ライフサイエンスコーパス: drug treatment

1 er clinical parameters (death by suicide and drug treatment).

2 major bleeding included events during study drug treatment.

3 and the impact of medical interventions like drug treatment.

4 netic diversity and improved adaptability to drug treatment.

5 target for the development of a translatable drug treatment.

6 cy of oncogenic pathways or sensitivity to a drug treatment.

7 creatitis (AP), a condition without specific drug treatment.

8 ization and regulation of histone PTMs after drug treatment.

9 ged as a result of natural genetic drift and drug treatment.

10 ity of distinct cancer cells to anti-mitotic drug treatment.

11 acogenetic interactions between genotype and drug treatment.

12 donovani evolution in the ISC in response to drug treatment.

13 els with parasitemia and its clearance after drug treatment.

14 e biological system in response to, such as, drug treatment.

15 topography, and consequently, the outcome of drug treatment.

16 ing to its prognosis and further response to drug treatment.

17 ect on diagnosis, diagnostic confidence, and drug treatment.

18 of breast cancer patients to Vinca alkaloid drug treatment.

19 tment rate and more intense antihypertensive drug treatment.

20 CA1 in response to individual or combination drug treatment.

21 ng of more than 1 million cancer cells under drug treatment.

22 rescue of the Parkinson's phenotype through drug treatment.

23 on with respect to both dose and duration of drug treatment.

24 that are known to be sensitive to anxiolytic drug treatment.

25 n-resistant cell line generated by long-term drug treatment.

26 1.3-fold changes, respectively, by day 5 of drug treatment.

27 NA (small interfering RNA) gene knockdown or drug treatment.

28 l anticoagulant, and combined antithrombotic drug treatment.

29 not cure HIV infection and requires lifelong drug treatment.

30 s in 2012, despite availability of effective drug treatment.

31 ections is poor due to the lack of effective drug treatment.

32 reported as possibly or probably related to drug treatment.

33 and drug resistance is often acquired after drug treatment.

34 increasing single-, mixed-, and alternating-drug treatment.

35 ately responding to chemodenervation or oral drug treatment.

36 e immune responses, and respond to antiviral drug treatment.

37 may influence susceptibility to disease and drug treatment.

38 y truncating the course of an infection with drug treatment.

39 failure of antiatrial fibrillation (anti-AF) drug treatment.

40 ts; neither were considered related to study drug treatment.

41 de novo or were experimentally added before drug treatment.

42 might be able to better survive chemotherapy drug treatment.

43 gene expression assay, and hypoxia-targeted drug treatment.

44 rotein translation, which was exaggerated by drug treatment.

45 n predict clinical course and sensitivity to drug treatment.

46 e and transmission dynamics and responses to drug treatment.

47 stratification of cell lines in response to drug treatment.

48 predicts which cells will ultimately resist drug treatment.

49 eveloping in some populations after years of drug treatment.

50 herapeutic agents for disease prevention and drug treatment.

51 st genetics to disease susceptibility and to drug treatment.

52 such as high-density asexual parasitemia or drug treatment.

53 untary movements (AIMs) after three weeks of drug treatment.

54 s persistent protection after termination of drug treatment.

55 forks that have undergone fork reversal upon drug treatment.

56 key proteins and their cellular response to drug treatment.

57 cells that proliferate in spite of cytotoxic drug treatment.

58 ype persists even when fission is induced by drug treatment.

59 to psychotherapy, rather than as stand-alone drug treatments.

60 e cells themselves, the microenvironment and drug treatments.

61 mited by scarcity of resources and effective drug treatments.

62 hen co-opted, enable cancer cells to survive drug treatments.

63 , as well as better access to effective, non-drug treatments.

64 trophil count at initiation, and concomitant drug treatments.

65 en into account when designing antimicrobial drug treatments.

66 ating the mechanism-based development of new drug treatments.

67 in response to hydroxyurea and various other drug treatments.

68 epilepsy either alone or as a complement to drug treatments.

69 ferent genes than under corresponding single-drug treatments.

70 of Chk1 in response to HU and various other drug treatments.

71 bjected inappropriately to potentially toxic drug treatments.

72 ory, and lipid-lowering and antihypertensive drug treatments.

73 tment, or for patients who are too frail for drug treatments.

74 Placebo compared with various experimental drug treatments.

75 lls derived from a wide range of cancers and drug treatments.

76 sympathetic activity and often resistance to drug treatments.

77 es, genotypes, environmental conditions, and drug treatments.

