ライフサイエンスコーパス: Candida

1 rophil's ability to contain clusters of live Candida.

2 e were coagulase-negative Staphylococcus and Candida.

3 in vitro cytokine production in response to Candida.

4 ignificance of oral mycobiome members beyond Candida.

5 ddition to regulating Th17 responses against Candida, a STAT1 gain-of-function mutant impedes antigen

6 with a clinical response, whereas decreased Candida abundance post-FMT was indicative of ameliorated

7 High Candida abundance pre-FMT was associated with a clinical

8 ccus (VRE), Pseudomonas aeruginosa (PA), and Candida albicans (CA)].

9 te a multivalent recombinant protein against Candida albicans (mvPC).

10 iverse isolates of the human fungal pathogen Candida albicans (Todd et al., 2019).

11 ells compared with polyclonal stimulation or Candida albicans Ag exposure.

12 Candida albicans and Aspergillus fumigatus are dangerous

13 Candida albicans and Candida glabrata are the 2 most pre

14 formed stable homotetramers, the mtSSBs from Candida albicans and Candida parapsilosis formed stable

15 Aspergillus fumigatus, Candida albicans and Mycosphaerella tassiana had the hig

16 erimental whole-genome mutation screening in Candida albicans and Pseudomonas aureginosa genomes, whi

17 The fungus Candida albicans and the Gram-positive bacterium S. aure

18 y childhood caries, Streptococcus mutans and Candida albicans are often co-isolated from carious lesi

19 d by the opportunistic human fungal pathogen Candida albicans Aside from its primary function of bloc

20 Candida albicans can cause systemic infection in immunoc

21 hibited markedly increased susceptibility to Candida albicans challenge.

22 The fungal pathogen Candida albicans displays striking genome dynamics durin

23 The genome of the meiosis-defective pathogen Candida albicans encodes an Rme1 homolog that is part of

24 al membrane integrity as the fungal pathogen Candida albicans expands.

25 Here, we reveal that the fungal pathogen Candida albicans exploits diverse host-associated signal

26 The opportunistic fungal pathogen Candida albicans expresses three copper-only SODs, and d

27 Despite a lack of activity against Candida albicans for these early de novo analogs, the sy

28 Centromeres of Candida albicans form on unique and different DNA sequen

29 Fungal pathogen Candida albicans has a complex cell wall consisting of a

30 SOD5 from the opportunistic fungal pathogen Candida albicans have revealed that the active-site stru

31 sin is a cytolytic peptide toxin secreted by Candida albicans hyphae and has significantly advanced o

32 e oral mucosa caused by the commensal fungus Candida albicans IL-17R signaling is essential to preven

33 eptococcus mutans, Streptococcus oralis, and Candida albicans in the saliva from mothers and their in

34 uently, dnTCF4 mice were more susceptible to Candida albicans infection and more sensitive to 5-fluor

35 results in enhanced defense against systemic Candida albicans infection and prolonged host survival.

36 During Candida albicans infection, mice lacking TAGAP mount def

37 ns, it is imperative that we investigate how Candida albicans interacts with blood components.

38 Candida albicans is a commensal fungus of human gastroin

39 Candida albicans is a commensal yeast able to cause life

40 Candida albicans is a fungal pathobiont, able to cause e

41 Candida albicans is a gut commensal and opportunistic pa

42 Candida albicans is a leading cause of systemic bloodstr

43 Candida albicans is a pervasive commensal fungus that is

44 recent study shows that the commensal fungus Candida albicans is an inducer of differentiation of hum

45 Candida albicans is an opportunistic yeast that can caus

46 The human pathogen Candida albicans is considered an obligate commensal of

47 Candida albicans is known to form polymicrobial biofilms

48 -> 2)-Inositol-1-P-(O -> 1)-phytoceramide of Candida albicans is reported.

49 PE produced from Escherichia coli membranes, Candida albicans mitochondria, or HeLa cell mitochondria

50 sistant Staphylococcus aureus ATCC 43300 and Candida albicans MTCC 227.

