ライフサイエンスコーパス: lower airway

1 identical to samples taken directly from the lower airway.

2 d, in particular their ability to infect the lower airway.

3 recold specimens from either the nose or the lower airway.

4 fference in NO. concentration present in the lower airway.

5 tween bacteria and the host occurring in the lower airway.

6 lia and, consequently, autonomic tone in the lower airways.

7 th shared and distinct between the upper and lower airways.

8 uring allergic inflammation in the upper and lower airways.

9 l children with a bacterial infection of the lower airways.

10 ant changes in the measured functions of the lower airways.

11 n both the patency and responsiveness of the lower airways.

12 ief among these are infections involving the lower airways.

13 esis and the interaction with both upper and lower airways.

14 caused materials to accumulate in upper and lower airways.

15 ex microbial communities (microbiome) in the lower airways.

16 ration may contribute to colonization of the lower airways.

17 ir respiratory tract deposited dose in their lower airways.

18 nation for CF lung disease in the gland-free lower airways.

19 urable humoral and cellular responses in the lower airways.

20 diatric respiratory disease in the upper and lower airways.

21 es may be informative about processes in the lower airways.

22 (40% and 36%, respectively), the skin (27%), lower airways (14%) and the gut (8%).

23 nse is proportional to that occurring in the lower airway and greater in the presence of a bacterial

24 atory viruses and bacteria, which infect the lower airway and increase airway inflammation.

25 Gas exchange was achieved at lower airway and intrathoracic pressures than those that

26 Also, the involvement of the lower airway and the potential role of IgE in the bronch

27 in sheep but in the epithelial cells of the lower airways and alveoli.

28 y nebulizing 1 mg ml(-1) bradykinin into the lower airways and by microinjecting 0.5 nmol capsaicin i

29 an important risk factor for HAdV(+) of the lower airways and influences the likelihood of bacterial

30 e is evidence that rhinovirus can infect the lower airways and may be associated with bronchiolitis a

31 ve in reducing S. aureus colonization in the lower airways and preventing VAT or VAP.

32 bjects underwent evaluation of the upper and lower airways and serologic analysis to determine the pr

33 ings suggest that RV can infect cells of the lower airway, and raise the possibility that such an eff

34 e severe viral respiratory infections of the lower airway, and thus increase the risk of exacerbation

35 uch as lymph nodes, that drain the upper and lower airways, and further B-cell expansion takes place

36 sal-associated lymphoid tissue (d-NALT), the lower airways, and the lung.

37 iruses trigger inflammatory responses in the lower airway are poorly understood, in particular their

38 Pneumococci that try to invade the lower airways are recognized by innate immune cells thro

39 zed by recurrent infections of the upper and lower airways, as well as by progressive lung failure an

40 ower lobe bronchiectasis was associated with lower airway bacterial colonization (p = 0.004), higher

41 ociated with more severe COPD exacerbations, lower airway bacterial colonization, and increased sputu

42 Lower airway bacterial community composition was assesse

43 smoking status, exacerbation frequency, and lower airway bacterial load.

44 uffer from recurrent infections of upper and lower airways because of highly reduced numbers of multi

45 on between RV DNA/RNA detection in the upper/lower airways before HCT and the occurrence of allo-LSs.

46 A, DB1 reduced viral titers in the upper and lower airways by 3.8 log10 total PFU and 2.7 log10 PFU/g

47 ere colonized with S. mucilaginosus in their lower airways by culture growth from bronchoalveolar lav

48 Colonization of lower airways by Staphylococcus aureus is a risk factor

49 Antigen exposure in the upper or lower airways can also drive expansion of B-lineage cell

50 Lower airways can be also involved.

51 yet the characteristics of RV replication in lower airway cells are incompletely understood.

52 us RNA was detected in both nasal lavage and lower airway cells from all eight subjects 2 to 4 d afte

53 R) and Southern blotting to detect RV RNA in lower airway cells from eight allergic volunteers experi

54 acity of pneumococci to adhere to and infect lower airway cells is mediated by host-expressed platele

55 Combining cytopathology of lower airway cells obtained at bronchoscopy with the bio

56 ) are due, in part, to secreted signals from lower airway cells that modify the immune response and t

57 be associated with the presence of virus in lower airway cells, we used the techniques of reverse tr

58 ndent pneumococcal adhesion and infection of lower airway cells.

59 and the host mucosal barrier function of the lower airways, combined with both innate and adaptive im

60 e therapeutic strategies targeting upper and lower airways concomitantly and improving the health of

61 play a role in diverse pathologies including lower airway conditions, but the exact mechanism of acti

62 us exercise in cold environments can lead to lower airway disease and suggest that racing sled dogs m

63 us are major etiological agents of upper and lower airway disease in horses.

64 ial virus (RSV) is the major cause of severe lower airway disease in infants and young children, but

65 tion may inhibit the development of allergic lower airway disease in mice.