78 considered probably or definitely related to drug treatment; 16 in the alteplase group, five were con

79 Almost all patients received drug treatment: 86% used statins, 90% used antihypertens

80 cost varied between 266euro and 375euro, and drug treatment accounted for 42-55% of the costs, depend

81 levels significantly higher than individual drug treatments acting alone.

82 orogenic MMP sensor peptide to determine how drug treatment affects melanoma cell MMP activity in thr

83 ical health, and mental health predictors of drug treatment allocation.

84 Control of the HCV pandemic with drug treatment alone is likely to fail due to limited ac

85 y demonstrated that successful antipsychotic drug treatment alters resting-state functional connectiv

86 ent in hypertension awareness (63.6%-67.7%), drug treatment among those aware (84.5%-87.5%), and BP c

87 of a control group continuing antiepileptic drug treatment and a consistent definition of long-term

88 hotosensitization is a common side effect of drug treatment and can be associated with an increased s

89 ependent individuals in maintenance-oriented drug treatment and employment is recommended to achieve

90 s in stage distribution following stress and drug treatment and in vivo in identifying immature and m

91 common background findings, observed without drug treatment and independent of diet or glycemic statu

92 the importance of studying MMP activity with drug treatment and its possible implications for unwante

93 ydrogels to examine the relationship between drug treatment and MMP activity.

94 hypertension control program administration, drug treatment and monitoring costs, disease-related cos

95 s identified GxE interactions in response to drug treatment and pathogen exposure.

96 and growth/kill rates, we modeled long-term drug treatment and performed parameter sweeps to analyze

97 generation, we demonstrated that antithyroid drug treatment and targeting iodothyronine deiodinases (

98 an detect heterogeneous cellular response to drug treatment and that the sum of single cell AR activi

99 tion between the molecular states induced by drug treatment and the cellular phenotypes controlled by

100 The aged liver is more sensitive to the drug treatments and has a high probability of developing

101 odel could be used to develop more efficient drug treatments and may form a basis for modeling pathog

102 we are to predict effectively the outcome of drug treatments and the development of abnormal phenotyp

103 of elderly people for invasive procedures or drug treatments and would be the basis for a shift in th

104 We therefore changed the procedure from drug-treatment and assay in the same buffer to sequentia

105 diovascular Disease Policy Model to simulate drug-treatment and monitoring costs, costs averted for t

106 vast amount of disease genomics, phenomics, drug treatment, and genetic pathway and uniquely reveale

107 ophageal reflux disease, safety of long-term drug treatment, and questions regarding the durability a

108 (10.1%) to surgery alone, 2 (1.6%) to other drug treatments, and 14 (10.9%) to no treatment.

109 mas, human cancer cell lines with or without drug treatments, and human breast and colon cancers.

110 g-drug interactions, suboptimum adherence to drug treatments, and other factors.

111 concerns about medicalisation and overuse of drug treatments are paramount.

112 Drug treatments are unsatisfactory but surgery may hold

113 ta support a potential role for antifibrotic drug treatment as adjunctive therapy with ART to improve

114 here is no licensed RSV vaccine or effective drug treatment available.

115 highly malignant cancer, with resistance to drug treatment based on molecular- and tissue-scale char

116 f establishing receptor activation following drug treatment both in vitro and in vivo but also allows

117 activated fraction of cells diminishes upon drug treatment, but active cells appear unperturbed), ve

118 elay in nursing home placement with dementia drug treatment, but findings from a previous randomised

119 ects the ability of tumor cells to die after drug treatment, but the effect of autophagy may be to pr

120 f the early ring-stage parasites can survive drug treatment by entering cell cycle arrest or dormancy

121 cidence of malaria, coverage of antimalarial drug treatment, case fatality rate, and population distr

122 However, the drug treatment caused a striking bias of CD4 T cell diff

123 rtunity where CDDCs coexisted with voluntary drug treatment centres (VTCs) providing methadone in Mal

124 New drug treatments, clinical trials, and standards of quali

125 ar at 17 Bangkok Metropolitan Administration drug-treatment clinics.

126 nuclear localization of BRCA1 in response to drug treatment, cofactors binding and p53 phosphorylatio

127 Drug treatment comprised plasma-derived C1 inhibitor (pd

128 phosphoquantitation in response to multiple drug treatment conditions and using limited primary pati

129 RNA expression for twenty-nine genes in four drug-treatment conditions and in untreated controls.

130 Inadequate response to drug treatments constitutes a substantial unmet need in

131 ls without induced periodontitis and without drug treatment (controls).

