ライフサイエンスコーパス: candidiasis

1 n and immunopathogenesis during vulvovaginal candidiasis.

2 hilis, bacterial vaginosis (BV), and vaginal candidiasis.

3 risk factor for haematogenously-disseminated candidiasis.

4 atment of experimental subacute disseminated candidiasis.

5 a useful tool for the diagnosis of invasive candidiasis.

6 are the preferred choice to treat a range of candidiasis.

7 icity testing and protection studies against candidiasis.

8 hospital mortality or occurrence of invasive candidiasis.

9 mmadelta T cells and resistance to cutaneous candidiasis.

10 bicans, the causative agent of oropharyngeal candidiasis.

11 ogen and can cause life-threatening systemic candidiasis.

12 of IL-17 during the early innate response to candidiasis.

13 guishable during hematogenously disseminated candidiasis.

14 T3, STAT1, CARD9) are prone to mucocutaneous candidiasis.

15 conversion in patients with proven invasive candidiasis.

16 eficiency in the neutrophil response to oral candidiasis.

17 potent activity in two mouse models of oral candidiasis.

18 al burden in a murine model of oropharyngeal candidiasis.

19 GM-CSF axis contributes to susceptibility to candidiasis.

20 idence of the composite of death or invasive candidiasis.

21 mitigated, but not eliminated, the threat of candidiasis.

22 s class of antifungal drug to treat invasive candidiasis.

23 neutropenia are typically not susceptible to candidiasis.

24 Lcn2 is not required for immunity to mucosal candidiasis.

25 diseases, recurrent aphthous stomatitis, and candidiasis.

26 predisposition to invasive aspergillosis and candidiasis.

27 ol that influences host survival in systemic candidiasis.

28 a are predominant fungi associated with oral candidiasis.

29 primary outcomes were mortality and invasive candidiasis.

30 till had infections, including mucocutaneous candidiasis.

31 s associated with increased risk of systemic candidiasis.

32 e been associated with chronic mucocutaneous candidiasis.

33 y underlie deep dermatophytosis and invasive candidiasis.

34 gated in blood culture-negative, deep-seated candidiasis.

35 FD), particularly invasive aspergillosis and candidiasis.

36 Immunized mice were protected from fatal candidiasis.

37 scribe a simple mouse model of oropharyngeal candidiasis.

38 and approved for treatment of human invasive candidiasis.

39 Four patients had recurrent mucocutaneous candidiasis.

40 17 responses in host defense against mucosal candidiasis.

41 tenuated virulence in a murine model of oral candidiasis.

42 Network study Early Diagnosis of Nosocomial Candidiasis.

43 tion to improve the outcomes of disseminated candidiasis.

44 nd is avirulent in a mouse model of systemic candidiasis.

45 d for optimal host defense against cutaneous candidiasis.

46 ealing in individuals with chronic cutaneous candidiasis.

47 virulence in a murine model of disseminated candidiasis.

48 r virulence in a mouse model of hematogenous candidiasis.

49 motes virulence in a mouse model of systemic candidiasis.

50 st resistance to hematogenously disseminated candidiasis.

51 an invasive, multicellular form that causes candidiasis.

52 an innate immune response in preventing oral candidiasis.

53 oimmune cytopenias and chronic mucocutaneous candidiasis.

54 ding invasive tuberculosis and mucocutaneous candidiasis.

55 s a useful alternative for the management of candidiasis.

56 thogen that causes mucosal and deep systemic candidiasis.

57 utic target for protection from disseminated candidiasis.

58 nt and prevention of candidemia and invasive candidiasis.

59 n oral infection but exacerbate vulvovaginal candidiasis.

60 and 22 (1.5%) exhibited documented invasive candidiasis.

61 duals, probably accounting for their chronic candidiasis.

62 nt and prevention of candidemia and invasive candidiasis.

63 phagocytosis and protect mice from systemic candidiasis.

64 l as biomarkers for anticipation of invasive candidiasis.

65 usceptibility of mice and humans to systemic candidiasis.

66 ne defense against both mucosal and systemic candidiasis.

67 icial mucosal to hematogenously disseminated candidiasis.

68 albicans and suggest therapeutic avenues for candidiasis.

