戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 resistance may be attributable to antifungal drug tolerance.
2 enter a reversible nonproliferative state of drug tolerance.
3 establishes a paradigm for antimycobacterial drug tolerance.
4 teins (P-gps, ABCB1) with a putative role in drug tolerance.
5 ost stresses induced only limited Salmonella drug tolerance.
6 es in cancer are limited by cells exhibiting drug tolerance.
7 rapeutic promise by eluding the formation of drug tolerance.
8 ising strategy to overcome plasticity-driven drug tolerance.
9 apy need to be taken in context of patient's drug tolerance.
10  associated with side effects, addiction and drug tolerance.
11 olic interactions and gains in antimicrobial drug tolerance.
12 revents receptor internalization, leading to drug tolerance.
13  of M. tuberculosis could contribute to this drug tolerance.
14 d stress granule proteins that contribute to drug tolerance.
15  stressful conditions like hypoxia and abets drug tolerance.
16 AD6 plays a universal role in platinum-based drug tolerance.
17 e responses establish a mutation-independent drug tolerance.
18 reveals miR-371-3p as a potent suppressor of drug tolerance.
19 nd benefits, with important implications for drug tolerance.
20  suggesting a combination strategy to target drug tolerance.
21 tential role for microRNAs in such transient drug tolerance.
22 rinciples underlying the emergence of cancer drug tolerance.
23  the rate of decline slowed >94%, indicating drug tolerance.
24 echanism for the transient emergence of such drug tolerance.
25 ains and is implicated in macrophage-induced drug tolerance.
26 s verapamil at inhibiting macrophage-induced drug tolerance.
27 (TLS), and recombination each play a role in drug tolerance.
28 tal lesions, stimulate survival and increase drug tolerance.
29 raction correlated with an increase of assay drug tolerance.
30 ells, the phenomenon known as persistence or drug tolerance.
31 ic regulation of phenotypic heterogeneity in drug tolerance.
32  account the important intermediate stage of drug tolerance.
33  the slo K(+) channel gene and induces rapid drug tolerance.
34 gesting that membrane CHS may play a role in drug tolerance.
35 istinct ability of various opioids to induce drug tolerance.
36 at the next higher dose level depending upon drug tolerance.
37 cells, which can promote metastasis and fuel drug tolerance.
38 supporting a role for biofilms in phenotypic drug tolerance.
39 iological parameters such as growth rate and drug tolerance.
40 and that biofilm formation can contribute to drug tolerance.
41 ree key mechanisms to treatment outcomes: 1) drug tolerance, 2) immune regulation, and 3) viral escap
42 role for non-genetic plasticity in transient drug tolerance(3) and the acquisition of stable resistan
43 e Mtb protein CinA as a major determinant of drug tolerance and as a potential target to shorten TB c
44 geting this convergence could overcome cross-drug tolerance and could emerge as a new paradigm in the
45 ors are related to their tendency to produce drug tolerance and dependence.
46 rther elucidate the biological mechanisms of drug tolerance and dependence.
47 portant for key biofilm processes, including drug tolerance and dispersion.
48 ess has been hampered by issues such as poor drug tolerance and drug resistance, several PI3K inhibit
49 oanatomical change accompanied by increasing drug tolerance and escalating intake, two behavioral par
50                        Thus, both phenotypic drug tolerance and genetic drug resistance are major obs
51  efflux pump inhibitors that inhibit in vivo drug tolerance and growth.
52 te the complex transcriptional regulation of drug tolerance and hypersusceptibility that cannot be ca
53 ribe the spectrum of changes associated with drug tolerance and inhibition of specific tolerant cell
54 ions are clinically latent, characterized by drug tolerance and little or no bacterial replication.
55 x pumps with verapamil reduces the bacterial drug tolerance and may enhance drug efficacy.
56 hose inhibition has the potential to prevent drug tolerance and persister formation.
57 phogenesis to enable invasive hyphal growth, drug tolerance and resistance, cell wall integrity, and
58  into the vital role of RAD6/TLS in platinum drug tolerance and reveal clinical benefits of targeting
59 itioning, fear conditioning, aggression, and drug tolerance and sensitization.
60 activity plays an important role in melanoma drug tolerance and the development of acquired resistanc
61           MP dose intensity was a marker for drug tolerance and toxicities and was defined as prescri
62 o determined in healthy animals to establish drug tolerances and withdrawal times in diseased animals
63 er cell dormancy characterised by anticancer drug tolerance, and activation of growth factor survival
64 y (noise), which contributes to bet-hedging, drug tolerance, and cell-fate switching.
65 e feed consumption, physiological responses, drug tolerance, and detection of low drug concentrations
66 g changes contribute to learning and memory, drug tolerance, and ischemic preconditioning.
67 luding energy metabolism, stress adaptation, drug tolerance, and microbial pathogenesis.
68 ting in unexpected difficulties with dosing, drug tolerances, and decreased patient compliance.
69  to identify compounds that block stress and drug tolerance, as opposed to traditional screens for co
70 ations triggered by drug exposure to produce drug tolerance become counter-adaptive after drug cleara
71 nts do not show canonical drug resistance or drug tolerance but instead shorten the post-antibiotic e
72 bolism is associated not only with transient drug-tolerance but also permanent drug-resistance, and s
73             Mechanistically, ASCL1 conferred drug tolerance by initiating an epithelial-to-mesenchyma
74 s a key target of miR-371-3p in establishing drug tolerance by regulating PLA2/PKCalpha activity and
75 ranscription of the nc-tgp1 lncRNA regulates drug tolerance by repressing the adjacent phosphate-resp
76 te that inhibiting a driver of MAPKi-induced drug tolerance could improve current approaches of targe
77 o elucidate the mechanisms underlying opiate drug tolerance, dependence, and addiction.