132 orted by the observation that an anti-formin drug treatment converts dextral snail embryos to a sinis

133 ically approximately 6.5 hours after initial drug treatment, correlating with clearance of parasitemi

134 (RBC) deformability, caused by infection or drug treatment, could influence the pathophysiological o

135 As we found evidence for drug treatment counteracting the effects of IL-13 on the

136 n increased chance of receiving antidementia drug treatment (DCM, 114 of 291 [39.2%] vs care as usual

137 in animal disease models and in response to drug treatments, demonstrating the power of mass spectro

138 Growth conditions and drug treatments determine the partitioning of ribosomes

139 The drug treatment did not affect performance of the control

140 PDX cells that survived in vitro anti-cancer drug treatment displayed transcriptome signatures consis

141 h a history of a long-term immunosuppressive drug treatment due to kidney transplantation and the sec

142 ot reverse the beneficial effects of chronic drug treatment during CUS, nor have any effect on baseli

143 ro physiological models studying disease and drug treatment effects are urgently needed as more relev

144 Simulation of drug treatment effects by perturbing the inferred cell-s

145 ovide new insights into the heterogeneity of drug treatment effects.

146 nique for monitoring disease progression and drug treatment efficacy in vivo.

147 acquire resistance, they respond to initial drug treatment either by undergoing apoptosis ('addictio

148 tocking prawns, coupled with infrequent mass drug treatment, eliminates schistosomiasis from high-tra

149 triamcinolone acetonide (TAA) is one of the drug treatments employed to ameliorate the inflammation

150 s drug and its potential use in the targeted drug treatment era are discussed.

151 ly, tracking the progression of Pol II after drug treatment establishes Pol II elongation rates at ov

152 No specific drug treatment exists for MERS and infection prevention

153 Drug treatment experiments targeting HER2 and components

154 The association of LRV1 with clinical drug treatment failure could serve to guide more-effecti

155 everity in animal models and humans and with drug treatment failures in humans.

156 odels and human disease, and associated with drug-treatment failures in Leishmania braziliensis and L

157 ual toxic effects related to active targeted drug treatment for cancer.

158 oing to elucidate the optimal indication and drug treatment for children.

159 LOX and FU/FA groups, respectively, received drug treatment for metastatic disease.

160 Optimal drug treatment for patients with resistant hypertension

161 als for ALS have failed to generate improved drug treatments for ALS patients.

162 Overall medical drug treatments for concurrent diabetes, hypertension, h

163 surveillance, advances in development of non-drug treatments for gastro-oesophageal reflux disease, s

164 With a clear clinical need for new drug treatments for HAT that address both the hemolympha

165 Effective drug treatments for many psychiatric diseases are lackin

166 ive trait that might suggest novel, targeted drug treatments for these diseases.

167 Besides drug treatments for tuberculosis and diabetes, other int

168 hange to the cellular lipid composition with drug treatment; furthermore, this response is not caused

169 Drug treatment had no effect on either anxiety-like or d

170 evaluate whether simultaneous or sequential drug treatment has maximal therapeutic efficacy, which i

171 a invasiveness and metastasis in relation to drug treatment has not been developed.

172 cine has existed for TB for a century, while drug treatments have been available for over 70 years; d

173 Meta-analyses of blinded trials of non-drug treatments have not yet proven the efficacy of such

174 Beyond state-of-the-art drug treatment, healthy eating was associated with a low

175 onditions of stress (i.e., serum starvation, drug treatment, hypoxia).

176 hin 4 weeks of the start of antituberculosis-drug treatment in a specialist centre in Minsk, Belarus.

177 nnectivity predict response to antipsychotic drug treatment in acutely psychotic patients.

178 role, efficacy, and benefit of ET-A targeted drug treatment in cardiovascular disease.

179 Drug treatment in FRDA patients demonstrated increased F

180 re forms of leishmaniasis and relapses after drug treatment in humans.

181 errin, was also significantly decreased upon drug treatment in MDA-MB-231 and MDA-MB-157 cells (P < 0

182 e pulmonary vascular efficacy of any ongoing drug treatment in patients with PAH.

183 phorylated and inactivated after antitubulin drug treatment in taxol-resistant cancer cells.

184 isease samples and of molecular changes upon drug treatment in various disease models.

185 histone modification analyses and epigenetic drug treatment in vitro We found that DNA methylation pa

186 tastasis or heterogeneous tumor responses to drug treatment in vivo is difficult to achieve.

187 ion and reduced the IC50 of chemotherapeutic drug treatments in AML cells.

