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1 eted and dysfunctional, resembling pulmonary alveolar proteinosis.
2 tic of atherosclerotic lesions and pulmonary alveolar proteinosis.
3 from six patients with idiopathic pulmonary alveolar proteinosis.
4 rupt surfactant clearance, causing pulmonary alveolar proteinosis.
5 bodies isolated from patients with pulmonary alveolar proteinosis.
6 contributor to the pathogenesis of pulmonary alveolar proteinosis.
7 omatous inflammation leading to fibrosis and alveolar proteinosis.
8 vital lung function that prevents pulmonary alveolar proteinosis.
9 with chronic inflammation, and two had focal alveolar proteinosis.
10 n 79% and ventilatory defects 63%, pulmonary alveolar proteinosis 18%, pulmonary arterial hypertensio
12 t a lung disorder similar to human pulmonary alveolar proteinosis, a rare disease with congenital, in
14 sufficient GM-CSF signaling caused pulmonary alveolar proteinosis and excessive IL-6 signaling promot
15 ions are impaired in patients with pulmonary alveolar proteinosis and that GM-CSF autoantibodies caus
16 e syndrome, cigarette smoking, and pulmonary alveolar proteinosis and the implications of obesity and
19 atherosclerosis, type 2 diabetes, pulmonary alveolar proteinosis, and obesity, have a chronic inflam
21 antibodies against GM-CSF underlie pulmonary alveolar proteinosis; associated infections are less wel
22 ing growth failure, renal disease, pulmonary alveolar proteinosis, autoimmune disorders and osteoporo
23 uman GM-CSF and IL-3 and developed pulmonary alveolar proteinosis because of elimination of mouse GM-
25 polyendocrine syndrome type I and pulmonary alveolar proteinosis, detecting ACAA levels consistent w
26 ptible to respiratory infections and develop alveolar proteinosis due to defects in innate immune fun
27 actant and cell debris in airways (pulmonary alveolar proteinosis) due to impaired development of alv
29 Neutrophils from subjects with pulmonary alveolar proteinosis had normal ultrastructure and diffe
31 l disorder identical to hereditary pulmonary alveolar proteinosis (hPAP) in children with CSF2RA or C
32 -/- mice resulting in complete correction of alveolar proteinosis in bitransgenic GM-/-, SP-C-GM+ mic
33 functional and prevented the development of alveolar proteinosis in mice transplanted with GM-Csf-re
35 monary chronic interstitial inflammation and alveolar proteinosis, inflammation of the glandular stom
38 Both human SP-A (isolated from normal and alveolar proteinosis lungs) and SP-D (recombinant protei
40 bronchiolitis obliterans (n = 21), pulmonary alveolar proteinosis (n = 12), pulmonary fibrosis (n = 1
41 idosis (occupational burden, 30%); pulmonary alveolar proteinosis (occupational burden, 29%); tubercu
42 ty from infection in patients with pulmonary alveolar proteinosis occurs in association with high lev
43 e at risk for later development of pulmonary alveolar proteinosis or other opportunistic infections,
44 hils are impaired in patients with pulmonary alveolar proteinosis, owing to the presence of GM-CSF au
45 erved that it is elevated in human pulmonary alveolar proteinosis (PAP) and in the GM-CSF knockout mo
46 -) mice, respectively) resulted in pulmonary alveolar proteinosis (PAP) but no hematologic abnormalit
47 rize the frequency and features of pulmonary alveolar proteinosis (PAP) in patients with ADA deficien
61 ystemic lupus erythematosus (SLE), pulmonary alveolar proteinosis (PAP) or multiple sclerosis) and co
63 utoantibodies are thought to cause pulmonary alveolar proteinosis (PAP), a rare syndrome characterize
64 d tomography is characteristic for pulmonary alveolar proteinosis (PAP), it is not specific and has n
65 rom five independent kindreds have pulmonary alveolar proteinosis (PAP), progressive polycystic lung
66 asis and how its disruption causes pulmonary alveolar proteinosis (PAP), we evaluated lipid compositi
72 phil dysfunction characteristic of pulmonary alveolar proteinosis was reproduced in a dose-dependent
73 ce of Stat5 signaling in AMs, mice developed alveolar proteinosis with altered lipid homeostasis.