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1 use, general drug use, and participation in drug treatment).
2 er clinical parameters (death by suicide and drug treatment).
3 itors, thereby promoting cell survival after drug treatment.
4 during acute infection, 7 and 28 days after drug treatment.
5 nd data analysis in CRISPR screens involving drug treatment.
6 -based whole-liver quantitative changes upon drug treatment.
7 effectively prevented by gene correction or drug treatment.
8 eir impact on therapeutic outcomes following drug treatment.
9 r cell pro-survival program responses during drug treatment.
10 that mimic those produced by antidepressant drug treatment.
11 llows cells to re-enter the cell cycle after drug treatment.
12 ts; neither were considered related to study drug treatment.
13 stratification of cell lines in response to drug treatment.
14 herapeutic agents for disease prevention and drug treatment.
15 key proteins and their cellular response to drug treatment.
16 netic diversity and improved adaptability to drug treatment.
17 ization and regulation of histone PTMs after drug treatment.
18 els with parasitemia and its clearance after drug treatment.
19 ing to its prognosis and further response to drug treatment.
20 of breast cancer patients to Vinca alkaloid drug treatment.
21 rescue of the Parkinson's phenotype through drug treatment.
22 l anticoagulant, and combined antithrombotic drug treatment.
23 de novo or were experimentally added before drug treatment.
24 might be able to better survive chemotherapy drug treatment.
25 gene expression assay, and hypoxia-targeted drug treatment.
26 rotein translation, which was exaggerated by drug treatment.
27 n predict clinical course and sensitivity to drug treatment.
28 e and transmission dynamics and responses to drug treatment.
29 predicts which cells will ultimately resist drug treatment.
30 eveloping in some populations after years of drug treatment.
31 st genetics to disease susceptibility and to drug treatment.
32 such as high-density asexual parasitemia or drug treatment.
33 untary movements (AIMs) after three weeks of drug treatment.
34 s persistent protection after termination of drug treatment.
35 forks that have undergone fork reversal upon drug treatment.
36 cells that proliferate in spite of cytotoxic drug treatment.
37 ype persists even when fission is induced by drug treatment.
38 major bleeding included events during study drug treatment.
39 and the impact of medical interventions like drug treatment.
40 target for the development of a translatable drug treatment.
41 - 0.12 to 0.12 +/- 0.06 (P = .04), following drug treatment.
42 cy of oncogenic pathways or sensitivity to a drug treatment.
43 creatitis (AP), a condition without specific drug treatment.
44 ged as a result of natural genetic drift and drug treatment.
45 ity of distinct cancer cells to anti-mitotic drug treatment.
46 acogenetic interactions between genotype and drug treatment.
47 donovani evolution in the ISC in response to drug treatment.
48 e biological system in response to, such as, drug treatment.
49 nge in (64)Cu-ATSM signal after redox-active drug treatment.
50 tal condition that currently has no specific drug treatment.
51 ir neural circuits over prolonged periods of drug treatment.
52 ct the response of tumor cells to a specific drug treatment.
53 ts during the acute attack and 42 days after drug treatment.
54 resolves following successful antimicrobial drug treatment.
55 cin, providing an epigenetic memory of prior drug treatment.
56 ent nuclear gene expression during genotoxic drug treatment.
57 egression and reverts acquired resistance to drug treatment.
58 to have less improvement with antipsychotic drug treatment.
59 the BCL-2 family of apoptotic proteins after drug treatment.
60 e and only five patients were withdrawn from drug treatment.
61 families of proteins present, regardless of drug treatment.
62 nduced pluripotent stem cells resulting from drug treatments.
63 cytic capabilities as compared to individual drug treatments.
64 sis in distant organs compared to individual drug treatments.
65 al properties and requires mutation-oriented drug treatments.
66 epilepsy either alone or as a complement to drug treatments.
67 tment, or for patients who are too frail for drug treatments.
