ライフサイエンスコーパス: blast

1 Five weeks after blast exposure, 8 of the 13 blasted rats exhibited chronic tinnitus.

2 atment morphologic evidence of disease (>=5% blasts in bone marrow).

3 treatment minimal residual disease (MRD; <5% blasts in bone marrow), and 10 patients had pretreatment

4 ic composition of these formulations after a blast.

5 ratory suggest that shockwaves produced by a blast can generate micron-sized bubbles in the tissue.

6 A supernova's explosion is driven by a blast wave causing the development of Rayleigh-Taylor an

7 used this single-cell approach to identify a blast-crisis-specific SC population, which was also pres

8 study of how the shockwave associated with a blast explosion impacts different brain regions.

9 stromal migration and the number of BCR-ABL blasts.

10 ecreased pTau levels in vitro, and abolished blast-induced elevation of pTau in vivo.

11 in insights into these injuries, an advanced blast simulator was used to expose rats to BOP and asses

12 ty and exposure frequency) using an advanced blast simulator.

13 ine methyl ester (L-NAME) administered after blast blocked BBB disruption and prevented CD4(+) T-cell

14 These changes were detected 30 days after blast exposure, suggesting the possibility of long-lasti

15 develop heterotopic ossification (HO) after blast-related extremity injury and traumatic injuries, r

16 levels in ApoE4 mice did not increase after blast TBI.

17 Deficits persisting up to 1 month after blast exposure were observed in the distortion product o

18 Five weeks after blast exposure, 8 of the 13 blasted rats exhibited chron

19 e P1-N1 amplitude reduction persisted in all blast-exposed rats.

20 We show that human B-ALL blasts alter a vascularized microenvironment promoting m

21 Third, T-cell ALL blasts are generally more resistant to conventional chem

22 l chemotherapeutic drugs than are B-cell ALL blasts.

23 enhance phagocytosis of patient-derived ALL blasts by human macrophages in vitro.

24 allele is preferentially retained in HD-ALL blasts consistent with inherited genetic variation contr

25 We report that HyperD-ALL blasts are low proliferative and show a delay in early m

26 n of target antigens between CARTs and T-ALL blasts leads to CART fratricide.

27 ction of collagens, potentially trapping ALL blasts.

28 -positive acute lymphoblastic leukemia (ALL) blasts, was approved for use in patients with relapsed o

29 mediated pro-survival signaling, dampens AML blast regeneration, and strongly synergizes with chemoth

30 ion associated with oncogenesis enhances AML blast binding to E-selectin and enable promotion of pro-

31 dly effective against a panel of primary AML blast cells, with low nanomolar IC(50)s and, based on co

32 stromal cells then feed back to promote AML blast survival and proliferation via the SASP.

33 ates bone marrow stromal cells (BMSC) to AML blast transfer of mitochondria through AML-derived tunne

34 e, we report a novel interaction between AML blasts and BM-MSCs, which benefits AML proliferation and

35 vivo in serially sorted peripheral blood AML blasts.

36 h BETi-P/R sAML cells or patient-derived AML blasts innately resistant to BETi.

37 erent AML cell lines and patient-derived AML blasts, whereas endothelial cells with low binding capac

38 show AHR signaling is repressed in human AML blasts and preferentially downregulated in LSC-enriched

39 ic cell divisions and differentiation in AML blasts and AML stem/progenitor cells, inhibited cell gro

40 ore, targeting protein palmitoylation in AML blasts could block MDSC accumulation to improve immune r

41 es the proliferative capacity of NPM1mut AML blasts in vitro and in vivo.

42 ion neoantigen is naturally presented on AML blasts and enables T cell recognition and killing of AML

43 ion of multiple costimulatory ligands on AML blasts at post-transplantation relapse (PD-L1, B7-H3, CD

44 e combination of MTP-PE and IFN-gamma on AML blasts generated an inflammatory cytokine profile and ac

45 as a frequently up-regulated antigen on AML blasts that is a critical regulator of blast function.

46 her to target AML cell lines and patient AML blasts.

