ライフサイエンスコーパス: candidiasis

1 ding invasive tuberculosis and mucocutaneous candidiasis.

2 s a useful alternative for the management of candidiasis.

3 thogen that causes mucosal and deep systemic candidiasis.

4 utic target for protection from disseminated candidiasis.

5 nt and prevention of candidemia and invasive candidiasis.

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

7 duals, probably accounting for their chronic candidiasis.

8 nt and prevention of candidemia and invasive candidiasis.

9 nity is essential to control oral and dermal candidiasis.

10 phagocytosis and protect mice from systemic candidiasis.

11 l as biomarkers for anticipation of invasive candidiasis.

12 usceptibility of mice and humans to systemic candidiasis.

13 ne defense against both mucosal and systemic candidiasis.

14 is avirulent in the mouse model of systemic candidiasis.

15 icial mucosal to hematogenously disseminated candidiasis.

16 albicans and suggest therapeutic avenues for candidiasis.

17 risk factor for haematogenously-disseminated candidiasis.

18 atment of experimental subacute disseminated candidiasis.

19 a useful tool for the diagnosis of invasive candidiasis.

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

21 hospital mortality or occurrence of invasive candidiasis.

22 mmadelta T cells and resistance to cutaneous candidiasis.

23 bicans, the causative agent of oropharyngeal candidiasis.

24 ogen and can cause life-threatening systemic candidiasis.

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

26 guishable during hematogenously disseminated candidiasis.

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

28 conversion in patients with proven invasive candidiasis.

29 eficiency in the neutrophil response to oral candidiasis.

30 GM-CSF axis contributes to susceptibility to candidiasis.

31 idence of the composite of death or invasive candidiasis.

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

33 neutropenia are typically not susceptible to candidiasis.

34 Lcn2 is not required for immunity to mucosal candidiasis.

35 ns reigning as the leading cause of invasive candidiasis.

36 diseases, recurrent aphthous stomatitis, and candidiasis.

37 predisposition to invasive aspergillosis and candidiasis.

38 ol that influences host survival in systemic candidiasis.

39 a are predominant fungi associated with oral candidiasis.

40 till had infections, including mucocutaneous candidiasis.

41 s associated with increased risk of systemic candidiasis.

42 e been associated with chronic mucocutaneous candidiasis.

43 y underlie deep dermatophytosis and invasive candidiasis.

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

45 FD), particularly invasive aspergillosis and candidiasis.

46 Immunized mice were protected from fatal candidiasis.

47 scribe a simple mouse model of oropharyngeal candidiasis.

48 and approved for treatment of human invasive candidiasis.

49 Four patients had recurrent mucocutaneous candidiasis.

50 f C. glabrata in the mouse model of invasive candidiasis.

51 ment of patients with candidemia or invasive candidiasis.

52 protected women from recurrent vulvovaginal candidiasis.

53 aspofungin for primary treatment of invasive candidiasis.

54 phosphorylation during murine oropharyngeal candidiasis.

55 cterial vaginosis, and 8.6% for vulvovaginal candidiasis.

56 ctic and therapeutic intervention of mucosal candidiasis.

57 nsible for approximately 20% of disseminated candidiasis.

58 cted compounds for treatment of disseminated candidiasis.

59 n and immunopathogenesis during vulvovaginal candidiasis.

60 oimmune cytopenias and chronic mucocutaneous candidiasis.

61 n oral infection but exacerbate vulvovaginal candidiasis.

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

63 icity testing and protection studies against candidiasis.

64 potent activity in two mouse models of oral candidiasis.

65 al burden in a murine model of oropharyngeal candidiasis.

66 s class of antifungal drug to treat invasive candidiasis.

67 primary outcomes were mortality and invasive candidiasis.

68 an innate immune response in preventing oral candidiasis.

69 ons of LAUP are as follows: bleeding (2.6%), candidiasis (0.3%), dryness (7.2%), dysgeusia (0.3%), dy

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

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 fungal disease associated with high morta

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

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

75 ause serious nosocomial infections including candidiasis and aspergillosis, some of which display red

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

77 Mucocutaneous candidiasis and dermatophyte infections occur either in

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

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

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

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

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

83 (GOF) mutations also have susceptibility to candidiasis and sinopulmonary infection, as well as auto

84 virulence in a mouse model for disseminated candidiasis and that the cellular functions of Mac1p ext

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

86 y manifesting most commonly as oropharyngeal candidiasis and vulvovaginal candidiasis (VVC).

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 hich are diseases that increase the risk for candidiasis, and MG serves as a regulatory signal in div

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

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

95 d-glucan assays in the diagnosis of invasive candidiasis, and the application of serology and antigen

96 f invasive pulmonary aspergillosis, invasive candidiasis, and the common endemic mycoses was systemat

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

98 g for bacterial vaginosis (BV), vulvovaginal candidiasis, and trichomoniasis.

