ライフサイエンスコーパス: ASM

1 ASM and mast cells expressed intracellular IL-33 and ST2

2 ASM area was higher in preschoolers with atopy than with

3 ASM area was lower in preschoolers than in schoolchildre

4 ASM cells from healthy individuals and nonsevere and sev

5 ASM cells from patients with COPD have reduced DeltaPsim

6 ASM enlargement occurred independently of features of ai

7 ASM is related to the concept we refer to as Fixed Solve

8 5 per thousand] immunoreactivity, P < .001), ASM-associated nerves (452.6 [25th-75th IQR, 196.0-811.2

9 ult SM patients (10 ISM, 2 BMM, 1 SSM, and 1 ASM-AHN) received omalizumab with a median duration of 1

10 Mimics of BET bromodomains inhibit aberrant ASM cell proliferation and inflammation with lesser effi

11 diseases whose etiology resides in abnormal ASM proliferation.

12 n schoolchildren, but nothing is known about ASM in preschool wheezers.

13 Analyses across ASM quartiles in patients with severe asthma demonstrate

14 In a murine model of lung adenocarcinoma, ASM deficiency reduced tumor development in a manner ass

15 g stalk mesenchyme can be induced to form an ASM niche by a lateral bud or by an airway tip plus foca

16 3 directly promotes mast cell activation and ASM wound repair but indirectly promotes ASM contraction

17 uscle (ASM) mass is increased in asthma, and ASM cells from patients with asthma are hyperproliferati

18 hosphatase PP5 in endobronchial biopsies and ASM cells.

19 ocytes migrated towards recombinant CCL2 and ASM supernatants.

20 Bronchial epithelium and ASM expressed IL-33 with the latter in asthma correlatin

21 Resealing is reduced by ASM inhibitors and ASM deficiency and enhanced or restored by extracellular

22 ship between cholinergic neuroplasticity and ASM contractile phenotypes that operates uniquely in ear

23 1/10, Ebf and Mrf differ between the OSM and ASM lineages.

24 purinergic nucleotide-mediated responses and ASM catalytic bioactivity, respectively.

25 regulatory mechanism for PI3K signaling and ASM proliferation and further suggests miR-10a as a pote

26 purely phasic smooth muscle of anococcygeus (ASM) vs. the truly tonic smooth muscle of IAS.

27 Partial genetic inhibition of ASM (ASM(+/-)) in a mouse model of familial AD (FAD; amyloid

28 eration and cytokine expression in asthmatic ASM cells by studying the effect of BET bromodomain mimi

29 we cannot conclude whether or not asthmatic ASM is hyperreactive.

30 ond, we investigated the association between ASM transcriptomic profiles and airway function.

31 We hypothesized that direct contact between ASM and CD4(+) T cells facilitated the transfer of anti-

32 ids and did not differ significantly between ASM cells from healthy and asthmatic individuals.

33 indicates epigenetic heterogeneity caused by ASM or CSM.

34 The chemokine most highly expressed by ASM from asthmatics compared with healthy controls was c

35 ynamic actomyosin-driven force generation by ASM cells.

36 in-stiffening of ECM and force generation by ASM yielding a highly nonlinear relationship between eff

37 The proportion of submucosa occupied by ASM was higher in both asthma groups (P = 0.021 and P =

38 Resealing is reduced by ASM inhibitors and ASM deficiency and enhanced or restor

39 nt an important target to modulate mast cell-ASM crosstalk in asthma.

40 ' IL-33 in asthma, but its role in mast cell-ASM interactions is unknown.

41 In cancer cells, ASM-mediated ceramide production is important for apopto

42 We sought to compare ASM area in control subjects and patients with mild-to-m

43 that a specific microRNA (miR-10a) controls ASM proliferation through directly inhibiting the phosph

44 Biochemical analysis of CD148-deficient ASM revealed hyperphosphorylation of the C-terminal inhi

45 mRNA and protein expression in human-derived ASM, epithelial and mast cells were assessed by qPCR, im

46 at tissue culture plates before lung derived ASM cells and fibroblasts from patients with pulmonary f

47 We have detected ASM activity in human CSF, established a sensitive quant

48 RNA of laser-dissected ASM from 96 bronchial biopsy specimens was sequenced wit

49 RNA of laser-dissected ASM was sequenced (RNA-Seq) using GS FLX+ (454/Roche).

50 In this study, we demonstrate elevated ASM activity in the lung tumor environment and blood ser

51 m, we revealed that upon lack of endothelial ASM activity, the phosphorylation of ezrin was perturbed

52 To study the role of endothelial ASM in transmigration, we generated brain endothelial ce

53 ese peptides, peptide 1C1 (FBLN1C1) enhanced ASM cell and fibroblast attachment.

