ライフサイエンスコーパス: single-drug

1 l antiangiogenic and antitumor strike with a single drug.

2 tance genes, each coding for resistance to a single drug.

3 ations may act as a more potent version of a single drug.

4 tration with drug combinations compared with single drugs.

5 ruton's tyrosine kinase inhibitor, has shown single-drug activity in relapsed or refractory B-cell ma

6 single-stranded oligonucleotide containing a single drug adduct at a T residue and to study its effec

7 that the study was based on deaths involving single drugs alone and changes in deaths involving presc

8 onth, 17.1% of all children were dispensed a single drug and 6.4% were dispensed two or more.

9 el, we predicted viability responses of many single drug and drug combinations in agreement with expe

10 nd compared them with patients allergic to a single drug and with healthy controls (HC).

11 profiles (exposure) observed in patients for single drugs and combinations, by evaluating exposure me

12 e relies largely on mass administration of a single drug, and the development of new drugs and vaccin

13 Currently, there is no single drug approved for the simultaneous treatment of b

14 be made a priority, as there is still not a single drug approved specifically for a nonclear cell in

15 nd may be beneficial even in tumors in which single drugs are inactive, as exemplified by the effect

16 tachycardia in infants can be refractory to single-drug as well as standard combination medical ther

17 orosis treatments are generally limited to a single drug at a fixed dose and frequency.

18 ries without low-income subsidies who take a single drug before and after the doughnut hole closes.

19 ping toxicity profiles so that doses of each single drug can be reduced below toxicity levels.

20 , a powerful tool to determine affinities of single drug candidates toward chosen targets, were recen

21 available, so the emergence of resistance to single drug classes and now multidrug resistance greatly

22 molecular interactions and properties within single drug classes are lacking.

23 articles published in symposia sponsored by single drug companies and articles from the parent journ

24 Symposia sponsored by single drug companies had more articles without methods

25 Articles in symposia sponsored by single drug companies were similar in quality and clinic

26 overage and demonstrate that even very small single-drug compartments lead to dramatically higher res

27 Although their single-drug components are well studied, the mechanisms

28 nation with first-line chemotherapy and as a single-drug continuation treatment for 18 cycles.

29 icacy, or augmented toxicity compared to the single drug counterparts.

30 el in which the frequencies of resistance to single drugs, cross-resistance, and epistasis combine to

31 Relaxation times for any single drug decrease with increasing tubulin concentrati

32 , but the proportion of children dispensed a single drug decreased (slope -.02%, p= .001).

33 Our study showed that a single drug delivery device loaded with a proprietary hy

34 els that were detectable after 16 hours of a single drug dose before any evidence of in situ cellular

35 ter six cycles of treatment, patients in the single-drug doxorubicin group were followed up expectant

36 d not improve overall survival compared with single-drug doxorubicin in patients with locally advance

37 rgistic combinations using easily obtainable single drug efficacy, no detailed mechanistic understand

38 itaxel (36- to 93-fold) was selected by this single drug exposure in all 9 stably resistant mutants.

39 stration, little work has investigated how a single drug exposure paired with withdrawal influences c

40 acokinetic parameters calculated following a single drug exposure.

41 nd the District of Columbia, was queried for single drug exposures in individuals 12 years and older

42 xy-Delta12,14-prostaglandin J2 compared with single drug exposures on the adenocarcinoma cell line A5

43 Single drug exposures to methiothepin or scopolamine did

44 the combined drug exposure, as compared with single-drug exposures.

45 and AG879, respectively, were compared with single drugs for inhibition of cell growth.

46 advantageous than a combination of targeted single drug formulations administered at the same drug r

47 ences of individual drugs between 3-in-1 and single drug formulations were eliminated.

48 was only one third of that achieved for the single drug formulations.

49 as optional crossover for patients in either single-drug group to receive combination treatment.

50 model in vivo than free DOX and GEM and the single drug HA conjugates.

51 Previous pharmacologic studies of single drugs have suggested that one factor contributing

52 Pharmacokinetic variability to a single drug in the regimen is significantly associated w

53 ic arterial and portal venous infusions of a single drug, in a cross-over fashion, at two dose rates

54 nce in Escherichia coli under selection with single drugs, including chloramphenicol, doxycycline and

55 Single-drug-induced and cross-reactive NSAID-Hs were pro

56 One simple reason why a single drug is indicated for so many age-related disease

57 Standard methodologies assume only a single drug is used, it acts only in its unconverted for

58 isease even with models developed based on a single drug known to treat the disease.

59 rs of 17-AAG were similar in both 3-in-1 and single drug-loaded PEG-b-PLA micelle formulations.

60 In contrast, when 3-in-1 and single drug-loaded PEG-b-PLA micelles were administrated

61 Single-drug maintenance after salvage therapy might be a

62 utations on the bacterial chromosome using a single drug marker.

