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1 hesized that 12/15-LOX is also active during invasive aspergillosis.
2 5-LOX (Alox15) are profoundly susceptible to invasive aspergillosis.
3 iconazole treatment failure in patients with invasive aspergillosis.
4 ogression and mortality in a murine model of invasive aspergillosis.
5 roup criteria classified these as "probable" invasive aspergillosis.
6 es in immunocompromised patients who develop invasive aspergillosis.
7 from those of the more commonly encountered invasive aspergillosis.
8 ssue-invasive hyphae, disseminate, and cause invasive aspergillosis.
9 ing as a causative agent of life-threatening invasive aspergillosis.
10 causal agent of the life-threatening disease invasive aspergillosis.
11 ctin inhibits excessive lung inflammation in invasive aspergillosis.
12 demonstrating improved outcomes of treating invasive aspergillosis.
13 osphamide-treated BALB/c mice with cutaneous invasive aspergillosis.
14 gliotoxin contributes to pathogenesis during invasive aspergillosis.
15 n synthesis and are used clinically to treat invasive aspergillosis.
16 or amphotericin B formulation as therapy for invasive aspergillosis.
17 corticosteroid-immunosuppressed mice against invasive aspergillosis.
18 iconazole has become the agent of choice for invasive aspergillosis.
19 apy is increasingly used in the treatment of invasive aspergillosis.
20 y available nonculture method for diagnosing invasive aspergillosis.
21 detection of invasive Candida infection and invasive aspergillosis.
22 diagnostic and therapeutic interventions in invasive aspergillosis.
23 ly deficit in CCR4 (CCR4-/-) did not develop invasive aspergillosis.
24 system, leading to the false presumption of invasive aspergillosis.
25 pergillus fumigatus, the leading etiology of invasive aspergillosis.
26 rulence of the wild type in a mouse model of invasive aspergillosis.
27 ature of the echinocandins, particularly for invasive aspergillosis.
28 1/CCL2 in the lungs of neutropenic mice with invasive aspergillosis.
29 posed them to doxycycline after the onset of invasive aspergillosis.
30 vising future therapeutic strategies against invasive aspergillosis.
31 tin-deficient mice in a neutropenic model of invasive aspergillosis.
32 ere the most common radiographic findings in invasive aspergillosis.
33 portant role in normal host defenses against invasive aspergillosis.
34 ms were associated with significant risk for invasive aspergillosis.
35 toxocariasis, congenital toxoplasmosis, and invasive aspergillosis.
36 tenuate fungal virulence in a mouse model of invasive aspergillosis.
37 ) increased the odds of early posttransplant invasive aspergillosis.
38 e different for invasive candidiasis and for invasive aspergillosis.
39 reduction in mortality in a murine model of invasive aspergillosis.
40 act the sensitivity of mcfDNA sequencing for invasive aspergillosis.
41 killing and, in turn, host susceptibility to invasive aspergillosis.
42 ation because of concerns for posttransplant invasive aspergillosis.
43 rtality up until day 42 in participants with invasive aspergillosis.
44 mbination therapy with azole monotherapy for invasive aspergillosis.
45 test that support the diagnosis of probable invasive aspergillosis.
46 g conditions, which overlap risk factors for invasive aspergillosis.
47 e developments in the molecular diagnosis of invasive aspergillosis.
48 rapy for invasive fungal infections, such as invasive aspergillosis.
49 ended as primary treatment for patients with invasive aspergillosis.
50 to voriconazole for the primary treatment of invasive aspergillosis.
51 12 weeks or less in the primary treatment of invasive aspergillosis.
52 and evaluated different case definitions of invasive aspergillosis.
53 ehold as potential source of azole-resistant invasive aspergillosis.
54 ecisions in patients with triazole-resistant invasive aspergillosis.
55 ungal burden in a neutropenic mouse model of invasive aspergillosis.
56 ce of EAPCRI protocols in an animal model of invasive aspergillosis.
57 of protective innate immune responses during invasive aspergillosis.
58 r donors for PTX3 SNPs modifying the risk of invasive aspergillosis.
59 and evaluated different case definitions of invasive aspergillosis.
60 protects CGD mice from colitis and also from invasive aspergillosis.
61 antly reduced virulence in a murine model of invasive aspergillosis.
62 rum GM quantification for early detection of invasive aspergillosis.
63 ith an increase in the 3-year probability of invasive aspergillosis (12% vs. 1%, P=0.02) and death th
64 fungal infections (36% vs. 7%, P=0.0007) and invasive aspergillosis (14% vs. 2%, P=0.02) was signific
65 ccesses by type of IFI included 7 of 12 with invasive aspergillosis, 2 of 2 with invasive fusariosis,
66 15), Pseudomonas aeruginosa (27%, 4 of 15), invasive aspergillosis (20%, 3 of 15), and Enterobacter
68 illus fumigatus) is the most common cause of invasive aspergillosis, a frequently fatal lung disease
71 be licensed was caspofungin, for refractory invasive aspergillosis (about 40% response rate) and the
72 haplotypes (S3 and S4) increased the risk of invasive aspergillosis (adjusted hazard ratio for S3, 2.
