ライフサイエンスコーパス: Candida

1 residual matrix from the specimen or yeast (Candida).

2 The most common single fungal isolate was Candida (4/16, 25%), but 75% of all isolates were molds.

3 erein, flowers of Bauhinia variegata L. var. candida alba Buch.-Ham were submitted to electron beam i

4 Most CUTS cases were caused by Candida albicans (52.7%), followed by Candida glabrata (

5 rine infection with microorganisms including Candida albicans (C.albicans).

6 rom Schizosaccharomyces pombe (Sp-Hsp104) or Candida albicans (Ca-Hsp104) also trimmed and cured the

7 In the human pathogen Candida albicans (which last shared a common ancestor wi

8 e Oma1 ortholog in the human fungal pathogen Candida albicans also alters TOR signaling and, unexpect

9 trated that medically relevant fungi such as Candida albicans and Aspergillus fumigatus also form bio

10 so increased the proportion of persisters in Candida albicans and Candida glabrata.

11 y against the opportunistic fungal pathogens Candida albicans and Cryptococcus neoformans However, th

12 Candida albicans and Fusobacterium nucleatum are well-st

13 iroscytalin showed moderate activity against Candida albicans and good activity against an export-def

14 MA, the calcium ionophore A23187, nigericin, Candida albicans and Group B Streptococcus.

15 The opportunistic fungal pathogen Candida albicans and lactic acid bacteria (LAB) are comm

16 The secondary outcome was the rate of Candida albicans and nonalbicans strains after treatment

17 us neoformans) to labeling at the bud sites (Candida albicans and Saccharomyces cerevisiae).

18 rthologues from Saccharomyces cerevisiae and Candida albicans and show that under nitrogen-sufficient

19 had recurrent mucocutaneous infections with Candida albicans and Staphylococcus aureus and chronic i

20 tin-1, mannose, and Toll-like receptors with Candida albicans and Staphylococcus epidermidis was 2.5-

21 sensitivity to early systemic infection with Candida albicans and T cell-mediated colitis.

22 The fungus Candida albicans and the bacterium Pseudomonas aeruginos

23 Although the dimorphic fungal species Candida albicans and the bacterium Staphylococcus aureus

24 s, whereas Th17 cells are protective against Candida albicans and to a lesser degree Staphylococcus a

25 Using the opportunistic fungal pathogen Candida albicans as a model, we identified a highly spec

26 is study evaluated the antifungal effects on Candida albicans ATCC90028, the cytotoxicity toward huma

27 Candida albicans biofilm formation is an important virul

28 alized to the nucleus of Pichia pastoris and Candida albicans but is cytoplasmic in Saccharomyces cer

29 The fungal pathogen Candida albicans can transition from budding to hyphal g

30 Candida albicans cells are often detected with Streptoco

31 his research was to evaluate the adhesion of Candida albicans cells onto PMMA surfaces by employing a

32 lla pneumophila, Streptococcus pneumonia and Candida albicans cleaved the N-terminus of immunoglobuli

33 The fungal pathogen Candida albicans colonizes basically all human epithelia

34 enhanced in patients with CF colonized with Candida albicans compared with that in noncolonized pati

35 human vaginal epithelium, and to the fungus Candida albicans Complementary crystallographic and biop

36 cell responses against Escherichia coli and Candida albicans displayed microbe-specific polyfunction

37 sponses to host cells in the fungal pathogen Candida albicans Eukaryotic Target of Rapamycin complex

38 Candida albicans excretes E,E-farnesol as a virulence fa

39 cently, we reported that the fungal pathogen Candida albicans expresses a novel copper-only SOD, know

40 The plasma membrane of the fungal pathogen Candida albicans forms a protective barrier that also me

41 nsition of the opportunistic fungal pathogen Candida albicans from budding to hyphal growth has been

42 e capacity of peach DMSO extracts to inhibit Candida albicans growth was more pronounced, especially,

43 ce of opportunistic fungal pathogens such as Candida albicans has increased.