51 ly important differences with human NatA and Candida albicans NatB, resolves key hNatB protein determ

52 growth in the opportunistic fungal pathogen Candida albicans Our results suggest that HHK3 regulates

53 rials, contains a recombinant version of the Candida albicans rAls3 N-terminus protein (rAls3p-N) in

54 mon causes of invasive mycotic disease, with Candida albicans reigning as the leading cause of invasi

55 Candida albicans scavenges environmental zinc via two pa

56 ability of the fungal opportunistic pathogen Candida albicans to adhere to denture material and invad

57 lles and stimulated with bacterial toxins or Candida albicans to induce NETosis.

58 drug library to sensitize an azole-resistant Candida albicans to the effect of fluconazole.

59 otocol for CRISPR-Cas9-based manipulation in Candida albicans using a modified gene-drive-based strat

60 Candida albicans utilizes chromosome missegregation to a

61 CaTOK (Candida albicans) and CnTOK (Cryptococcus neoformans neo

62 two species of Candida (Cornus glabrata and Candida albicans) from Candida-spiked blood samples.

63 l as with heat-inactivated and viable fungi (Candida albicans).

64 e in the CTG clade of ascomycetes, including Candida albicans, a human pathogen.

65 Candida albicans, a major opportunistic fungal pathogen,

66 Candida albicans, a ubiquitous commensal fungus that col

67 e separase homologue Esp1p in the ascomycete Candida albicans, an important pathogen of humans, is es

68 h responses against Clostridium perfringens, Candida albicans, and Bacteroides vulgatus were also cou

69 efflux in highly azole-resistant strains of Candida albicans, another human fungal pathogen, increas

70 , a stronger cytokine response compared with Candida albicans, but a lower macrophage lysis capacity.

71 ad-spectrum synergistic interactions against Candida albicans, Candida auris, Cryptococcus neoformans

72 ely colonized by pathobiont microbes such as Candida albicans, capable of invasive disseminated infec

73 levels of effector cytokines in response to Candida albicans, compared to CD69(-) T cells.

74 man fungal pathogens (Aspergillus fumigatus, Candida albicans, Cryptococcus neoformans and Coccidioid

75 cterium, Pseudomonas aeruginosa and a yeast, Candida albicans, induce the resistance of the latter to

76 erant fungi, including filamentous fungi and Candida albicans, is associated with poor lung function

77 In the human fungal pathogen Candida albicans, mating of diploid cells generates tetr

78 In Candida albicans, stress triggers adaptive chromosome de

79 With the opportunistic fungal pathogen Candida albicans, the Cu-sensing transcription factor Ma

80 ulates virulence of pathogenic fungi such as Candida albicans, the underlying mechanisms have remaine

81 hin a population of macrophages encountering Candida albicans, there are distinct host-pathogen traje

82 e of circulating Cryptococcus neoformans and Candida albicans, thereby reducing fungal dissemination

83 In the opportunistic fungal pathogen Candida albicans, transcriptional regulatory networks re

84 rms expressed by Cryptococcus neoformans and Candida albicans, two pathogenic fungi of major clinical

85 For the fungal pathogen Candida albicans, utilization of amino acids has been sh

86 e of Trl1 KIN-CPD from the pathogenic fungus Candida albicans, which adopts an extended conformation

87 CD82 and Dectin-1 on the plasma membrane of Candida albicans-containing phagosomes independent of ph

88 ononuclear cells, these molecules suppressed Candida albicans-induced production of the cancer-promot

89 n mentagrophytes, Aspergillus fumigatus, and Candida albicans.

90 n yeast species identified in all groups was Candida albicans.

91 n different cellular systems stimulated with Candida albicans.

92 il recruitment during invasion of the CNS by Candida albicans.

93 ganisms including the human fungal pathogen, Candida albicans.

94 of Hsp90 in a leading human fungal pathogen, Candida albicans.

95 ning and integration into a neutral locus in Candida albicans.

96 from the most common human fungal pathogen, Candida albicans.

97 rived dendritic cells (moDCs) that presented Candida albicans.

98 upstream sensors activated in the context of Candida and Aspergillus infections are unknown.

99 enus-level community types (mycotypes), with Candida and Malassezia as the main taxa driving cluster

100 antimicrobial resistance genes, and both Pan Candida and Pan Gram-Negative targets that are unique to

101 sitive percent agreement and NPA for the Pan Candida and Pan Gram-Negative targets were 92.4% and 95.

