ライフサイエンスコーパス: proteinosis

1 herosclerotic lesions and pulmonary alveolar proteinosis.

2 patients with idiopathic pulmonary alveolar proteinosis.

3 nic inflammation, and two had focal 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 ventilatory defects 63%, pulmonary alveolar proteinosis 18%, pulmonary arterial hypertension 9%), de

11 studied 12 subjects with pulmonary alveolar proteinosis, 61 healthy control subjects, and 12 control

12 disorder similar to human pulmonary alveolar proteinosis, a rare disease with congenital, infantile,

13 om healthy donors and patients with alveolar proteinosis also binds to M.tb.

14 impaired in patients with pulmonary alveolar proteinosis and that GM-CSF autoantibodies cause the dys

15 e, cigarette smoking, and pulmonary alveolar proteinosis and the implications of obesity and obstruct

16 ytogenetic abnormalities, pulmonary alveolar proteinosis, and myeloid leukemias.

17 lerosis, type 2 diabetes, pulmonary alveolar proteinosis, and obesity, have a chronic inflammatory co

18 ssion profile of a variant causal for lipoid proteinosis, and with a simulation study to assess our m

19 SF and IL-3 and developed pulmonary alveolar proteinosis because of elimination of mouse GM-CSF.

20 d to the pathogenesis of congenital alveolar proteinosis (CAP).

21 crine syndrome type I and pulmonary alveolar proteinosis, detecting ACAA levels consistent with those

22 pe of decreased GM-CSF function is pulmonary proteinosis due to aberrant function of alveolar macroph

23 respiratory infections and develop alveolar proteinosis due to defects in innate immune function and

24 al amygdala pathology as a sequela of lipoid proteinosis due to Urbach-Wiethe disease.

25 Prdx6 and SP-A isolated from human alveolar proteinosis fluid were studied.

26 ophils from subjects with pulmonary alveolar proteinosis had normal ultrastructure and differentiatio

27 Hereditary pulmonary alveolar proteinosis (hPAP) caused by granulocyte-macrophage colo

28 r identical to hereditary pulmonary alveolar proteinosis (hPAP) in children with CSF2RA or CSF2RB mut

29 resulting in complete correction of alveolar proteinosis in bitransgenic GM-/-, SP-C-GM+ mice.

30 al and prevented the development of alveolar proteinosis in mice transplanted with GM-Csf-receptor-de

31 by homologous recombination caused alveolar proteinosis in mice.

32 ronic interstitial inflammation and alveolar proteinosis, inflammation of the glandular stomach and s

33 Idiopathic pulmonary alveolar proteinosis is caused by autoantibodies against granuloc

34 However, lipoid proteinosis is clinically heterogeneous with affected in

35 ice lacking beta c show a pulmonary alveolar proteinosis-like disease and reduced numbers of peripher

36 Lipoid proteinosis (LP), also known as hyalinosis cutis et muco

37 uman SP-A (isolated from normal and alveolar proteinosis lungs) and SP-D (recombinant protein and pro

38 t protein and protein isolated from alveolar proteinosis lungs) bound the conidia.

39 itis obliterans (n = 21), pulmonary alveolar proteinosis (n = 12), pulmonary fibrosis (n = 15), and o

40 nfection in patients with pulmonary alveolar proteinosis occurs in association with high levels of au

41 for later development of pulmonary alveolar proteinosis or other opportunistic infections, and that

42 impaired in patients with pulmonary alveolar proteinosis, owing to the presence of GM-CSF autoantibod

43 t it is elevated in human pulmonary alveolar proteinosis (PAP) and in the GM-CSF knockout mouse, a mu

44 respectively) resulted in pulmonary alveolar proteinosis (PAP) but no hematologic abnormalities.

45 frequency and features of pulmonary alveolar proteinosis (PAP) in patients with ADA deficiency.

46 Pulmonary alveolar proteinosis (PAP) is a rare disease characterized by an

47 Pulmonary alveolar proteinosis (PAP) is a rare disorder in which surfactant

48 Pulmonary alveolar proteinosis (PAP) is a rare lung disease characterized b

49 Pulmonary alveolar proteinosis (PAP) is a rare lung disorder in which surfa

50 Pulmonary alveolar proteinosis (PAP) is a rare lung syndrome caused by the

51 Pulmonary alveolar proteinosis (PAP) is a rare syndrome characterized by ac

52 Primary pulmonary alveolar proteinosis (PAP) is a rare syndrome characterized by ac

53 Pulmonary alveolar proteinosis (PAP) is an idiopathic lung disease in which

54 In patients with pulmonary alveolar proteinosis (PAP) syndrome, disruption of granulocyte/ma

55 dies are thought to cause pulmonary alveolar proteinosis (PAP), a rare syndrome characterized by myel

56 phy is characteristic for pulmonary alveolar proteinosis (PAP), it is not specific and has not been c

57 how its disruption causes pulmonary alveolar proteinosis (PAP), we evaluated lipid composition in alv

58 gitis who later developed pulmonary alveolar proteinosis (PAP).

59 l function in patients with primary alveolar proteinosis (PAP).

60 ells and severe secondary pulmonary alveolar proteinosis (PAP).

61 a slightly more severe mucocutaneous lipoid proteinosis phenotype, but neurological features do not

62 The autosomal recessive disorder lipoid proteinosis results from mutations in extracellular matr

63 f extracts from normal human skin and lipoid proteinosis skin (lacking ECM1).

64 hat partially rescued the pulmonary alveolar proteinosis syndrome.

65 s, distinguishing the disorder from alveolar proteinosis syndromes.

66 in 10 further unrelated patients with lipoid proteinosis to extend genotype-phenotype correlation and

67 unction characteristic of pulmonary alveolar proteinosis was reproduced in a dose-dependent fashion i

68 larities between lichen sclerosus and lipoid proteinosis, which results from mutations in extracellul

69 t5 signaling in AMs, mice developed alveolar proteinosis with altered lipid homeostasis.

70 Five patients developed pulmonary alveolar proteinosis without mutations in the granulocyte-macroph