54 Compared to methods that do not account for ASM, our approach increases statistical power to detect

55 atients with severe asthma were analyzed for ASM area, basement membrane thickness, vessels, eosinoph

56 Of the 2.2 million CpGs tested for ASM, mQTL, and genotype-independent effects, we identify

57 One hundred and seventy four ASM genes were differentially expressed between asthma p

58 Transfer of GFP-tagged Mcl-1 from ASM cells to CD4(+) T cells via the nanotubes confirmed

59 Direct transfer of Mcl-1 from ASM to CD(+) T cells via nanotubes is involved in T cell

60 pha and greatly enhances PGE2 secretion from ASM cells.

61 e-restricted ASM, and among them are 188 hap-ASM DMRs and 933 mQTLs located near GWAS signals for imm

62 phocytes, and placenta, and identify 795 hap-ASM differentially methylated regions (DMRs) and 3,082 s

63 inding sites were over-represented among hap-ASM DMRs and mQTLs, and analysis of the human data, supp

64 been mechanistically linked to mQTLs and hap-ASM.

65 Targeted bis-seq confirmed hap-ASM in 12/13 loci tested, including CCDC155, CD69, FRMD1

66 e-dependent allele-specific methylation (hap-ASM) can impact disease susceptibility, but maps of this

67 pendent allele-specific DNA methylation (hap-ASM), have become a major focus in the post-genome-wide-

68 is an underlying mechanism, and maps of hap-ASM and mQTLs reveal regulatory sequences underlying sup

69 These results show that hap-ASM is highly tissue specific; an important trans-acting

70 demonstrated that patients with the highest ASM quartile (median value of ASM area, 26.3%) were youn

71 eration, and immune modulation, highlighting ASM as a potential multimodal therapeutic target.

72 Human ASM cells were isolated from bronchial biopsy specimens

73 We hypothesized that HLMC and human ASM cell (HASMC) responsiveness to beta2-AR agonists wou

74 and mitochondrial function in mice and human ASM cells were measured with and without the presence of

75 ssion of Sema3E receptor, plexinD1, in human ASM cells (HASMCs); effect of Sema3E on basal and platel

76 lerin increased BK channel activity in human ASM cells (V50 shifted by 73.5+/-13.5 and 71.8+/-14.6 mV

77 he expression of more than 80 genes in human ASM cells, including several genes known to be involved

78 ted GRK2/3 knockdown was performed, in human ASM cultures, and agonist-induced signaling was assessed

79 In primary cultures of isolated human ASM, we identified mRNA expression for multiple ORs.

80 t airway remodelling by stimulation of human ASM cell proliferation.

81 eling, as well as the proliferation of human ASM cells.

82 Olipudase alfa, a recombinant form of human ASM, is being developed as enzyme replacement therapy to

83 resistance) analyses were performed on human ASM cells and murine airways/whole animal subject to bet

84 were absent in OR51E2-deleted primary human ASM.

85 Here we present the human ASM holoenzyme and product bound structures encompassing

86 tion of TNF-alpha-induced COX-2 by IL-17A in ASM cells and show that is not via increased COX-2 gene

87 Genetic alterations in ASM lead to ASM deficiency (ASMD) and have been linked t

88 ative selectivity of GRKs for the beta2AR in ASM and the ability to exploit GRK2/3 functional domains

89 Thus a focus on early changes in ASM might be important in understanding the subsequent d

90 ive to both fluticasone and dexamethasone in ASM cells from severe asthmatic compared to that in heal

91 role of VASP in regulating actin dynamics in ASM is not known.

92 eroxide induced mitochondrial dysfunction in ASM cells from healthy subjects.

93 Because it is selectively expressed in ASM within the lung and does not promote inflammation, R

94 se cellular responses in vitro were found in ASM from non-asthmatics and asthmatics, and were absent

95 Increase in ASM mass, possibly involving aberrant expression and act

96 Levels of PP5 were increased in ASM cells from severe asthmatics and PP5 knockdown using

97 novel mechanism driving GC insensitivity in ASM in severe asthma.

98 the primary fibronectin-binding integrin in ASM, and alpha5beta1-specific blockade inhibited focal a

99 M transgenic mice and undetectable levels in ASM knock-out mice prove that the measured ASM activity

100 enhanced GPCR-induced Ca(2+) mobilization in ASM.