69 immunodeficiency SCID mice from disseminated candidiasis (100% survival in BCG-vaccinated mice vs. 30

70 ood cultures among patients with deep-seated candidiasis (88% and 62% vs 17%; P = .0005 and .003, res

71 , but PCR was more sensitive for deep-seated candidiasis (89% vs 53%; P = .004).

72 da albicans is the leading cause of systemic candidiasis, a disease with poor prognosis affecting imm

73 da albicans is the leading cause of systemic candidiasis, a fungal disease associated with high morta

74 ifestations, including chronic mucocutaneous candidiasis, AI, and asplenia, respectively, in 49 of 12

75 viously shown to produce IL-17 during dermal candidiasis and are known to mediate host defense at muc

76 nvasive mycosis in order of importance after candidiasis and aspergillosis in patients with hematolog

77 disease manifestations such as disseminated candidiasis and chronic mucocutaneous candidiasis (CMC).

78 Mucocutaneous candidiasis and dermatophyte infections occur either in

79 will also be useful for ruling out invasive candidiasis and discontinuing unnecessary antifungal the

80 of neutropenic mice with lethal disseminated candidiasis and inhalational aspergillosis.

81 psilosis is a frequent cause of disseminated candidiasis and is associated with significant morbidity

82 Two HIV-related diagnoses, oesophageal candidiasis and Kaposi's sarcoma, rose from almost zero

83 ndreds of different ethnic origins with both candidiasis and mycobacteriosis.

84 ription 1 (STAT1) with chronic mucocutaneous candidiasis and PML was reported previously.

85 een linked to increased resistance to murine candidiasis and to restriction of fungal growth in vivo.

86 had opportunistic infections (excluding oral candidiasis and tuberculosis).

87 Five patients showed esophageal candidiasis, and 2 had eosinophilic esophagitis.

88 Pneumocystis jiroveci pneumonia, esophageal candidiasis, and disseminated Mycobacterium avium comple

89 l virulence in a mouse model of disseminated candidiasis, and Git3 sequence orthologs are present in

90 d 96% of patients were free of IFD, invasive candidiasis, and invasive aspergillosis at 1 year.

91 ed TH17 differentiation, cured mucocutaneous candidiasis, and maintained remission of immune-mediated

92 ood vessel wall by yeast during disseminated candidiasis, and N-WASP may play a key role in the proce

93 e particularly high in patients with HIV and candidiasis, and that these cells expand and produce IL-

94 cans, the role of IL-17-mediated immunity in candidiasis, and the implications for clinical therapies

95 were hypovirulent in fly and mouse models of candidiasis, and this phenotype correlated with the cell

96 ple endocrine failure, chronic mucocutaneous candidiasis, and various ectodermal defects.

97 As an example, in the treatment of invasive candidiasis, antifungal therapy with intravenous micafun

98 tment based on surrogate markers of invasive candidiasis are warranted.

99 nd as effective in experimental disseminated candidiasis as once-daily therapy in neutropenic hosts.

100 tative role for the Th17 response in mucosal candidiasis as well as S100 alarmin induction, this stud

101 had increased susceptibility to disseminated candidiasis, as indicated by decreased survival and incr

102 ndida infection in a murine model of mucosal candidiasis, as well as in the modulation of host immuni

103 IL17R in patients with chronic mucocutaneous candidiasis, as well as neutralizing autoantibodies agai

104 tory pathology in a gastric model of mucosal candidiasis, but is host protective in disseminated dise

105 Fluconazole prophylaxis reduces candidiasis, but its effect on mortality and the safety

106 e been associated with chronic mucocutaneous candidiasis, but the role of CARD9 in intestinal inflamm

107 ice or humans leads to chronic mucocutaneous candidiasis, but the specific downstream mechanisms of I

108 species have emerged as causes of nosocomial candidiasis, but there is little information about their

109 ete IL-17 are highly susceptible to systemic candidiasis, but we found that temporary blockade of the

110 the incidence of proven or probable invasive candidiasis by EORTC/MSG criteria in patients who did no

111 cultures are limited for diagnosing invasive candidiasis by poor sensitivity and slow turn-around tim

112 Candidiasis carries a significant risk of death or neuro

113 Vulvovaginal candidiasis, caused primarily by Candida albicans, prese

114 Congenital cutaneous candidiasis (CCC) is a challenging diagnosis due to vari

115 al pathogen Candida albicans causes invasive candidiasis, characterized by fatal organ failure due to

116 Chronic mucocutaneous candidiasis (CMC) is characterized by recurrent or persi

117 been shown to underlie chronic mucocutaneous candidiasis (CMC), while inborn errors of caspase recrui

118 7F) or IL-17RA display chronic mucocutaneous candidiasis (CMC).

