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1 dysfunctional, resembling pulmonary alveolar proteinosis.
2 herosclerotic lesions and pulmonary alveolar proteinosis.
3  patients with idiopathic pulmonary alveolar proteinosis.
4 actant clearance, causing pulmonary alveolar proteinosis.
5 olated from patients with pulmonary alveolar proteinosis.
6 ore represent a recurrent mutation in lipoid proteinosis.
7 or to the pathogenesis of pulmonary alveolar proteinosis.
8 st common sites for ECM1 mutations in lipoid proteinosis.
9 nflammation leading to fibrosis and alveolar proteinosis.
10 nic inflammation, and two had focal alveolar proteinosis.
11 ng function that prevents pulmonary alveolar proteinosis.
12  ventilatory defects 63%, pulmonary alveolar proteinosis 18%, pulmonary arterial hypertension 9%), de
13  studied 12 subjects with pulmonary alveolar proteinosis, 61 healthy control subjects, and 12 control
14 disorder similar to human pulmonary alveolar proteinosis, a rare disease with congenital, infantile,
15 om healthy donors and patients with alveolar proteinosis also binds to M.tb.
16 ar macrophages, thereby underlying pulmonary proteinosis and airborne infections, type I interferon v
17 t GM-CSF signaling caused pulmonary alveolar proteinosis and excessive IL-6 signaling promoted bone m
18 impaired in patients with pulmonary alveolar proteinosis and that GM-CSF autoantibodies cause the dys
19 e, cigarette smoking, and pulmonary alveolar proteinosis and the implications of obesity and obstruct
20 s infections, lymphedema, pulmonary alveolar proteinosis, and myelodysplasia.
21 ytogenetic abnormalities, pulmonary alveolar proteinosis, and myeloid leukemias.
22 lerosis, type 2 diabetes, pulmonary alveolar proteinosis, and obesity, have a chronic inflammatory co
23 ssion profile of a variant causal for lipoid proteinosis, and with a simulation study to assess our m
24                Autoimmune pulmonary alveolar proteinosis (aPAP) is a rare lung disorder involving pro
25 s against GM-CSF underlie pulmonary alveolar proteinosis; associated infections are less well charact
26 h failure, renal disease, pulmonary alveolar proteinosis, autoimmune disorders and osteoporosis, are
27 SF and IL-3 and developed pulmonary alveolar proteinosis because of elimination of mouse GM-CSF.
28 d to the pathogenesis of congenital alveolar proteinosis (CAP).
29 crine syndrome type I and pulmonary alveolar proteinosis, detecting ACAA levels consistent with those
30 pe of decreased GM-CSF function is pulmonary proteinosis due to aberrant function of alveolar macroph
31  respiratory infections and develop alveolar proteinosis due to defects in innate immune function and
32 al amygdala pathology as a sequela of lipoid proteinosis due to Urbach-Wiethe disease.
33 d cell debris in airways (pulmonary alveolar proteinosis) due to impaired development of alveolar mac
34  Prdx6 and SP-A isolated from human alveolar proteinosis fluid were studied.
35 ophils from subjects with pulmonary alveolar proteinosis had normal ultrastructure and differentiatio
36                Hereditary pulmonary alveolar proteinosis (hPAP) caused by granulocyte-macrophage colo
37 r identical to hereditary pulmonary alveolar proteinosis (hPAP) in children with CSF2RA or CSF2RB mut
38 resulting in complete correction of alveolar proteinosis in bitransgenic GM-/-, SP-C-GM+ mice.
39 al and prevented the development of alveolar proteinosis in mice transplanted with GM-Csf-receptor-de
40  by homologous recombination caused alveolar proteinosis in mice.
41 ronic interstitial inflammation and alveolar proteinosis, inflammation of the glandular stomach and s
42                Idiopathic pulmonary alveolar proteinosis is caused by autoantibodies against granuloc
43                              However, lipoid proteinosis is clinically heterogeneous with affected in
44 ice lacking beta c show a pulmonary alveolar proteinosis-like disease and reduced numbers of peripher
45                                       Lipoid proteinosis (LP), also known as hyalinosis cutis et muco
46 uman SP-A (isolated from normal and alveolar proteinosis lungs) and SP-D (recombinant protein and pro
47 t protein and protein isolated from alveolar proteinosis lungs) bound the conidia.
