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1 killing and, in turn, host susceptibility to invasive aspergillosis.
2 ungal burden in a neutropenic mouse model of invasive aspergillosis.
3 causal agent of the life-threatening disease invasive aspergillosis.
4 demonstrating improved outcomes of treating invasive aspergillosis.
5 osphamide-treated BALB/c mice with cutaneous invasive aspergillosis.
6 gliotoxin contributes to pathogenesis during invasive aspergillosis.
7 n synthesis and are used clinically to treat invasive aspergillosis.
8 ce of EAPCRI protocols in an animal model of invasive aspergillosis.
9 or amphotericin B formulation as therapy for invasive aspergillosis.
10 corticosteroid-immunosuppressed mice against invasive aspergillosis.
11 iconazole has become the agent of choice for invasive aspergillosis.
12 apy is increasingly used in the treatment of invasive aspergillosis.
13 y available nonculture method for diagnosing invasive aspergillosis.
14 detection of invasive Candida infection and invasive aspergillosis.
15 diagnostic and therapeutic interventions in invasive aspergillosis.
16 ly deficit in CCR4 (CCR4-/-) did not develop invasive aspergillosis.
17 system, leading to the false presumption of invasive aspergillosis.
18 rulence of the wild type in a mouse model of invasive aspergillosis.
19 ature of the echinocandins, particularly for invasive aspergillosis.
20 1/CCL2 in the lungs of neutropenic mice with invasive aspergillosis.
21 posed them to doxycycline after the onset of invasive aspergillosis.
22 vising future therapeutic strategies against invasive aspergillosis.
23 ere the most common radiographic findings in invasive aspergillosis.
24 portant role in normal host defenses against invasive aspergillosis.
25 ms were associated with significant risk for invasive aspergillosis.
26 toxocariasis, congenital toxoplasmosis, and invasive aspergillosis.
27 r donors for PTX3 SNPs modifying the risk of invasive aspergillosis.
28 ehold as potential source of azole-resistant invasive aspergillosis.
29 protects CGD mice from colitis and also from invasive aspergillosis.
30 antly reduced virulence in a murine model of invasive aspergillosis.
31 rum GM quantification for early detection of invasive aspergillosis.
32 ecisions in patients with triazole-resistant invasive aspergillosis.
33 iconazole treatment failure in patients with invasive aspergillosis.
34 roup criteria classified these as "probable" invasive aspergillosis.
35 es in immunocompromised patients who develop invasive aspergillosis.
36 from those of the more commonly encountered invasive aspergillosis.
37 ing as a causative agent of life-threatening invasive aspergillosis.
38 ith an increase in the 3-year probability of invasive aspergillosis (12% vs. 1%, P=0.02) and death th
39 fungal infections (36% vs. 7%, P=0.0007) and invasive aspergillosis (14% vs. 2%, P=0.02) was signific
40 ccesses by type of IFI included 7 of 12 with invasive aspergillosis, 2 of 2 with invasive fusariosis,
41 15), Pseudomonas aeruginosa (27%, 4 of 15), invasive aspergillosis (20%, 3 of 15), and Enterobacter
43 illus fumigatus) is the most common cause of invasive aspergillosis, a frequently fatal lung disease
46 be licensed was caspofungin, for refractory invasive aspergillosis (about 40% response rate) and the
47 haplotypes (S3 and S4) increased the risk of invasive aspergillosis (adjusted hazard ratio for S3, 2.
48 onor haplotype S4 also increased the risk of invasive aspergillosis (adjusted odds ratio, 2.49; 95% C
49 ifungal immunity result in increased risk of invasive aspergillosis after chemotherapy or transplanta
50 orphisms were shown to influence the risk of invasive aspergillosis among hematopoietic stem cell tra
51 of TLR polymorphisms in conferring a risk of invasive aspergillosis among recipients of allogeneic he
52 the donor TLR4 haplotype S4 and the risk of invasive aspergillosis among recipients of hematopoietic
57 s a critical early host defense mechanism in invasive aspergillosis and demonstrate NK cells to be an
59 ine dilution into account, reliably detected invasive aspergillosis and may be a promising diagnostic
62 escribe the case of a patient with improving invasive aspergillosis and paradoxically rising serum ga
63 Furthermore, nosocomial infections such as invasive aspergillosis and Pseudomonas aeruginosa occurr
65 fungal infections, invasive mold infections, invasive aspergillosis, and invasive candidiasis during
66 tional amphotericin B as primary therapy for invasive aspergillosis, and is the new standard of care
67 as performed, radiology data consistent with invasive aspergillosis, and the timing of initiation of
68 early IFN-gamma in the lungs in neutropenic invasive aspergillosis, and this is an important mechani
69 to be effective in reducing the incidence of invasive Aspergillosis as compared with no prophylaxis.