44 fection, and opportunistic pathogens such as Candida albicans have evolved complex circuitry to sense

45 The secreted aspartyl proteinases of Candida albicans have long been implicated in virulence

46 organisms in the oral cavity, while TM7x and Candida albicans have served as crucial paradigms for CP

47 d NETs in response to fungal beta-glucan and Candida albicans hyphae when presented with extracellula

48 The most commonly isolated pathogen was Candida albicans in 20% of the patients.

49 shown that S. mutans is often detected with Candida albicans in early childhood caries.

50 ons of amphotericin B after inoculation with Candida albicans in light-exposed and light-protected co

51 ether the recently observed sensitization to Candida albicans in patients with EoE is owing to pre-ex

52 ns in the most common human fungal pathogen: Candida albicans In this organism, the histone deacetyla

53 Candida albicans infection produces elongated hyphae res

54 o demonstrated in a murine model of systemic Candida albicans infection with a significant fungal loa

55 e than wild-type control mice in response to Candida albicans infection, and the expression of JNK1 i

56 or clusters of miRNAs in countering systemic Candida albicans infection.

57 The oral cavity is a unique niche where Candida albicans infections occur in immunocompetent as

58 onal replacement therapy predispose women to Candida albicans infections.

59 Candida albicans is a dimorphic commensal fungus that co

60 Candida albicans is a ubiquitous mucosal commensal that

61 mmune response, and yet the commensal fungus Candida albicans is able to colonize immuno competent in

62 Candida albicans is among the most common human fungal p

63 Candida albicans is an opportunistic fungal pathogen col

64 Candida albicans is an opportunistic fungal pathogen fou

65 Candida albicans is an opportunistic human fungal pathog

66 Candida albicans is an opportunistic pathogen, typically

67 The cell wall of Candida albicans is composed largely of polysaccharides.

68 ith its mammalian host, the pathogenic yeast Candida albicans is exposed to a range of stresses such

69 Candida albicans is frequently detected with heavy infec

70 Candida albicans is normally a commensal fungus of the h

71 The Hog1 SAPK in Candida albicans is robustly phosphorylated in response

72 Candida albicans is the leading cause of fungal infectio

73 Candida albicans is the most common fungal pathogen in h

74 Although Candida albicans is the predominant organism found in pa

75 Candida albicans is the single most prevalent cause of f

76 Notably, experiments against Candida albicans mutants lacking those genes showed resi

77 NOPE1 encodes a functional homologue of the Candida albicans N-acetylglucosamine (GlcNAc) transporte

78 e ability of these cells to kill/phagocytose Candida albicans or Escherichia coli cells both ex vivo

79 tears and protected the eye from pathogenic Candida albicans or Pseudomonas aeruginosa infection.

80 overturned by mono-colonization with either Candida albicans or Saccharomyces cerevisiae.

81 us oralis forms robust mucosal biofilms with Candida albicans that have increased pathogenic potentia

82 e circuitry that enables the fungal pathogen Candida albicans to couple cell cycle dynamics with resp

83 and long-lasting antifungal effects against Candida albicans to the PMMA resin, and it has low toxic

84 The fungal pathogen Candida albicans undergoes morphogenetic switching from

85 a mouse model of KD (induced by a cell wall Candida albicans water-soluble fraction [CAWS]), we iden

86 nase domain of Trl1 from the fungal pathogen Candida albicans with GDP and Mg2+ in the active site.

87 e exhibited good antifungal activity against Candida albicans with MIC of 15.6mug/mL.

88 The interaction of Candida albicans with the innate immune system is the ke

89 (methicillin-resistant S. aureus (MRSA) and Candida albicans) and standard (Pseudomonas aeruginosa 1

90 ive (Escherichia coli) bacteria and a fungi (Candida albicans) were examined; which showed good antib

91 was immunized (Mycobacterium tuberculosis or Candida albicans).

92 is essential for GlcNAc signalling (NGS1) in Candida albicans, a commensal and pathogenic yeast of hu

93 cus faecalis, a Gram-positive bacterium, and Candida albicans, a fungus, occupy overlapping niches as

94 roteins, as a potential antifungal target in Candida albicans, a major human fungal pathogen.