68 Placebo compared with various experimental drug treatments.
69 lls derived from a wide range of cancers and drug treatments.
70 sympathetic activity and often resistance to drug treatments.
71 ficult, despite the availability of curative drug treatments.
72 es, genotypes, environmental conditions, and drug treatments.
73 to psychotherapy, rather than as stand-alone drug treatments.
74 eemergence of LF transmission after stopping drug treatments.
75 repair, and the efficacy of pharmacological drug treatments.
76 To date, there are no effective drug treatments.
77 with PDAC who may benefit by HSP90-targeting drugs treatment.
79 to quantify the effects on ER morphology of drug treatments, abiotic stress and over-expression of E
80 zo-1 fusion-defective mutants or after acute drug treatment accelerates actin-based wound closure.
81 cost varied between 266euro and 375euro, and drug treatment accounted for 42-55% of the costs, depend
85 y demonstrated that successful antipsychotic drug treatment alters resting-state functional connectiv
86 of a control group continuing antiepileptic drug treatment and a consistent definition of long-term
90 g, P < .01; n = 57), and by a combination of drug treatment and lifestyle interventions over 6 months
92 and growth/kill rates, we modeled long-term drug treatment and performed parameter sweeps to analyze
93 generation, we demonstrated that antithyroid drug treatment and targeting iodothyronine deiodinases (
94 an detect heterogeneous cellular response to drug treatment and that the sum of single cell AR activi
95 tion between the molecular states induced by drug treatment and the cellular phenotypes controlled by
96 expression noise is important for improving drug treatment and the performance of synthetic biologic
97 nisms could affect population survival under drug treatment and thereby explain observed discrepancie
98 h to decreased probability of survival under drug treatment and underestimation of mutation rates in
100 nse of individual patient-based organoids to drug treatments and find that temporally-modified drug t
101 we are to predict effectively the outcome of drug treatments and the development of abnormal phenotyp
102 fected mice with further accumulation during drug treatment, and exhibit a reversible transcriptional
103 vast amount of disease genomics, phenomics, drug treatment, and genetic pathway and uniquely reveale
106 h mutations accumulate are known from cancer drug treatment, and order constraints for species invasi
107 ophageal reflux disease, safety of long-term drug treatment, and questions regarding the durability a
109 mas, human cancer cell lines with or without drug treatments, and human breast and colon cancers.
111 auses malaria is not available, antimalarial drug treatments are critical in fighting the disease.
112 ential drawbacks and barriers to combination drug treatment as initial therapeutic strategy will also
116 rmacologically inhibited-remain sensitive to drug treatment, because new KRAS(G12C) is either not ava
118 f establishing receptor activation following drug treatment both in vitro and in vivo but also allows
119 activated fraction of cells diminishes upon drug treatment, but active cells appear unperturbed), ve
120 f the early ring-stage parasites can survive drug treatment by entering cell cycle arrest or dormancy
121 treatments and find that temporally-modified drug treatments can be more effective than constant-dose
122 ion in the immune system or heterogeneity in drug treatment, can impact within-host pathogen evolutio
123 cidence of malaria, coverage of antimalarial drug treatment, case fatality rate, and population distr
126 decreased in most settings, particularly in drug treatment centers and primary care settings, where
127 rtunity where CDDCs coexisted with voluntary drug treatment centres (VTCs) providing methadone in Mal
132 orted by the observation that an anti-formin drug treatment converts dextral snail embryos to a sinis
136 al lipidome during cellular infection and/or drug treatment could reflect a mechanism to fine-tune M.
138 ion of tumor hypoxia with the heme-targeting drug treatments create important opportunities for image
139 n increased chance of receiving antidementia drug treatment (DCM, 114 of 291 [39.2%] vs care as usual
140 BP control is the limited use of combination drug treatment, despite evidence of its superior ability
141 etween species in a manner that would render drug treatments developed in nonprimate species entirely
145 h a history of a long-term immunosuppressive drug treatment due to kidney transplantation and the sec
146 r D-cycloserine augmentation of psychotropic drug treatment each improved psychotic and mood symptoms
147 ro physiological models studying disease and drug treatment effects are urgently needed as more relev
149 o provide a deeper understanding of apparent drug treatment efficacy in preclinical NASH studies.
