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1 hancing the oxidative burst in patients with chronic granulomatous disease.
2 nts with primary immunodeficiency other than chronic granulomatous disease.
3 rms of severe combined immune deficiency and chronic granulomatous disease.
4 sed association of autoimmune disorders with chronic granulomatous disease.
5 id organ transplantation, advanced AIDS, and chronic granulomatous disease.
6 and association of autoimmune diseases with chronic granulomatous disease.
7 patches from eosinophils from a patient with chronic granulomatous disease.
8 and neutrophils from a patient with X-linked chronic granulomatous disease.
9 e of antifungal agents in the prophylaxis of chronic granulomatous disease.
10 novel approach in the molecular treatment of chronic granulomatous disease.
11 hylaxis against serious fungal infections in chronic granulomatous disease.
12 em cells derived from patients with X-linked chronic granulomatous disease.
13 organisms known to have unusual virulence in chronic granulomatous disease.
14 f gene therapy protocols being developed for chronic granulomatous disease.
15 into the X-linked gene CYBB, thereby causing chronic granulomatous disease.
16 tracts of patients with cystic fibrosis and chronic granulomatous disease.
17 ents suffering from cystic fibrosis (CF) and chronic granulomatous disease.
18 gp91(phox)) gives rise to the known types of chronic granulomatous disease.
19 promoter have been detected in patients with chronic granulomatous disease.
20 r in stimulated monocytes from patients with chronic granulomatous disease.
21 ne deficiency, Wiskott-Aldrich syndrome, and chronic granulomatous disease.
22 nia or phagocyte functional defects, such as chronic granulomatous disease.
23 h defective ROS production machinery develop chronic granulomatous disease.
24 cess caused by a Phellinus sp. in a boy with chronic granulomatous disease.
25 e and efficacious in high-risk patients with chronic granulomatous disease.
26 ng dectin-1 deficiency, CARD9 deficiency, or chronic granulomatous disease.
27 ytic functions, such as the genetic disorder chronic granulomatous disease.
28 ealthy volunteers with that in patients with chronic granulomatous disease.
29 is a predictor of survival in patients with chronic granulomatous disease.
30 might be linked to survival in patients with chronic granulomatous disease.
31 ents with X-linked (NOX2) or autosomal (p47) chronic granulomatous disease.
32 nt genetic defect causing p47-phox-deficient chronic granulomatous disease (A47 degrees CGD) is a GT
36 ents of this complex have been implicated in chronic granulomatous disease and Crohn's disease, highl
38 unctive therapy in genetic disorders such as chronic granulomatous disease and infectious diseases su
40 advances in development of gene therapy for chronic granulomatous disease and leukocyte adhesion def
42 th brain abscess formation in a patient with chronic granulomatous disease and review the literature
43 n conducted for other forms of PID including chronic granulomatous disease and Wiskott-Aldrich syndro
45 educes the frequency of fungal infections in chronic granulomatous disease, but monitoring for long-t
47 intermediates (ROIs) is the major defect in chronic granulomatous disease, causing recurrent infecti
48 ying immunocompromising condition, including chronic granulomatous disease (CGD) (n=4), diabetes mell
51 ties in circulating B cells in patients with chronic granulomatous disease (CGD) and those with HIV i
52 xhibits a phenotype similar to that of human chronic granulomatous disease (CGD) and, thus, is an exc
54 utation in p47-phox-deficient (A47 degrees ) chronic granulomatous disease (CGD) as a result of the i
58 Data from a registry of 368 patients with chronic granulomatous disease (CGD) documenta shift in t
59 monstrated in human patients who suffer from chronic granulomatous disease (CGD) due to defective NAD
62 onuclear leukocytes (PMN) from patients with chronic granulomatous disease (CGD) fail to produce micr
63 ls are reduced in the blood of patients with chronic granulomatous disease (CGD) for reasons and cons
68 than 6 years of age) often resembles that of chronic granulomatous disease (CGD) in extent and featur
91 invasive aspergillosis (IA) in patients with chronic granulomatous disease (CGD) is Aspergillus fumig
99 PB in normal volunteers and in patients with chronic granulomatous disease (CGD) or adenosine deamina
100 ogically inhibited oxidase, or isolated from chronic granulomatous disease (CGD) patients and mice, f
103 eotide phosphate (NADPH) oxidase predisposes chronic granulomatous disease (CGD) patients to infectio
104 inucleotide (NADPH) oxidase in patients with chronic granulomatous disease (CGD) results in susceptib
105 utrophils and neutrophils from patients with chronic granulomatous disease (CGD) that are completely
106 uency of serious infections in patients with chronic granulomatous disease (CGD) through an unknown m
107 is a Gram-negative pathogen in patients with chronic granulomatous disease (CGD), a deficiency in the
108 altered B cell compartment in patients with chronic granulomatous disease (CGD), a disorder of phago
109 during prolonged neutropenia or in cases of chronic granulomatous disease (CGD), a primary immunodef
110 de phosphate oxidase 2 (NOX2) function cause chronic granulomatous disease (CGD), a primary immunodef
111 e a major threat for patients suffering from chronic granulomatous disease (CGD), a primary immunodef
112 egative bacterium that infects patients with chronic granulomatous disease (CGD), a primary immunodef
113 n of either p22(phox) or gp91(phox) leads to chronic granulomatous disease (CGD), a severe immune dis
114 ox), both of which are mouse models of human chronic granulomatous disease (CGD), also lack LTP.
