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 frequencies are increased in cancers versus matched

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

9 5 per thousand] immunoreactivity, P < .001), ASM-associated nerves (452.6 [25th-75th IQR, 196.0-811.2

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

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

12 Analyses across ASM quartiles in patients with severe asthma demonstrate

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

14 ctor binding from ChIP-seq is enriched among ASM loci, but most ASM differentially methylated regions

15 3 directly promotes mast cell activation and ASM wound repair but indirectly promotes ASM contraction

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

17 hosphatase PP5 in endobronchial biopsies and ASM cells.

18 pecific and different roles for ceramide and ASM secreted by irradiated endothelial cells opens new p

19 icient humans with Niemann-Pick disease, and ASM activity in healthy humans correlates with iNKT cell

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 ignificantly reduced in blood leucocytes and ASM obtained from patients with asthma compared to cells

23 e, OR2W3-evoked [Ca(2+)](i) mobilization and ASM relaxation required Ca(2+) flux through the store-op

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

25 and ETV1, which are both induced in NPC and ASM patient cells.

26 e increase of KLF2 protein levels in NPC and ASM stems from impaired signaling downstream sphingosine

27 1/10, Ebf and Mrf differ between the OSM and ASM lineages.

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

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

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

31 cer cells show increased allele switching at ASM loci, but disruptive SNPs in specific classes of CTC

32 Because ASM/ceramide were secreted by primary endothelial cells,

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

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

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

36 indicates epigenetic heterogeneity caused by ASM or CSM.

37 ynamic actomyosin-driven force generation by ASM cells.

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 , there are no effective therapies to combat ASM cell proliferation, which contributes to bronchocons

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

44 Activated Sludge Model-Electron Competition (ASM-EC)].

45 nformative "chromatin deserts." CONCLUSIONS: ASM is increased in cancers but occurs by a shared mecha

46 ng, the data pinpoint 15,112 high-confidence ASM differentially methylated regions, of which 1838 con

47 (NPC) and acid sphingomyelinase deficiency (ASM), in patient cells and mouse tissues.

48 Dense ASM mapping in normal plus cancer samples reveals candid

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

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

51 (NIR-ASM) by conjugating dicyanoisophorone (ASM) fluorophore with the NQO1 substrate quinone propion

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

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

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

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

56 Adding exogenous ASM or ceramide enhanced epithelial cell growth arrest a

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

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

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

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

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

62 pha and greatly enhances PGE2 secretion from ASM cells.

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

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

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

66 been mechanistically linked to mQTLs and hap-ASM.

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

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

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

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

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

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

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

74 Human ASM cells were isolated from bronchial biopsy specimens

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

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

77 sed ECM deposition and MMP activity in human ASM cells, which was significantly reduced with WAY trea

78 citation-contraction (E-C) coupling in human ASM cells.

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 Primary human ASM cells isolated from asthmatics and nonasthmatics wer

85 were absent in OR51E2-deleted primary human ASM.

86 We found that human ASM cells and mouse airway tissues exposed to insulin ex

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

88 (P < 0.001) and AP-1 (P < 0.01, P < 0.05) in ASM cells from asthmatics and nonasthmatics.

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

90 , or in combination with LPS or TNF-alpha in ASM.

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

92 ion and restores the levels of iNKT cells in ASM-deficient mice.

93 event or treat beta(2) AR desensitization in ASM.

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

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

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

97 lpha- or PDGF-induced ECM gene expression in ASM cells was significantly reduced with WAY (P < 0.001)

98 ) and reduced fibronectin mRNA expression in ASM layers but did not reduce inflammation per se.

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

100 EC survival was 53% higher in ASM (P < 0.001), structural and functional proteins of E

101 asing intracellular calcium ([Ca(2+)](i)) in ASM cells, some of which were (paradoxically) associated

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

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

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

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

106 eceptor agonists, absinthin alone (1 mum) in ASM cells does not induce Ca(2+) signals but reduces his

107 nd decreased iNKT cells are also observed in ASM-deficient humans with Niemann-Pick disease, and ASM

108 corneas, 1 was stored in OC and the other in ASM, using the same medium.

109 roteins of ECs were much better preserved in ASM, and it prevented the constant major edema of OC.

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

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

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

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

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

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

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

117 , collagen production, and IL-6 secretion in ASM cells.

118 he compartmentalization of cAMP signaling in ASM.

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

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

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

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

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

124 dictates the odorant receptor OR2W3-induced ASM relaxation and identify a previously unrecognized E-

125 10 years, volcanic eruptions have influenced ASM variations on an inter-decadal timescale via telecon

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

127 Instead, ASM olfactory responses to the monoterpene nerol were pr

128 vestigate this mechanism, we introduced into ASM cells aequorin-based Ca(2+) probes targeted to the c

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

130 -1 expression was increased in cells lacking ASM activity, we measured a significant decrease in T ly

131 901-1935 and 1963-1993), significantly lower ASM precipitation was observed compared with that during

132 culture (OC), of an active storage machine (ASM) that restores intraocular pressure and medium renew

133 s to reduce the approximate string matching (ASM) problem to the single net routing (SNR) problem in

134 tively reversed impaired beta(2) AR-mediated ASM relaxation in an obesity mouse model induced by a hi

135 Mapping of allele-specific DNA methylation (ASM) can be a post-GWAS strategy for localizing regulato

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

137 d for detecting allele-specific methylation (ASM) events within segments of DNA containing clusters o

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

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

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

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

142 rs of the American Society for Microbiology (ASM) concerning detailed verification strategies for SAR

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

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

145 ), according to the activation strain model (ASM) and energy decomposition analysis (EDA), we were ab

146 Increased ECM production modulates ASM cell proliferation and leads to airway remodeling.

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

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

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

150 span and patterns of age-specific mortality (ASM).