66 ntry skiers, have an increased prevalence of lower airway disease that is hypothesized to result from

67 with BPEx was sufficient to inhibit allergic lower airway disease with minimal collateral lung inflam

68 to elicit protection against murine allergic lower airway disease.

69 iscuss the role of TGF-beta in the upper and lower airway diseases.

70 ude that inflammatory responses of upper and lower airways during RV-16 colds are similar in asthmati

71 conclude that MIP-1-alpha is present in the lower airways during severe RSV disease.

72 the lower airway, these results suggest that lower airway dysfunction occurs through this mechanism i

73 nce of allergy is a risk factor for enhanced lower airway effects during RV infection, we experimenta

74 at these factors contribute to the increased lower airway effects of RV infection in subjects with as

75 bility of rhinovirus to infect a transformed lower airway epithelial cell line (A549) and to induce I

76 erns of chemokine expression in RSV-infected lower airway epithelial cells (A549 and SAE).

77 ls in upper airway tissues and indicate that lower airway epithelial cells have a similar susceptibil

78 mporal changes in expression by RSV-infected lower airway epithelial cells of chemokines, chemotactic

79 sms occurring in the upper airway may mirror lower airway events.

80 Parental tobacco smoking is associated with lower airway function and an increased incidence of whee

81 y hyperreactivity, which could contribute to lower airway function and the increased wheezy illnesses

82 osure to parental smoking is associated with lower airway function but not increased airway reactivit

83 on did not produce detectable alterations in lower airway function in health AR and non-AR subjects.

84 ratio of wall to lumen area correlated with lower airway function.

85 rotracheal intubation (thereby isolating the lower airway gas from ambient air contamination or gas c

86 Lower airway gas, sampled through the bronchoscope durin

87 al vascular density was increased at mid- to lower airway generations, which was independent of chang

88 plice variant was significantly increased at lower airway generations.

89 idia, TLR9(-/-) mice exhibited significantly lower airway hyper-responsiveness compared to the TLR9(+

90 eficient (CD8-/-) mice develop significantly lower airway hyperresponsiveness (AHR), eosinophilic inf

91 bumin showed less pulmonary inflammation and lower airway hyperresponsiveness than genetically matche

92 the thickened basement membrane of asthmatic lower airways, (ii) around smooth muscle cells of the as

93 ); however, it has also been detected in the lower airway in the stable state, but the consequences o

94 Remodelling has been long identified in the lower airways in asthma and is characterized by epitheli

95 d standard for detection of pathogens in the lower airways in cystic fibrosis (CF).

96 educed inflammatory cell accumulation to the lower airways in response to inhaled LPS.

97 sts that differences exist between upper and lower airways in the polarity of available receptors for

98 approach we confirmed the involvement of the lower airways in the response to aerosolized methacholin

99 Cytokine levels in nasal and lower airways in young cystic fibrosis (CF) patients wer

100 idence of bloodstream infection was 20.1 and lower airway infection 9.1 episodes per 1,000 patient da

101 ained impaired exercise tolerance; recurrent lower airways infection; and therapy-resistant, irrevers

102 Here, we use cystic fibrosis (CF) lower airway infections as a model system to examine how

103 the sampling method for the investigation of lower airway infections.

104 Of the different lower airway-infiltrating immune cells that participate

105 y inflammation correlated with the degree of lower airway inflammation (e.g., nasal wash/sputum myelo

106 c inflammation correlated with the degree of lower airway inflammation (e.g., serum IL-6/sputum IL-8;

107 eveloped significant airflow obstruction and lower airway inflammation after CDE inhalation.

108 ons can cause asthma exacerbations and alter lower airway inflammation and physiology, it is unclear

109 ficant determinant of airflow obstruction or lower airway inflammation following CDE inhalation.

110 n bronchial hyperreactivity and eosinophilic lower airway inflammation in asthmatic compared with nor

111 cal recovery, we note surprisingly extensive lower airway inflammation with persistent viral antigen

112 To determine the role of bacterial DNA in lower airway inflammation, we intratracheally instilled

113 d air may represent a noninvasive measure of lower airway inflammation.

114 pect to clinical problems and the pattern of lower airway inflammation.

115 tly related to neutrophilic and eosinophilic lower airway inflammation.

116 treatments to attempt to attenuate asthmatic lower airway inflammation.

117 sought to determine the relationship between lower airway inflammatory biomarkers, specifically inter

118 ocess, the observed S. aureus fitness in the lower airways is due to its intrinsic resistance to resi

119 Repeated monthly administration to mouse lower airways is feasible without loss of gene expressio

120 esting that the bacterial communities of the lower airways may act as persistent stimuli for repetiti

121 whether the composition and structure of the lower airway microbiome correlated with clinical charact

122 at compositionally and structurally distinct lower airway microbiomes are associated with discrete lo

123 Just as in the lower airways, objective and subjective evaluation gives

124 dren, Rint was increased in the patient with lower airway obstruction and five of six patients withou

125 unction tests revealed air trapping and mild lower airway obstruction in the ECMO group, compared wit

126 six with parenchymal lung disease; one with lower airway obstruction) and six without primary lung d

127 Parasympathetic ganglia neurons in the lower airway of laboratory animals have membrane propert

128 Pseudomonas aeruginosa (Pa) density from the lower airway of young children with cystic fibrosis.

129 different inflammatory changes in upper and lower airways of asthmatic and healthy subjects, we inoc

130 nin, and the B2 receptor agonist, BK, in the lower airways of asthmatics and in the upper airways of

131 ormed molecular sequencing of HAdVs from the lower airways of children with chronic endobronchial sup

132 -C is the major HAdV species detected in the lower airways of children with PBB and BE.

