ライフサイエンスコーパス: airway resistance

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

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

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

4 djusted to double and quadruple the baseline airway resistance.

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

6 sequent ventilation-related control of nasal airway resistance.

7 an inability to overcome increases in upper airway resistance.

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

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

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

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

12 and validate it against gold-standard upper airway resistance.

13 -1-phosphate) were associated with increased airway resistance.

14 ing (SDB), which arises from nocturnal upper airway resistance.

15 an untapped therapeutic reserve for managing airway resistance.

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

17 imitation in the LFEV(1) is due to increased airway resistance.

18 ticularly during sleep, and modulating upper airway resistance.

19 n bronchoalveolar lavage fluid and decreased airway resistance.

20 vasodilation, gastrointestinal motility, and airway resistance.

21 th endotracheal tube diameter and peripheral airway resistance.

22 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

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

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

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

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

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

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

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

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

31 Increased airway resistance and airway hyperresponsiveness induced

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

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

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

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

36 irway hyper-responsiveness (AHR) in terms of airway resistance and compliance to methacholine challen

37 utide inhibited Lys-ASA-induced increases in airway resistance and decreased markers of platelet acti

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

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

40 These colonized mice had decreased airway resistance and fewer inflammatory cells, less sev

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

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

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

44 Dupilumab decreased frequency dependence of airway resistance and improved reactance area at week 24

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

46 Increased airway resistance and increased airway mucin production

47 There is evidence of increased large-airway resistance and lower midexpiratory airflow, but i

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

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

50 parasympathetic pulmonary nerves to decrease airway resistance and mucus hypersecretion.Objectives: T

51 However, central airway resistance and mucus metaplasia remained elevated

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

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

54 inflammation in BALB/c mice, 4-OI alleviated airway resistance and reduced eosinophil recruitment to

55 he thermoregulatory system, causing specific airway resistance and reflex bronchoconstriction via act

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

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

58 The printed airway resistance and standardised volume reactance conf

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

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

61 zymes, with a concomitant reduction in small airway resistance and tissue elastance.

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

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

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

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

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

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

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

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

70 ovalbumin (OVA) allergy model and increased airways resistance and mucus production in a house dust

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

72 er, in addition to lower spirometry, greater airways resistance and reactance, and more air trapping

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

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

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

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

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

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

79 olar simplification, normalized alveolar and airway resistance, and normalized weight gain compared w

80 lysine-aspirin (Lys-ASA)-induced changes in airway resistance, and platelet-derived mediator release

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

82 pathway that modulates airway inflammation, airway resistance, and tissue remodeling in the HDM muri

83 Although there was a very small effect on airway resistance as measured by impulse oscillometry, t

84 % CI, 0.13% to 10.62%, P = .045); peripheral airway resistance as the difference between 5 and 20 Hz,

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

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

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

88 (95% CI, 1.56% to 13.43%, P = .02); central airway resistance at 20 Hz, 5.37% (95% CI, 0.13% to 10.6

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

90 ures included total, large airway, and small airway resistance at 5 Hz, 20 Hz, and the difference in

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

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

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

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

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

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

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

98 nduced collagen, goblet cell hyperplasia and airway resistance compared to saline-challenged CD2-IL5

99 rways reactance (X5Hz) and peripheral/distal airways resistance (D5-D20%) via IOS, averaging - 1369%

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

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

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

103 148+/-33 mm Hg, P=0.01); lung compliance and airway resistance did not differ significantly.

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

105 engagement on ILC2s, which lead to improved airway resistance, dynamic compliance and eosinophilia.

106 We conclude that airway resistance estimated from Ztr measurements compri

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

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

109 as strongly correlated with normalized upper airway resistance in both test sets (set 1: cubic adjust

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

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

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

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

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

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

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

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

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

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

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

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

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

123 CR5 inhibitor (maraviroc) with assessment of airway resistance, inflammatory cell recruitment by flow

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

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

126 ted TLC 134.8% vs 109.6%; P < .05) and lower airway resistance (mean %of predicted Raw 101.9% vs 199.

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

128 ymphocyte phenotype on lung function through airway resistance measures.

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

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

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

132 Significant decrease in airways resistance occurred after administration of albu

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

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

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

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

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

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

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

140 trongly linked to Ptc(CO(2)) (P < 0.012) and airway resistance (P < 0.013) but not respiratory work (

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

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

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

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

145 interval [CI] = -0.39, -0.11), higher large airway resistance (R20 z-score: beta = 0.34; 95% CI = 0.

146 = 0.16; 95% CI = 0.01, 0.31) and lower small airway resistance (R5-20 z-score: beta = -0.15; 95% CI =

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

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

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

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

151 The key model parameter was airway resistance, Raw.

152 city (FEF(25%-75%)), frequency dependence of airway resistance, reactance area, airway wall area and

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

154 Airway resistance responses (Raw) to the muscarinic agon

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 associated with the median normalized upper airway resistance (set 1: linear adj.

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

171 provide forced expiration and reduced upper airway resistance simultaneously.

172 Specific airway resistance (sR(aw) ) was significantly higher in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 thma endotype with early onset and increased airway resistance that is characterized by reduced sphin

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

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

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

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

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

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

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

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

202 ing, CD274 expression by flow cytometry, and airway resistance using the Buxco FinePointe RC system.

203 ction, as a surrogate of gold-standard upper airway resistance, using hallmarks of upper airway obstr

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

205 Airway resistance was determined with a mechanical venti

206 Airway resistance was not changed.

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

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

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

210 tion or bronchodilation or during changes in airway resistance were common across all age groups and

211 Airway inflammation and airway resistance were evaluated.

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

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

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

215 proportionally enlarged airways and reduced airway resistance, while airflow limitation in the LFEV(

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

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