151 hIP-seq is enriched among ASM loci, but most ASM differentially methylated regions lack such annotati

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

153 wever, it protects the airway smooth muscle (ASM) against a loss of smooth muscle myosin heavy chain

154 -AR desensitization in airway smooth muscle (ASM) and compromises airway relaxation responsiveness to

155 e contractile state of airway smooth muscle (ASM) and uncovered a complex mechanism of odorant-evoked

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

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

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

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

160 Increased airway smooth muscle (ASM) cell mass and secretory functions are characteristi

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

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

163 calizations, including airway smooth muscle (ASM) cells, in which TAS2R have been reported to induce

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

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

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

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

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

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

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

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

172 tility [ via increased airway smooth muscle (ASM) intracellular calcium [Ca(2+)](i)] and remodeling (

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

174 Altered airway smooth muscle (ASM) mass and extracellular matrix (ECM) deposition in a

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

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

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

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

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

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

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

182 ed to play a role in arterial smooth muscle (ASM), we find that one of the largest contributors to me

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

184 ension transmission in airway smooth muscle (ASM).

185 ogenously expressed in airway smooth muscle (ASM).

186 odulatory functions in airway smooth muscle (ASM).

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

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

189 NIR-ASM was successfully used to detect and image the endoge

190 d emission (646 nm) in response to NQO1, NIR-ASM was capable of monitoring NQO1 activity in vitro and

191 NQO1)-activatable NIR fluorescent probe (NIR-ASM) by conjugating dicyanoisophorone (ASM) fluorophore

192 electivity, and nontoxic properties, the NIR-ASM appears to be a promising agent with clinical applic

193 QO1 to be the sole target activating the NIR-ASM in cell cultures.

194 only the A549 malignancies activated the NIR-ASM probe with a strong signal.

195 We successfully employed the NIR-ASM to differentiate cancer cells from normal cells base

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

197 these same motif classes track with de novo ASM.

198 00/mm were also usable for emergency, 58% of ASM corneas were usable versus 33% in OC.

199 eration during the contractile activation of ASM.

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

201 Previous studies defined the association of ASM with the pathogenesis of T(H) 1-directed lung diseas

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

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

204 Inhibition of ASM elevates cellular sphingomyelin and reduces cellular

205 Ceramide and the two isoforms of ASM were acutely secreted in the blood serum of wild-typ

206 nt supplies of nations and their patterns of ASM.

207 to affect the immunomodulatory potential of ASM.

208 ronutrient supplies are strong predictors of ASM even after correction for time and economic factors.

209 vation of the ERK1/2 are major regulators of ASM cell proliferation and airway remodeling in asthma.

210 d increases in [Ca(2+)](i) and relaxation of ASM cells.

211 Here, we define the role of ASM in T(H) 2-regulated allergic bronchial asthma.

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

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

214 itable for transplantation, but one-third of ASM corneas were compliant (ECD > 2000/mm).

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

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 As such, our ASM analysis approach can potentially lead to biological

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

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

222 Pharmacological ASM administration facilitates antigen presentation and

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

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

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

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

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

228 en insulin and beta(2) AR signaling promotes ASM beta(2) AR desensitization in obesity through upregu

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

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

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

232 )-beta, which upon activation down-regulated ASM proliferation, implicating an important role for est

233 identify 32% as being genetically regulated (ASM or mQTL) and 14% as being putatively epigenetically

234 ellular calcium [Ca(2+)](i)] and remodeling (ASM proliferation and extracellular matrix formation) in

235 e conductance in both conduit and resistance ASMs has been inadvertently overlooked.

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

237 Use of enteroid models revealed ASM and ceramide-mediated deleterious mode-of-action: wh

238 This study identifies secreted ASM and ceramide as paracrine factors enhancing intestin

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

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

241 nd is no longer evident in hTAS2R46-silenced ASM cells, indicating that it is hTAS2R46-dependent.

242 nd its related enzyme acid sphingomyelinase (ASM) are secreted by irradiated endothelial cells and ac

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

244 Acid sphingomyelinase (ASM) is a key regulator of the sphingolipid pathway.

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

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

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

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

249 and mice deficient in acid sphingomyelinase (ASM), an enzyme that degrades sphingomyelin.

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

251 enteroids without affecting their structure, ASM induced a significant decrease of enteroid growth wi

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 We show that ASM absence in mice leads to diminished CD1d-restricted

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

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

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

262 Our previous studies showed that ASM from patients with asthma exhibited increased expres

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

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

265 The ASM extended storage to 3 months with unprecedented endo

266 The ASM-EC model uses fewer parameters compared to existing

267 The ASM-EC model was calibrated with data from batch experim

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

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

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

271 decadal predictions of future changes in the ASM.

272 By extending graft survival to 3 months, the ASM will optimize eye banking and open up new perspectiv

273 in a common hyperosmotic medium, but not the ASM corneas, which had remained thin.

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

275 and the influence of external factors on the ASM.

276 Reducing the ASM problem into SNR also makes SneakySnake efficient to

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

278 a) , which increases the excitability of the ASMs.

279 bility; IK(Na) is the largest contributor to ASM cell resting conductance.

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

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

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

283 this approach, and the mechanisms underlying ASM in normal and neoplastic cells, remain to be clarifi

284 ecular basis of Mrf activation in OSM versus ASM.

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

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

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

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

289 hobiological characteristics associated with ASM enlargement.

290 f which were (paradoxically) associated with ASM relaxation.

291 are unrelated, and atopy is associated with ASM.

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

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

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

295 binding motifs are similarly correlated with ASM in cancer and non-cancer.

296 el therapeutic strategies, for example, with ASM blockade.

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

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

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

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