ライフサイエンスコーパス: airway resistance

1 nt increase of lung volumes, compliance, and airway resistance.

2 ur in HIB, including increases in peripheral airway resistance.

3 djusted to double and quadruple the baseline airway resistance.

4 ate either no change or a slight increase in airway resistance.

5 sequent ventilation-related control of nasal airway resistance.

6 an inability to overcome increases in upper airway resistance.

7 and flow dependence were opposite to that of airway resistance.

8 ishes, which is likely to cause an increased airway resistance.

9 degrees of sleep-induced increases in upper airway resistance.

10 tion, goblet cell hyperplasia, and increased airway resistance.

11 er type of hyperventilation had an effect on airway resistance.

12 ticularly during sleep, and modulating upper airway resistance.

13 n bronchoalveolar lavage fluid and decreased airway resistance.

14 vasodilation, gastrointestinal motility, and airway resistance.

15 th endotracheal tube diameter and peripheral airway resistance.

16 y airflow, which they do by regulating upper-airway resistance.

17 trol 2.7 [1.9, 3.6], p < 0.001) and specific airway resistance (1.65 z-scores [0.96, 2.33], p < 0.001

18 raining lung (lung compliance, 50 mL/cm H2O; airway resistance, 5 cm H2O/L/sec), adjustable lower eso

19 e +66%), reduced DL(CO) (-21%), and elevated airway resistance (+76%) that resembled advanced human E

20 terol were associated with improved specific airway resistance (abeta coefficient, -0.11 kPa/s; 95% C

21 I, -0.24 to -0.03 L/s; P = .01) and specific airway resistance (abeta coefficient, 0.06 kPa/s; 95% CI

22 ory cell infiltration, mucus production, and airway resistance after challenge.

23 nvolved in long-term airway inflammation and airway resistance after RSV infection through mediating

24 e-1 null mice exhibit sustained increases in airway resistance, along with lung mast cell (MC) activa

25 in suspended airway), and in vivo (invasive airway resistance) analyses were performed on human ASM

26 Increased airway resistance and airway hyperresponsiveness induced

27 cle conditional knock-out of Plk1 attenuated airway resistance and airway smooth muscle hyperreactivi

28 rated that anti-MCP-1 Abs inhibit changes in airway resistance and attenuate histamine release into t

29 Because of the oscillatory pattern of upper airway resistance and breathing during sleep in patients

30 hat a human IL-15 agonist (ALT-803) improved airway resistance and compliance in an experimental asth

31 ulmonary function characterized by increased airway resistance and decreases in minute volume, lung c

32 Further, measurements of airway resistance and dynamic compliance at baseline and

33 onse to arousal is influenced by pre-arousal airway resistance and gender.

34 In addition to improving airway resistance and histopathologic presentation and r

35 ction, helium-oxygen (He-O2) mixtures reduce airway resistance and improve ventilation, but their inf

36 ted significant increases in bilateral nasal airway resistance and in ipsilateral and contralateral h

37 Increased airway resistance and increased airway mucin production

38 expressing mice demonstrated normal baseline airway resistance and markedly increased airway hyperres

39 The increases in airway resistance and MC products were blocked by antago

40 However, central airway resistance and mucus metaplasia remained elevated

41 IL-13Ralpha1 regulates aeroallergen-induced airway resistance and mucus production but not IgE and T

42 in mild disease in C57BL/6 mice that had low airway resistance and mucus production with little pulmo

43 , periostin deficiency resulted in increased airway resistance and significantly enhanced mucus produ

44 nally, treatment with CTTN-I peptide reduced airway resistance and smooth muscle hyperreactivity in a

45 Ralpha1 is required for aeroallergen-induced airway resistance and that allergen-induced chemokine pr

46 m a nasal cannula identifies increased upper airway resistance and the presence of flow limitation.

47 after bronchial airway responses) may detect airway resistance and ventilation perfusion ratio inequa

48 Mean values of the airway resistance and work of breathing from periods 1 a

49 al tube resulted in significant decreases in airway resistance and work of breathing, which has the p

50 of the Kolobow tube will result in decreased airway resistance and work of breathing.

51 ng was set up to mimic a series of different airway resistances and lung compliances as would be seen

52 udy suggests that in various combinations of airway resistances and lung compliances, auto-PEEP can b

53 s revealed significant increases in baseline airways resistance and airways hyperresponsiveness (AHR)

54 lly resistant to IL-25-induced AHR, restored airways resistance and lung cell infiltration.

55 at 2-mo-old transgene (+) mice had increased airways resistance and non-specific airways hyperrespons

56 en-induced airway hyperresponsiveness (AHR), airway resistance, and compliance in response to methach

57 cytokines and improves allergen-induced AHR, airway resistance, and compliance.

58 ia and leukocytes in lungs, experienced more airway resistance, and died of the infection.

