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1 antibody detection for chronic and allergic aspergillosis.
2 for PTX3 SNPs modifying the risk of invasive aspergillosis.
3 remaining 165 patients no invasive pulmonary aspergillosis.
4 lent in a murine model of invasive pulmonary aspergillosis.
5 CGD mice from colitis and also from invasive aspergillosis.
6 ich remains the diagnostic gold standard for aspergillosis.
7 uced virulence in a murine model of invasive aspergillosis.
8 antification for early detection of invasive aspergillosis.
9 ransplant recipients with invasive pulmonary aspergillosis.
10 treatment failure in patients with invasive aspergillosis.
11 potential source of azole-resistant invasive aspergillosis.
12 ithm judged 86 of 115 cases to have putative aspergillosis.
13 eria classified these as "probable" invasive aspergillosis.
14 unocompromised patients who develop invasive aspergillosis.
15 detrimental immunopathology that is seen in aspergillosis.
16 se of the more commonly encountered invasive aspergillosis.
17 pathology-controlled patients, 79 had proven aspergillosis.
18 spergillus fumigatus, the causative agent of aspergillosis.
19 in patients with triazole-resistant invasive aspergillosis.
20 Four patients had allergic bronchopulmonary aspergillosis.
21 asthma that mimics allergic bronchopulmonary aspergillosis.
22 causative agent of life-threatening invasive aspergillosis.
23 s fumigatus is responsible for most cases of aspergillosis.
24 not protect immunosuppressed recipients from aspergillosis.
25 d mice from experimentally induced pulmonary aspergillosis.
26 hogenic fungus Aspergillus fumigatus, called aspergillosis.
27 al disseminated candidiasis and inhalational aspergillosis.
28 distinct murine models of invasive pulmonary aspergillosis.
29 genously disseminated and invasive pulmonary aspergillosis.
30 ent of the life-threatening disease invasive aspergillosis.
31 ificant challenge in effective management of aspergillosis.
32 ating improved outcomes of treating invasive aspergillosis.
33 -treated BALB/c mice with cutaneous invasive aspergillosis.
34 ro and in mouse models of invasive pulmonary aspergillosis.
35 contributes to pathogenesis during invasive aspergillosis.
36 is and are used clinically to treat invasive aspergillosis.
37 virulence in an experimental murine model of aspergillosis.
38 ericin B formulation as therapy for invasive aspergillosis.
39 eroid-immunosuppressed mice against invasive aspergillosis.
40 istic in the treatment of invasive pulmonary aspergillosis.
41 nd, in turn, host susceptibility to invasive aspergillosis.
42 den in a neutropenic mouse model of invasive aspergillosis.
43 e the diagnosis of allergic bronchopulmonary aspergillosis.
44 CRI protocols in an animal model of invasive aspergillosis.
45 modulatory therapy to improve the outcome of aspergillosis.
46 se fungal rhinosinusitis or bronchopulmonary aspergillosis.
47 atus avirulent in a mouse model of pulmonary aspergillosis.
48 r in vitro or in a murine model of pulmonary aspergillosis.
49 8 eyes of 8 patients with isolated, orbital aspergillosis.
50 mprehension of the pathogenesis of pulmonary aspergillosis.
51 ausative agent of allergic broncho-pulmonary aspergillosis.
52 vancement in the diagnosis and management of aspergillosis.