101 teroid-resistant, pro-remodelling pathway in ASM cells.

102 llular reactive oxygen species production in ASM cells, and inhibited nuclear translocation of the an

103 s4B mislocalization is also recapitulated in ASM-deficient Neimann-Pick type A and B fibroblasts.

104 and relaxant G-protein-coupled receptors in ASM.

105 zipper (GILZ) were significantly reduced in ASM cells from severe asthmatics compared to responses i

106 al benefit was accompanied by a reduction in ASM area (median values before and after BT, respectivel

107 ulation of Mcl-1 by small interfering RNA in ASM cells significantly increased T cell apoptosis, wher

108 tion, and angiogenesis, although its role in ASM cell function is not investigated.

109 on by expression of the mutant VASP S157A in ASM tissues suppressed VASP phosphorylation and membrane

110 protein-coupled receptor (GPCR) signaling in ASM could mediate enhanced contractility.

111 tical positive regulator of SFK signaling in ASM.

112 n smooth muscle via ROCK2: a lack of tone in ASM may be associated with the suppression of ROCK2 by h

113 ) cells leading to hyperplasia and increased ASM mass is one of the most characteristic features of a

114 ways promotes Orai1 hyperactivity, increased ASM contraction and airway hyperresponsiveness.

115 activated by IL-33 increased agonist-induced ASM contraction, and in vivo IL-33 induced AHR in a mous

116 MitoQ and Tiron inhibited TGF-beta-induced ASM cell proliferation and CXCL8 release.

117 and I-BET762 inhibited FCS+TGF-beta-induced ASM cell proliferation and IL-6 and CXCL8 release in hea

118 10 years, volcanic eruptions have influenced ASM variations on an inter-decadal timescale via telecon

119 ther, chymase cleaved fibronectin, inhibited ASM adhesion, and attenuated focal adhesion phosphorylat

120 ited from these tip pools differentiate into ASM around airway stalks; flanking stalk mesenchyme can

121 we generated brain endothelial cells lacking ASM activity using a lentiviral shRNA approach.

122 -1 expression was increased in cells lacking ASM activity, we measured a significant decrease in T ly

123 CSF localized ASM activities were comparable to corresponding serum AS

124 901-1935 and 1963-1993), significantly lower ASM precipitation was observed compared with that during

125 n ASM knock-out mice prove that the measured ASM activity originates from the ASM-encoding gene SMPD1

126 age, 7.3 years [range, 5.9-11 years]; median ASM, 0.07 [range, 0.02-0.23]; P=.007).

127 age, 8.2 years [range, 6-10.4 years]; median ASM, 0.12 [range, 0.08-0.16]) compared with that seen in

128 hat is due in part to growth factor-mediated ASM cell proliferation and migration.

129 In case of anesthesia-sensitive memory (ASM) we identified a characteristic two-step mechanism t

130 ent analyses of allele-specific methylation (ASM) and non-allelic methylation (mQTL).

131 originate from allele-specific methylation (ASM) or cell-specific methylation (CSM).

132 etect potential allele-specific methylation (ASM) patterns, which can greatly enhance the detection a

133 not account for allele-specific methylation (ASM).

134 manual of American Society for Microbiology (ASM) and their antibiotic susceptibility test, performed

135 rt of the American Society for Microbiology (ASM) Evidence-Based Laboratory Medicine Practice Guideli

136 with the American Society for Microbiology (ASM) in meeting the future challenges faced by our disci

137 ent and discuss the Activation Strain Model (ASM).

138 ch we refer to as Active Solvent Modulation (ASM).

139 in the form of alternative splicing modules (ASMs), where transcript isoforms diverge.

140 y Circulation (WC) and Asian Summer Monsoon (ASM) are likely to promote the precipitation respectivel

141 Asian summer monsoon (ASM) precipitation is the primary water resource for agr

142 )]i responsiveness in betaAR knock-out mouse ASM.

143 expression of the GRK2 C terminus in murine ASM enabled approximately 30-50% greater beta-agonist-me

144 ions were assessed for airway smooth muscle (ASM) area, subepithelial basement membrane thickness, ne

145 the cholinergic nerve-airway smooth muscle (ASM) axis that underlies prolonged airway hyperreactivit

146 heir relocation to the airway smooth muscle (ASM) bundles.