63 A single drug, MCC-134, opens surface K(ATP) channels but

64 Outcomes were reported for 42 single-drug measures in the independent RCTs, with just

65 Binding of a single drug molecule is observed to cause a 2.4 A decrea

66 We hypothesized that a single drug molecule-a novel Toll-like receptor 9 (TLR9)

67 bility of MdfA to exchange two protons for a single drug molecule.

68 s (n=7), patients with hypersensitivity to a single drug (monoallergic, n=6), and healthy controls (H

69 t examined the effects of approximately 1300 single drugs on several human cancer cell lines.

70 eted dual-drug combination NPs over NPs with single drug or nontargeted NPs.

71 Within this group, selective responses to a single drug or responders to several APs may exist, sugg

72 disaggregated ES-2 tumor spheroids, whereas single drugs or 2-drug combinations only slowed growth o

73 ogue carrier and cytotoxic radical AN-201 as single drugs or as an unconjugated mixture) had no signi

74 iotic resistance under treatment regimens of single drugs or drug combinations.

75 In contrast to the limited efficacy of the single drugs, or any two drugs in combination, the three

76 The treatment relies on a single drug, praziquantel (PZQ), making the discovery of

77 eatment relies predominantly on the use of a single drug, praziquantel.

78 aimed to assess the efficacy and safety of a single-drug regimen with oral rivaroxaban compared with

79 l, toxic effects were tolerable with the two single-drug regimens.

80 Triple antithrombotic therapy emerged as the single drug-related predictor of GIB in addition to pati

81 rtant bacteria are characterized not only by single drug resistance but also by multiple antibiotic r

82 g selection and their rapid selection as the single drug resistance mutation during therapy with gefi

83 tment failure is caused by the fixation of a single drug resistance mutation.

84 lity at each sequence position suggests: (i) single drug resistance mutations are likely to occur at

85 so had equivalent potency against a panel of single-drug resistant strains of Mtb and remarkably sele

86 DR mutations rapidly became undetectable and single-drug-resistant (SDR) viruses emerged as minority

87 s are resolved by linearly interpolating the single drug responses, while for the antagonistic drug p

88 benznidazole-resistant clones derived from a single drug-selected population.

89 ical trials of patients with cancer assigned single-drug sorafenib at 400 mg twice daily with data on

90 Antiretroviral changes (single drug substitutions and regimen switches) limit tr

91 persaturation attained by dissolution of the single drug systems.

92 sed in doping control is more efficient than single drug target analysis (SDTA).

93 corresponded to patients' renin profile vs a single drug that corresponded to patients' age-race subg

94 ieving goal DBP (<90 mm Hg) in response to a single drug that corresponded to patients' renin profile

95 is the first biological treatment given as a single drug that has survival benefits in patients with

96 For single drugs, the best GEA method (Precision: .92/Recall

97 to be more effective in curing patients than single drugs, the impact of such treatments on the evolu

98 BQR was the most potent single drug: the 4.0 or 8.0 mg/kg/day BQR doses delivere

99 n sometimes treat recalcitrant diseases when single-drug therapies fail.

100 or additive antiviral effects compared with single drug therapy.

101 or hepatitis B surface antigen) compared to single drug therapy.

102 ADCT), and adequate empirical and definitive single-drug therapy (AESD, ADSD).

103 wledge of biochemical targets has brought to single-drug therapy and creates a statistical and experi

104 filing and age-race subgroup may help select single-drug therapy for stage 1 and stage 2 hypertension

105 not reduce the mortality risk compared with single-drug therapy in PA bloodstream infections.

106 lity testing is not routinely performed, and single-drug therapy is used for the treatment of most in

107 Single-drug therapy with paclitaxel or suramin did not r

108 (P<.001) significantly predicted response to single-drug therapy, whereas renin profile was of border

109 s, because they often have poor responses to single-drug therapy.

110 py is less likely to yield an advantage over single-drug therapy.

111 enously with chemotherapy and continued as a single drug thereafter (total 54 weeks).

112 tem is believed to belong to the category of single-drug transporters.

113 essed dose-dependent activity of rifampin in single-drug treatment during 3 weeks.

114 and potentiator activities may be useful for single-drug treatment of cystic fibrosis caused by Delta

115 0-min intravenous infusion every 3 weeks) or single-drug treatment of physician's choice.

116 ation was observed for rifampin after 3-week single-drug treatment.

117 Single drug treatments were cytostatic, but only DDP and

118 Responses to single-drug treatments were temporary, whereas combinati

119 in different genes than under corresponding single-drug treatments.

120 ects on strengthening muscles, compared with single-drug treatments.

121 ltiple drugs of abuse could be detected in a single drug user hair scan with confirmation of identity

122 stic combinations, most drugs average extant single-drug variations in therapeutic response.

123 ystemically trigger HIV-1 reactivation using single drugs were unsuccessful.

124 , or 150 mg/m(2)/d) administered as a 3-day, single-drug window before initiation of standard, multid

125 Thus, single drugs with durable antiviral activity can provide

126 tiple genes, each coding for resistance to a single drug, within a single cell.

127 herefore took an epigenetic approach where a single drug would simultaneously affect the expression o