102 codons decoded by I*A and U*G wobble in both Candida and Saccharomyces.

103 population reported all blood cultures with Candida, and a standard case definition was applied to i

104 core-shell biocatalyst by immobilization of Candida antarctica B lipase is reported, coating single-

105 By employing Candida antarctica lipase B (CALB) as the model enzyme w

106 ilized and commercially available food-grade Candida antarctica lipase B, Lipozyme(R) 435, was used a

107 Candida antarctica lipase B-catalysed synthesis of lipop

108 ower was esterified with octanoic acid using Candida antarctica lipase B.

109 utanol as a solvent, 20 g/L of lipase B from Candida Antarctica, and vinyl cinnamate as acyl donor at

110 ctivity was observed for lipase AK Amano 20, Candida antartica lipase B, and Mucor miehei lipase.

111 Although we detected elevated anti-Candida antibodies in placebo recipients, this increase

112 provide enhanced protection against complex candida antigens.

113 Physiological races of the oomycete Albugo candida are biotrophic pathogens of diverse plant specie

114 A variety of fungi, including species of Candida, Aspergillus, Exserohilum, Cryptococcus, Histopl

115 The MPA-Candida assay can also be coupled to a pan-Fungal assay

116 Candida-associated denture stomatitis (DS) is a persiste

117 itional albicans and non-albicans pathogenic Candida at genus level.

118 f additional drug-resistant species, such as Candida auris and Candida glabrata, further threatens th

119 al outbreaks of drug-resistant fungi such as Candida auris are thought to be due at least in part to

120 The emerging yeast Candida auris can be highly drug resistant, causing inva

121 Since the identification of the first 2 Candida auris cases in Chicago, Illinois, in 2016, ongoi

122 tropicalis and the emerging fungal pathogen Candida auris contain a single SOD5-like SOD rather than

123 The multidrug-resistant yeast pathogen Candida auris continues to cause outbreaks and clusters

124 Candida auris is a multidrug-resistant yeast associated

125 Candida auris is a multidrug-resistant yeast which has e

126 Candida auris is a pathogen of considerable public healt

127 Candida auris is among the most important emerging funga

128 Candida auris is an emerging fungal pathogen that exhibi

129 Candida auris is an emerging human fungal pathogen that

130 Candida auris is an emerging multi-drug resistant yeast

131 Candida auris is an emerging multi-drug-resistant human

132 Candida auris is an emerging multidrug-resistant fungal

133 Candida auris is an emerging multidrug-resistant yeast t

134 t coverage in the mainstream media of global Candida auris outbreaks has provided the general public

135 Candida auris was isolated from 37 of 322 (11%) environm

136 Candida auris, a multidrug-resistant fungal pathogen, is

137 potent antifungal effects against strains of Candida auris, an emerging multidrug-resistant fungus th

138 istic interactions against Candida albicans, Candida auris, Cryptococcus neoformans, and Aspergillus

139 fectious diseases, such as pandrug-resistant Candida auris.

140 actor Mrr1, best known for its regulation of Candida azole resistance genes such as MDR1, regulates o

141 gent of oral mucosal candidiasis, in which a Candida-bacteriome partnership plays a key role.

142 deaths occurred within 7 days of a positive Candida blood culture, and 5628 (95% CI, 2465-8791) deat

143 Patients with Candida bloodstream infection experienced a prior marked

144 Candida bloodstream infection is associated with high mo

145 egral part of clinical care of patients with candida bloodstream infection.

146 eligibility, we analysed 1691 patients with candida bloodstream infection; 776 (45.9%) who had an in

147 antifungal prophylaxis; however, IC and non-Candida breakthrough IFIs were observed, most often repr

148 n mucosal and Th17-mediated immunity against Candida, but mechanisms of impaired antiviral immunity h

149 matous disease produce larger swarms against Candida, but their release of NETs is delayed, resulting

150 ver, the mtSSBs from Candida nivariensis and Candida castellii formed tetramers at high protein conce

151 riments with 1 mum polystyrene particles and Candida cells.

152 We find that neutrophil swarming over Candida clusters delays germination through the action o

153 It is believed to ensue from Candida colonization, breach of the intestinal epithelia

154 lower fungal diversity with an overgrowth of Candida compared with controls.