73 onor haplotype S4 also increased the risk of invasive aspergillosis (adjusted odds ratio, 2.49; 95% C
74 ifungal immunity result in increased risk of invasive aspergillosis after chemotherapy or transplanta
75 orphisms were shown to influence the risk of invasive aspergillosis among hematopoietic stem cell tra
76 of TLR polymorphisms in conferring a risk of invasive aspergillosis among recipients of allogeneic he
77 the donor TLR4 haplotype S4 and the risk of invasive aspergillosis among recipients of hematopoietic
82 s a critical early host defense mechanism in invasive aspergillosis and demonstrate NK cells to be an
84 ting may be useful for the diagnosis of both invasive aspergillosis and invasive candidiasis, when in
85 ine dilution into account, reliably detected invasive aspergillosis and may be a promising diagnostic
86 r mold-active triazoles for the treatment of invasive aspergillosis and mucormycosis after solid orga
90 escribe the case of a patient with improving invasive aspergillosis and paradoxically rising serum ga
91 Furthermore, nosocomial infections such as invasive aspergillosis and Pseudomonas aeruginosa occurr
93 fungal infections, invasive mold infections, invasive aspergillosis, and invasive candidiasis during
94 tional amphotericin B as primary therapy for invasive aspergillosis, and is the new standard of care
95 as performed, radiology data consistent with invasive aspergillosis, and the timing of initiation of
96 early IFN-gamma in the lungs in neutropenic invasive aspergillosis, and this is an important mechani
97 to be effective in reducing the incidence of invasive Aspergillosis as compared with no prophylaxis.
100 is considered a significant risk factor for invasive aspergillosis but is almost always associated w
102 NK cells mediate their protective effect in invasive aspergillosis by acting as the major source of
103 above the threshold considered positive for invasive aspergillosis by the recently licensed double s
104 addition to its emergence in the therapy of invasive aspergillosis by triazole medicines, it has bee
107 rate variability in the numbers of diagnosed invasive aspergillosis cases in oncology centers, and a
111 using multiple pulmonary diseases, including invasive aspergillosis, chronic necrotizing aspergillosi
112 festations of Aspergillus infections include invasive aspergillosis, chronic pulmonary aspergillosis
113 ransplant recipients with proven or probable invasive aspergillosis collected as part of the Transpla
114 tive azoles against 731 AFM isolates causing invasive aspergillosis collected in Europe (EU; n = 449)
121 embolism, pneumonia, secondary peritonitis, invasive aspergillosis, endocarditis and myocardial infa
122 , A. fumigatus is the most frequent agent of invasive aspergillosis, followed by A. lentulus and A. v
123 ients with a potentially low pretest risk of invasive aspergillosis following effective antimold prop
125 d comparison clinical trial for treatment of invasive aspergillosis found that the efficacy of isavuc
126 infections is still limited, mouse models of invasive aspergillosis fulfill a critical void for study
128 ared them with contemporaneous patients with invasive aspergillosis (group B; n = 54) and with matche
129 cy of the echinocandins for the treatment of invasive aspergillosis has been based on historically co
133 branching hyphae, suggesting a diagnosis of invasive aspergillosis; however, occasional yeast-like c
136 unit (ICU) patients with probable or proven invasive aspergillosis (IA) and 100 ICU patients without
137 l study, 211 samples from 10 proven/probable invasive aspergillosis (IA) and 2 possible IA cases and
138 entified 93 patients with proven or probable invasive aspergillosis (IA) and GM values of >or=0.50 fr
139 between clinical cases from colonization of invasive aspergillosis (IA) and major building construct
141 iral therapy (cART), roughly 50% of cases of invasive aspergillosis (IA) associated with human immuno
144 dy, 124 DNA extracts from 14 proven/probable invasive aspergillosis (IA) cases, 2 possible IA cases,
149 methodologies for the molecular detection of invasive aspergillosis (IA) have been established by the
151 s DNA for the early diagnosis and therapy of invasive aspergillosis (IA) in high-risk hematological p
154 tus, a ubiquitous mold, is a common cause of invasive aspergillosis (IA) in immunocompromised patient
155 hoalveolar lavage (BAL) for the diagnosis of invasive aspergillosis (IA) in lung transplant recipient
156 of statin use on the risk of development of invasive aspergillosis (IA) in lung transplant recipient
176 y (LFA) is a rapid test for the diagnosis of invasive aspergillosis (IA) that has been almost exclusi
177 tivity of the GM LFA for proven and probable invasive aspergillosis (IA) was 100% (95% CI, 51.0 to 10
178 tool in children at high risk of developing invasive aspergillosis (IA) who are not receiving mold-a
179 nsplant recipients are at increased risk for invasive aspergillosis (IA), a disease with poor outcome
180 he most devastating infections after HSCT is invasive aspergillosis (IA), a life-threatening disease
181 8 ng/ml) of mice with experimentally induced invasive aspergillosis (IA), and levels decreased with a
183 onic necrotizing pulmonary aspergillosis, or invasive aspergillosis (IA), depending on the host's imm
184 ollowing four groups of patients: those with invasive aspergillosis (IA), those with other mold infec
185 ods have long been used for the diagnosis of invasive aspergillosis (IA), variable performance in cli
186 s, and A. terreus, account for most cases of invasive aspergillosis (IA), with A. nidulans, A. niger,
192 ression of one such ligand, KC, in mice with invasive aspergillosis improves the outcome of disease.