95 revisit this concept from the perspective of Candida albicans, a microbial pathogen uniquely adapted

96 the N-terminal domain of Tps2 (Tps2NTD) from Candida albicans, a transition-state complex of the Tps2

97 aphylococcus aureus, Listeria monocytogenes, Candida albicans, and Candida parapsilosis isolates were

98 ey pattern-recognition receptors for sensing Candida albicans, and their downstream kinase SYK, thus

99 gal models such as Saccharomyces cerevisiae, Candida albicans, and Ustilago maydis.

100 t fungal infections, caused most commonly by Candida albicans, Aspergillus fumigatus and Cryptococcus

101 tly lost in the Metschnikowiaceae, including Candida albicans, but became more complex in the Sacchar

102 Candida albicans, Candida glabrata, and Candida parapsil

103 The fungal pathogens Candida albicans, Cryptococcus neoformans, and Aspergill

104 In the human pathogen Candida albicans, deep sequencing of mutants lacking the

105 Infection with Candida albicans, disseminated disease, pneumonia, and c

106 For the leading human fungal pathogen Candida albicans, filamentation is thought to be require

107 ogenicity of the clinically important yeast, Candida albicans, is dependent on robust responses to ho

108 In the fungal commensal and pathogen, Candida albicans, little is known of how these pathways

109 an be extended to other systems such as e.g. Candida albicans, or selected plant cells.

110 e in which the loss of an ABC transporter in Candida albicans, orf19.4531 (previously named ROA1), in

111 ha-mannoside, found in Saccharopolyspora and Candida albicans, respectively, induced the activation o

112 y (EIS) that allows multiplexed detection of Candida albicans, Streptococcus agalactiae and Chlamydia

113 Surprisingly, we found that the genome of Candida albicans, the predominant human fungal pathogen,

114 ntage of the minimal MT nucleation system of Candida albicans, we reconstituted the interactions of M

115 epigenetic states, "white" and "opaque." In Candida albicans, white cells are essentially sterile, w

116 rofoundly resistant to systemic infection by Candida albicans, with resistance characterized by enhan

117 In Candida albicans-infected resident peritoneal macrophage

118 clusively on immune stimulation, including a Candida albicans-specific master regulator at the CR1 lo

119 lucans on the surface of the fungal pathogen Candida albicans.

120 s to cell wall stress in the fungal pathogen Candida albicans.

121 irulence factor of the human fungal pathogen Candida albicans.

122 antarum and the opportunistic human pathogen Candida albicans.

123 rium oxysporum, Saccharomyces cerevisiae and Candida albicans.

124 athogenesis of many fungal pathogens such as Candida albicans.

125 equired for clearance of the fungal pathogen Candida albicans.

126 ith DNA repeats in the human fungal pathogen Candida albicans.

127 of temperature stress in the fungal pathogen Candida albicans.

128 mmune responses to Aspergillus fumigatus and Candida albicans.

129 peptide toxin in the opportunistic pathogen Candida albicans.

130 ose residues that cap the glycan produced by Candida albicans.

131 d no significant effect after challenge with Candida albicans.

132 ingle Dig1 orthologue in the fungal pathogen Candida albicans.

133 Resistance mechanisms for Candida and Aspergillus species have been extensively de

134 Azole resistance among Candida and Aspergillus species is one of the greatest c

135 centration (MIC) values against non-albicans Candida and Aspergillus strains.

136 igation of antifungal immunity (primarily to Candida and Aspergillus) and will also examine the emerg

137 eningoencephalitis but not colitis caused by Candida and Exophiala species.

138 iocordyceps, Verticillium, Pseudallescheria, Candida and Ilyonectria Not surprisingly, the genus Ophi

139 antibiotic consumption, incidence density of Candida and multidrug-resistant (MDR) bacteria bloodstre

140 gher relative abundance of particular fungi (Candida and Rhodotorula) and a distinct fecal metabolome

141 Lipases B from Candida antarctica (CALB), Rhizomucor miehei (RML) and T

142 The fatty acid selectivity of Candida antarctica lipase A (CAL-A) was applied to produ

143 The reactions were catalyzed by immobilized Candida antarctica lipase B in acetonitrile.

144 racemic amines have been investigated using Candida antarctica lipase type B as biocatalyst.

145 on the optimum conditions using immobilised Candida antartica lipase.

146 emerging threats such as multidrug resistant Candida auris are also alarming.