53 crease in the 3-year probability of invasive aspergillosis (12% vs. 1%, P=0.02) and death that was no
55 y type of IFI included 7 of 12 with invasive aspergillosis, 2 of 2 with invasive fusariosis, 1 of 1 w
56 gorithm judged 199 patients to have putative aspergillosis (38.0%) and 246 to have Aspergillus coloni
57 udy Group criteria, 32 patients had probable aspergillosis (6.1%) and 413 patients were not classifia
59 igatus) is the most common cause of invasive aspergillosis, a frequently fatal lung disease primarily
60 e displayed high susceptibility to pulmonary aspergillosis, a phenotype associated with a proinflamma
62 t has previously been reported that invasive aspergillosis, a prototypic opportunistic infection in n
63 o the diagnosis of allergic bronchopulmonary aspergillosis (ABPA) and fungal sensitisation, but how t
64 g diseases such as allergic bronchopulmonary aspergillosis (ABPA) and severe asthma with fungal sensi
66 illosis (CCPA) and allergic bronchopulmonary aspergillosis (ABPA) in overtly immunocompetent and atop
71 nsitization and/or allergic bronchopulmonary aspergillosis (ABPA), which affects pulmonary function a
73 s (S3 and S4) increased the risk of invasive aspergillosis (adjusted hazard ratio for S3, 2.20; 95% c
74 otype S4 also increased the risk of invasive aspergillosis (adjusted odds ratio, 2.49; 95% CI, 1.15 t
75 mmunity result in increased risk of invasive aspergillosis after chemotherapy or transplantation.
76 were shown to influence the risk of invasive aspergillosis among hematopoietic stem cell transplant r
79 lymorphisms in conferring a risk of invasive aspergillosis among recipients of allogeneic hematopoiet
80 r TLR4 haplotype S4 and the risk of invasive aspergillosis among recipients of hematopoietic-cell tra
86 f TLR3 was associated with susceptibility to aspergillosis and concomitant failure to activate memory
89 multiplex real-time PCR capable of detecting aspergillosis and genetic markers associated with azole
90 the etiological agent of invasive pulmonary aspergillosis and had reduced in vitro susceptibilities
91 ion into account, reliably detected invasive aspergillosis and may be a promising diagnostic tool for
92 gets for the treatment of invasive pulmonary aspergillosis and may potentiate both innate immunity an
96 more, nosocomial infections such as invasive aspergillosis and Pseudomonas aeruginosa occurred during
97 highlights the magnitude of azole-resistant aspergillosis and resistance mechanisms implicated in th
98 ood conditions are allergic bronchopulmonary aspergillosis and severe asthma with fungal sensitizatio
99 spergillus include allergic bronchopulmonary aspergillosis and severe asthma with fungal sensitizatio
100 seen, and 1 trial indicated a lower rate of aspergillosis and survival benefits in patients with AML
101 about the pathogenesis of invasive pulmonary aspergillosis and the relationship between the kinetics
103 ors (e.g., asthma, allergic bronchopulmonary aspergillosis, and chronic obstructive pulmonary disease
105 lammatory response during invasive pulmonary aspergillosis, and in particular the IL-1 axis, drives t
106 chondrial respiration in the pathogenesis of aspergillosis, and lay the foundation for future researc
108 , the use of molecular (PCR) diagnostics for aspergillosis, and the crucial role of antibody detectio
109 med, radiology data consistent with invasive aspergillosis, and the timing of initiation of antifunga
110 N-gamma in the lungs in neutropenic invasive aspergillosis, and this is an important mechanism in the
111 treatment of chronic pulmonary and allergic aspergillosis are also required, as well as new potent d
113 proven or probable IA from patients without aspergillosis, as determined by European Organization fo
114 is particularly true for invasive pulmonary aspergillosis, as so far, sources of (macro)elements tha
117 and validate novel methods for diagnosis of aspergillosis based on detection of galactomannan requir
118 patients without allergic broncho-pulmonary aspergillosis but sensitized to A. fumigatus and in nine
119 are important in the innate defense against aspergillosis, but little is known about their molecular
120 vaccine-induced protection from experimental aspergillosis, but the molecular mechanisms leading to t
121 mediate their protective effect in invasive aspergillosis by acting as the major source of IFN-gamma
122 as the potential to improve the diagnosis of aspergillosis by offering more rapid and sensitive ident
124 ability in the numbers of diagnosed invasive aspergillosis cases in oncology centers, and a persisten
126 A recent report on several cases of invasive aspergillosis caused by Neosartorya udagawae suggested d