48 itis obliterans (n = 21), pulmonary alveolar proteinosis (n = 12), pulmonary fibrosis (n = 15), and o
49 ccupational burden, 30%); pulmonary alveolar proteinosis (occupational burden, 29%); tuberculosis (oc
50 nfection in patients with pulmonary alveolar proteinosis occurs in association with high levels of au
51 B, and C in lavage fluids from patients with proteinosis of different causes in comparison with healt
52  for later development of pulmonary alveolar proteinosis or other opportunistic infections, and that
53 impaired in patients with pulmonary alveolar proteinosis, owing to the presence of GM-CSF autoantibod
54 t it is elevated in human pulmonary alveolar proteinosis (PAP) and in the GM-CSF knockout mouse, a mu
55 respectively) resulted in pulmonary alveolar proteinosis (PAP) but no hematologic abnormalities.
56 frequency and features of pulmonary alveolar proteinosis (PAP) in patients with ADA deficiency.
57                           Pulmonary alveolar proteinosis (PAP) is a devastating lung disease caused b
58                           Pulmonary alveolar proteinosis (PAP) is a rare disease characterized by an
59                Autoimmune pulmonary alveolar proteinosis (PAP) is a rare disease characterized by mye
60                           Pulmonary alveolar proteinosis (PAP) is a rare disease with frequently favo
61                           Pulmonary alveolar proteinosis (PAP) is a rare disorder in which surfactant
62                           Pulmonary alveolar proteinosis (PAP) is a rare lung disease characterized b
63                           Pulmonary alveolar proteinosis (PAP) is a rare lung disorder in which surfa
64                           Pulmonary alveolar proteinosis (PAP) is a rare lung syndrome caused by the
65                           Pulmonary alveolar proteinosis (PAP) is a rare syndrome characterized by ac
66                   Primary pulmonary alveolar proteinosis (PAP) is a rare syndrome characterized by ac
67                           Pulmonary alveolar proteinosis (PAP) is a syndrome characterized by the acc
68                           Pulmonary alveolar proteinosis (PAP) is an idiopathic lung disease in which
69                Rationale: Pulmonary alveolar proteinosis (PAP) is characterized by filling of the alv
70 upus erythematosus (SLE), pulmonary alveolar proteinosis (PAP) or multiple sclerosis) and coronavirus
71          In patients with pulmonary alveolar proteinosis (PAP) syndrome, disruption of granulocyte/ma
72 dies are thought to cause pulmonary alveolar proteinosis (PAP), a rare syndrome characterized by myel
73 phy is characteristic for pulmonary alveolar proteinosis (PAP), it is not specific and has not been c
74 independent kindreds have pulmonary alveolar proteinosis (PAP), progressive polycystic lung disease,
75 how its disruption causes pulmonary alveolar proteinosis (PAP), we evaluated lipid composition in alv
76 ells and severe secondary pulmonary alveolar proteinosis (PAP).
77 gitis who later developed pulmonary alveolar proteinosis (PAP).
78 l function in patients with primary alveolar proteinosis (PAP).
79  a slightly more severe mucocutaneous lipoid proteinosis phenotype, but neurological features do not
80      The autosomal recessive disorder lipoid proteinosis results from mutations in extracellular matr
81 f extracts from normal human skin and lipoid proteinosis skin (lacking ECM1).
82 hat partially rescued the pulmonary alveolar proteinosis syndrome.
83 s, distinguishing the disorder from alveolar proteinosis syndromes.
84 in 10 further unrelated patients with lipoid proteinosis to extend genotype-phenotype correlation and
85 unction characteristic of pulmonary alveolar proteinosis was reproduced in a dose-dependent fashion i
86 larities between lichen sclerosus and lipoid proteinosis, which results from mutations in extracellul
87 t5 signaling in AMs, mice developed alveolar proteinosis with altered lipid homeostasis.
88   Five patients developed pulmonary alveolar proteinosis without mutations in the granulocyte-macroph