147 Candida auris is an emerging multidrug-resistant fungal

148 Candida auris is an emerging, often multidrug-resistant

149 merging multidrug-resistant pathogenic yeast Candida auris represents a serious threat to global heal

150 Candida auris, a multidrug-resistant yeast that causes i

151 emergence of the multidrug-resistant species Candida auris, identification of Candida to species leve

152 t notably Candida glabrata and more recently Candida auris.

153 large-scale production and isolation of the Candida biofilm extracellular matrix.

154 While single-species Candida biofilms have been well studied, considerably le

155 nd treating for <10 days was associated with Candida bloodstream dissemination.

156 Candida bloodstream infections (BSI) are associated with

157 ffectiveness of T2DT was highly dependent on Candida BSI prevalence and the cost of antifungal therap

158 endent direct molecular detection method for Candida BSIs (T2Candida).

159 d by fusobacterial membrane protein RadD and Candida cell wall protein Flo9.

160 xis reduced the odds of IC or death, IC, and Candida colonization during the drug exposure period com

161 xis is effective and safe in reducing IC and Candida colonization in premature infants, and has no im

162 ying illness, severity, invasive procedures, Candida colonization), and using a marginal structural m

163 oints evaluated were IC or death, IC, death, Candida colonization, and fluconazole resistance among t

164 patients with ICU-acquired sepsis, multiple Candida colonization, multiple organ failure, exposed to

165 e in healthy controls, both with and without Candida colonization.

166 ure Assessment (SOFA) score, 3 for number of Candida-colonized sites, and 99 pg/mL for level of (1-3)

167 milation test procedures and using CHROMagar Candida culture.

168 lves hydrolysis of vegetable oil blend using Candida cylindracea followed by esterification with glyc

169 vated amounts of formate and the presence of Candida-derived farnesol, which is commonly known to exh

170 Candida-derived IL-17A was indistinguishable from murine

171 ys to identify C. auris and related species: Candida duobushaemulonii, Candida haemulonii, and Candid

172 fections (coagulase-negative Staphylococcus, Candida, Fusarium, and Propionibacterium species).

173 The Candida Genome Database is a freely available online res

174 ven other closely related diploid pathogenic Candida genomes encode the two TAF12 paralogs.

175 sed by Candida albicans (52.7%), followed by Candida glabrata (25.6%) and Candida tropicalis (16.3%).

176 the potentially multidrug-resistant pathogen Candida glabrata against anidulafungin and fluconazole.

177 red in several Candida species, most notably Candida glabrata and more recently Candida auris.

178 The fungal pathogen Candida glabrata has emerged as a major health threat si

179 vival, and virulence in the pathogenic yeast Candida glabrata Here, we demonstrate PI3-kinase (CgVps3

180 rtance of SUMOylation in the human pathogen, Candida glabrata We identified the enzymes involved in s

181 Candida albicans, Candida glabrata, and Candida parapsilosis endophthalmit

182 nt forms of the Tom40 protein from the yeast Candida glabrata, and truncated constructs lacking the N

183 recognition of an emerging fungal pathogen, Candida glabrata, by the human NK cytotoxic receptor NKp

184 tivity of VT-1161 against Candida krusei and Candida glabrata, pathogens that are intrinsically resis

185 her-level resistance has been reported among Candida glabrata, which is also frequently resistant to

186 ortion of persisters in Candida albicans and Candida glabrata.

187 d in the clinically important human pathogen Candida glabrata.

188 tance among some Candida species, especially Candida glabrata.

189 The opportunistic yeast Candida glabratais increasingly refractory to antifungal

190 Detectable Candida growth in donor rim cultures, associated with a

191 with regard to room temperature exposure on Candida growth in optisol-gentamicin and streptomycin (G

192 Candida guilliermondii was isolated from sterile specime

193 d related species: Candida duobushaemulonii, Candida haemulonii, and Candida lusitaniae Targeting rDN

194 evidence of strain-dependent differences in Candida-host interactions that may affect virulence.

195 her analysis revealed that the inhibition of Candida hyphal morphogenesis is mediated via RadD and Fl

196 that the F. nucleatum-induced inhibition of Candida hyphal morphogenesis promotes C. albicans surviv

197 ofungin and voriconazole decreased growth of Candida in a species-dependent manner.