119 ctions and suffer with chronic mucocutaneous candidiasis (CMC).

120 inated candidiasis and chronic mucocutaneous candidiasis (CMC).

121 ypomorphic alleles) to chronic mucocutaneous candidiasis (CMC; hypermorphic alleles).

122 suspected IFI was the diagnosis of invasive candidiasis confirmed.

123 reatment of invasive aspergillosis, invasive candidiasis, cryptococcal meningitis and mucosal and uri

124 infections, viral infections, mucocutaneous candidiasis, cutaneous warts, and skin abscesses.

125 to contribute to hematogenously disseminated candidiasis (DC) after several days in the standard mous

126 The most common form of oral candidiasis, denture-associated stomatitis, involves bio

127 to antifungal drugs, making the treatment of candidiasis difficult, especially in immunocompromised o

128 le, some patients with chronic mucocutaneous candidiasis disease might also have viral or intracellul

129 iption 1 (STAT1) cause chronic mucocutaneous candidiasis disease.

130 In patients with chronic mucocutaneous candidiasis, disease-associated polymorphisms in DECTIN1

131 y also be incorporated in Sap inhibitors for Candidiasis drugs targeting to lysosomes.

132 s are the recommended treatment for invasive candidiasis due to Candida glabrata.

133 Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) is an autoimmu

134 ither APECED (autoimmune polyendocrinopathy, candidiasis, ectodermal dystrophy syndrome) or thymoma.

135 Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a monogenic

136 Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) syndrome is a

137 Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) syndrome, whic

138 Humans with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED), a T cell-driv

139 patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy, directly impair IL-17

140 disease called autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy.

141 ontrols from a multicenter study of neonatal candidiasis enrolled from 2001 to 2003 were included in

142 dose of micafungin could clear disseminated candidiasis, even though the micafungin half-life in suc

143 tions of exposure, except for LRTI and local candidiasis, for which it was much higher during the fir

144 ion, as well as for the clearance of mucosal candidiasis from the tongue or lower gastrointestinal (G

145 In patients with chronic mucocutaneous candidiasis, gain-of-function STAT1 mutations shift the

146 ntrations in urine of patients with invasive candidiasis (>220 muM).

147 Disseminated candidiasis has become one of the leading causes of hosp

148 rrently used rat and mouse models of vaginal candidiasis have generated a large mass of data on patho

149 Most cases of donor-derived candidiasis have occurred in kidney transplant recipient

150 sk of mortality or of occurrence of invasive candidiasis (hazard ratio, 1.05; 95% confidence interval

151 a mouse model of hematogenously disseminated candidiasis (HDC) and episodes of vulvovaginal candidias

152 order characterized by chronic mucocutaneous candidiasis, hypoparathyroidism, and adrenal insufficien

153 on, Norwegian scabies, chronic mucocutaneous candidiasis, hypothyroidism, and esophageal squamous cel

154 studied the pathogenesis of intra-abdominal candidiasis (IAC) in mice that were infected intraperito

155 -abdominal infection are at risk of invasive candidiasis (IC) and candidates for preemptive antifunga

156 terized isolates from patients with invasive candidiasis (IC) breaking through >or=3 doses of micafun

157 Delayed antifungal therapy for invasive candidiasis (IC) contributes to poor outcomes.

158 Rates of invasive candidiasis (IC) in children between 2003 and 2011 were

159 Invasive candidiasis (IC) is an important cause of sepsis in prem

160 Invasive candidiasis (IC) is an important healthcare-related infe

161 ty of blood cultures for diagnosing invasive candidiasis (IC) is poor.