47 105 prevented the engraftment of primary AML blasts and inhibited leukemia progression following dise

48 (+)HLA-A2(+) leukaemia cells and primary AML blasts, but not NPM1c(-)HLA-A2(+) leukaemia cells or HLA

49 AML cell line or patient-derived primary AML blasts.

50 senchymal stromal cells (BM-MSC) protect AML blasts from spontaneous and chemotherapy-induced apoptos

51 Targeting MEK1/2 sensitizes AML blasts to genotoxic agents, indicating a role for NCAM1

52 oid leukemia (AML) mouse models, we show AML blasts release inflammatory mediators that upregulate en

53 We show that AML blasts alter metabolic processes in adipocytes to induce

54 Here, we report that AML blasts induce a senescent phenotype in the stromal cells

55 We further show that AML blasts secrete EGFL7 protein and that higher levels of E

56 ansfer of fatty acids from adipocytes to AML blasts.

57 In vivo AML blasts with highest E-selectin binding potential are 12-

58 ion profiles of acute myeloid leukemia (AML) blasts purified from patients at serial time-points duri

59 were stratified according to donor, age, and blast count.

60 the re-establishment of EZH2 expression and blast clearance.

61 rd PCR amplifications, Sanger sequencing and blast analysis, the proposed strategy was demonstrated t

62 smear revealed anemia, thrombocytopenia, and blast cells, and a diagnosis of acute myeloid leukemia w

63 S1, no blasts; CNS2a to 2c, < 5 WBCs/muL and blasts with/without >/= 10 RBCs/muL or >/= 5 WBCs/muL pl

64 tanical remains are reinterpreted in part as blast deposits that resulted from several episodes of ai

65 oblastic acute myeloid leukaemia (defined as blasts >=20% but <=30%) refractory to hypomethylating ag

66 emonstrated enhanced responses to autologous blasts in vitro, and primed CD56bright cells controlled

67 phenotypically resemble antigen-activated B-blasts.

68 In vivo similar B-blasts can differentiate to become memory B cells (MBC),

69 ent with human data showing that battlefield blasts might be associated with molecular changes before

70 mputational pipeline to predict PPIs between blast fungus and rice.

71 n given to the possible relationship between blast exposure and decreased sound tolerance in Service

72 L-NAME also blocked blast-induced increases in intercellular adhesion molecu

73 d a concomitant increase in peripheral blood blast cells.

74 ize, and high leukocyte and peripheral-blood blast counts.

75 had cytopenias, and 12.0% presented >/=5% BM blast cells.

76 e chronic myelogenous leukemia (CP-CML), but blast crisis CML (BC-CML) and acute myeloid leukemias (A

77 nces in spatial cognition were observed, but blasted rats as a whole exhibited increased anxiety.

78 s, and the top seven subnetworks affected by blast fungus through PPIs were investigated.

79 Traumatic brain injury generated by blast may induce long-term neurological and psychiatric

80 er the generation of invasive force to cause blast disease.

81 The fungus Magnaporthe oryzae causes blast, the most devastating disease of cultivated rice.

82 system, in which primary human CD8(+) T cell blasts are stimulated by recombinant peptides presented

83 ected subjects of HBHA-induced CD4(+) T cell blasts that degranulate, as measured by surface capture

84 S-causative p110delta variants and in T-cell blasts derived from patients.

85 9)/L, platelets < 100 x 10(9)/L, circulating blasts >/= 2%, bone marrow fibrosis grade >/= 2, constit

86 The most common blast injury pattern was of a secondary type in the curr

87 All concussive blast injuries met the Department of Defense definition

88 Worsening of symptoms in concussive blast TBI was also observed on measures of posttraumatic

89 Thirty-six of 50 patients with concussive blast TBI (72%) had a decline in the GOS-E from the 1- t

90 nificantly worse in patients with concussive blast TBI compared with combat-deployed controls, wherea

91 g that PTEN acts non-autonomously to control blast cell quiescence may be relevant to its function as

92 day-29 minimal residual disease < 0.1%, CSF blast, regardless of cell count, was an independent adve

93 In the devastating blast fungus Magnaporthe oryzae(1), powerful glycoprotei

94 hase in a patient who subsequently developed blast crisis.

95 hat were genomically similar to the dominant blast populations at diagnosis and were fully clonally r

96 neurobehavioral changes 2 weeks after double blast exposure is a relevant finding, consistent with hu

97 n rats 2 weeks after explosive-driven double-blast exposure.

