ライフサイエンスコーパス: drug tolerance

1 stressful conditions like hypoxia and abets drug tolerance.

2 AD6 plays a universal role in platinum-based drug tolerance.

3 nd benefits, with important implications for drug tolerance.

4 suggesting a combination strategy to target drug tolerance.

5 tential role for microRNAs in such transient drug tolerance.

6 rinciples underlying the emergence of cancer drug tolerance.

7 the rate of decline slowed >94%, indicating drug tolerance.

8 echanism for the transient emergence of such drug tolerance.

9 ains and is implicated in macrophage-induced drug tolerance.

10 s verapamil at inhibiting macrophage-induced drug tolerance.

11 (TLS), and recombination each play a role in drug tolerance.

12 tal lesions, stimulate survival and increase drug tolerance.

13 e responses establish a mutation-independent drug tolerance.

14 raction correlated with an increase of assay drug tolerance.

15 ells, the phenomenon known as persistence or drug tolerance.

16 ic regulation of phenotypic heterogeneity in drug tolerance.

17 account the important intermediate stage of drug tolerance.

18 the slo K(+) channel gene and induces rapid drug tolerance.

19 gesting that membrane CHS may play a role in drug tolerance.

20 istinct ability of various opioids to induce drug tolerance.

21 at the next higher dose level depending upon drug tolerance.

22 reveals miR-371-3p as a potent suppressor of drug tolerance.

23 ors are related to their tendency to produce drug tolerance and dependence.

24 rther elucidate the biological mechanisms of drug tolerance and dependence.

25 oanatomical change accompanied by increasing drug tolerance and escalating intake, two behavioral par

26 ions are clinically latent, characterized by drug tolerance and little or no bacterial replication.

27 x pumps with verapamil reduces the bacterial drug tolerance and may enhance drug efficacy.

28 hose inhibition has the potential to prevent drug tolerance and persister formation.

29 into the vital role of RAD6/TLS in platinum drug tolerance and reveal clinical benefits of targeting

30 itioning, fear conditioning, aggression, and drug tolerance and sensitization.

31 MP dose intensity was a marker for drug tolerance and toxicities and was defined as prescri

32 o determined in healthy animals to establish drug tolerances and withdrawal times in diseased animals

33 g changes contribute to learning and memory, drug tolerance, and ischemic preconditioning.

34 ations triggered by drug exposure to produce drug tolerance become counter-adaptive after drug cleara

35 s a key target of miR-371-3p in establishing drug tolerance by regulating PLA2/PKCalpha activity and

36 ranscription of the nc-tgp1 lncRNA regulates drug tolerance by repressing the adjacent phosphate-resp

37 te that inhibiting a driver of MAPKi-induced drug tolerance could improve current approaches of targe

38 d phenotypes, such as body mass index (BMI), drug tolerance, EEG patterns, and externalizing traits,

39 These mechanisms can also reverse epigenetic drug tolerance following drug washout.

40 SCI rats manifested no drug tolerance following repeated bolus i.p. or chronic

41 While biofilm drug tolerance has been considered to be multifactorial,

42 Drug tolerance in bacteria is widely believed to be due

43 ine systemic infection model, and antifungal drug tolerance in C. lusitaniae.

44 epresents a new type of molecule influencing drug tolerance in eukaryotes.

45 We recently showed that drug tolerance in fission yeast Schizosaccharomyces pomb

46 Thus, transcription of an lncRNA governs drug tolerance in fission yeast.

47 gesting that it contributes to the burden of drug tolerance in human tuberculosis.

48 spring number of F0-daphnids and resulted in drug tolerance in the F1 generation.

49 he long-standing counter-adaptive theory for drug tolerance in which homeostatic adaptations triggere

50 Drug tolerance likely represents an important barrier to

51 A study in this issue of Cell reveals a drug tolerance mechanism in replicating mycobacteria tha

52 t activators, plays a role in the high-level drug tolerance of biofilms formed by Pseudomonas aerugin

53 ctivators that contributes to the high-level drug tolerance of Pseudomonas aeruginosa biofilms.

54 We evaluated strategies to improve drug tolerance of surface plasmon resonance (SPR) assays

55 lycol(PEG)-V-I-Adnectin and did not increase drug tolerance of the ADA assay.

56 Low pH increased drug tolerance of the assay relative to pH 7.4 but cause

57 eptors, could mitigate pain without invoking drug tolerance or dependence by stimulating cholinergic

58 It has been suggested that drug tolerance represents a form of learning and memory,

59 Persistence, manifested as drug tolerance, represents a significant obstacle to glo

60 er of an early non-mutational and reversible drug-tolerance state, which is induced by PAX3-mediated

61 sensitization is a strategy to safely induce drug tolerance to a specific drug to limit the possibili

62 noma inflammatory niches adapt to and confer drug tolerance toward BRAF and MEK inhibitors early duri

63 Drug tolerance was better among previously untreated pat

64 e redundancies can lead to poor efficacy and drug tolerance when addressing a single molecule.