155 Cross-talk between Candida-confronted monocyte-derived dendritic cells (moD

156 d (STEM method) by recovering two species of Candida (Cornus glabrata and Candida albicans) from Cand

157 Candida counts and salivary IL-6, IL-8, and TNF-a levels

158 ological parameters of CP, reduction of oral Candida counts, and improvement of HIV-infection status.

159 these deaths are attributable to species of Candida, Cryptococcus, and Aspergillus Treating fungal i

160 msel for intermediate Nugent) scores for BV, Candida cultures and DNA sequencing for VVC, and a compo

161 e antifungal treatment caused by inefficient Candida diagnosis contributes to its notoriously high mo

162 The availability of better Candida diagnostic tools would positively impact patient

163 Surprisingly, inoculation with Candida dubliniensis and S. aureus resulted in minimal m

164 In addition to Candida dubliniensis, several other low-virulence Candid

165 C. auris, n = 35; Candida haemulonii, n = 5; Candida duobushaemulonii, n = 4) were tested by three di

166 Candida endocarditis (OR, 1.84), cirrhosis (OR, 1.93), d

167 ts in part the younger demographic; however, Candida endocarditis seen among approximately 40% unders

168 Endogenous Candida endophthalmitis (ECE) has been established with

169 h between C. auris, C. duobushaemulonii, and Candida famata were obtained in an average of 27% of sam

170 F. candida feeds on the Streptomyces colonies and dissemina

171 ng systemic antifungal prophylaxis targeting Candida for up to 90 days after transplant and extending

172 of being diagnosed with EE in the setting of Candida fungemia.

173 2], Mucorales [2], Fusarium species [2], and Candida glabrata [1]) occurred, representing 8.3% of pat

174 ll as two clinically relevant yeast species (Candida glabrata and Cryptococcus neoformans), is shown.

175 meostasis in macrophages upon infection with Candida glabrata and exacerbate infection.

176 The human fungal pathogen Candida glabrata appears to utilise unique stealth, evas

177 Candida albicans and Candida glabrata are the 2 most prevalent Candida specie

178 -cell interaction, the human fungal pathogen Candida glabrata harbors a large family of more than 20

179 Candida glabrata's ability to adhere to host tissue is m

180 culture-proven infectious endophthalmitis (2 Candida glabrata, 2 coagulase-negative Staphylococcus, 1

181 the Candida species group, 4% for VVC due to Candida glabrata, and 10% for T. vaginalis Sensitivity a

182 resistant species, such as Candida auris and Candida glabrata, further threatens the limited armament

183 Candida glabratais an opportunistic pathogen in humans,

184 These patients were less likely to present Candida growth in all 3 sets of blood cultures (15.4% vs

185 olates of Candida species (C. auris, n = 35; Candida haemulonii, n = 5; Candida duobushaemulonii, n =

186 IL-1beta/IL-1Ra and TNF-alpha/IL-10 ratio in Candida hyphae-stimulated PBMCs were significantly highe

187 to an exaggerated vaginal immune response to Candida hyphae.

188 IQR] 16-56 days) after transplant, while non-Candida IFIs occurred later, at a median of 86 days (IQR

189 1.4% (95% CI 9.2-13.6%), and the rate of non-Candida IFIs was 8.8% (95% CI 6.9-10.8%).

190 Activation of human NK cells in response to Candida in human blood mainly occurs indirectly by media

191 iasis, which is caused by several species of Candida, in addition to a limited number of systemic myc

192 necrosis factor-alpha [TNF-alpha]), and oral Candida infection (colony forming units and species) wer

193 enhanced molecular diagnosis of bloodstream Candida infection and especially compared it with the co

194 rophage phagocytosis, clearance of secondary Candida infection, and mortality.

195 improved molecular diagnosis of bloodstream Candida infection.

196 osuppression and susceptibility to secondary Candida infection.

197 ated with the later development of secondary Candida infection.

198 the body's immune response against invasive candida infections.

199 s novel antifungal agents for drug-resistant Candida infections.

200 he true burden of invasive infections due to Candida is higher.