198 The effects of the three quinaldines on F. candida in soil were similar, with EC50 values ranging f

199 confirmed the negative prognostic impact of Candida in the bile in pancreatic cancer patients.

200 cter globiformis and the Collembola Folsomia candida in two exposure scenarios, with and without soil

201 1) is important for control of early mucosal Candida infection and plays a critical role in the induc

202 Following oral Candida infection, Il17ra(DeltaK13) mice exhibited funga

203 taining regimens had higher risk of invasive Candida infection.

204 Diagnosis of antifungal-resistant Candida infections is critical to the successful managem

205 Because much of the treatment for Candida infections is empirical, some institutions do no

206 Invasive Candida infections remain an important cause of morbidit

207 ia, invasive aspergillosis, and disseminated Candida infections were frequently reported.

208 incidence rates of grade 3 or 4 neutropenia, candida infections, and Crohn's disease were 0.7, 0.9, a

209 gold standard diagnostic method for invasive Candida infections, have low specificity and take up to

210 Implicating the role of vitamin D in Candida infections, we showed that candidemic patients h

211 paucity of clinical evidence suggesting true Candida infections.

212 ously unknown physical component of the host-Candida interaction that might change during antifungal

213 Candida is the third most common cause of bloodstream in

214 apid and accurate identification of clinical Candida isolates is fundamental in ensuring timely and e

215 rapidly and accurately identify 153 clinical Candida isolates to species level.

216 s, including the activity of VT-1161 against Candida krusei and Candida glabrata, pathogens that are

217 concentration (MFC) were established against Candida krusei isolates.

218 da duobushaemulonii, Candida haemulonii, and Candida lusitaniae Targeting rDNA region nucleotide sequ

219 Candida albicans, Candida glabrata, and Candida parapsilosis endophthalmitis isolates were each

220 (S)-carbonyl reductase II (SCRII) from Candida parapsilosis is a short-chain alcohol dehydrogen

221 isteria monocytogenes, Candida albicans, and Candida parapsilosis isolates were detected in volumes a

222 n health care settings compared with that of Candida parapsilosis, a species known to colonize the sk

223 We demonstrate a novel mechanism for Candida parapsilosis-mediated induction of IL-27 in a TL

224 s to facilitate and accelerate research into Candida pathogenesis and biology, by curating the scient

225 actorial manipulation of fungivore (Folsomia candida) presence, nitrogen availability, and fungal ass

226 on for >/=14 days prevents dissemination and Candida-related mortality.

227 ough there was a suggestive association with Candida-related oral mucosal lesions in males (hazard ra

228 we present a scalable methodology to create Candida rugosa lipase-immobilized magnetic nanoparticles

229 A commercial preparation of Candida rugosa lipases (CRL) was tested for the producti

230 auses the naturally abundant and sustainable Candida rugose lipase to ordered-assemble into nanoparti

231 rly diagnosis of fungal infections caused by Candida sp. yeasts.

232 A total of 104 blood cultures with different Candida species (28% C. albicans, 27% C. parapsilosis, 2

233 ication; this assay detects seven pathogenic Candida species (C. albicans, C. glabrata, C. parapsilos

234 The interactions between invasive fungi (eg, Candida species and Aspergillus species) and pathogenic

235 Several pathogenic Candida species are capable of heritable and reversible

236 Lethal systemic fungal infections of Candida species are increasingly common, especially in i

237 Infections caused by non-albicans Candida species are on the rise, but surprisingly little

238 Candida species are one of the leading causes of nosocom

239 y less is known about the dynamics of mixed- Candida species biofilms and how these dynamics are alte

240 ne the precise species composition of mixed- Candida species biofilms formed by clinical isolates and

241 e was not effective against preformed mixed- Candida species biofilms while amphotericin B was potent

242 As a general trend, in mixed- Candida species biofilms, C. albicans lost dominance in

243 ific non- albicans Candida species in mixed- Candida species biofilms.

244 in testing the caspofungin susceptibility of Candida species by both the CLSI and EUCAST broth microd

245 cally ill patients with ICU-acquired sepsis, Candida species colonization at multiple sites, and mult

246 differentiation of major clinically relevant Candida species directly from blood culture.