98 ML-DS blast cells ex vivo have increased sensitivity to cytara

99 e exposure conditions and combinations (i.e. blast overpressure (BOP) intensity and exposure frequenc

100 abilizes MDM2 transcripts, thereby enhancing blast crisis progenitor propagation.

101 many months, suggesting that MDS with excess blasts could be viewed as an overlap between a dysplasti

102 In the presence of excessive blasts and other poor prognostic factors, hypomethylatin

103 s, on a timescale comparable to an explosive blast but with minimal pressure transients.

104 Brain injuries caused by an explosive blast or blunt force is typically presumed to associate

105 e identified at both days 1 and 28 following blast, and are associated with inner ear mechanotransduc

106 ell infiltration in the cerebellum following blast exposure.

107 activation in the sub-acute stages following blast.

108 uidelines establishing cumulative limits for blast exposure numbers and intensities in military perso

109 nic RNA binding protein that is required for blast crisis CML.

110 e effectiveness of the 2NS translocation for blast resistance and emphasizes the urgent need to ident

111 In primary human AML, exposure of fresh blast cells to daunorubicin activated the stress-respons

112 Injury from blast exposure is becoming a more prevalent cause of dea

113 s of such exposure include overpressure from blast explosions or high-intensity focused ultrasound (H

114 primary ocular blast exposure resulting from blast wave pressure has been reported among survivors of

115 ng neurological impairments that result from blasts are significant and lifelong.

116 , we show that the decision of somatic gonad blast cells (SGBs) and germline stem cells (GSCs) to be

117 The use of ground granulated blast-furnace slag (GGBS) in Ontario was studied, and an

118 After 6 months, grit-blasted acid-etched (GBAE) PS implants with and without

119 the accumulation of primitive hematopoietic blast cells in the blood and bone marrow.

120 anemia, thrombocytopenia, leukopenia, higher blast count, symptoms, large splenomegaly, and unfavorab

121 of its kind drilling program on a historical blast furnace slag heap at Consett, U.K., are reported.

122 traits and in human veterans exposed to IED blasts in theater with behavioral, cognitive, and/or mem

123 the hierarchical differentiation of immature blast cells into mature, functional cell types and linea

124 ocess leading to an accumulation of immature blasts in the blood.

125 tic syndrome, acute myeloid leukemia, and in blast crisis transformation of chronic myeloid leukemia.

126 However, in blast crisis chronic myeloid leukemia progenitors, loss

127 ncogenic function through BCAA production in blast crisis CML cells.

128 GFL7 mRNA and EGFL7 protein are increased in blasts of patients with acute myeloid leukemia (AML) com

129 patient each: myalgia (one [2%]), increased blast cell count (one [2%]), and general physical health

130 In this study, using HBHA-induced blast formation as a readout of specific T lymphocyte ac

131 long-term repopulating LSCs and infiltrating blast cells, conferring a survival advantage in preclini

132 We found that 300-kPa blasts yielded no detectable cognitive or motor deficits

133 Rats received two 30-psi (~ 207-kPa) blasts 24 h apart or were handled identically without bl

134 t-blast interval (24-71 hours after the last blast) also prevented sensorimotor impairment on a rotar

135 ogenitor infant acute lymphoblastic leukemia blast cells.

136 induces dramatic differentiation of leukemia blast cells as shown by cellular morphology and cell sur

137 tivity of mebendazole using primary leukemia blast cells isolated from human acute myeloid leukemia (

138 Leukemia blasts show a myeloid differentiation phenotype when the

139 ating active viral transcription in leukemia blasts as well as intact virions in serum.

140 -derived B-cell acute lymphoblastic leukemia blasts compared with standard TCR transfer.

141 ction of B-cell acute lymphoblastic leukemia blasts during CART19 manufacturing can lead to CAR19+ le

142 ith Alox5 overexpression in MLL-AF9-leukemic blast cells; inhibition of the above signaling pathways

143 hat may result from infiltration of leukemic blast cells (LBCs) into lung parenchyma and interstitium

144 ene expression patterns in purified leukemic blast cells.

145 ls, leukemic stem cells [LSCs], and leukemic blasts).

146 ce of the undifferentiated state in leukemic blasts.

147 lows adequate protein production in leukemic blasts.

148 Patients with 25% or more leukemic blasts after induction (early nonresponders) had the poo

149 is not expressed on the majority of leukemic blasts but instead on a subpopulation of supportive cell

150 rine mechanism supporting growth of leukemic blasts in patients with AML.

