ライフサイエンスコーパス: nasal lavage

1 hils, eosinophils, and interleukin (IL)-6 in nasal lavage.

2 miRNAs could be confirmed in EVs from human nasal lavages.

3 ollowed by standard dose of virus and serial nasal lavages.

4 ined by quantification of S. pneumoniae from nasal lavage and analysis of sinus tissue, respectively.

5 merase chain reaction analysis on cells from nasal lavage and induced sputum samples from all subject

6 Rhinovirus RNA was detected in both nasal lavage and lower airway cells from all eight subje

7 ssociation between ChoP(+) expression in the nasal lavage and the development of OM with culture-posi

8 al loads, and cytokines were quantified from nasal lavages and blood, and correlated to clinical seve

9 t spirometry, methacholine challenge (PC20), nasal lavage, and sputum induction at baseline and on Da

10 5-75%pred) ), thus lower sEV-miRNA levels in nasal lavages associated with airway obstruction.

11 Nasal lavages at 0, 15, 60, and 120 min after lysine-asp

12 Nasosorption, nasal lavage, blood samples, forced expiratory volume 1

13 f which conducted an additional visit with a nasal lavage collected and subjected to bulk RNA-sequenc

14 In addition, one rhinovirus from a nasal lavage contained an identical nucleic acid sequenc

15 Nasal lavage cytokine levels of IL-4 (P < 0.01), IL-5, a

16 We analysed cytokine levels in nasal lavage fluid (NLF) in 59 subjects (46 with asthma)

17 IL-8 levels were measured in nasal lavage fluid and serum on randomization, day 8, an

18 ction through analysis of cytokine levels in nasal lavage fluid and stimulated peripheral blood monon

19 tion of macrophage inflammatory protein 2 in nasal lavage fluid and subsequent recruitment of neutrop

20 Viral load was measured in nasal lavage fluid at day 3, 6 and 14.

21 Nasal lavage fluid cells were analyzed for inflammatory

22 the mouse, human CD49d(+) PMNs isolated from nasal lavage fluid during a viral respiratory tract infe

23 +) PMN frequency was significantly higher in nasal lavage fluid during acute respiratory symptoms in

24 We collected nasal tissue and nasal lavage fluid from patients with CRS and control su

25 = .6) but resulted in a greater decrease in nasal lavage fluid IL-8 levels by day 15 (P = .03).

26 Nasal lavage fluid levels of interleukin (IL)-6, tumor n

27 Nasal lavage fluid myeloperoxidase (another neutrophil m

28 and measured the total leukocyte content of nasal lavage fluid obtained from 10 min to 4 h after the

29 cell differential counts were evaluated from nasal lavage fluid obtained from wild-type and IL-17A-de

30 nts with acute bronchiolitis was elevated in nasal lavage fluid on both Days 1-2 (p = 0.014) and Days

31 ning cytokine and chemokine levels in serial nasal lavage fluid samples from 15 volunteers experiment

32 higher level of NTHI 2019 per milliliter of nasal lavage fluid than chinchillas colonized with predo

33 The percentage of leukocytes observed in nasal lavage fluid was significantly increased 12, 24, 4

34 ncreased levels of inflammatory cytokines in nasal lavage fluid, and confirmed olfactory dysfunction

35 antibodies was measured in tissue extracts, nasal lavage fluid, and sera by using multiplex bead arr

36 histologic assessment, cytokine analysis of nasal lavage fluid, olfactory behavioral tests, and gene

37 IL-8, IFN-alpha, TGF-beta, and TNF-alpha in nasal lavage fluid, plasma, and serum obtained serially

38 leukotriene (cysLT) levels were measured in nasal lavage fluid.

39 y response (measured by the albumin level in nasal-lavage fluid) to nasal provocation.

