, a drug resistant cell line, suggested that PEG5

176 and are also able to identify promising new ADRs.

177 Rs) and 32 spontaneously reported nonserious ADRs were submitted, approximately half of which are ide

178 iated COX-2 expression, only 6.6 +/- 0.4% of ADR-treated cells underwent apoptosis.

179 Further analysis of ADR-induced p53 response showed that stable Rad6-p53-p14

180 e; or (d) mice treated with a combination of ADR + 2-DG.

181 implicate mtDNA damage in the development of ADR toxicity and identify Prkdc as a MDDS modifier gene

182 Healthy mice were exposed to acute doses of ADR and ADR with mRQ.

183 med an unbiased assessment of the effects of ADR-2, the only A-to-I editing enzyme in C. elegans, on

184 le maintaining or increasing the efficacy of ADR against cancer cell lines in vitro.

185 ance were associated with a low frequency of ADR.

186 The annual incidence of ADR declined over the study period.

187 ADR), and secular trends in the incidence of ADR were assessed.

188 All the animals received an injection of ADR, except half of the control group, which were given

189 regimens in patients, and expected rates of ADR, as well as a proposal of new susceptibility breakpo

190 r and varies by drug, as well as the type of ADR.

191 ngdom) aims to evaluate the value and use of ADR and determine its future position in contemporary ch

192 tudies reported rates ranging from 7%-98% of ADRs being either definitely/possibly avoidable.

193 , and illustrate how comparative analysis of ADRs can reveal underlying mechanisms.

194 nsidered a risk marker to the development of ADRs to immunotherapy.

195 cogenomics have been applied to the field of ADRs for both predictable ADRs and hypersensitivity drug

196 In postapproval experience, the frequency of ADRs spontaneously reported was less than 1 per 10,000 d

197 wer for every 5 percentage-point increase of ADRs and for mortality, 12.8% (95% CI, 11.1%-13.7%) lowe

198 sitized the patients and the total number of ADRs (P = 0.004) occurred locally (P = 0.003) and system

199 significantly improve the predictability of ADRs.

200 from a community-based health care system on ADR variation and cancer risk among 57,588 patients exam

201 longer survival) than the control, 2-DG, or ADR treatments (P < 0.0001).

202 iated with either microbiological failure or ADR in the clinic.

203 reventing microbiologic failure, relapse, or ADR, in evidence-based medicine.

204 Our ADR in both genders meets and exceeds the recommended co

205 Bail-out ADR strategies were successful in 63% (n=133/210).

206 ul restoration of drug sensitivity of OVCAR8/ADR cells to Pgp-transportable cytotoxic agents.

207 In 2012, overall ADR reached 31.3% and 20.1% in men and women, respective

208 onal criterion involving P-gp overexpressing ADR-RES cells.

209 ed to the field of ADRs for both predictable ADRs and hypersensitivity drug reactions.

210 g interactions (DDI) is necessary to prevent ADR, the rapid pace of drug discovery makes it challengi

211 a machine learning classifier to prioritize ADRs for approved drugs and pre-clinical small-molecule

212 t cardiomyocytes (H9C2) showed that RES:QUE: ADR at 10:10:1 ratio was synergistic in SKOV-3 cells and

213 reaching or maintaining the highest quintile ADR category (such as an ADR > 24.56%) decreased the adj

214 The adenoma detection rate (ADR) is an important quality indicator of screening colo

215 The adenoma detection rate (ADR) was 19.4%, with a higher rate in men (25.8% vs 16.7

216 mance is measured by adenoma detection rate (ADR).

217 ed to calculate the adenoma detection rates (ADR), and assess the quality of colonoscopies in an oppo

218 center variation in adenoma detection rates (ADRs) was observed in the U.K.

219 ity, as measured by adenoma detection rates (ADRs), varies widely among physicians, with unknown cons

220 efficacy, inefficacy, adverse drug reaction (ADR), and other medical causes.

221 Adverse drug reactions (ADRs) accounted for the majority of drug substitutions o

222 sly reported serious adverse drug reactions (ADRs) and 32 spontaneously reported nonserious ADRs were

223 LA associations with adverse drug reactions (ADRs) and one for the examination of infectious and auto

224 Adverse drug reactions (ADRs) are a central consideration during drug developmen

225 Adverse drug reactions (ADRs) are a relatively common cause of morbidity and mor

226 Immune-mediated (IM) adverse drug reactions (ADRs) are an underrecognized source of preventable morbi

227 Adverse drug reactions (ADRs) are commonplace and occur when a drug binds to its

228 Idiosyncratic adverse drug reactions (ADRs) are one of the most common causes of pharmaceutica

229 investigate whether adverse drug reactions (ADRs) during immunotherapy with a grass extract (AVANZ(R

230 Adverse drug reactions (ADRs) pose critical public health issues, affecting over

231 1 is associated with adverse drug reactions (ADRs), including hepatotoxicity; oxidative metabolism of

232 ts experienced minor adverse drug reactions (ADRs), of which 2 cases demonstrated flap necrosis.

233 incidence of serious adverse drug reactions (ADRs).

234 the investigators as adverse drug reactions (ADRs).

235 py because of severe adverse drug reactions (ADRs); leukopenia is one of the most serious ADRs.