188 Testing potential drug treatments in animal disease models is a decisive s

189 D2R is a prominent target for drug treatments in disorders where dopamine function is

190 y explain why the virus is less sensitive to drug treatments in prolonged chronic HCV infections that

191 Weight-control interventions, including drug treatment, in pregnant women who are obese or overw

192 hnology offers many possibilities to improve drug treatments, including with regard to drug pharmacol

193 urring JCV sequence variation, together with drug treatment-induced cellular changes, may synergize t

194 his axis, oxidative stress induced by cancer drug treatment is attenuated, leading to increased resis

195 cal problem for which currently no effective drug treatment is available.

196 unocompromised individuals, and no effective drug treatment is currently available for those who need

197 Clinical response to antipsychotic drug treatment is highly variable, yet prognostic biomar

198 d is fibre-type independent, suggesting that drug treatment is modulating utrophin transcription in e

199 ts myeloma cell growth and their response to drug treatment is poorly understood.

200 of all human primary brain cancers, in which drug treatment is still one of the most effective treatm

201 quantify cell viability and its change under drug treatment is thus of significant importance in both

202 The relationship between MMP activity and drug treatment is unknown, and therefore we used an in s

203 ine health care settings, where adherence to drug treatment is unsupervised and therefore may be subo

204 ot have access to effective psychosocial and drug treatments is questionable.

205 s typically terminated through antiepileptic drug treatment, leads to hippocampus dysfunction typifie

206 imals with induced periodontitis and without drug treatment (LG); and 4) animals without induced peri

207 improvement in clinical status during study drug treatment (< 10% difference).

208 osure, indicating that brief pulses of daily drug treatment may be sufficient for long-term efficacy.

209 tion, which can potentially be influenced by drug treatment, may in part explain the heterogeneous cl

210 Additionally, upon chemotherapy drug treatment, miR-7 down-regulated p53-dependent apopt

211 to support diagnostic assays and methods for drug treatment monitoring.

212 10), TAC (n = 12), MET (metoprolol, positive drug treatment, n = 7) and XML (XML treatment, n = 14).

213 nzodiazepine), and no maternal depression or drug treatment (no exposure).

214 Drug treatment of diseases of the human nail remains a d

215 PIM resistance engineered through prolonged drug treatment of MOLM16 cell lines and successfully val

216 dala is implicated in the susceptibility and drug treatment of mood disorders.

217 zing early transcriptional changes following drug treatment of mutant EGFR-addicted cells, we identif

218 ll modern advances in medicine, an effective drug treatment of obesity has not been found yet.

219 ntravenous infusion every 3 weeks) or single-drug treatment of physician's choice.

220 patients that were modulated by combination-drug treatment of SS cells.

221 harmacological treatment, and to what extent drug treatment of the associated morbidities (e.g., diab

222 gnificant differences in MCTS diameter under drug treatment of varying duration.

223 eloped countries, but the impact of improved drug treatment on blood pressure (BP) control in the pop

224 ) determine the effects of key mutations and drug treatments on actin and regulator assembly.

225 who have a specific history like a long-term drug treatment or a palpable tumour should be approached

226 duals with diminished CCR2 responses (due to drug treatment or other reasons) may also be at risk of

227 he characterization of chromatin response to drug treatment or physiological processes.

228 ds for selective protein degradation require drug treatment or take hours for protein removal, limiti

229 es aimed at preventing virus growth, such as drug treatment or vaccination approaches, e.g., in HIV i

230 Here, we found that drug treatments or a genetic deficiency in the thioredox

231 ons or activations that simulate knock-outs, drug treatments or over-expressions) can have over signa

232 erventions for prevention and improvement of drug treatment outcomes have lagged behind.

233 parable growth curve for MCTS under constant drug treatment over 13 days with those treated for only

234 omized, and a 3-week wash out separated each drug treatment period.

235 ncludes rainfall and temperature covariates, drug treatment periods, and population variability is ca

236 e MI, younger age, depression, and a complex drug treatment plan are associated with lower medication

237 ailure were treatment history (antiepileptic drug treatment prior to randomisation), EEG result, seiz

238 or heroin (N = 10,784) at entry to 1 of 150 drug treatment programs in 48 states completed an anonym

239 Cellular stress induced by drug treatment promotes adaptation, which contributes to

240 osis rates of dementia and in the quality of drug treatment provided to those diagnosed.

241 Drug treatment providers should employ contingency manag

242 aroxysmal AF without previous antiarrhythmic drug treatment, radiofrequency ablation compared with an

243 The drug treatment reduced the total feed consumed per day,

244 sing disease progression and for stratifying drug treatment regimes.