147 nsensitive pathways in airway smooth muscle (ASM) caused by a defect in GC receptor (GRalpha) functio

148 receptors (TAS2Rs) in airway smooth muscle (ASM) causes a stronger bronchodilation in vitro and in v

149 bmucosa and disrupting airway smooth muscle (ASM) cell-extracellular matrix (ECM) interactions.

150 Contact between airway smooth muscle (ASM) cells and activated CD4(+) T cells, a key interacti

151 force when applied to airway smooth muscle (ASM) cells and tissue strips.

152 eased proliferation of airway smooth muscle (ASM) cells leading to hyperplasia and increased ASM mass

153 Airway smooth muscle (ASM) cells play important physiological roles in the lun

154 In immortalized human airway smooth muscle (ASM) cells, Sul-121 dose-dependently prevented cigarette

155 terial exacerbation in airway smooth muscle (ASM) cells, we show that activation of toll-like recepto

156 nd PGE2 secretion from airway smooth muscle (ASM) cells.

157 exposed mice and human airway smooth muscle (ASM) cells.

158 wound healing in human airway smooth muscle (ASM) cells.

159 means of manipulating airway smooth muscle (ASM) contractile state, we assessed the specificity of G

160 gy of inflammation and airway smooth muscle (ASM) contractility have identified several potential nov

161 secretion and abnormal airway smooth muscle (ASM) contraction.

162 inflammation-triggered airway smooth muscle (ASM) contraction.

163 nscriptomic profile of airway smooth muscle (ASM) distinguishes atopic asthma from atopic healthy con

164 mAChRs and beta2ARs in airway smooth muscle (ASM) helps determine the contractile state of the muscle

165 Airway smooth muscle (ASM) hyperplasia is a feature of airway remodelling and

166 o a 2-fold increase in airway smooth muscle (ASM) innervation (P<0.05) and persistent airway hyperrea

167 Increased airway smooth muscle (ASM) is a feature of established asthma in schoolchildre

168 alter, the increase in airway smooth muscle (ASM) mass and cellular remodeling that occur in asthma a

169 The increase in airway smooth muscle (ASM) mass is an essential component of airway remodeling

170 Airway smooth muscle (ASM) mass is increased in asthma, and ASM cells from pat

171 acterized by increased airway smooth muscle (ASM) mass that is due in part to growth factor-mediated

172 ociated with increased airway smooth muscle (ASM) mass.

173 ates the relaxation of airway smooth muscle (ASM) observed with beta-agonist treatment.

174 Airway smooth muscle (ASM) plays a key role in airway hyperresponsiveness (AHR

175 Airway smooth muscle (ASM) progenitors map exclusively to mesenchyme ahead of

176 aoral cells, including airway smooth muscle (ASM) where they evoke relaxation.

177 uctural cells, such as airway smooth muscle (ASM), contribute to the asthmatic diathesis.

178 brane (RBM) thickness, airway smooth muscle (ASM), mucus gland area, vascularity, and epithelial inte

179 elease of eotaxin from airway smooth muscle (ASM), similar to effects of these inhibitors on ASM cont

180 ocalization within the airway smooth muscle (ASM)-bundle plays an important role in the development o

181 ogenously expressed in airway smooth muscle (ASM).

182 ter gene expression of airway smooth muscle (ASM).

183 ension transmission in airway smooth muscle (ASM).

184 ing the contraction of airway smooth muscle (ASM); however, the role of VASP in regulating actin dyna

185 hat myogenesis in the atrial siphon muscles (ASMs) and oral siphon muscles (OSMs), which control the

186 eral ASM best practices guidelines and a non-ASM practice guideline from the Emergency Nurses Associa

187 ans is attributed to an intrinsic ability of ASM to maintain shortening during a progressive decrease

188 eration during the contractile activation of ASM.

189 Analyses of ASM cell and tissue contraction demonstrate that PKA inh

190 reatly enhance the detection and analysis of ASM patterns; 4) by linking directly with other popular

191 ificantly increased activities in the CSF of ASM transgenic mice and undetectable levels in ASM knock

192 levels of chemokines in primary cultures of ASM cells from asthmatics vs healthy controls and to ass

193 critical time window for the development of ASM hypercontractility after cholinergic stimulation.

194 otentially contributes to the development of ASM hyperplasia in asthma.

195 and migration, leading to downregulation of ASM remodeling.

196 hat NT4 was necessary for hyperreactivity of ASM induced by early-life OVA exposure.

