ライフサイエンスコーパス: antifungals

1 tentially a powerful alternative to standard antifungals.

2 ally relevant C. albicans isolates against 4 antifungals.

3 . albicans lost dominance in the presence of antifungals.

4 development of more efficient broad-spectrum antifungals.

5 P5218 to be only a secondary target of azole antifungals.

6 se 2 is crucial for the development of novel antifungals.

7 resent a potential target for developing new antifungals.

8 m of action distinct from currently marketed antifungals.

9 as antitumor agents, immunosuppressants and antifungals.

10 ffered lumbar puncture (LP) and treated with antifungals.

11 validation of therapeutic efficacy of novel antifungals.

12 er assay was reduced in animals treated with antifungals.

13 here was no significant difference among the antifungals.

14 ceptibility to the triazole and echinocandin antifungals.

15 ty of 47 isolates of dermatophytes against 8 antifungals.

16 ion about their in vitro susceptibilities to antifungals.

17 da species were susceptible to the available antifungals.

18 -fold with no effect on sensitivity to other antifungals.

19 articularly in combination with conventional antifungals.

20 lobosa CYP51 was strongly inhibited by azole antifungals (0.15 to 0.35 muM).

21 who did not receive preventative mold-active antifungals (87.5%).

22 sistance to all currently available triazole antifungals after a course of FLC treatment.

23 We report the in vitro activities of eight antifungals against 64 Rhodotorula isolates collected in

24 ro antifungal susceptibility pattern of nine antifungals against a selected group of isolates.

25 veral of the newer triazole and echinocandin antifungals against isolates of C. dubliniensis.

26 ignaling and potentiates the activity of the antifungals amphotericin B and micafungin.

27 We also offer perspectives for the use of 2 antifungals, amphotericin B products and posaconazole, w

28 y utilized the model to test the efficacy of antifungals, analyze transcriptional patterns, and exami

29 A. fumigatus sensitive to the azole class of antifungals and a strain displaying an azole-resistant p

30 charomyces cerevisiae, LMP can be induced by antifungals and endoplasmic reticulum stressors when cal

31 The lack of a sufficient number of effective antifungals and our incomplete understanding of the path

32 rol 14alpha-demethylase (the target of azole antifungals) and a putative fatty acid metabolism protei

33 amilies of clinically important antibiotics, antifungals, and anticancer agents are actually present

34 , comorbidities, exposure to antibiotics and antifungals, and ICU factors such as total parenteral nu

35 ctor (VEGF) agents, antibiotics, antivirals, antifungals, and methotrexate.

36 s tested were susceptible to the majority of antifungals, and only flucytosine showed poor antifungal

37 ion to statins, our screen found that SERMs, antifungals, and several antipsychotic medications reduc

38 sceptibility testing was performed against 7 antifungals (anidulafungin, caspofungin, micafungin, flu

39 hey include antibiotics, immunosuppressants, antifungals, antihypercholesterolemics, and cytotoxins.

40 h intravaginal formulations of topical azole antifungals are first-line treatment for pregnant women,

41 Current commercially available antifungals are limited by their insufficient potency, s

42 ers who used systemic antibiotics or vaginal antifungals (aRR = 0.81, 95% CI 0.57, 1.14).

43 The FMICs of both antifungals, as measured by the DiOC6 membrane probe, sh

44 utline complexity in administering new azole antifungals, assisting in optimizing outcomes.

45 oven/probable IFI and no need for additional antifungals) at end of prophylaxis (EOP).

46 es the acquisition of resistance to multiple antifungals, at least partially explaining the elevated

47 ell survival in response to several clinical antifungals (azoles, allylamines, echinocandins) that ta

48 Most patients were treated with antifungals before presentation without resolution of ni

49 s were all susceptible in vitro to the azole antifungals, but had elevated MICs with caspofungin.

50 important, because treatment with imidazole antifungals can provide significant benefit.

51 Few antifungals can treat C. neoformans infections, and drug

52 ombine placebo-controlled and direct topical antifungals comparison trials.

53 tistically significant differences among the antifungals concerning the outcome of mycologic cure at

54 ndicated macrolide antibiotics and imidazole antifungals continues to occur.