162 Neonatal invasive candidiasis (IC) presenting in the first week of life is

163 G) levels with clinical outcomes in invasive candidiasis (IC) remains unknown.

164 with C. kefyr, with 8 (9.6%) having invasive candidiasis (IC).

165 ta-D-glucan (BG) is a biomarker for invasive candidiasis (IC).

166 trategies are needed for diagnosing invasive candidiasis (IC).

167 We report here the clinical signs of candidiasis in 35 patients with IL-12Rbeta1 deficiency.

168 increased susceptibility to intra-abdominal candidiasis in a homogenous prospective cohort of high-r

169 kin infection promoted more rapid healing of candidiasis in both wild-type mice and mice deficient in

170 ommended as first-line treatment in invasive candidiasis in children and infants.

171 sis (OPC) compared with systemic and vaginal candidiasis in female patients with AIDS has been a para

172 reat candidaemia and other forms of invasive candidiasis in human patients.

173 imics that of pseudomembranous oropharyngeal candidiasis in humans.

174 rugs used to treat fungal infections such as candidiasis in humans.

175 any antifungal use versus placebo to prevent candidiasis in ICU patients were performed.

176 Antifungal prevention of systemic candidiasis in immunocompetent critically ill adults did

177 g Administration for prophylaxis of invasive candidiasis in patients undergoing bone marrow transplan

178 d numbers of T(H)17 cells, causing localized candidiasis in patients with hyper-IgE syndrome.

179 Invasive candidiasis in premature infants causes death and neurod

180 clinical trials to reduce the occurrence of candidiasis in some patient populations, including high-

181 c mucocutaneous candidiasis, suggesting that candidiasis in subjects with AD-HIES is not driven solel

182 The incidence of proven/probable invasive candidiasis in the placebo and caspofungin arms was 16.7

183 anti-IL-22 autoantibodies and mucocutaneous candidiasis in the setting of either APECED (autoimmune

184 The clinical features and outcome of candidiasis in these patients have not been described be

185 f a previously established model of invasive candidiasis in Toll mutant flies.

186 l mutants, we investigated a murine model of candidiasis in which repressing essential genes in the h

187 ty of fungal infections, especially invasive candidiasis, in patients in the intensive care unit sett

188 ource of IL-17 in HIV-infected patients with candidiasis, in whom CD4(+) Th17 responses are impaired.

189 ortant advances in the diagnosis of invasive candidiasis include rapid species identification and imp

190 xpression of 49 genes during intra-abdominal candidiasis, including previously unidentified Rim101 ta

191 During murine systemic candidiasis, interruption of CCR2-dependent inflammatory

192 CMC, invasive candidiasis, invasive aspergillosis, deep dermatophytosi

193 the most frequent species to be isolated in candidiasis, involves a well-characterized Dectin-1/casp

194 Oropharyngeal candidiasis is a frequent cause of morbidity in patients

195 Invasive candidiasis is a serious infection in hospitalized infan

196 Vaginal candidiasis is common during pregnancy.

197 andida albicans in a mouse model of invasive candidiasis is dependent on the phospholipids phosphatid

198 nnan antibody in host resistance to systemic candidiasis is influenced by its IgG subclass.

199 Reduction in the incidence of invasive candidiasis is observed even when prophylaxis is limited

200 The pathogenesis of intra-abdominal candidiasis is poorly understood.

201 ortant line of defense against oropharyngeal candidiasis is the oral microbiota that prevents infecti

202 Invasive candidiasis is the third most common bloodstream infecti

203 A mouse model of intra-abdominal candidiasis is valuable for studying pathogenesis and C.

204 The relative risk of LRTI and local candidiasis is very high during the first weeks of gluco

205 Species should be identified for invasive candidiasis isolates, and species-level identification c

206 ondary and safety outcomes included invasive candidiasis, liver function, bacterial infection, length

207 Candidiasis may be the first clinical manifestation in t

208 ndings from this study demonstrate that oral candidiasis may constitute a risk factor for disseminate

209 Centers with a low incidence of invasive candidiasis may not benefit from fluconazole prophylaxis

210 Furthermore, in a model of systemic candidiasis, mice lacking group V sPLA(2) had an increas

211 In a murine acute systemic candidiasis model, C albicans strongly stimulated hepcid

212 mation and decreases virulence in a systemic candidiasis model, suggesting a role for post-transcript

213 with proven OPC in 2 episodes, and cutaneous candidiasis (n = 2) with OPC in 1 patient, whereas isola

214 with IC had candidemia (n = 17), deep-seated candidiasis (n = 33), or both (n = 5).