40 We sought to compare MP types and levels in nasal lavage fluids (NLFs) from controls and patients wi

41 Ethmoid tissues and nasal lavage fluids (NLFs) were obtained from control pa

42 e assessed, the inflammatory cell content in nasal lavage fluids estimated, and the activation patter

43 tase protein was also elevated in NPs and in nasal lavage fluids from patients with CRSwNP.

44 ergen significantly increased NGF protein in nasal lavage fluids of subjects with allergic rhinitis,

45 We found that IL-6 and IFN-alpha levels in nasal lavage fluids peaked early (day 2) and correlated

46 ores, and concentrations of IL-6 and IL-8 in nasal lavage fluids were compared between treatment grou

47 The concentrations of NGF protein in nasal lavage fluids were not affected by provocation wit

48 Sinonasal tissues and nasal lavage fluids were obtained from control patients

49 er baseline concentrations of NGF protein in nasal lavage fluids, compared with control subjects.

50 Nasal lavage for flow cytometry and nasal swabs for vira

51 ers kept a daily diary of symptoms and had a nasal lavage for polymerase chain reaction once each wee

52 We collected nasal lavages from ragweed sensitized subjects at differ

53 eron-gamma, and RANTES were detected only in nasal lavages from two asthmatic subjects, who had the m

54 t during RSV bronchiolitis reduces serum and nasal lavage IL-8 levels and the occurrence of postbronc

55 ECP in the nasal lavage increased after the NAC-P in the group A (P

56 te immune profile characterized by increased nasal lavage monocyte chemotactic protein-3, IFN-alpha2,

57 l cells and proinflammatory cytokines in the nasal lavage (NAL) and bronchoalveolar lavage (BAL) flui

58 Nasal lavage (NAL) fluid samples were obtained from five

59 Biomarkers in nasal lavage (NL) fluid may be useful in determining the

60 Nasal lavage (NL) samples from 20 subjects who were expo

61 r proteins were recovered during presurgical nasal lavage of patients at a sinus clinic.

62 olated by size-exclusion chromatography from nasal lavages of children with mild-to-moderate (n = 8)

63 d serum on randomization, day 8, and day 15 (nasal lavage only).

64 specific IgE, IgG, and IgG4 were measured in nasal lavage samples at the conclusion of the sensitizat

65 se in prion seeding activity was observed in nasal lavage samples following nasotoxic treatment.

66 ct illness at 3-month intervals and analyzed nasal lavage samples for respiratory tract viruses at th

67 Nasal lavage samples from building occupants with upper

68 s of 105 DNA samples extracted from archived nasal lavage samples from high-risk infants/young childr

69 2 x 10(3) PFU, genomic diversity present in nasal lavage samples increased from 1 to 3 days postinfe

70 ofiled global patterns of gene expression in nasal lavage samples obtained during an acute, moderate,

71 Sputum and nasal lavage samples were analysed using long-read metag

72 Peripheral blood and nasal lavage samples were collected at baseline and duri

73 Nasal lavage samples were processed without prior manipu

74 both OMP and prion proteins were present in nasal lavage samples.

75 ch is specific for ORNs, was not detected in nasal lavage samples.

76 roximately 1000 kDa was found in all patient nasal lavage samples.

77 Nasal lavage specimens were assayed for interferon-gamma

78 leukocyte or interleukin-8 concentrations in nasal-lavage specimens, or on quantitative-virus titer.

79 analyze the presence of virus in cells from nasal lavage, sputum, bronchoalveolar lavage, bronchial

80 V species and types were determined in 1,445 nasal lavages that were prospectively collected from 209

81 A nasal lavage was collected before and after the NACs to

82 Nasal lavage was performed before exposure (Day 0) and o

83 Nasal lavage was performed for moderate to severe respir

84 sal biopsies, and Th1 and Th2 cytokines from nasal lavage were assessed in subjects with severe PAR (

85 arated by at least 3 wk; bronchoalveolar and nasal lavages were performed on three occasions: immedia

86 of rats in which the ORNs were destroyed by nasal lavage with ZnSO(4), D2-like radioligand binding w