201 So far, Candida is the only genus demonstrated to reach a signif

202 We then repeated Candida killing assays with thrombin-stimulated or unsti

203 Pre-FMT Candida levels may identify FMT responders.

204 d the remaining 9% of which were reported as Candida lusitaniae /C. duobushaemulonii.

205 dies in Clavispora lusitaniae, also known as Candida lusitaniae, showed that Mrr1 regulates expressio

206 eterm infants by Saccromycetes, specifically Candida, may suggest a pathologic association with prete

207 this method was applied in the detection of Candida metapsilosis and Zygosaccharomyces bailii, both

208 ments, with aciduric species enriched in the Candida mycotype and inflammophilic bacteria increased i

209 The Candida mycotype had lower diversity than the Malassezia

210 ng bacterial communities associated with the Candida mycotype showed lower diversity than those assoc

211 Moreover, the mtSSBs from Candida nivariensis and Candida castellii formed tetrame

212 We detail the generation of Candida-optimized Cas9-based plasmids for gene deletion,

213 dent, each dominated by only 1 genus, either Candida or Malassezia.

214 ramers, the mtSSBs from Candida albicans and Candida parapsilosis formed stable homodimers.

215 lated Candida sojae, Candida viswanathii and Candida parapsilosis indicates loss of ancestral HIR-ass

216 However, antibiotics promoted emergence of Candida parapsilosis, a collagenase-producing microorgan

217 The strains Candida parapsilosis, Torulaspora delbrueckii and Pichia

218 ed peritoneum and to phagocytose heat-killed Candida particles.

219 However, decreased Candida post-treatment was associated with improved dise

220 computational tools, we screened the entire candida proteome (6030 proteins) and identified the most

221 g showed that resistance to an isolate of A. candida race 2 (Ac2V) can be explained in each accession

222 t the adult leaf stage to white rust (Albugo candida) races that infect the crop species Brassica jun

223 ciated with improved disease-suggesting that Candida reductions are associated with less inflammation

224 In the case of Candida-related sepsis, Candida species and major blood

225 strate ulcerative colitis patients with high Candida responded best to fecal microbial transplant (FM

226 ms were tested to give a target yeast strain Candida rugosa for further evaluation of MICs on the iso

227 ssezia species-but not species in the genera Candida, Saccharomyces or Aspergillus-accelerated oncoge

228 syndrome-associated multiorgan failure with Candida sepsis on day +40 following HSCT.

229 Candida serves as the main etiological agent of oral muc

230 ncluding testing for aerobic vaginitis (AV), Candida, sexually transmitted infections (STI), and BV (

231 Candida showed relative resistance to these compounds, r

232 n of putative centromeres in closely related Candida sojae, Candida viswanathii and Candida parapsilo

233 ion, polyploidy and host domestication in A. candida specialization on distinct plant species.

234 Sensitivity and specificity of detection of Candida species (C. albicans, C. auris, C. dubliniensis,

235 A panel of 44 isolates of Candida species (C. auris, n = 35; Candida haemulonii, n

236 da dubliniensis, several other low-virulence Candida species (C. glabrata, C. auris, and C. albicans

237 Candida species (predominantly C. albicans) were more of

238 In the case of Candida-related sepsis, Candida species and major blood cells (i.e., red blood c

239 To effectively retrieve a majority of Candida species and remove most of the interfering blood

240 e biological activity against four different Candida species and showed no toxicity in vivo.

241 Candida species are a leading source of healthcare infec

242 Candida species are among the most common causes of inva

243 and the rising frequency of azole-resistant Candida species are growing challenges to human medicine

244 the biofilm-forming abilities of the tested Candida species by up to 73%, and successfully reduced t

245 nd Candida glabrata are the 2 most prevalent Candida species causing bloodstream infections.

246 for simultaneous detection of sepsis-causing Candida species directly in whole blood.

247 Isolates from other Candida species displayed heterogeneity in MG resistance

248 plied this inertial sorting device to purify Candida species from whole blood sample for enhanced mol

249 samples: 49% for BV, 29% for VVC due to the Candida species group, 4% for VVC due to Candida glabrat

250 espectively, for BV; 91.7% and 94.9% for the Candida species group; 84.7% and 99.1% for C. glabrata;

251 Secondary outcomes included Candida species isolated from culture or detected on the

252 s and elaborate on the resistance mechanisms Candida species possess that render them recalcitrant to

253 es revealed the ability of the low-virulence Candida species that conferred protection to invade the

254 teria, 58%; Gram-negative bacteria, 78%; and Candida species, 83%.