193 reviews the presentation and epidemiology of invasive aspergillosis in children and adolescents with
196 leading causative agent of life-threatening invasive aspergillosis in immunocompromised individuals.
197 man fungal pathogen causing life-threatening invasive aspergillosis in immunocompromised patients.
198 tions have been used for prophylaxis against invasive aspergillosis in lung transplant recipients.
203 caspofungin when used as primary therapy for invasive aspergillosis in organ transplant recipients ha
204 eutrophils and may contribute to the risk of invasive aspergillosis in patients treated with HSCT.
206 ession may not be a relevant risk factor for invasive aspergillosis in the 1990s due to less frequent
208 o be the "gold standard" in the treatment of invasive aspergillosis in the immunocompromised host.
209 he immunocompetent host but can cause lethal invasive aspergillosis in the immunocompromised host.
210 ver a potential mechanism for development of invasive aspergillosis in the setting of CGD and cortico
211 ssessed the performance of any PCR assay for invasive aspergillosis in whole blood or serum and that
212 with influenza and COVID-19 with or without invasive aspergillosis in whom BAL for bacterial culture
215 se antigens expanded in patients with active invasive aspergillosis, indicating their contribution to
217 lly bioavailable agents for the treatment of invasive aspergillosis, invasive candidiasis, cryptococc
219 icin B and triazoles is antagonistic against invasive aspergillosis is a controversial issue that is
225 protects immunocompromised patients against invasive aspergillosis is a novel approach to a universa
235 ics of fungal cfDNA PCR for the diagnosis of invasive aspergillosis, mucormycosis, and Pneumocystis p
236 onazole for a median of 58.0 days because of invasive aspergillosis (n = 71) or mucormycosis (n = 10)
237 that, in the lungs of neutropenic mice with invasive aspergillosis, NK cells were the major populati
239 roups (11.0 vs. 7.4 vs. 2.8 days, P=0.0003.) Invasive aspergillosis occurred in 44% of the lowest IgG
241 ), tissue-invasive cytomegalovirus (P=0.01), invasive aspergillosis (P=0.001), total fungal infection
245 nd caspofungin (n=40) as primary therapy for invasive aspergillosis (proven or probable) in a prospec
248 ersistently immunosuppressed murine model of invasive aspergillosis resulted in hypovirulence, while
249 inistration of heme to mice with neutropenic invasive aspergillosis resulted in markedly increased lu
250 KC in the lung in the setting of established invasive aspergillosis results in improved host defense
251 subsets of organ transplant recipients with invasive aspergillosis, such as those with renal failure
252 on (ITT participants with proven or probable invasive aspergillosis) supported this conclusion: 31 (1
253 aluation of therapeutic strategies to combat invasive aspergillosis that closely mimic human disease
254 t we believe is a novel defense mechanism in invasive aspergillosis that is the result of alterations
256 tigen detection for cryptococcal disease and invasive aspergillosis, the use of molecular (PCR) diagn
257 ke early therapeutic decisions when treating invasive aspergillosis using changes in biomarkers as a
258 of A. fumigatus and unique susceptibility to invasive aspergillosis via incompletely characterized me
259 r cumulative incidence of proven or probable invasive aspergillosis was 0.5% (95% CI, 0.1%-3.5%) with
262 transplant patients with proven or probable invasive aspergillosis was available from the Transplant
264 lity of galactomannan antigen for diagnosing invasive aspergillosis was evaluated in 154 liver transp
265 n's eggs and leucopenic mice, the outcome of invasive aspergillosis was similar to that described for
269 nsitivities and specificities for diagnosing invasive aspergillosis were 81.6% and 91.6%, and 76.9% a
270 y failure, malignant organ infiltration, and invasive aspergillosis were associated with higher hospi
271 ungal infections and invasive candidiasis or invasive aspergillosis (when possible) within 1 y posttr
272 lungs of cortisone-treated mice during early invasive aspergillosis, whereas gene expression returned
274 and 54% were on dialysis before the onset of invasive aspergillosis, which suggest that overall sever
275 nic mice provided a protective effect during invasive aspergillosis, which was further enhanced with
276 sufficient sensitivity for the screening of invasive aspergillosis while maintaining methodological
277 ix hospitalized patients with no evidence of invasive aspergillosis who were receiving antibiotics an
280 lerated and effective against IFIs including invasive aspergillosis, zygomycosis, fusariosis, and cry