150 acquire resistance, they respond to initial drug treatment either by undergoing apoptosis ('addictio
151 n, barrier methods, and the costly antiviral drug treatments, eliminating or at least reducing recurr
152 triamcinolone acetonide (TAA) is one of the drug treatments employed to ameliorate the inflammation
156 odels and human disease, and associated with drug-treatment failures in Leishmania braziliensis and L
163 surveillance, advances in development of non-drug treatments for gastro-oesophageal reflux disease, s
166 naptic vesicle physiology, pathogenesis, and drug treatments for neuronal disorders where glutamate i
168 ting "driver" mutations that will respond to drug treatment from much more abundant but inconsequenti
169 hange to the cellular lipid composition with drug treatment; furthermore, this response is not caused
171 evaluate whether simultaneous or sequential drug treatment has maximal therapeutic efficacy, which i
172 cine has existed for TB for a century, while drug treatments have been available for over 70 years; d
174 mental stresses, disease progression, and/or drug treatment; however, most methods are limited by low
178 errin, was also significantly decreased upon drug treatment in MDA-MB-231 and MDA-MB-157 cells (P < 0
179 as enhanced apoptosis, compared with single-drug treatment in models of human and murine NPM1mut and
181 ing morbidity and mortality by rationalizing drug treatment in the critically ill is of paramount imp
185 histone modification analyses and epigenetic drug treatment in vitro We found that DNA methylation pa
189 nome-wide alterations in uracil pattern upon drug treatments in human cancer cell line models derived
190 Weight-control interventions, including drug treatment, in pregnant women who are obese or overw
192 for subtyping, alongside recommendations for drug treatment, including new development in the field,
193 hnology offers many possibilities to improve drug treatments, including with regard to drug pharmacol
194 constitutive heterochromatic regions, while drug treatment induced a shift of incorporated uracil to
196 e that persistent FOXM1 expression following drug treatment is a biomarker of resistance to PI3Kalpha
197 his axis, oxidative stress induced by cancer drug treatment is attenuated, leading to increased resis
198 unocompromised individuals, and no effective drug treatment is currently available for those who need
202 rgical intervention as an adjunct to medical drug treatment is required in certain circumstances.
203 ine health care settings, where adherence to drug treatment is unsupervised and therefore may be subo
205 trials have shown that a single-dose, triple-drug treatment (ivermectin with diethylcarbamazine and a
206 s typically terminated through antiepileptic drug treatment, leads to hippocampus dysfunction typifie
207 osure, indicating that brief pulses of daily drug treatment may be sufficient for long-term efficacy.
208 lar drug uptake, metabolism, and response to drug treatment may have profound effects on cellular sur
209 at has been learned in previous studies, and drug treatments may have differentially impacted finding
210 that a combination of this stimulation with drug treatment might be useful to treat memory impairmen
211 a that establishes a historic record of past drug treatments (mitochondrial memory) and renders the c
212 , we find the opposite at early times during drug treatment: most senescence-fated cells express much
213 10), TAC (n = 12), MET (metoprolol, positive drug treatment, n = 7) and XML (XML treatment, n = 14).