215 Controls had mucosal candidiasis (n = 5), Candida colonization (n = 48), or n

216 Esophageal candidiasis (n = 7) was associated with proven OPC in 2

217 functions and which has been linked to oral candidiasis (OC), the most prevalent oral lesion in huma

218 The first episode of candidiasis occurred earlier in life (median age+/-stand

219 Invasive candidiasis occurred less frequently in the fluconazole

220 Invasive candidiasis occurs in the gastrointestinal tract, especi

221 issue from 25 autopsy patients with invasive candidiasis of the gastrointestinal tract was stained wi

222 Oropharyngeal candidiasis (OPC [thrush]) is an opportunistic infection

223 e disproportionate increase in oropharyngeal candidiasis (OPC) compared with systemic and vaginal can

224 IL-17R) is required to prevent oropharyngeal candidiasis (OPC) in mice and humans.

225 Oropharyngeal candidiasis (OPC) is among the most common opportunistic

226 Oropharyngeal candidiasis (OPC) is an opportunistic fungal infection c

227 Isolated oropharyngeal candidiasis (OPC) was the most common presentation (59 e

228 Oropharyngeal candidiasis (OPC), caused by the commensal fungus Candid

229 albicans is the major cause of oropharyngeal candidiasis (OPC).

230 fungus Candida albicans causes oropharyngeal candidiasis (OPC; thrush) in settings of immunodeficienc

231 Oropharyngeal candidiasis (OPC; thrush) is an opportunistic fungal inf

232 normal flora confirmed by Gram stain with no candidiasis or trichomoniasis).

233 with persistent neutropenia and disseminated candidiasis, otherwise fatal, demonstrated that a single

234 extended the survival of mice with systemic candidiasis (P < 0.001).

235 ted mice against hematogenously disseminated candidiasis (P = .001).

236 occal infection (P=0.01), oral or esophageal candidiasis (P=0.02), death of unknown cause (P=0.03), a

237 quencing to analyze 43 isolates from 11 oral candidiasis patients.

238 ypoparathyroidism, and chronic mucocutaneous candidiasis plus autoantibodies neutralizing IL-17, IL-2

239 t for tuberculosis, and was largest for oral candidiasis, Pneumocystis pneumonia, and toxoplasmosis.

240 ped to investigate whether the onset of oral candidiasis predisposes the host to secondary staphyloco

241 te of death or definite or probable invasive candidiasis prior to study day 49 (1 week after completi

242 t 25% of patients also display mucocutaneous candidiasis, probably owing to impaired interleukin 23-d

243 endent activity in a mouse model of invasive candidiasis, reducing kidney burden by three logs after

244 r basis of host defense against disseminated candidiasis remains elusive, and treatment options are l

245 sual susceptibility to chronic mucocutaneous candidiasis resulting from T(H)17 deficiency have confir

246 terleukin-17 signalling during oropharyngeal candidiasis, resulting in more severe disease.

247 d with development of recurrent vulvovaginal candidiasis (RVVC) in women.

248 including spontaneous central nervous system candidiasis (sCNSc).

249 In a murine model of disseminated candidiasis, serum Cu was seen to progressively rise ove

250 fficacy studies in a mouse model of systemic candidiasis showed that AM2 (5) successfully cured all t

251 idney of antibody-treated mice with systemic candidiasis showed uniform binding of each variant, indi

252 Sap6 is important for virulence during oral candidiasis since it degrades host tissues to release nu

253 Oral candidiasis specifically, characterized by hyphal invasi

254 findings demonstrated that in mice with oral candidiasis, subsequent exposure to S. aureus resulted i

255 cts with mosaicism had chronic mucocutaneous candidiasis, suggesting that candidiasis in subjects wit

256 re superior to blood cultures in deep-seated candidiasis, suggesting they may identify currently undi

257 t assess a patient's risk of having invasive candidiasis, tests will facilitate preemptive antifungal

258 l trial of fluconazole for the prevention of candidiasis that was performed at the same institution.