197 ial damage and is related to infiltration of ASM with eosinophils and T lymphocytes, but is unrelated

198 Partial genetic inhibition of ASM (ASM(+/-)) in a mouse model of familial AD (FAD; amy

199 Inhibition of ASM activity by pharmacological blockers or knockdown of

200 Inhibition of ASM elevates cellular sphingomyelin and reduces cellular

201 dentify a pathway for specific inhibition of ASM hypercontractility in asthma.

202 by pharmacological blockers or knockdown of ASM abrogates STAT3 signaling, thereby limiting IL-17 pr

203 that accounts for the two-step mechanism of ASM acquisition.

204 l, these results reveal a novel mechanism of ASM pathogenesis in AD that leads to defective autophagy

205 alized to the plasma membrane and nucleus of ASM in both healthy controls and asthmatic patients, irr

206 to affect the immunomodulatory potential of ASM.

207 s in the lung, and abnormal proliferation of ASM directly contributes to the airway remodeling during

208 ts, all of which contribute to relaxation of ASM.

209 ere noted after pharmacologic restoration of ASM to the normal range in APP/PS1 mice.

210 tentially explain the reduced sensitivity of ASM cells to GC in severe asthmatics.

211 In studies of ASM mechanics, rapid cross-talk was confirmed at the phy

212 th the highest ASM quartile (median value of ASM area, 26.3%) were younger (42.5 vs >/=50 years old i

213 to the active site of beta2-adrenoceptors on ASM, which triggers a signaling cascade that results in

214 the prorelaxant effects of beta-agonists on ASM.

215 anoid-dependent beta2 -AR desensitization on ASM cells.

216 r JQ1/SGCBD01 nor I-BET762 had any effect on ASM cell viability.

217 Thus, whereas inflammatory effects on ASM alone are insufficient for AHR, Muc5ac-mediated plug

218 ), similar to effects of these inhibitors on ASM contractility.

219 that Mfge8 binding to integrin receptors on ASM opposes the effect of allergic inflammation on RhoA

220 Finally, we use our ASM datasets for functional interpretation of disease-as

221 t stem cells (iPSCs) was restored by partial ASM inhibition.

222 sosomal biogenesis and suggests that partial ASM inhibition is a potential new therapeutic interventi

223 owing and bronchial reactivity, particularly ASM, neuroendocrine epithelial cells, and bronchial nerv

224 The enzyme resembles plasmatic ASM including protein stability and Zn(2+)-dependence bu

225 We found that postnatal ASM innervation required neurotrophin (NT)-4 signaling t

226 Coinciding with postnatal ASM maturation, there was a critical time window for the

227 We found that fendiline, a potent ASM inhibitor, reduces the phosphatidylserine (PtdSer) a

228 able biopsy specimen had increased preschool ASM area fraction (n=8; median age, 8.2 years [range, 6-

229 Chemokine concentrations released by primary ASM were measured by MesoScale Discovery platform.

230 nd 2 (CCL2) levels were increased in primary ASM supernatants from asthmatics compared with healthy c

231 nchoalveolar lavage fluid, mucin production, ASM mass, and subepithelial collagen deposition.

232 psilonR1 cross-linking and directly promoted ASM wound repair.

233 and ASM wound repair but indirectly promotes ASM contraction via upregulation of mast cell-derived IL

234 Concordantly, delivery of recombinant ASM or exogenous ceramide to fendiline-treated cells rap

235 e to the ASM region and subsequently reduces ASM precipitation.

236 Arrestin subtypes differentially regulate ASM GPCRs and beta-arrestin-1 inhibition represents a no

237 dentify 32% as being genetically regulated (ASM or mQTL) and 14% as being putatively epigenetically

238 exploit GRK2/3 functional domains to render ASM hyporesponsive to contractile agents while increasin

239 half of these DMRs have cell type-restricted ASM, and among them are 188 hap-ASM DMRs and 933 mQTLs l

240 ities were comparable to corresponding serum ASM levels at their respective optimal reaction conditio

241 tee and results from their review of several ASM best practices guidelines and a non-ASM practice gui

242 In parallel, the levels of several ASM mitogenic factors, including the PAR-2 ligands, mast

243 l leukemia (MCL; n = 12), and aggressive SM (ASM; n = 7).

244 association augments acid sphingomyelinase (ASM) activity upon stimulation of CD4(+) T cells.