255 sensitivities for Gram-negative bacteria and Candida species, and elevated positivity rates during an

256 uboptimal codon pairs extends to two related Candida species, fungi that diverged from Saccharomyces

257 ifungal drugs combined with the isolation of Candida species, namely C. albicans and C. auris, exhibi

258 For Candida species, their inability to maintain plasmids, u

259 -FP panel correctly identified an additional Candida species, undetected by standard-of-care methods.

260 etion abolishes chlamydosporulation in three Candida species, whereas its overexpression bypasses the

261 955p, an uncharacterized protein specific to Candida species.

262 d differences for Gram-negative bacteria and Candida species.

263 central role in chlamydospore development in Candida species.

264 or marked intestinal expansion of pathogenic Candida species; this expansion consisted of a complex d

265 The expansion of Candida-specific IFNgamma-producing T cells together wit

266 Analysis of Candida-specific T-cell responses using enzyme-linked im

267 (Cornus glabrata and Candida albicans) from Candida-spiked blood samples.

268 Among 263 fungal infections, Candida spp (60%) prevailed as digestive tract pathogens

269 omonas aeruginosa (80%), S. aureus (77%) and Candida spp (71%) but lower reductions for E. coli (54%)

270 by P. aeruginosa (81%), S. aureus (79%) and Candida spp (72%), with lower reductions for the colifor

271 bacterial vaginosis alone or with concurrent Candida spp infections had high rates of coinfection wit

272 oodstream infection caused by either rGNB or Candida spp were associated with detrimental transitions

273 lture with a higher mortality risk (rGNB and Candida spp).

274 ve bacilli (sGNB), resistant GNB (rGNB), and Candida spp.

275 el yeast Saccharomyces cerevisiae than other Candida spp.

276 ve bacteria (sGNB), resistant GNB (rGNB) and Candida spp.

277 ed by Enterococcus spp. (32.2%, 39/121), and Candida spp. (9.1%, 11/121).

278 The intestinal expansion of pathogenic Candida spp. was associated with a substantial loss in b

279 oodstream infection caused by either rGNB or Candida spp. were associated with detrimental transition

280 lture with a higher mortality risk (rGNB and Candida spp.).

281 ydia trachomatis, Trichomonas vaginalis, and Candida spp., as well as their interactions with the hos

282 ainst a panel of 28 fungal strains including Candida spp., Cryptococcus spp., Aspergillus spp., and F

283 stant (MDR) strains of C. albicans and other Candida spp., highlighting the urgent need of new antifu

284 e Th-dependent adaptive immune response upon Candida stimulation.

285 Patients with LTBI had lower odds of having candida stomatitis (adjusted odds ratio (OR) = 0.68, p =

286 isms including Staphylococcus aureus and two Candida strains.

287 study provides a novel biophysical aspect of Candida-streptococcal interaction whereby extracellular

288 Candida thrives in the presence of lower oral pH and is

289 Our data suggest that FMT might reduce Candida to contain pro-inflammatory immunity during inte

290 is were tested with the Aptima BV and Aptima Candida/Trichomonas vaginitis (CV/TV) assays.

291 We present structures of the Candida Trl1 KIN domain at 1.5 to 2.0 angstrom resolutio

292 Interestingly, Candida tropicalis and the emerging fungal pathogen Cand

293 DNA sequences but a closely related species, Candida tropicalis, possesses homogenized inverted repea

294 Microscopic identification of Candida versus that by qPCR had 94% agreement (9 positiv

295 entromeres in closely related Candida sojae, Candida viswanathii and Candida parapsilosis indicates l

296 High pre-FMT Candida was associated with increased bacterial diversit

297 Candida was the most abundant genus in the fecal mycobio

298 Microscopy results for BV and Candida were compared to those from two molecular approa

299 he antennae of the model springtail Folsomia candida, which is also attracted to both compounds.

300 the molecular detection and cultivability of Candida, while cultivation showed low sensitivity for de