72 is considered a significant risk factor for invasive aspergillosis but is almost always associated w
74 NK cells mediate their protective effect in invasive aspergillosis by acting as the major source of
75 above the threshold considered positive for invasive aspergillosis by the recently licensed double s
77 rate variability in the numbers of diagnosed invasive aspergillosis cases in oncology centers, and a
80 festations of Aspergillus infections include invasive aspergillosis, chronic pulmonary aspergillosis
81 ransplant recipients with proven or probable invasive aspergillosis collected as part of the Transpla
86 embolism, pneumonia, secondary peritonitis, invasive aspergillosis, endocarditis and myocardial infa
87 , A. fumigatus is the most frequent agent of invasive aspergillosis, followed by A. lentulus and A. v
88 ients with a potentially low pretest risk of invasive aspergillosis following effective antimold prop
90 d comparison clinical trial for treatment of invasive aspergillosis found that the efficacy of isavuc
91 infections is still limited, mouse models of invasive aspergillosis fulfill a critical void for study
93 ared them with contemporaneous patients with invasive aspergillosis (group B; n = 54) and with matche
94 cy of the echinocandins for the treatment of invasive aspergillosis has been based on historically co
97 branching hyphae, suggesting a diagnosis of invasive aspergillosis; however, occasional yeast-like c
99 unit (ICU) patients with probable or proven invasive aspergillosis (IA) and 100 ICU patients without
100 l study, 211 samples from 10 proven/probable invasive aspergillosis (IA) and 2 possible IA cases and
101 entified 93 patients with proven or probable invasive aspergillosis (IA) and GM values of >or=0.50 fr
103 iral therapy (cART), roughly 50% of cases of invasive aspergillosis (IA) associated with human immuno
105 dy, 124 DNA extracts from 14 proven/probable invasive aspergillosis (IA) cases, 2 possible IA cases,
109 methodologies for the molecular detection of invasive aspergillosis (IA) have been established by the
111 s DNA for the early diagnosis and therapy of invasive aspergillosis (IA) in high-risk hematological p
113 hoalveolar lavage (BAL) for the diagnosis of invasive aspergillosis (IA) in lung transplant recipient
129 he most devastating infections after HSCT is invasive aspergillosis (IA), a life-threatening disease
130 8 ng/ml) of mice with experimentally induced invasive aspergillosis (IA), and levels decreased with a
132 onic necrotizing pulmonary aspergillosis, or invasive aspergillosis (IA), depending on the host's imm
133 ollowing four groups of patients: those with invasive aspergillosis (IA), those with other mold infec
134 ods have long been used for the diagnosis of invasive aspergillosis (IA), variable performance in cli
135 s, and A. terreus, account for most cases of invasive aspergillosis (IA), with A. nidulans, A. niger,
137 ression of one such ligand, KC, in mice with invasive aspergillosis improves the outcome of disease.
138 reviews the presentation and epidemiology of invasive aspergillosis in children and adolescents with
141 man fungal pathogen causing life-threatening invasive aspergillosis in immunocompromised patients.
142 tions have been used for prophylaxis against invasive aspergillosis in lung transplant recipients.
147 caspofungin when used as primary therapy for invasive aspergillosis in organ transplant recipients ha
148 eutrophils and may contribute to the risk of invasive aspergillosis in patients treated with HSCT.
150 ession may not be a relevant risk factor for invasive aspergillosis in the 1990s due to less frequent
152 o be the "gold standard" in the treatment of invasive aspergillosis in the immunocompromised host.
153 he immunocompetent host but can cause lethal invasive aspergillosis in the immunocompromised host.
154 ver a potential mechanism for development of invasive aspergillosis in the setting of CGD and cortico
155 ssessed the performance of any PCR assay for invasive aspergillosis in whole blood or serum and that
158 se antigens expanded in patients with active invasive aspergillosis, indicating their contribution to
159 lly bioavailable agents for the treatment of invasive aspergillosis, invasive candidiasis, cryptococc
161 icin B and triazoles is antagonistic against invasive aspergillosis is a controversial issue that is
167 protects immunocompromised patients against invasive aspergillosis is a novel approach to a universa
177 that, in the lungs of neutropenic mice with invasive aspergillosis, NK cells were the major populati
179 roups (11.0 vs. 7.4 vs. 2.8 days, P=0.0003.) Invasive aspergillosis occurred in 44% of the lowest IgG
181 ), tissue-invasive cytomegalovirus (P=0.01), invasive aspergillosis (P=0.001), total fungal infection
185 nd caspofungin (n=40) as primary therapy for invasive aspergillosis (proven or probable) in a prospec
187 ersistently immunosuppressed murine model of invasive aspergillosis resulted in hypovirulence, while
188 KC in the lung in the setting of established invasive aspergillosis results in improved host defense
189 subsets of organ transplant recipients with invasive aspergillosis, such as those with renal failure
190 aluation of therapeutic strategies to combat invasive aspergillosis that closely mimic human disease
191 t we believe is a novel defense mechanism in invasive aspergillosis that is the result of alterations
193 tigen detection for cryptococcal disease and invasive aspergillosis, the use of molecular (PCR) diagn
194 ke early therapeutic decisions when treating invasive aspergillosis using changes in biomarkers as a
195 of A. fumigatus and unique susceptibility to invasive aspergillosis via incompletely characterized me
198 transplant patients with proven or probable invasive aspergillosis was available from the Transplant
200 lity of galactomannan antigen for diagnosing invasive aspergillosis was evaluated in 154 liver transp
201 n's eggs and leucopenic mice, the outcome of invasive aspergillosis was similar to that described for
204 nsitivities and specificities for diagnosing invasive aspergillosis were 81.6% and 91.6%, and 76.9% a
205 y failure, malignant organ infiltration, and invasive aspergillosis were associated with higher hospi
206 lungs of cortisone-treated mice during early invasive aspergillosis, whereas gene expression returned
208 and 54% were on dialysis before the onset of invasive aspergillosis, which suggest that overall sever
209 nic mice provided a protective effect during invasive aspergillosis, which was further enhanced with
210 sufficient sensitivity for the screening of invasive aspergillosis while maintaining methodological
211 ix hospitalized patients with no evidence of invasive aspergillosis who were receiving antibiotics an
213 lerated and effective against IFIs including invasive aspergillosis, zygomycosis, fusariosis, and cry
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