127 fumigatus causes chronic cavitary pulmonary aspergillosis (CCPA) and allergic bronchopulmonary asper
128 atus may result in allergic bronchopulmonary aspergillosis, chronic necrotizing pulmonary aspergillos
129 osis, two each with acute invasive pulmonary aspergillosis, chronic necrotizing pulmonary aspergillos
130 s of Aspergillus infections include invasive aspergillosis, chronic pulmonary aspergillosis and bronc
131 tive GM (serologic allergic bronchopulmonary aspergillosis); class 3 (n = 19, 14.6%) represented pati
132 recipients with proven or probable invasive aspergillosis collected as part of the Transplant-Associ
135 ves survival of mice with invasive pulmonary aspergillosis, demonstrating the potential of CalA as an
136 ally, in the context of neutropenic invasive aspergillosis, depletion of DCs resulted in impaired fun
138 The calibrator can be used to standardize aspergillosis diagnostic assays which detect and/or quan
140 ortunistic animal and human pathogen causing aspergillosis diseases with incidence increasing in the
144 , pneumonia, secondary peritonitis, invasive aspergillosis, endocarditis and myocardial infarction.
146 gatus is the most frequent agent of invasive aspergillosis, followed by A. lentulus and A. viridinuta
147 h a potentially low pretest risk of invasive aspergillosis following effective antimold prophylaxis.
149 son clinical trial for treatment of invasive aspergillosis found that the efficacy of isavuconazole w
150 elped distinguish allergic broncho-pulmonary aspergillosis from A. fumigatus sensitization with good
151 s is still limited, mouse models of invasive aspergillosis fulfill a critical void for studying treat
153 echinocandins for the treatment of invasive aspergillosis has been based on historically controlled
156 U) patients with probable or proven invasive aspergillosis (IA) and 100 ICU patients without IA.
157 211 samples from 10 proven/probable invasive aspergillosis (IA) and 2 possible IA cases and 27 contro
158 93 patients with proven or probable invasive aspergillosis (IA) and GM values of >or=0.50 from Januar
160 apy (cART), roughly 50% of cases of invasive aspergillosis (IA) associated with human immunodeficienc
162 NA extracts from 14 proven/probable invasive aspergillosis (IA) cases, 2 possible IA cases, and 33 co
165 Screening of high-risk patients for invasive aspergillosis (IA) has the potential to decrease the use
166 gies for the molecular detection of invasive aspergillosis (IA) have been established by the European
167 the early diagnosis and therapy of invasive aspergillosis (IA) in high-risk hematological patients r
169 r lavage (BAL) for the diagnosis of invasive aspergillosis (IA) in lung transplant recipients is not
171 Despite suffering an outbreak of invasive aspergillosis (IA) in the intensive care unit due to ext
177 The testing of an animal model of invasive aspergillosis (IA) overcomes the low incidence of diseas
182 evastating infections after HSCT is invasive aspergillosis (IA), a life-threatening disease caused by
183 ansplant recipients are at risk for invasive aspergillosis (IA), associated with a significant mortal
184 otizing pulmonary aspergillosis, or invasive aspergillosis (IA), depending on the host's immune statu
185 four groups of patients: those with invasive aspergillosis (IA), those with other mold infections (Fu
186 long been used for the diagnosis of invasive aspergillosis (IA), variable performance in clinical pra
189 galactomannan (GM) for diagnosing pulmonary aspergillosis in 73 nonimmunocompromised patients with p
190 but also triggers allergic bronchopulmonary aspergillosis in a subset of otherwise healthy individua
191 phylaxis trials have shown trends of reduced aspergillosis in BMT patients; however, no survival bene
194 he presentation and epidemiology of invasive aspergillosis in children and adolescents with acquired
197 re, we evaluated susceptibility to pulmonary aspergillosis in globally NADPH oxidase-deficient mice v
206 in order of importance after candidiasis and aspergillosis in patients with hematological and allogen
207 ly associated with allergic bronchopulmonary aspergillosis in patients with severe asthma in which ch
211 ential mechanism for development of invasive aspergillosis in the setting of CGD and corticosteroid-i
213 he performance of any PCR assay for invasive aspergillosis in whole blood or serum and that used the
214 ns expanded in patients with active invasive aspergillosis, indicating their contribution to infectio
215 ogeny of adaptive immune responses to murine aspergillosis infection in relation to vaccination.