151 characterized by overproduction of leukemic blasts.

152 citabine in AML cell lines, primary leukemic blasts, and xenograft models.

153 against KIR ligand-matched primary leukemic blasts.

154 h or differentiation and sensitized leukemic blasts toward genotoxic agents in vitro and in vivo.

155 veral of these studies suggest that leukemic blasts occupy specific cellular and biochemical "niches.

156 By comparing LSCs to leukemic blasts and healthy HSPCs, we validate candidate LSC mark

157 ures in rats exposed to repetitive low-level blast that develop chronic anxiety-related traits and in

158 Rats exposed to repetitive low-level blasts accumulated abnormal hyperphosphorylated tau in n

159 hese findings suggest an association linking blast injury, tauopathy, and neuronal injury.

160 acterization of functionally validated LSCs, blasts, and healthy HSPCs, representing a valuable resou

161 (CML)-like disease manifesting in "lymphoid blast crisis." The biological heterogeneity of BCR-ABL1-

162 nsplant cytopenias, but not with bone marrow blast count, MDS treatment history, or history of prior

163 Reductions in blood and bone marrow blast percentages were observed, together with induction

164 During the venetoclax prephase, marrow blast reductions (>= 50%) were noted in NPM1-, IDH2-, an

165 ll subclones that were not detectable in MDS blasts became dominant upon AML progression.

166 and MDS-SC contributing to generation of MDS blasts or progression to AML, respectively.

167 The mean blast index of lines with and without the 2NS translocat

168 ement of the OsMYB30 gene in bsr-d1-mediated blast resistance.

169 Mild blast traumatic brain injury (B-TBI) induced lasting cog

170 of understanding the pathophysiology of mild blast-induced traumatic brain injury and identifying the

171 our study, we utilized a mouse model of mild blast-related TBI (bTBI) to investigate TBI-induced chan

172 erized by the accumulation of clonal myeloid blast cells unable to differentiate into mature leukocyt

173 When recalibrated for myelomonocytic blast enumeration, this approach is superior to flow cyt

174 ing burnout was sent via email or newsletter blast with responses received from 680 CCSC members, inc

175 F status was designated as follows: CNS1, no blasts; CNS2a to 2c, < 5 WBCs/muL and blasts with/withou

176 benefits for participants with tonal and non-blast induced tinnitus at the end of 6 (24.3% vs. 2%, p

177 lying debris are more common, primary ocular blast exposure resulting from blast wave pressure has be

178 Although secondary ocular blast injuries due to flying debris are more common, pri

179 asts are detected in vitro around day 1.5 of blast colony differentiation, within the cell population

180 Magnaporthe oryzae, the causal agent of blast disease, is one of the most destructive plant path

181 roaches to prevent or treat similar cases of blast-induced auditory damage in human subjects.

182 P protein level was greater in cerebellum of blast vs control rats (p < 0.05).

183 c hyperactivity, the non-auditory effects of blast and potential traumatic brain injury may also exer

184 for understanding the subsequent effects of blast exposure in a sample of Florida National Guard mem

185 le deficiency, myelodysplasia with excess of blast cells, and various developmental aberrations, we i

186 Meanwhile, the pathogenic genes of blast fungus were enriched in the predicted PPIs network

187 ased superoxide production within 4 hours of blast.

188 es were observed, together with induction of blast cell differentiation, in particular, in patients w

189 gus proteins in response to the infection of blast fungus.

190 oxidative stress assay and a mouse model of blast-induced indirect traumatic optic neuropathy (bITON

191 l system in both humans and animal models of blast injury.

192 article provide insight into the process of blast fungus infection.

193 fferentiation and impairs the propagation of blast crisis CML both in vitro and in vivo.

194 n AML blasts that is a critical regulator of blast function.

195 nt need to identify novel non-2NS sources of blast resistance.

196 fferentiate would produce an accumulation of blasts.

197 ndrome with refractory anemia with excess of blasts, in CR/CR with incomplete hematologic recovery (C

198 ified endoglin expression on the majority of blasts from patients with acute myeloid leukemia (AML) a

199 To determine the prognostic significance of blasts, and of white and red blood cells, in CSF samples

200 ely, that substantiates its strong effect on blast resistance.