236 alyzing sets of artifactual duplicate reads (ADRs), a known by-product of both sequencing platforms.

237 levels of the alpha(1D) adrenergic receptor (ADR) and we have previously demonstrated that alpha(1d)

238 alpha1d adrenergic receptor (ADR) mRNA is expressed at high levels in the hippocampal

239 ns of gene variants in adrenergic receptors (ADRs) with GAD, with the involvement of stressful events

240 pharmacogenomics and their role in reducing ADRs, especially those caused by drug hypersensitivity r

241 evices for antegrade dissection and reentry (ADR) of chronic total occlusions has improved historical

242 sing its importance; correlation of reported ADRs with public events, regulatory announcements, and w

243 stabilized monoubiquitinated p53 and rescued ADR-induced downregulation of Hdm2.

244 and suppression of acquired drug resistance (ADR) and informed predictions about optimal clinical dos

245 le of adherence in acquired drug resistance (ADR) and that very high levels of nonadherence are neede

246 lure, relapse, and acquired drug resistance (ADR) for 4 dosing schedules: daily throughout, thrice we

247 ing treatment, and acquired drug resistance (ADR) in patients with HIV and active tuberculosis.

248 cs associated with acquired drug resistance (ADR), and secular trends in the incidence of ADR were as

249 tures to ascertain acquired drug resistance (ADR).

250 ltidrug-resistant MCF7/adriamycin-resistant (ADR) human breast carcinoma cells, causing massive apopt

251 losporin-associated allergy, and all serious ADRs.

252 phalosporin-associated "allergy" and serious ADRs.

253 Twenty-five serious ADRs associated with 22 oncology drugs were identified a

254 ADRs); leukopenia is one of the most serious ADRs.

255 Five of the seven ADRs lacking PI changes occurred with off-label use, for

256 These revisions often differed for similar ADRs that occurred with drugs of the same class.

257 eaving colonoscopists, and relatively stable ADRs among continuing colonoscopists).

258 nce, and to identify an attainable, standard ADR to which endoscopists could aspire.

259 , further work is needed to address how such ADRs may be prevented.

260 Here it is demonstrated that ADR (also known as doxorubicin; 1 microg/ml) induced apo

261 -induced RAD6B transcription indicating that ADR-induced effects on RAD6B transcription result from a

262 This is the first study showing that ADR variants are susceptibility factors for GAD, further

263 These data suggest that ADR-induced degradation of Hdm2 occurs via the ubiquitin

264 The ADR for gastroenterologists was higher than for nongastr

265 The ADR technique was used in 23% (n=292/1253) of the RECHAR

266 The ADR types were adapted from a DDI corpus, including i) a

267 We assessed trends in the ADR in the first 10 years of the German screening colono

268 , outcomes, and low complication rate of the ADR technique and its subtypes confirm the benefit and v

269 Additional information relating to the ADR was collected: associated drug classification; clini

270 Starting with small or large tumors, the ADR + 2-DG combination treatment resulted in significant

271 The ADRs for gastroenterologists and nongastroenterologists

272 roach achieves an F-score of 0.87 across the ADRs classification using only the DDI features.

273 s been implicated in the pathogenesis of the ADRs.

274 the adr1 triple mutant, suggesting that the ADRs are required for TNL downstream signaling.

275 ing initiation with colonoscopy according to ADR quintiles (averages 15.3%, quintile 1; 21.3%, quinti

276 mber have been identified as contributors to ADR-induced injury.

277 vel of apoptosis in GMC that were exposed to ADR.

278 aling pathways for SF-mediated resistance to ADR.

279 ic RAD6B are significantly more resistant to ADR and cisplatin as compared to empty vector-transfecte

280 expression was induced early in response to ADR in mice and cultured human podocytes, and prevented

281 Here, we found that sensitivity to ADR nephropathy in mice was produced by a mutation in th

282 Many factors can contribute to ADRs, including genetics.

283 The degree to which genetics contributes to ADRs is not entirely clear and varies by drug, as well a

284 increased hazard of drug substitution due to ADRs.

285 ally lower rate of drug substitutions due to ADRs.

286 athioprine exhibited the highest DR owing to ADRs.

287 ine was associated with a higher DR owing to ADRs.

288 marked mtDNA depletion in renal tissue upon ADR treatment.

289 We used ADR quintiles in the whole data set to categorize the an

290 127 micelles (mRQ) when co-administered with ADR, will be cardioprotective in vitro and in vivo, whil

291 es indicated that mRQ did not interfere with ADR caspase activity in SKOV-3 cells but significantly d

292 between baseline isolates and isolates with ADR.

293 Concurrent administration of mRQ with ADR at 10:10:1 ratio provides a viable strategy to mitig

294 hemical estimations the presence of mRQ with ADR conferred full cardioprotection in these mice.

295 urrent dosing of these natural products with ADR is limited due to their low solubility, and low oral

296 a) untreated controls; (b) mice treated with ADR alone; (c) mice treated with 2-DG alone; or (d) mice

297 However, treatment with ADR or cisplatin is accompanied by a significant increas

298 y reported therapeutic class associated with ADRs in children admitted to hospital (17 studies; 12 st

299 were frequently reported as associated with ADRs in outpatient children (13 studies; 6 studies respe

300 utic classes most frequently associated with ADRs, further work is needed to address how such ADRs ma