245 o treatment regimens accounting for costs of drugs, treatment-related medical care, retreatment for i

246 nge their integrin repertoire in response to drug treatment renders this approach vulnerable to the d

247 Although drug treatment represents a confounding factor, ACVD sta

248 tes to predict patient-specific responses to drug treatments requires that they maintain inter-indivi

249 of those receiving triple-drug compared to 2-drug treatment respectively (P = .021); all resolved wit

250 Molecular dissection of the consequences of drug treatment revealed a critical role for CBP/p300 in

251 istent with a palatability-selective effect, drug treatment selectively reduced the rate and regulari

252 d participants at 12 National Health Service drug treatment services in the UK that provided opioid s

253 ate that the addition of small thiols to Mtb drug treatment shifted the menaquinol/menaquinone balanc

254 ecently, mesenchymal stem cells (MSCs) and a drug treatment stimulating endogenous stem cells (GM-CSF

255 the role of TIM in established and emerging drug treatment strategies may help provide rationales fo

256 utinib-resistant CLL cells may provide novel drug treatment strategies to overcome ibrutinib resistan

257 ing their unique properties when considering drug treatment strategies.

258 ng phenotype provides a valuable readout for drug treatment studies.

259 ement in quality of life is a good marker of drug treatment success and complete elimination of atria

260 Here we probed the relationship of LRV1 to drug treatment success and disease in 97 L. braziliensis

261 e to block virus assembly soon (<12 h) after drug treatment, suggesting that they rapidly engage with

262 studies will be discussed, and combinatorial drug treatments targeting mu-ORs and specific PFC subcor

263 altered allele, and it was activated only by drug treatments that derepress gene silencing by reversi

264 servations to recapitulate this effect using drug treatments that enhance the amplitude of EPSPs; how

265 nsistent with this hypothesis, mutations and drug treatments that perturb dNTP pool levels disproport

266 F-actin turnover via gene depletion or acute drug treatments that slow F-actin turnover destabilized

267 Following drug treatment, the H274Y resistance mutation fixed repr

268 ly contained in most cases by antiretroviral drug treatment, there is no satisfactory treatment for t

269 Before the availability of antimalarial drug treatment, there was evidence of concurrent 48-hour

270 rts, indicating that resistant cells escaped drug treatments through one or more mechanisms leading t

271 ed mouse skin cell proliferation, induced by drug treatment, through in vivo counting of the mitotic

272 ly affected in Alzheimer's disease (AD), and drug treatment to enhance cholinergic signaling is widel

273 patients who are most likely to benefit from drug treatment to prevent fracture.

274 gime of limiting dilution at early stages of drug treatment to probe two antimalarial imidazolopipera

275 siRNA modulation of profilin expression and drug treatments to interfere with actin dynamics.

276 fitness of individuals to using antiparasite drug treatments to test directly the consequences of inf

277 analyse data from a single experiment (e.g. drug treatment versus control), creating a need for comp

278 The median duration of drug treatment was 1.48 y (interquartile range 0.64-3.43

279 r, the response of cell viability during the drug treatment was able to be traced by the impedance me

280 Information on drug treatment was collected by the physician.

281 When drug treatment was combined with primary tumor resection

282 reatment period and rapidly disappeared when drug treatment was discontinued.

283 The response to drug treatment was evaluated by measuring plasma lactate

284 de, diagnostic confidence was estimated, and drug treatment was provided.

285 No drug treatment was significantly different from placebo

286 tween cell lines with respect to response to drug treatments, we generated gefitinib-resistant H1650

287 Heterogeneous cellular responses to drug treatment were also resolved in organoids.

288 Combinatorial drug treatments were able to abrogate ERK1/2 phosphoryla

289 Single drug treatments were cytostatic, but only DDP and PTX we

290 patients' exposure to the risks and costs of drug treatment when there is little prospect of long-ter

291 t had detrimental effects within 10 hours of drug treatment, whereas the effects of the other LRAs we

292 We also modified the internal cues using drug treatments, which modified the protrusion activity.

293 lthough the currently approved antipsychotic drug treatments, which primarily modulate dopaminergic f

294 ed the testing of combining an antipsychotic drug treatment with a second psychotropic medication.

295 e is moderate evidence to support initiating drug treatment with an angiotensin-converting enzyme inh

296 increased only in the presence of recent new drug treatment with antiepileptics or allopurinol, respe

297 The only safe drug treatment with substantial curative activity agains

298 n be used to predict complexome changes upon drug treatment with the example of bortezomib.

299 e majority, approximately 70%, of sequential drug treatments with 2-4 drugs promote resistance to the

300 burdensome long-term dietary exclusions, or drug treatments with uncertain efficacy or serious side-