245 Acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to ceramide and phosphocho

246 We show that acid sphingomyelinase (ASM) is increased in fibroblasts, brain, and/or plasma f

247 ipid hydrolase enzyme acid sphingomyelinase (ASM) is required for the conversion of the lipid cell me

248 ow that inhibition of acid sphingomyelinase (ASM) mislocalizes both the K-Ras isoforms K-Ras4A and K-

249 Acid sphingomyelinase (ASM) released from lysosomes induces endocytosis of inju

250 In particular, acid sphingomyelinase (ASM), a critical enzyme in the production of the bioacti

251 We stimulated ASM cells and tissues with the contractile agonist acety

252 helial cultures (HBECs), where it suppresses ASM contractility by binding to and inhibiting the Ca(2+

253 Targeting ASM using bronchial thermoplasty has provided undeniable

254 Our findings indicate that targeting ASM in NSCLC can act by tumor cell-intrinsic and -extrin

255 M), with the important difference being that ASM allows toggling of the diluent stream during each (2

256 We believe that ASM will significantly ease method development for 2D-LC

257 In this article, we hypothesize that ASM controls T cell migration by regulating ICAM-1 funct

258 In conclusion, in this article, we show that ASM coordinates ICAM-1 function in brain endothelial cel

259 In this work, we show that ASM eliminates the major drawbacks of FSM including comp

260 We showed that ASM continued to mature until approximately 3 wk after b

261 lts indicate that it is highly unlikely that ASM half-maximum effective concentration (EC50) or Vmax

262 We will support the view that ASM sensitivity to glucocorticoid therapy can be blunted

263 The ASM can be used in conjunction with any quantum chemical

264 The ASM establishes the desired causal relationship between

265 First, we compared the ASM transcriptomic profiles of endobronchial biopsies be

266 he measured ASM activity originates from the ASM-encoding gene SMPD1.

267 to the selectivity of the enzyme and how the ASM domains collaborate to complete hydrolysis.

268 el chemo-mechanical signaling network in the ASM and serve as a proof-of-concept that a specific rece

269 ivo PP5 expression was also increased in the ASM bundles in endobronchial biopsies in severe asthmati

270 ing and crosstalk, focusing on events in the ASM cell but also addressing the function of these recep

271 In the ASM, the potential energy surface DeltaE(zeta) along the

272 decadal predictions of future changes in the ASM.

273 rescent substrate was applied to measure the ASM activity in cerebrospinal fluid (CSF) collected from

274 ions on both the internal variability of the ASM and the influence of external factors on the ASM.

275 tallic chemistry illustrate the power of the ASM as a unifying concept and a tool for rational design

276 ized that the gene expression profile of the ASM layer in endobronchial biopsies of patients with ast

277 ays a critical role in the alteration of the ASM phenotype during postnatal growth, thereby linking e

278 ole of microRNAs in the proliferation of the ASM.

279 and the influence of external factors on the ASM.

280 Pacific that transports less moisture to the ASM region and subsequently reduces ASM precipitation.

281 Genetic alterations in ASM lead to ASM deficiency (ASMD) and have been linked to Niemann-Pi

282 (i) promote fibrocyte (FC) migration towards ASM and (ii) are increased in blood from subjects with a

283 le of this chemokine in FC migration towards ASM was investigated by chemotaxis assays.

284 Main bronchi and tracheal ASM were significantly hyposensitive in subjects with as

285 raction in diseases such as asthma, triggers ASM cell proliferation and enhances T cell survival.

286 ecular basis of Mrf activation in OSM versus ASM.

287 of patients with and without asthma, ex vivo ASM, mast cells, cocultured cells and in a mouse model s

288 senger (calcium, cAMP generation)], ex vivo (ASM tension generation in suspended airway), and in vivo

289 Ex vivo, ASM shortening was largely maintained during a progressi

290 with epithelial barrier impairment, whereby ASM cells respond directly to inhaled environmental alle

291 d human bronchial rings to determine whether ASM can maintain shortening during a progressive decreas

292 anisms and clinical outcomes associated with ASM enlargement remain elusive.

293 hobiological characteristics associated with ASM enlargement.

294 are unrelated, and atopy is associated with ASM.

295 Coculture of mast cells with ASM activated by IL-33 increased agonist-induced ASM con

296 subjects, when activated and cocultured with ASM cells for 24 h, formed nanotubes that were visualize

297 nclusion, activated T cells communicate with ASM cells via nanotube formation.

298 r patients with SM-AHNMD, 43% for those with ASM, and 17% for those with MCL.

299 airways responses likely via effects within ASM cells and within non-lymphocyte cells involved in ly

300 cent history of clinical microbiology within ASM and then some current challenges we face.

301 the Activated Sludge Model for Xenobiotics (ASM-X)) with representative measured data from literatur

302 and Activated Sludge Model for Xenobiotics (ASM-X).