99 antifungals predominantly used for invasive candidiasis, antibacterial agents posing the highest ris

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

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

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

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

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

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

106 egens strain's activity in an in vivo murine candidiasis assay led to the discovery of a family of hi

107 rom treatment were infrequent and minor (eg, candidiasis) but were slightly more common with active t

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

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

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

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

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

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

114 in vivo experimental models of disseminated candidiasis, C. auris was less virulent than C. albicans

115 Candidiasis carries a significant risk of death or neuro

116 Vulvovaginal candidiasis, caused primarily by Candida albicans, prese

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

118 Chronic disseminated candidiasis (CDC) is a rare disease that mostly occurs a

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

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

121 e been associated with chronic mucocutaneous candidiasis (CMC), as well as with increased susceptibil

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

123 inated candidiasis and chronic mucocutaneous candidiasis (CMC).

124 7F) or IL-17RA display chronic mucocutaneous candidiasis (CMC).

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

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

127 suspected IFI was the diagnosis of invasive candidiasis confirmed.

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

129 Esophageal candidiasis developed in 12% of patients receiving OVB a

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

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

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

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

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

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

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

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

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

139 dry mouth; and autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED).

140 Patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy show diverse endocrine

141 patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy suffer from early-onset

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

143 e skin of both autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy-like kinase-dead Ikkalp

144 patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy.

145 disease called autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy.

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

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

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

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

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

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

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

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

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

155 phae/hyphae is required to determine vaginal candidiasis; however, it may be not sufficient to induce

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

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

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

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

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

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

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

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

164 Invasive candidiasis (IC) is the most common nosocomial infection

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

166 The prevalence rate of invasive candidiasis (IC) was 11.4% (95% CI 9.2-13.6%), and the r

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

168 for treatment of candidemia and/or invasive candidiasis (IC).

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

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

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

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

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

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

175 imics that of pseudomembranous oropharyngeal candidiasis in humans.

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

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

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

179 Invasive candidiasis in premature infants causes death and neurod

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

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

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

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

184 s the main etiological agent of oral mucosal candidiasis, in which a Candida-bacteriome partnership p

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

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

187 bers of bacterial vaginosis and vulvovaginal candidiasis infections.

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

189 CMC, invasive candidiasis, invasive aspergillosis, deep dermatophytosi

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

191 Invasive candidiasis is a medical condition that is challenging t

192 Invasive candidiasis is a serious infection in hospitalized infan

193 Invasive candidiasis is an increasingly frequent cause of serious

194 Vaginal candidiasis is common disease affecting women; however,

195 Vaginal candidiasis is common during pregnancy.

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

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

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

199 Invasive candidiasis is one of the most common nosocomial fungal

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

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

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

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

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

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

216 Invasive candidiasis occurred less frequently in the fluconazole

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

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

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

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

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

222 Oropharyngeal candidiasis (OPC) is an opportunistic infection of the o

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

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

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

226 de effects of blocking these cytokines (oral candidiasis or tuberculosis).

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

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

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

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

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

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

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

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

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

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

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

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

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

240 Recurrent vulvovaginal candidiasis (RVVC) affects up to 8% of women.

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

242 including spontaneous central nervous system candidiasis (sCNSc).

243 y 61.6%, specificity 46.0%; and vulvovaginal candidiasis sensitivity 74.6%, specificity 50.6%.

244 sensitivity and specificity for vulvovaginal candidiasis (sensitivity 64.4%, specificity 69.4%).

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

246 old staphylococcal lesions and mucocutaneous candidiasis, severe allergy, and skeletal abnormalities.

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

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

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

250 Oral candidiasis specifically, characterized by hyphal invasi

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

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

253 identified that causes chronic mucocutaneous candidiasis, suggesting the existence of essential antif

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

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

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

257 ause candidemia is only one form of invasive candidiasis, the true burden of invasive infections due

258 though DS is the most prevalent form of oral candidiasis, there are currently no feasible therapeutic

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

260 and 3639037 visits occurred for non-invasive candidiasis (total cost $1.6 billion).

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

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

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

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

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

266 The diagnosis of vulvovaginal candidiasis (VVC) by the Affirm and Candida vaginitis Ho

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

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

269 Acute vulvovaginal candidiasis (VVC) is common among women, but current azo

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

271 Bacterial vaginosis (BV) and vulvovaginal candidiasis (VVC) present serious reproductive health ri

272 ue to bacterial vaginosis (BV), vulvovaginal candidiasis (VVC), and Trichomonas vaginalis accounts fo

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

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

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

276 s oropharyngeal candidiasis and vulvovaginal candidiasis (VVC).

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

280 Clinically manifested candidiasis was suspected in 16.2% of patients in the BO

281 Candidiasis was the first documented infection in 19 of

282 Vulvovaginal candidiasis was treated presumptively.

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

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

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

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

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

288 riers, and symptomatic patients with vaginal candidiasis were enrolled in this study.

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

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

291 nalis, bacterial vaginosis, and vulvovaginal candidiasis were the gold standard, and all patients pro

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

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

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

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

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

297 number and are focused mainly on diagnosing candidiasis, which is caused by several species of Candi

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

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