55 re antifungals with placebo instead of other antifungals, conventional meta-analysis is insufficient

56 y relevant concentrations of 3 commonly used antifungals: fluconazole, caspofungin, and amphotericin

57 d be an important addition to our arsenal of antifungals for the treatment of invasive fungal disease

58 ndomized trials comparing the effect of >/=2 antifungals for treatment of IC.

59 The search for new molecular targets for antifungals has generated considerable research using mo

60 and the side effects of currently available antifungals have restricted their use as long-term proph

61 IRIS developed 2-12 months after starting antifungals in 8 patients, who presented with new/enlarg

62 Treatment consisted of surgery in 59% and antifungals in 87% of cases (liposomal amphotericin B in

63 antifungals in all patients and intravitreal antifungals in 9 eyes.

64 Initial treatment included systemic antifungals in all patients and intravitreal antifungals

65 The growing use of antifungals in prophylaxis and treatment influences whic

66 s have been avoided as adjunctive therapy to antifungals in the treatment of acute respiratory distre

67 conazole with placebo in addition to topical antifungals in the treatment of filamentous fungal kerat

68 nsitizes drug-resistant C. glabrata to azole antifungals in vitro and in animal models for disseminat

69 tion was detected in response to other azole antifungals, in related Candida species, and in an in vi

70 e found to be distinct from other classes of antifungals, including the azole drugs, pointing toward

71 ls and strategies that allow targeted use of antifungals is essential to preserve drug effectiveness.

72 Long-term use of systemic antifungals is not optimal due to emerging evidence of l

73 The most important group of antifungals is the azoles (e.g. miconazole), which act b

74 elvamicin resembles the clinically important antifungals nystatin A1 and amphotericin B, but it has s

75 the ability to monitor the effectiveness of antifungals on Histoplasma yeasts, the morphological for

76 Because of the different costs of the antifungals, pharmacoeconomic analysis is required to id

77 h significantly enhanced the activity of the antifungals posaconazole, amphotericin B, and caspofungi

78 With the introduction of new antifungals, rapid, accurate identification of pathogeni

79 alutamide, sedative dexmedetomidine, and two antifungals ravuconazole and posaconazole.

80 biofilm resistance and acts by sequestering antifungals, rendering cells resistant to their action.

81 often have prolonged or repeated exposure to antifungals resulting in either the well-documented sele

82 ts intrinsic or acquired resistance to azole antifungals such as fluconazole.

83 toma has no acceptable treatment at present; antifungals such as ketoconazole and itraconazole have b

84 s specific for this drug because other azole antifungals, such as ketoconazole and econazole, did not

85 le alone, and none of 8 (0%) who received no antifungals survived.

86 The in vitro activities of 10 antifungals tested against 19 isolates representing 18 s

87 g HPLC-MS/MS, with up to 6.4 mug/L for azole antifungals that indirectly affect corticosteroid signal

88 These data suggest that azole antifungals, through differential inhibition of hepatic

89 R mutation, supporting the potential role of antifungals to halt progressive CF lung disease.

90 Impaired delivery of antifungals to hyphae within necrotic lesions is thought

91 ungal posaconazole could improve delivery of antifungals to the sites of established infection and im

92 ly useful for developing diagnostics and new antifungals to treat biofilm-based infections.

93 s grown in planktonic form, are resistant to antifungals used to treat denture stomatitis.

94 metabolism by certain macrolide antibiotics, antifungals, verapamil, diltiazem, and isoniazid.

95 Reduction of unnecessary use of antifungals via antifungal stewardship is critical to li

96 nt for Candida mastitis with oral or topical antifungals was ineffective in 20(91%).

97 icans were susceptible (50% RMA for the same antifungals was obtained at 0.25, 1.0, 4.0, and 0.5 micr

98 mpairs resistance to mechanistically diverse antifungals, we examined the effect of similarly modest

99 Empiric antibiotics, antivirals, and antifungals were administered in 85.8%, 53.4%, and 7.8%,

100 Patients treated with antifungals were more severely ill than untreated patien

101 n DCs A. terreus conidia were protected from antifungals, whereas A. fumigatus conidia were efficient

102 sed in an effort to identify novel cytotoxic antifungals which target this enzyme.

103 sis require the protracted administration of antifungals, which can result in significant toxicities

104 Seven antifungals with activity against dermatophytes were tes

105 ized controlled trials that compared topical antifungals with one another or with placebo in dermatop

106 at most randomized controlled trials compare antifungals with placebo instead of other antifungals, c