59 ma, reduced lung compliance, increased basal airway resistance, and hyperresponsiveness to methacholi

60 ases in symptoms, sneezes, ipsilateral nasal airway resistance, and ipsilateral histamine in the earl

61 ric plethysmography, invasive measurement of airway resistance, and isometric force measurements in i

62 n by eosinophils and polymorphs), atopy, and airway resistance, and produce proinflammatory cytokines

63 % CI, 0.13% to 10.62%, P = .045); peripheral airway resistance as the difference between 5 and 20 Hz,

64 airway resistance at 5 Hz, 177%; peripheral airway resistance as the difference between 5 and 20 Hz,

65 ion prevented increases in lung collagen and airway resistance as well as decreases in lung complianc

66 se, as measured by increased weight loss and airway resistance, as compared with control mice.

67 (95% CI, 1.56% to 13.43%, P = .02); central airway resistance at 20 Hz, 5.37% (95% CI, 0.13% to 10.6

68 rced vital capacity (FEF(25-75)), 48%; total airway resistance at 5 Hz, 177%; peripheral airway resis

69 s between formoterol and salmeterol in total airway resistance at 5 Hz, 7.50% (95% CI, 1.56% to 13.43

70 There was a trend towards the upper airway resistance being highest in NREM sleep compared w

71 not primarily responsible for differences in airway resistance between controls and abr-null mutants.

72 Mice expressing IL-4 had greater baseline airway resistance but did not demonstrate hyperreactivit

73 We previously showed that upper airway resistance can be inferred from the inspiratory f

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

75 ppm for 3 hr) or HA followed by analysis of airway resistance, cellular inflammation, and total prot

76 sting altered lung function, e.g., increased airway resistance, decreased lung compliance, or both.

77 struction, and quantified regions of bimodal airway resistance demonstrating lung compensation.

78 Ohmic airway resistance did not change, but the component of l

79 148+/-33 mm Hg, P=0.01); lung compliance and airway resistance did not differ significantly.

80 ice and was associated with increased distal airway resistance, down-regulation of antioxidant genes,

81 We conclude that airway resistance estimated from Ztr measurements compri

82 , challenged CCR6-deficient mice had reduced airway resistance, fewer eosinophils around the airway,

83 limitation events (transient elevated upper airway resistance identified by characteristic flattenin

84 tion that IL-15 deficiency promotes baseline airway resistance in naive mice.

85 A deep inspiration causes a decrease in airway resistance in normal subjects, whereas asthmatics

86 ecome activated during conditions that alter airway resistance in order to stabilise airway patency.

87 nd HDM-sensitized mice (47% decrease in peak airway resistance in OVA-asthma animals, P<0.01; 54% dec

88 avage (BAL) fluid eosinophil counts, reduced airway resistance in response to allergen challenge, and

89 ia, reduced lung inflammation, and decreased airway resistance in response to house dust mite allerge

90 found that colonization with NTHi amplified airway resistance in response to increasing doses of a b

91 osol, gVPLA2 caused dose-related increase in airway resistance in saline-treated mice; in allergic mi

92 osol necessary to produce a 150% increase in airway resistance in sensitized monkeys.

93 ant decrease in inflammatory cell counts and airways resistance in a murine model of allergic asthma.

94 ability of bradykinin to increase peripheral airways resistance in asthmatic, but not in normal, subj

95 We found that airways resistance in this mouse was not different to co

96 ivity rises above baseline as PCO2 rises and airway resistance increases.

97 nidase release, IgG, or methacholine-induced airway resistance, it significantly decreased mucus cont

98 clinical conditions (e.g., increased distal airway resistance, mainstem intubation) may increase obs

99 Raw-z was compared with airway resistance measured with whole-body plethysmograp

100 ymphocyte phenotype on lung function through airway resistance measures.

101 th muscle relaxation, and decreased baseline airway resistance (measures of putative PAR(2) "protecti

102 Furthermore, we demonstrate that increased airway resistance, mucus, TGF-beta, and eotaxin(s) produ

103 minished bronchial hyperresponsiveness (lung airway resistance); numbers of eosinophils, neutrophils,

104 Significant decrease in airways resistance occurred after administration of albu

105 ast, the IOS parameter R20, a marker of mean airway resistance of both large and small airways, appea

106 In contrast, markers of total (R5) and mean airway resistance of large and small airways (R20) were

107 inhaled SO2 (an 8-unit increase in specific airway resistance on inhaling an SO2 concentration of <

108 rly expiratory airflow (i.e. increased upper airway resistance) only during wake.

109 Ptm', arguing that LVRS has little effect on airway resistance or closure; and (3) large changes in P

110 ges in the pulmonary circulation could alter airway resistance or tissue mechanics, we hypothesized t

111 kg, responders showed a greater fall in mean airway resistance (p < .05) than nonresponders.

112 There was a 59% decrease in total airway resistance (p = .001) and 45% decrease in the wor

113 epiglottic pressures (Pchoa and Pepi), upper airway resistance, phasic and tonic GG EMG, and the GG r

114 Biomarkers in exhaled breath condensate and airway resistance (pre- and post- bronchodilator) did no

115 ed to assess whether elevated sleeping upper airway resistance (R(UA)) alters the ventilatory respons

116 titioning of total lung resistance (RL) into airway resistance (Raw) and tissue resistance (Rti) in p

117 essure with time that yielded information on airway resistance (Raw), final plateau pressure (Pp), an

118 in plethysmographic FRC, initial inspiratory airway resistance (Raw), or respiratory system complianc

119 different combinations of tidal volume (VT), airways resistance (Raw), FRC, and mask leak.

