ライフサイエンスコーパス: antifungals

1 ceptibility to the triazole and echinocandin antifungals.

2 ty of 47 isolates of dermatophytes against 8 antifungals.

3 ion about their in vitro susceptibilities to antifungals.

4 da species were susceptible to the available antifungals.

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

6 articularly in combination with conventional antifungals.

7 ally relevant C. albicans isolates against 4 antifungals.

8 human fungal pathogen, C. albicans, to azole antifungals.

9 gement of pharmacokinetic DDIs with triazole antifungals.

10 pment of new pharmaceutical and agrochemical antifungals.

11 ng poor in vitro activity for most available antifungals.

12 l can yield potent and renal-sparing polyene antifungals.

13 atient improved post-operatively on systemic antifungals.

14 d likelihood of evolving resistance to other antifungals.

15 ch display reduced susceptibility to current antifungals.

16 41 (34%) were prescribed antibiotics and/or antifungals.

17 tile ground for discovery of antibiotics and antifungals.

18 bitors opens up prospects for a new class of antifungals.

19 lly important compounds like antibiotics and antifungals.

20 res, offering an alternative to conventional antifungals.

21 tance of C. albicans to cell wall-perturbing antifungals.

22 linked to the widespread agricultural use of antifungals.

23 e EFE (75%) were treated initially with oral antifungals.

24 ilitates the development of defensin-mimetic antifungals.

25 t the ergosterol-active triazole and polyene antifungals.

26 renewed optimism for the discovery of novel antifungals.

27 ivities of ergosterol biosynthesis-targeting antifungals.

28 t host toxicities that preclude their use as antifungals.

29 ons to support decisions for safely stopping antifungals.

30 resent a potential target for developing new antifungals.

31 tentially a powerful alternative to standard antifungals.

32 . albicans lost dominance in the presence of antifungals.

33 development of more efficient broad-spectrum antifungals.

34 riteria that predict when it is safe to stop antifungals.

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

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

37 om survival without therapy to death despite antifungals.

38 m of action distinct from currently marketed antifungals.

39 as antitumor agents, immunosuppressants and antifungals.

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

41 validation of therapeutic efficacy of novel antifungals.

42 conazole when used in combination with those antifungals.

43 er assay was reduced in animals treated with antifungals.

44 here was no significant difference among the antifungals.

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

46 aerobes [12.7%]), antivirals (14.5%), and/or antifungals (3.6%); and antimicrobial narrowing in 27.3%

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

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

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

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

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

52 ructure may contribute to the development of antifungals against phytopathogens and, with the afc gen

53 dentified as a potential drug target for new antifungals against systemic candidiasis.

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

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

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

57 a continuing challenge due to few effective antifungals and a rise in resistance.

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

59 ortant clinical applications as antibiotics, antifungals and anti-cancer agents.

60 ds as promising leads for development of new antifungals and as pharmacological tools for the study o

61 Here, we describe our current arsenal of antifungals and elaborate on the resistance mechanisms C

62 costs, owing to rising resistance to current antifungals and emergence of multidrug-resistant fungal

63 s are difficult to treat due to a paucity of antifungals and emerging resistances.

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

65 We discuss different antifungals and fungicides, their modes of action and re

66 reby affecting its survival upon exposure to antifungals and host immune response.

67 e fungal cell wall is the primary target for antifungals and is recognized by host immune cells.

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

69 lbicans resistant to first-line echinocandin antifungals and potentiate non-curative echinocandin tre

70 ystems can provide discovery pathways to new antifungals and structurally intriguing metabolites.

71 The patient received additional intravitreal antifungals and systemic therapy.

72 oles, which is the most widely used class of antifungals and the only available oral treatment option

73 The limited number of antifungals and the rising frequency of azole-resistant

74 ay be exploited for the development of novel antifungals and therapies are discussed.

75 These biofilms are tolerant to antifungals and to the host immune system.

76 ment requires combination of antibiotics and antifungals and, even with prompt diagnosis and treatmen

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

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

79 In contrast, co-trimoxazole, doxycycline, antifungals, and antivirals had less impact on microbiom

80 ng antihistamines, mucolytics, antitussives, antifungals, and decongestants.

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

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

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

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

85 We find that B-lactams, fluoroquinolones, antifungals, and, surprisingly, calcimimetics, phenothia

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

87 ly used in clinical settings as antibiotics, antifungals, anticancer agents, and immunosuppressants.

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

89 s (aOR, 3.14; 95% CI, 1.41-6.98), receipt of antifungals (aOR, 5.35; 95% CI, 1.7-16.91), and lymphocy

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

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

92 Currently, conventional antifungals are often ineffective as Candida spp. have d

93 Azole antifungals are vital therapeutic options for treating i

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

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

96 complete biosynthetic pathways of the potent antifungals AS2077715 (1) and funiculosin (2) are recons

97 o researchers who conduct clinical trials of antifungals, assess diagnostic tests, and undertake epid

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

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

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

101 rther threatens the limited armamentarium of antifungals available to treat these serious infections.