247 rst week (</=7 days), with identification of Candida species from skin or mucous membrane cultures, a

248 favors the growth of specific non- albicans Candida species in mixed- Candida species biofilms.

249 ion of antifungal agents decreased growth of Candida species in optisol-GS and should be further expl

250 d following ICU admission, colonization with Candida species on surveillance cultures from 3 sites as

251 incubation of optisol-GS increased growth of Candida species over time.

252 ingoencephalitis, colitis, or both caused by Candida species remain unexplained.

253 Given the notable length of time Candida species survive and persist outside their host,

254 at this may also be a greater issue for some Candida species than for others.

255 is also raised the question of whether other Candida species that are unable to form hyphae are as vi

256 Candida species were cultured in 40 cases (56.3%).

257 irst description of active PAMP masking by a Candida species, a process that reduces the visibility o

258 Antifungal resistance, especially among Candida species, aggravates the problem.

259 rotein and sequence information for multiple Candida species, along with web-based tools for accessin

260 carbapenem-resistant Enterobacteriaceae, and Candida species, are a major cause of morbidity, mortali

261 gainst a panel of pathogenic fungi including Candida species, Aspergillus fumigatus, and Cryptococcus

262 This protocol has been used for Candida species, but, using the troubleshooting guide pr

263 nocandin and multidrug resistance among some Candida species, especially Candida glabrata.

264 caspofungin MICs using 209 isolates of four Candida species, including 16 C. albicans and 11 C. glab

265 ation and infections caused by non- albicans Candida species, including C. glabrata, C. dubliniensis,

266 surface of C. albicans and other pathogenic Candida species, is modulated in response to changes in

267 ndins, and polyenes have occurred in several Candida species, most notably Candida glabrata and more

268 , in addition to fungicidal activity against Candida species, shows promising and broad antifungal in

269 Oral infections caused by Candida species, the most commonly isolated human fungal

270 Unlike most other Candida species, this organism appears to be commonly tr

271 al resistance or emergence of drug-resistant Candida species.

272 phic CARD9 mutation causes susceptibility to Candida species.

273 the CNS, digestive tract, or both caused by Candida species.

274 ance, although it is a rare event among most Candida species.

275 ovide useful models for the sexual cycles of Candida species.

276 ibitory to fluconazole-resistant isolates of Candida species.

277 o regulate sexual reproduction in pathogenic Candida species.

278 L-23 are important for host immunity against Candida spp.

279 s showing potent antifungal activity against Candida spp.

280 ced by myeloid cells in response to selected Candida spp.

281 and was not significantly different between Candida spp.

282 eriaceae (42%), Enterococcus spp. (24%), and Candida spp. (15%) were predominant pathogens.

283 Candida spp. adhere to medical devices, such as catheter

284 fungus in air conditioning unit A and B were Candida spp. and Cladosporium spp., and two fungus were

285 Candida spp. elicit cytokine production downstream of va

286 Fungal infections caused by Candida spp. represent an emerging problem during treatm

287 A high load of Candida spp. was found in a symptomatic control sample i

288 Specifically, representation of Candida spp. was reduced, while Aspergillus, Wallemia, a

289 (BCID) that included 19 bacterial species, 5 Candida spp., and 4 antimicrobial resistance genes were

290 Common causes include Candida spp., Fusarium spp. and Aspergillus spp..

291 The majority of isolated yeast were Candida spp., which were usually detected by automated s

292 Members of the genus Candida, such as C. albicans and C. parapsilosis, are im

293 istance mechanisms are not exchanged between Candida; thus, acquired resistance either emerges in res

294 ant species Candida auris, identification of Candida to species level has new clinical relevance.

295 empirical, some institutions do not identify Candida to species level.

296 with other forms of severe disease caused by Candida, Trichophyton, Phialophora, and Exophiala specie

297 %), followed by Candida glabrata (25.6%) and Candida tropicalis (16.3%).

298 Candida was the single most common isolate, but the majo

299 cell count less than 100 cells/mm(3) or non-Candida World Health Organization stage 4 event (with CD

300 tomated systems, whereas the most common non-Candida yeast was Malassezia furfur, which the automated