120 The key model parameter was airway resistance, Raw.

121 vivo studies showed a significantly blunted airway resistance response to the inhaled bronchoconstri

122 Airway resistance responses (Raw) to the muscarinic agon

123 the forced oscillation technique to measure airway resistance reveals that PAR(2) activation protect

124 Upper airway resistance (Rua), lower airway resistance (RIa), and lung volume did not change

125 have previously demonstrated that peripheral airway resistance (Rp) rises more in asthmatics than in

126 On Day 5, peripheral airway resistance (Rp) was measured followed by lavage.

127 Peripheral airway resistance (RP) was measured using a wedged bronc

128 ich is characterized by increased peripheral airway resistance (RP), eicosanoid mediator production,

129 i.e., dry air challenge [DAC]) on peripheral airway resistance (Rp), reactivity, and inflammation.

130 ope technique to measure baseline peripheral airway resistance (Rp).

131 f ASF volume, ASF osmolality, and peripheral airway resistance (Rp).

132 ed in anesthetized dogs to record peripheral airway resistance (Rp); to test airway reactivity to NK

133 bronchoscopy with measurement of peripheral airways resistance (Rp) at 4:00 P.M. and at 4:00 A.M.

134 Peripheral airways resistance (Rp) was measured at baseline and aft

135 Baseline peripheral airways resistance (Rp) was measured in the right upper

136 Upper airway resistance (Rua), lower airway resistance (RIa),

137 eatly improved pulmonary function as adults (airway resistance similar to SHAM).

138 provide forced expiration and reduced upper airway resistance simultaneously.

139 0) and to nitrogen dioxide (NO2) on specific airway resistance (sR(aw)) and forced expiratory volume

140 Specific airway resistance (SR(aw)) and pulmonary function were m

141 Plethysmographic measurement of specific airway resistance (sR(aw)) is feasible in this age group

142 sured the children's lung function (specific airways resistance [sR(aw)], forced expiratory volume in

143 in percent change in FEV1, FVC, and specific airway resistance (SRaw) across the single-day exposure

144 stionnaires, skin testing, IgE, and specific airway resistance (sRaw) measurement were completed at t

145 inflammatory cells in lung tissues; specific airway resistance (sRaw) response to methacholine; and u

146 In a population-based birth cohort, specific airway resistance (sRaw) was assessed at age 3 (n = 560)

147 the particles, and by the subject's specific airway resistance (sRAW).

148 ing plethysmographic measurement of specific airway resistance (sRaw).

149 nary function tests (FEV1, FVC, and specific airway resistance [SRaw]) were performed before, during,

150 Lung function (specific airway resistance [sRaw]; kPa/second) was assessed at ag

151 parallel analysis of the immunophenotype and airway resistance (standard resistance of the airways [S

152 asthmatic phenotype characterized by marked airway resistance, strong Th2 cytokine, and mucus produc

153 BP was more prevalent in subjects with upper airway resistance syndrome (UARS) (23%) than in subjects

154 Upper airway resistance syndrome (UARS) is defined by excessiv

155 Ten symptomatic patients (snoring, upper airway resistance syndrome [UARS], or OSAS) and four asy

156 New syndromes, such as the upper airway resistance syndrome, have recently been described

157 hacholine and allergen (Aspergillus)-induced airway resistance, Th2 cytokine levels, and atopy and ac

158 er methacholine-induced increases in central airway resistance than allergen-treated WT mice.

159 n piglets with cystic fibrosis had increased airway resistance that was accompanied by luminal size r

160 flexiVent was used to determine airway resistance to methacholine in these mice.

161 r19F because it induces mucus production and airway resistance, two manifestations of RSV infection i

162 ted muscle activity, ventilation , and upper airway resistance (UAR) during wakefulness and sleep ons

163 on, upper airway muscle activation and upper airway resistance (UAR) in middle-aged and younger healt

164 siveness (60% reduced P(enh) and 58% reduced airway resistance upon challenge with 25 and 100 mg meth

165 mice were transferred to wild-type animals, airway resistance upon challenge with CRA was significan

166 mpliance was further documented by increased airway resistance upon methacholine challenge.

167 esult in a significant reduction in specific airway resistance was 3 and 30 micrograms/ml for misopro

168 Airway resistance was determined with a mechanical venti

169 Airway resistance was not changed.

170 Increased airway resistance was produced late (24 h) after Ag chal

171 The decrease in airway resistance was sustained for 60 min in the group

172 Airway obstruction, including AHR and airway resistance, was diminished in allergen-challenged

173 Airway inflammation and airway resistance were evaluated.

174 Peak expiratory flow rate and mean airway resistance were measured while subjects received

175 ganic compounds (VOCs), gene expression, and airway resistance were measured.

176 gh and rapid shallow breathing and increased airway resistance, which was reversed by albuterol aeros

177 correlated with the concomitant increase of airway resistance with both modes of mechanical ventilat

178 The decrease in airway resistance with four puffs of albuterol was compa