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

103 or future research, including a hope for new antifungals based on metals.

104 ity to develop resistance to next generation antifungals because of variants in the DNA mismatch repa

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

106 age by exposure to triazole and echinocandin antifungals but not by exposure to amphotericin B or flu

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

108 Echinocandins are frontline antifungals, but rising resistance limits their efficacy

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

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

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

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

113 ndicated macrolide antibiotics and imidazole antifungals continues to occur.

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

115 rgosterol biosynthesis and susceptibility to antifungals could set the stage for the development of n

116 o antifungal drugs and the limited number of antifungals currently available highlight the need for n

117 ong with severe side effects of the existing antifungals demands for new effective antimycotics.

118 uture applications including strain specific antifungals, diagnostic tools, and immunomodulators.

119 ically resistant to the latest generation of antifungals, echinocandins, while Candida auris, a notor

120 elucidated how chemical modifications of the antifungals encode desired inhibitor conformation and co

121 is a severe lack of effective and accessible antifungals, especially in regions with limited resource

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

123 Identifying new antifungals for cryptococcal meningitis is a priority gi

124 e-counter sialagogues for dry mouth, topical antifungals for oral candidiasis, and topical corticoste

125 species which reflects the widespread use of antifungals for prophylaxis and therapy, and in the case

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

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

128 tients in the treatment arm received empiric antifungals from d9 tod28 (42.4% v 63.9%; P = .02) and d

129 Triazole antifungals function as ergosterol biosynthesis inhibito

130 ely reported for its multidrug resistance to antifungals, further complicating its clinical managemen

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

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

133 most cost-effective approach of the studied antifungals; however, the CEA was sensitive to potential

134 New antifungals, ibrexafungerp and oteseconazole, are now av

135 ncluded immunomodulation in 60 decedents and antifungals in 50 decedents.

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

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

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

139 Widespread use of azole antifungals in agriculture has been linked to resistance

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

141 lem due to the prospect of dual use of novel antifungals in clinical and agricultural settings.

142 ource of infection, days of therapy (DOT) of antifungals in patients with discordant results, and ove

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

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

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

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

147 However, our tests revealed that these antifungals, in fact, enhance SARS-CoV-2 infection by fa

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

149 States, which rapidly acquires resistance to antifungals, in vitro and in vivo.

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

151 epidemiologic cutoff values (ECVs) for eight antifungals, including those commonly used to treat chro

152 third of patients due to poor penetration of antifungals into the nail plate.

153 Reduced susceptibility to antifungals is common among members of genera Scedospori

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

155 r suggest that resistance to next-generation antifungals is more likely to emerge within organisms th

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

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

158 The calculated ECVs for the commonly used antifungals itraconazole and terbinafine were 0.5 and 0.

159 xhibiting resistance to all three classes of antifungals magnifies the need for novel therapeutic int

160 s, prompt ART initiation, and more intensive antifungals may reduce mortality among asymptomatic CrAg

161 ss of the current reserve of antibiotics and antifungals, methodological advances open additional ave

162 d C. auris, exhibiting resistance to current antifungals necessitates the development of new therapeu

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

164 RNA-based antifungals offer a sustainable and environmentally frie

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

166 at SOT, prior hospital admission, receipt of antifungals or lymphocyte-specific antibodies.

167 ndicate the potential of bio-oils as natural antifungals, particularly the licuri-derived extracts, w

168 polychlorobiphenyls, pesticides, herbicides, antifungals, pharmaceuticals, artificial sweeteners, and

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

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

171 f SAARs for narrow-spectrum B-lactam agents, antifungals predominantly used for invasive candidiasis,

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

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

174 Azole antifungals remain the treatment of choice for uncomplic

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

176 Azole antifungals represent first-line therapeutics for most o

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

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

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

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

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

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

183 The other antifungals tested had no impact on SARS-CoV-2 infection

184 tors will accelerate the design of selective antifungals that can be deployed to combat life-threaten

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

186 lta strain exhibits several sensitivities to antifungals that target lipid metabolism.

187 s the synthesis of extended "long-arm" azole antifungals that were evaluated against wild-type and re

188 Next-generation antifungals therefore are needed urgently.

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

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

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

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

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

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

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

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

197 Resistance to multiple antifungals was frequent, and three isolates were recove

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

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

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

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

202 Voriconazole, caspofungin, and combination antifungals were less cost-effective than amphotericin B

203 ous efforts to develop renal-sparing polyene antifungals were misguided by the classic membrane perme

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

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

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

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

208 and resistance, it is unclear whether these antifungals will replace fluconazole.

209 Seven antifungals with activity against dermatophytes were tes

210 nhibitor hybrids are a novel class of potent antifungals with clinical potential.

211 fungal peptides represent a useful source of antifungals with novel mechanisms-of-action, and potenti

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

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

214 comitant administration of CYP3A4-inhibiting antifungals with respect to adverse effects and remissio

215 more likely to be resistant to agricultural antifungals with unrelated modes of action.

216 is, halving the number of patients receiving antifungals without excess mortality or IFDs.