217 ailable agents for the treatment of invasive aspergillosis, invasive candidiasis, cryptococcal mening
218 s and optimal therapy for invasive pulmonary aspergillosis (IPA) after kidney transplantation (KT) re
220 fluid in the diagnosis of invasive pulmonary aspergillosis (IPA) among solid-organ transplant recipie
224 olved inflammation during invasive pulmonary aspergillosis (IPA) is associated with a poor outcome.
235 d triazoles is antagonistic against invasive aspergillosis is a controversial issue that is not likel
250 hough the number of cases of azole-resistant aspergillosis is still limited, resistance mechanisms co
251 the strategies to improve the management of aspergillosis is the adoptive transfer of antigen-specif
253 d that in a murine model of bronchopulmonary aspergillosis, maternal exposure to mainstream CS increa
259 the lungs of neutropenic mice with invasive aspergillosis, NK cells were the major population of cel
261 e in patients with allergic bronchopulmonary aspergillosis or cystic fibrosis are among the major rec
262 aspergillosis, chronic necrotizing pulmonary aspergillosis, or invasive aspergillosis (IA), depending
263 burdens in a rat model of invasive pulmonary aspergillosis (p<0.05) compared to treatment with the ca
265 e mortality and morbidity caused by invasive aspergillosis present a major obstacle to the successful
266 The diagnosis of allergic bronchopulmonary aspergillosis relies on criteria first established in 19
268 ly immunosuppressed murine model of invasive aspergillosis resulted in hypovirulence, while analysis
269 rve as an S source during invasive pulmonary aspergillosis since a sulfate transporter mutant strain
270 eve is a novel defense mechanism in invasive aspergillosis that is the result of alterations in DC tr
272 ection for cryptococcal disease and invasive aspergillosis, the use of molecular (PCR) diagnostics fo
274 ine patients with allergic broncho-pulmonary aspergillosis (two with cystic fibrosis and seven with a
276 therapeutic decisions when treating invasive aspergillosis using changes in biomarkers as a surrogate
277 igatus and unique susceptibility to invasive aspergillosis via incompletely characterized mechanisms.
282 nt patients with proven or probable invasive aspergillosis was available from the Transplant-Associat
288 and leucopenic mice, the outcome of invasive aspergillosis was similar to that described for A. fumig
289 ance of phagocyte NADPH oxidase in resisting aspergillosis, we found no evidence of this mechanism in
290 investigate the role of CCR7 during invasive aspergillosis, we used a well-characterized neutropenic
291 f two significant resources: the Aspergillus/Aspergillosis website and the Central Aspergillus Data R
292 es and specificities for diagnosing invasive aspergillosis were 81.6% and 91.6%, and 76.9% and 89.4%,
293 , malignant organ infiltration, and invasive aspergillosis were associated with higher hospital morta
294 cortisone-treated mice during early invasive aspergillosis, whereas gene expression returned rapidly
296 provided a protective effect during invasive aspergillosis, which was further enhanced with the adopt
297 nt sensitivity for the screening of invasive aspergillosis while maintaining methodological simplicit
298 tremely susceptible to mucormycosis, but not aspergillosis, while sodium bicarbonate reversed this su
300 nd effective against IFIs including invasive aspergillosis, zygomycosis, fusariosis, and cryptococcos
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