201 Current research on blast and other injuries sustained by United States Serv

202 Overall, blast exposure increased the likelihood of participants

203 stitutively activated in primary AML patient blasts but not in normal mononuclear cells.

204 iR-99 inhibition induced primary AML patient blasts to undergo differentiation.

205 death in AML cell lines, primary AML patient blasts, and isolated AML patient leukemic progenitor/ste

206 promote proliferation of primary AML patient blasts.

207 Ribavirin slows increases in peripheral blasts in KMT2A-R infant ALL xenograft-bearing mice.

208 uation revealed pancytopenia with peripheral blasts, and acute myeloid leukemia (AML; French-American

209 versified B cell repertoire for rapid plasma blast responses.

210 er of RBCs; CNS3a to 3c, >/= 5 WBCs/muL plus blasts with/without >/= 10 RBCs/muL or clinical signs of

211 thout >/= 10 RBCs/muL or >/= 5 WBCs/muL plus blasts, with WBCs >/= 5 times the number of RBCs; CNS3a

212 developed a system that couples a pneumatic blast to a microfluidic channel to precisely and reprodu

213 le injuries collectively known as polytrauma/blast-related injury (PT/BRI).

214 that the most adequate way to describe post blast polymer samples is that they are less oxygenated a

215 and 7 days, and were restored by day 28 post-blast.

216 vulnerable) immediately and four hours post-blast exposure.

217 delayed-onset BBB disruption (72 hours post-blast) in cerebellum.

218 as a significant, sub-acute (four hours post-blast) pathological change in bTBI.

219 dysfunction during this acute/subacute post-blast interval (24-71 hours after the last blast) also p

220 xidative stress occurs at the same time post-blast when the BBB permeability changes.

221 tested if down-regulation of synj1 prevented blast-induced Tau hyper-phosphorylation.

222 jury and neuronal inflammation after primary blast exposure.

223 d leukemia (AML) cell line cells and primary blast AML cells in vitro.

224 Rats were injured by primary blast waves in a compressed gas-driven shock tube at 180

225 H2 expression in resistant cells and primary blasts from a subset of relapsed AML patients resulted f

226 nd FLT3-resistant AML cell lines and primary blasts from AML patients, while showing no cytotoxicity

227 ll lines and coT-ALL patient-derived primary blasts.

228 Finally, primary blasts derived from leukemia patients experiencing chemo

229 nsecutive complete haematological remission (blast counts <5% in bone marrow) or myelodysplastic synd

230 ted behavioral changes from primary repeated blast lung injury under appropriate exposure conditions

231 vice members and Veterans who did not report blast exposure, 28% and 34% respectively, also reported

232 Of those who reported blast exposure, 33% of Service members (adjusted OR = 1.

233 a high throughput screen using Msi2-reporter blast crisis chronic myeloid leukemia (bcCML) and identi

234 Down-regulation of synj1 rescues blast-induced phospholipid dysregulation and prevents de

235 Rice blast disease caused by the fungus Magnaporthe grisea (M

236 als against Septoria tritici blotch and rice blast disease.

237 feeds half the world's population, and rice blast is often a destructive disease that results in sig

238 A key factor causing rice blast disease and defense might be protein-protein inter

239 y understanding the role of glycerol in rice blast disease.

240 iosynthesis inhibitors not only prevent rice blast disease, but also show effective, broad-spectrum f

241 nicity of filamentous fungi such as the rice blast fungus (Magnaporthe oryzae) remains unclear.

242 al metabolic sources of glycerol in the rice blast fungus and how appressorium turgor is focused as p

243 ly, we grouped field populations of the rice blast fungus Magnaporthe oryzae (syn: Pyricularia oryzae

244 The rice blast fungus Magnaporthe oryzae elaborates a specialized

245 The pathogenic life cycle of the rice blast fungus Magnaporthe oryzae involves a series of mor

246 appressorium-mediated infection in the rice blast fungus Magnaporthe oryzae, requires very-long-chai

247 rane trafficking in pathogenesis of the rice blast fungus Magnaporthe oryzae, we identified MoGlo3 as

248 acterised the function of MoHMT1 in the rice blast fungus, Magnaporthe oryzae.

249 the physiology and pathogenicity of the rice blast fungus.

250 ssorium-mediated plant infection by the rice blast fungus.