133 The lower airways of children with severe asthma display a d

134 M. pneumoniae was present in the lower airways of chronic, stable asthmatics with greater

135 a link between bacterial colonization of the lower airways of COPD sufferers and an increase in exace

136 y despite heavy attenuation in the upper and lower airways of cotton rats.

137 airway epithelial cells and in the upper and lower airways of cotton rats.

138 he cellular immune responses observed in the lower airways of humans with pneumotypeSPT indicate a ro

139 demonstrate the frequent colonization of the lower airways of stable CB patients with multiple strain

140 gnificant proportion of T lymphocytes in the lower airways of subjects with asthma expressed high lev

141 e and effective for significant reduction of lower airway Pa density in young children with cystic fi

142 Rhinovirus (RV) infections can alter lower airway physiology and inflammation, yet the charac

143 , and baseline PD20 influence the changes in lower airway physiology caused by RV infection and raise

144 Sputum samples containing lower airway plugs were obtained from 10 healthy childre

145 airway cross-sectional area was decreased by lowering airway pressure.

146 Surprisingly, these IL-5 TG mice showed lower airway reactivity to methacholine.

147 oprost therapy, 36% stopped iloprost, due to lower airway reactivity, clinical deterioration, or deat

148 tribute to inflammation, adversely effecting lower airway remodeling and asthma severity.

149 cells is a key determinant in the control of lower airway remodeling posttransplantation.

150 Here, we examine how, in the lower airways, resident cell populations contribute to t

151 Upper airway resistance (Rua), lower airway resistance (RIa), and lung volume did not c

152 Upper and lower airway resistance can increase the risk for sleep-

153 '-NT and NS AP mRNA dominating in higher and lower airways, respectively.

154 induce clinical, physiologic, and pathologic lower airway responses typical of an asthma exacerbation

155 mice, CD8(-/-) mice developed significantly lower airway responsiveness to inhaled methacholine and

156 mice, BLT1 -/- mice developed significantly lower airway responsiveness to inhaled methacholine, low

157 lenge, fB-/- mice demonstrated significantly lower airway responsiveness to methacholine and less air

158 treated C57BL/6 mice injected with OC-20 had lower airways responsiveness than HDM-treated mice injec

159 in RSV-infected WD-PBECs reflected those in lower airway samples from RSV-hospitalized infants.

160 il secretory ribonucleases, were detected in lower airway secretions from RSV-infected patients; ECP

161 alpha, RANTES, and IL-8 were also present in lower airway secretions obtained from patients with RSV

162 serve as a useful model for the analysis of lower-airway secretions and their role in host defense a

163 as a determinant for infection spread to the lower airways, severity of accompanying inflammatory sym

164 id prevalence of infections of the upper and lower airway, skin/soft tissue, and urinary tract (all P

165 ed to the upper airway, yet can cause severe lower airway symptoms in children and adults with asthma

166 n origin and in which sinus, pharyngeal, and lower airway symptoms, although frequently present, are

167 upper airway disease is also associated with lower airway symptoms.

168 ffline in 391 children aged 3-47 months with lower airway symptoms.

169 s characterized by an acute infection of the lower airways that may progress rapidly to organ failure

170 ve been shown to reflect colonization of the lower airways, the actual site of inflammation in asthma

171 In the lower airways, the Na+ concentrations were 80-85 meq/lit

172 ecrease of the bacterial colonization of the lower airways, there was pervasive trachea-bronchial-lun

173 n confirming that RV can infect cells in the lower airway, these results suggest that lower airway dy

174 location, and frequency of RV appearance in lower airway tissues during an acute infection, immunohi

175 These results confirm that infection of lower airway tissues is a frequent finding during a cold

176 Sampling various compartments within the lower airways to examine human bronchial epithelial cell

177 measured the effects on the response of the lower airways to histamine.

178 tinent to allergic diseases of the upper and lower airways, to function as professional APCs, those s

179 NTHi causes upper and lower airway tract infections in individuals with compro

180 Similar measurements made on the lower airway via the bronchoscope have been successful i

181 of strong relationships between virus load, lower airway virus-induced inflammation and asthma exace

182 The reduced concentration of cells in the lower airways was associated with enhanced apoptosis of

183 er airway isolated from and connected to the lower airway were performed before and following bilater

184 e review demonstrates that several upper and lower airway work-related diseases may present with chro