215 and activated by irradiation or chemotherapy drug treatment, NSC194598 inhibited p53 DNA binding and
222 l lobe are potential targets for symptomatic drug treatment of frontotemporal dementia and progressiv
223 with notable success, for decades focused on drug treatment of infected human populations, but a rece
224 PIM resistance engineered through prolonged drug treatment of MOLM16 cell lines and successfully val
229 andscape analysis, we examined the impact of drug treatment on the cellular environment at a genome-w
230 who have a specific history like a long-term drug treatment or a palpable tumour should be approached
233 llular differentiation status in response to drug treatments or genetic perturbations is crucial for
234 ons or activations that simulate knock-outs, drug treatments or over-expressions) can have over signa
235 e dopamine transporter rescued antipsychotic drug treatment outcomes, supporting the hypothesis that
236 parable growth curve for MCTS under constant drug treatment over 13 days with those treated for only
237 multivariable analysis, not having been in a drug treatment program in the past year was associated w
238 re not treated, 5 were discontinued from the drug treatment program or did not follow up after the ev
242 ntal illness, 44.85% of children who receive drug treatment receive benzodiazepines, tricyclic antide
244 rected medical therapy and other recommended drug treatment regimens, the reader is advised to follow
246 tes to predict patient-specific responses to drug treatments requires that they maintain inter-indivi
247 departments with harm reduction services and drug treatment resources offers an opportunity to impact
248 of those receiving triple-drug compared to 2-drug treatment respectively (P = .021); all resolved wit
249 Molecular dissection of the consequences of drug treatment revealed a critical role for CBP/p300 in
250 ulating ssd1Delta defects with combinatorial drug treatment selectively blocked proliferation of wild
251 istent with a palatability-selective effect, drug treatment selectively reduced the rate and regulari
252 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
258 ension, even when the latter is resistant to drug treatment, strategies to screen patients for PA ear
260 Here we probed the relationship of LRV1 to drug treatment success and disease in 97 L. braziliensis
261 studies will be discussed, and combinatorial drug treatments targeting mu-ORs and specific PFC subcor
263 that cells grown in 3D are more tolerant to drug treatment than those grown in dispersion, but the m
264 esistance arises and the initial response to drug treatment that promotes cell survival is unknown.
265 ctious disease practice calls for aggressive drug treatment that rapidly eliminates the pathogen popu
266 dentified molecular mechanisms and potential drug treatments that merit further molecular and clinica
267 nsistent with this hypothesis, mutations and drug treatments that perturb dNTP pool levels disproport
268 ons in the probability that children receive drug treatments that raise a red flag when viewed throug
270 ly contained in most cases by antiretroviral drug treatment, there is no satisfactory treatment for t
271 tentially improve efficacy of new innovative drug treatments through effective patient selection, str
272 rts, indicating that resistant cells escaped drug treatments through one or more mechanisms leading t
273 e used the approach of removing infection by drug treatment to establish this and to understand the u
275 gime of limiting dilution at early stages of drug treatment to probe two antimalarial imidazolopipera
276 ling defects likely to require combinatorial drug treatment to suppress patient phenotypes and sympto
277 abolic regulators at points across 5 days of drug treatment to uncover a cell-state landscape with tw
278 ur system provides combinatorial and dynamic drug treatments to hundreds of cultures and enables real
280 tal manipulation of fatty acid metabolism by drug treatment turns a mouse into a cat in the "eye" of
286 dition, metabolic heterogeneity upon various drug treatments was also revealed and evaluated at the s
287 p21 dynamics before, during, and days after drug treatment, we link three distinct patterns of early
288 ichodysplasia spinulosa polyomaviruses after drug treatment were determined by immunoblotting, proxim
291 t had detrimental effects within 10 hours of drug treatment, whereas the effects of the other LRAs we
292 long-term infections that are refractory to drug treatment, which we refer to as 'persister-like cel
293 rsity analysis showed minimal changes due to drug treatment, which were transient and quickly returne
294 ed the testing of combining an antipsychotic drug treatment with a second psychotropic medication.
295 increased only in the presence of recent new drug treatment with antiepileptics or allopurinol, respe
296 atment for active tuberculosis (TB) requires drug treatment with at least four drugs over six months.
297 through CRISPR genomic alteration or through drug treatment with micelle encapsulated thiostrepton, l
299 r results indicate that supplementing annual drug treatments with "slash and clear" can significantly
300 understood to derive from cells that survive drug treatment without selection of genetically heritabl