251 avus, and appressorium formation in the rice blast pathogen Magnaporthe grisea.

252 aracterize two nuclear effectors of the rice blast pathogen Magnaporthe oryzae.

253 SODs in miR398b-regulated resistance to rice blast disease, and uncover an integrative regulatory net

254 Patient-derived, post-MPN, CD34+ sAML blasts exhibiting relative resistance to BETi, as compar

255 nce to BETi, as compared with sensitive sAML blasts, displayed higher messenger RNA and protein expre

256 vels, inducing loss of viability of the sAML blasts.

257 Sixty-two of 77 patients had secondary blast injuries caused by shrapnel.

258 coefficient was measured following simulated blast-induced microcavitation.

259 Repetitive, but not single blast exposure, induced delayed-onset BBB disruption (72

260 in bone marrow) or myelodysplastic syndrome (blast counts <20% in bone marrow), Karnofsky index of 60

261 erility, a stress condition known as "tassel blasting." We identified a mutant, necrotic upper tips1

262 rotic upper tips1 (nut1), that mimics tassel blasting and drought stress and reveals the genetic mech

263 Using this system, we demonstrate that blast-like shear transients produced with minimal pressu

264 en collectively, these results indicate that blast provokes delayed-onset of NOS-dependent pathogenic

265 analysis of 20 human primary AML showed that blasts generating high levels of ROS have increased gluc

266 The blast fungus Magnaporthe oryzae gains entry to its host

267 The blast injuries were observed in the head and neck (16/77

268 miR398b-regulated rice immunity against the blast fungus Magnaporthe oryzae.

269 om chronic phase CML patients as well as the blast crisis phase cell lines, Kcl-22 and K562, formed f

270 Here we show how, in the blast fungus Magnaporthe oryzae, terminating rice innate

271 analysis of host species determinants in the blast fungus resulted in the cloning of avirulence genes

272 omparable to neuropathologic findings in the blast-exposed mice.

273 er studies on altered gene expression in the blast-injured rat cochlea may provide insights into new

274 tion, discover subdiffusive character of the blast wave-induced interfacial mixing, and reveal the me

275 ML) progressed from the chronic phase to the blast crisis phase, and was associated with the poor pro

276 equencing provides advantages over using the blast count, which underestimates tumor burden, and coul

277 ructed for their fast identification through blast analysis.

278 ntly higher subclonal complexity compared to blast cells and contained a large number of aging-relate

279 wave produced by shear forces consequent to blast shock waves passing through density inhomogeneity

280 Traumatic brain injury due to blast exposure is currently the most prevalent of war in

281 evaluate brain injury following exposure to blast is also highlighted.

282 Exposure to blast overpressure from improvised explosive devices (IE

283 with repetitive head impacts or exposure to blast waves.

284 that confers non-race-specific resistance to blast.

285 e cerebellum as a brain region vulnerable to blast-induced mTBI.

286 , rapidly fatal, and serially transplantable blast population, phenotypically and transcriptionally s

287 ic brain injury resulting from blunt trauma, blast exposure, and highly physically demanding tasks un

288 ms and tinnitus were directly dependent upon blast exposure, with both acting as bridge symptoms to o

289 Wheat blast caused by the fungus Magnaporthe oryzae pathotype

290 Wheat blast first emerged in Brazil in the mid-1980s and has r

291 destructive new fungal disease called wheat blast and stress the importance of open-science platform

292 at cultivation in Brazil, suggest that wheat blast emerged due to widespread deployment of rwt3 wheat

293 Taken together, our data suggest that while blast-induced tinnitus may play a role in auditory and l

294 is the most prevalent injury associated with blast overpressure exposure (BOP) in Warfighters and civ

295 opo IIbeta was significantly associated with blast percentage in marrow or blood (P = 0.0001), CD7 (P

296 To identify genomic regions associated with blast resistance against MoT isolates in Bolivia and Ban

297 s from Veterans/military Servicemembers with blast-related TBI, we found marked Purkinje cell dendrit

298 nts with CNS3 disease (CSF WBC >= 5/muL with blasts or cranial nerve palsies, brain/eye involvement,

299 overt CNS disease (CNS3; >= 5 WBCs/muL with blasts) received HDMTX and were randomly assigned to rec

300 h apart or were handled identically without blast.