259 lls both ex vivo and in vivo During systemic candidiasis, the absence of alphaXbeta2 resulted in the

260 IL-17, confers the dominant response to oral candidiasis through neutrophils and antimicrobial factor

261 s also associated with chronic mucocutaneous candidiasis, through as yet undetermined mechanisms invo

262 nts, summary risk was highest (>5%) for oral candidiasis, tuberculosis, herpes zoster, and bacterial

263 p = 0.005) or occurrence of intra-abdominal candidiasis (tumor necrosis factor-alpha rs1800629, haza

264 n patients affected by chronic mucocutaneous candidiasis underscore the preponderant role of IL-17 re

265 l for protection of the host against mucosal candidiasis, underscoring the dependence on different ma

266 ts who are deficient in IL-12Rbeta1 may have candidiasis, usually mucocutaneous, which is frequently

267 Vulvovaginal candidiasis (VVC) caused by Candida albicans affects a s

268 ndidiasis (HDC) and episodes of vulvovaginal candidiasis (VVC) in humans, we found evidence that many

269 Vulvovaginal candidiasis (VVC) is a high-incidence disease seriously

270 Vulvovaginal candidiasis (VVC) is an insidious infection that afflict

271 using a reference standard for vulvovaginal candidiasis (VVC) of yeast culture plus exclusion of alt

272 obacilli may reduce the risk of vulvovaginal candidiasis (VVC), but supporting data are limited.

273 Vulvovaginal candidiasis (VVC), caused by Candida albicans, affects w

274 Vulvovaginal candidiasis (VVC), caused by Candida species, is a signi

275 uding bacterial vaginosis (BV), vulvovaginal candidiasis (VVC), or Trichomonas vaginalis (TV), were r

276 ly bacterial vaginosis (BV) and vulvovaginal candidiasis (VVC), particularly in the setting of treatm

277 in 1 patient, whereas isolated vulvovaginal candidiasis (VVC; n = 3) was not.

278 osite primary end point of death or invasive candidiasis was 16% (95% CI, 11%-22%) vs 21% in the plac

279 ty of a positive BG for identifying invasive candidiasis was 87%, with a 73% specificity.

280 Intra-abdominal candidiasis was defined by the presence of clinical symp

281 nti-Candida activity, in treating esophageal candidiasis was tested in a double-blind study versus or

282 Candidiasis was the first documented infection in 19 of

283 By using a mouse model of oropharyngeal candidiasis we found that IL-17A and IL-17F, which are b

284 rains of C. albicans in two models of murine candidiasis, we demonstrate that neutrophils derived fro

285 Here, using a mouse model of systemic candidiasis, we found that resident macrophages accumula

286 ssect the role of neutrophils during mucosal candidiasis, we took advantage of a new, transparent zeb

287 Patients who had invasive candidiasis were allowed to break the blind and receive

288 Five episodes of proven invasive candidiasis were documented in 4 patients; 1 of these ep

289 ons and development of chronic mucocutaneous candidiasis were extensively studied.

290 Most (n = 71) of the 76 episodes of candidiasis were mucocutaneous.

291 ed for at least 5 days, and free of invasive candidiasis, were included.

292 Infections, including candidiasis, were more common with secukinumab than with

293 d tended to reduce the incidence of invasive candidiasis when used for prophylaxis, but the differenc

294 leukin-17F (IL-17A/F) underlie mucocutaneous candidiasis, whereas inborn errors of interferon-gamma (

295 have long been implicated in defense against candidiasis, whereas the role of Th17 cells remains cont

296 uding recurrent infections and mucocutaneous candidiasis, which are suggestive of TH17 cell dysfuncti

297 re limited by the low prevalence of invasive candidiasis, which mandates that results be interpreted

298 a mouse model of hematogenously disseminated candidiasis, while the double mutant was rapidly cleared

299 he current standard of treatment of invasive candidiasis with echinocandins requires once-daily thera

300 A simplified score that excluded BV and candidiasis yielded an AUC of 0.76 (95% CI, .67-.85); HI