78 d phenotypes, such as body mass index (BMI), drug tolerance, EEG patterns, and externalizing traits,
79                           Cells that acquire drug tolerance exhibit a more neuronally differentiated
80 nt by increasing metabolic heterogeneity and drug tolerance, facilitating drug resistance.
81 These mechanisms can also reverse epigenetic drug tolerance following drug washout.
82                       SCI rats manifested no drug tolerance following repeated bolus i.p. or chronic
83 ause of their association with analgesia and drug tolerance, GIRK channels and receptor internalizati
84                                While biofilm drug tolerance has been considered to be multifactorial,
85                                              Drug-tolerance has emerged as one of the major non-genet
86 utations, reversible mechanisms that lead to drug tolerance have emerged.
87        While there is evidence of concurrent drug tolerance, immune regulation, and viral escape, the
88  activity were shown to revert mycobacterial drug tolerance in an in vitro M. tuberculosis biofilm mo
89                                              Drug tolerance in bacteria is widely believed to be due
90 hat macrophage internalization induces cidal drug tolerance in C. glabrata, expanding the persister r
91 ine systemic infection model, and antifungal drug tolerance in C. lusitaniae.
92 o biologics and chemotherapy agents, monitor drug tolerance in desensitisation, and predict and addre
93 epresents a new type of molecule influencing drug tolerance in eukaryotes.
94                      We recently showed that drug tolerance in fission yeast Schizosaccharomyces pomb
95     Thus, transcription of an lncRNA governs drug tolerance in fission yeast.
96 gesting that it contributes to the burden of drug tolerance in human tuberculosis.
97 orylation, which are critical for sustaining drug tolerance in leukemia cells.
98 rogeneous and context-specific mechanisms of drug tolerance in lung cancer that could lead to the dev
99 f genetically encoded but rapidly reversible drug tolerance in M. tuberculosis caused by transient fr
100                                  MAF induced drug tolerance in Mtb, remodeled its transcriptome, and
101                           We aimed to target drug tolerance in order to delay the development of acqu
102 sis isolates, we assessed macrophage-induced drug tolerance in strains from lineages 1-3, representin
103 ds was less impacted, supporting an enhanced drug tolerance in the 3D microenvironment.
104 spring number of F0-daphnids and resulted in drug tolerance in the F1 generation.
105 he long-standing counter-adaptive theory for drug tolerance in which homeostatic adaptations triggere
106                                              Drug-tolerance in Mycobacterium tuberculosis (Mtb) may d
107 analyses revealed that a further increase in drug tolerance is achieved by structural evolution of ec
108                            We show that this drug tolerance is associated with non-proliferation and
109  of evidence suggest that macrophage-induced drug tolerance is mediated by mycobacterial drug efflux
110                                              Drug tolerance likely represents an important barrier to
111 that affords bacterial adhesion-cohesion and drug tolerance, making them difficult to treat using con
112      A study in this issue of Cell reveals a drug tolerance mechanism in replicating mycobacteria tha
113                            Here, we report a drug tolerance mechanism regulated by the germ-cell-spec
114 t activators, plays a role in the high-level drug tolerance of biofilms formed by Pseudomonas aerugin
115 ctivators that contributes to the high-level drug tolerance of Pseudomonas aeruginosa biofilms.
116           We evaluated strategies to improve drug tolerance of surface plasmon resonance (SPR) assays
117 lycol(PEG)-V-I-Adnectin and did not increase drug tolerance of the ADA assay.
118                             Low pH increased drug tolerance of the assay relative to pH 7.4 but cause
119 efficiency of magnesium without the risks of drug tolerance or addiction.
120 eptors, could mitigate pain without invoking drug tolerance or dependence by stimulating cholinergic
121                             Either long-term drug tolerance or viral escape (or some combination ther
122                   It has been suggested that drug tolerance represents a form of learning and memory,
123                   Persistence, manifested as drug tolerance, represents a significant obstacle to glo
124 t, because C. albicans can initiate a strong drug tolerance response that allows some cells to grow a
125 uely to them about exposures that may affect drug tolerance, safety, and effectiveness (eg, nonprescr
126 ne at position 37, but its role in promoting drug tolerance specifically depends on its mitochondrial
127 er of an early non-mutational and reversible drug-tolerance state, which is induced by PAX3-mediated
128                                          The drug tolerance study on BALB/c mice showed good toleranc
129 als fundamental insights into the biology of drug tolerance, the plasticity of cells through TKI trea
130 sensitization is a strategy to safely induce drug tolerance to a specific drug to limit the possibili
131 A) anticodon loop as essential for mediating drug tolerance to cytarabine and venetoclax (Ven) in acu
132 noma inflammatory niches adapt to and confer drug tolerance toward BRAF and MEK inhibitors early duri
133  that GlpK phase variation may contribute to drug tolerance, treatment failure, and relapse in human
134 etabolism studies suggest that CinA mediates drug tolerance via cleavage of NAD-drug adducts.
135                                              Drug tolerance was better among previously untreated pat
136 ecurrent emergence of prpR mutation-mediated drug tolerance was detected.
137 e redundancies can lead to poor efficacy and drug tolerance when addressing a single molecule.
138 induces icl1 expression which contributes to drug tolerance whereas blaI downregulates cydA, which co
139 tive features of either tumour initiation or drug tolerance within the same cancer population.

 
Page Top