116 Progress in development of gene therapy for chronic granulomatous disease (CGD), an inherited defect
118 nactivating mutations in this enzyme lead to chronic granulomatous disease (CGD), associated with inc
119 ntation (HSCT) is a successful treatment for chronic granulomatous disease (CGD), but the safety and
121 t p40(phox), have been described in cases of chronic granulomatous disease (CGD), defining their esse
122 id (BALF) and lungs of A. fumigatus-infected chronic granulomatous disease (CGD), hydrocortisone-trea
123 t in PMNs from six individuals with X-linked chronic granulomatous disease (CGD), p47phox and p67phox
124 a respiratory burst, ie, from a patient with chronic granulomatous disease (CGD), was strongly inhibi
125 so referred to as NOX2), are associated with chronic granulomatous disease (CGD), which is characteri
137 -deficient, and respiratory burst-deficient (chronic granulomatous disease [CGD]) neutrophils killed
138 deficiencies in the oxidative burst seen in chronic granulomatous disease, could lead to pathologic
139 nied with Duchenne muscular dystrophy (DMD), chronic granulomatous disease (CYBB), retinitis pigmento
141 of a lesion at the RP3 locus, in addition to chronic granulomatous disease, Duchenne muscular dystrop
145 neficial gene therapy correction of X-linked chronic granulomatous disease in two adult patients was
146 d in neutrophils isolated from patients with chronic granulomatous disease incubated with a caspase i
155 ditions such as Wiskott-Aldrich syndrome and chronic granulomatous disease, offering curative engraft
156 , p40(phox), p47(phox), p67(phox) (autosomal chronic granulomatous disease), or gp91(phox) (X-linked
157 ns, which compromise p40(phox) function in a chronic granulomatous disease patient, also perturbed cl
158 ad no effect on endothelial function in NOX2-chronic granulomatous disease patients (-0.9; 95% confid
159 -mediated dilatation was not observed in p47-chronic granulomatous disease patients (-1.5%; 95% confi
161 H(+) currents in granulocytes from X-linked chronic granulomatous disease patients lacking gp91(phox
162 he reduced Mo-DC differentiation observed in chronic granulomatous disease patients lacking p22phox.
163 p1 is normally activated in neutrophils from chronic granulomatous disease patients that lack cytochr
168 tients with the p47(phox) deficiency form of chronic granulomatous disease received intravenous infus
169 graft is a feasible option for patients with chronic granulomatous disease, recurrent life-threatenin
170 rors of the phagocyte NADPH oxidase complex (chronic granulomatous disease), severe congenital neutro
171 atus of gene therapy for immunodeficiencies, chronic granulomatous disease, suicide gene therapy for
173 ent (p47(phox-/-)) mice are a model of human chronic granulomatous disease; these mice are prone to d
174 ciency (SCID), Wiskott-Aldrich syndrome, and chronic granulomatous disease through retrospective, pro
175 ulomas and the susceptibility of humans with chronic granulomatous disease to mycobacterial infection
176 atients, five children and five adults, with chronic granulomatous disease underwent peripheral-blood
178 Using Transwells and cells of patients with chronic granulomatous disease, we show that this downreg
180 s (median age 12.7 years; IQR 6.8-17.3) with chronic granulomatous disease were enrolled from June 15
181 nulomatous disease), or gp91(phox) (X-linked chronic granulomatous disease), which result in variable
182 ecies (ROS) because cells from patients with chronic granulomatous disease, which are defective in RO
183 donium and in neutrophils from patients with chronic granulomatous disease, which lack NADPH oxidase.
184 This was also observed in individuals with chronic granulomatous disease, who lack NADPH oxidase ac
185 n patients with the NADPH oxidase deficiency chronic granulomatous disease, who require antibiotic an
188 severe G6PD deficiency can be a phenocopy of chronic granulomatous disease with regard to the cellula
190 sing an established murine model of X-linked chronic granulomatous disease (X-CGD) created by homolog
191 or) was used in a clinical trial of X-linked chronic granulomatous disease (X-CGD) gene therapy to ac
192 ietic stem cells from patients with X-linked chronic granulomatous disease (X-CGD) give rise to X-CGD
193 ratory previously demonstrated that X-linked chronic granulomatous disease (X-CGD) mice develop exagg
197 or this model, because in mice with X-linked chronic granulomatous disease (X-CGD) that lack oxidase
198 atory-burst oxidase cytochrome b-558, mimics chronic granulomatous disease (X-CGD) to study the role
199 m cells (iPSCs) from a patient with X-linked chronic granulomatous disease (X-CGD), a defect of neutr
204 tory burst-deficient gp91(phox)-/- (X-linked chronic granulomatous disease [X-CGD]) mice and inducibl
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