ライフサイエンスコーパス: PAH

1 PAH concentrations in personal air and on skin accounted

2 PAH concentrations were higher at wildland fires compare

3 PAH enzyme activity was reduced in the presence of DNAJC

4 PAHs concentrations that decline more rapidly with incre

5 PAHs in the cuticles and inner tissues were distinguishe

6 PAHs in the inner tissues became concentrated with the i

7 PAHs on the adaxial and abaxial sides of a leaf were dif

8 (other heavy metals (r = 0.43, p = <0.001)), PAHs (r = 0.20, p = 0.050), and PCBs (r = 0.19, p = 0.02

9 PM samples with 22 PAH compounds obtained from residential areas close to i

10 ere exceeded for BaP in 12%, and for total 4 PAHs in 28%, with a greater contribution of adulterated

11 oluene resulted in desorption of 13 +/- 0.4% PAH.

12 Consecutive 46 PAH males and 94 females were age matched with a represe

13 ow-valent zirconocene reagent, which gives a PAH with one or more annulated zirconacyclopentadienes (

14 SBE experiments revealed an accessible PAH fraction of 41 +/- 1% ( summation operator16 US EPA

15 (SBE) was applied to quantify the accessible PAH fraction in industrially contaminated soil with and

16 robically incubated soil from two additional PAH-contaminated sites and was formed from pyrene by two

17 riability in bioavailability of CNM-adsorbed PAHs is largely driven by PAH size, configuration and su

18 reduction in bioavailability of CNM-adsorbed PAHs was negatively correlated with the amount of CNM su

19 Although it appeared that GN adsorbed PAHs indiscriminately compared to MWCNTs, the subsequent

20 he subsequent bioavailability of GN-adsorbed PAHs was more sensitive to PAH morphology than MWCNTs.

21 ermining the bioavailability of the adsorbed PAHs to Pimphales promelas using bile analysis via fluor

22 of CNM surface area covered by the adsorbed-PAHs.

23 Applying the method using Stockholm air PAH samples indicated MPFs with orders of magnitude high

24 mixture potency factors (MPFs) for airborne PAHs.

25 to assess whole mixture samples of airborne PAHs to improve health risk assessment.

26 es per year in Stockholm are due to airborne PAHs.

27 sis membrane is not sufficient to remove all PAH polymers.

28 All PAHs and metal ions modulated the Abeta aggregation proc

29 sed risks via inhalation exposure to ambient PAHs.

30 ubation, the changes in the total alkane and PAH contents in the NAPL residue were quantified.

31 distinctive differences between controls and PAH patients.

32 Lung immune complexes were isolated and PAH target antigens were identified by liquid chromatogr

33 ardiopulmonary tissues from PAH patients and PAH rat models, respectively.

34 52 grew by utilizing the bulk of alkanes and PAHs in the fuel; however, biofilm formation was incipie

35 rties (elemental composition, delta(13)C and PAHs signatures, chemical recalcitrance, density and por

36 BPCAs (soot) and PAHs (precursors of soot) trace fossil fuel-derived PyC.

37 mately 70%, but had little impact on angular PAHs.

38 given in combination with currently approved PAH therapies.

39 icularly vulnerable in early life stages, as PAH toxicity causes developmental cardiac abnormalities

40 with (n = 17) and without (n = 5) associated PAH using Optical Coherence Tomography during Right Hear

41 LDL-C was lower in both PAH (2.6 +/- 0.8 mmol/l) and CTEPH (2.7 +/- 0.7 mmol/l)

42 On the basis of the PM-bound PAH concentrations and their activities reported in HTS

43 ty of CNM-adsorbed PAHs is largely driven by PAH size, configuration and surface area coverage.

44 e unable to successfully remove carcinogenic PAHs from contaminated soils to concentrations below the

45 ncy factors (PEFs) for targeted carcinogenic PAHs.

46 However, the precise identity of cardiotoxic PAHs, and the mechanisms underlying contractile dysfunct

47 y a crucial role in the synthesis of complex PAHs in circumstellar envelopes of dying carbon-rich sta

48 strategies were most effective for degrading PAHs and estimated the cancer risks associated with PAH-

49 Further analyses extending to differentially PAH-resistant subpopulations showed organismal level bio

50 wo ecologically relevant levels of dissolved PAHs.

51 pollutant species (PM, NOx, trace elements, PAHs); the pros and cons of biomagnetic monitoring of at

52 n of 41 +/- 1% ( summation operator16 US EPA PAHs + 5 further PAHs).

53 cal inhibition of HDAC6 improved established PAH in two experimental models and can be safely given i

54 , we examined the consequences of a familial PAH-associated frameshift mutation in CAV1, P158PfsX22,

55 eased in subjects with scleroderma following PAH development.

56 model predicted a higher energetic cost for PAH-resistant subpopulations when seeking an optimum hab

57 asticus appears to lack the genes needed for PAH degradation.

58 the ascending aorta (3.4 versus 2.3 m/s for PAH and controls, respectively; P=0.001) and reduced aor

59 ss the effectiveness of DMF as a therapy for PAH using patient-derived cells and murine models.

60 hlorobenzene and semiquantitative values for PAHs with a high molecular weight.

61 ectrometry and mass-defect filtering to four PAH-contaminated samples from geographically distant sit

62 Four PAHs, benzo[a]anthracene (BaA), chrysene (Chr), benzo[b]

63 date a method for the quantification of four PAHs [benzo(a)anthracene, chrysene, benzo(b)fluoranthene

64 lungs, distal PAs, and isolated PASMCs from PAH patients and animal models.

65 was reduced in cardiopulmonary tissues from PAH patients and PAH rat models, respectively.

66 summation operator16 US EPA PAHs + 5 further PAHs).

67 mean degradation of 44% across the B2 group PAHs.

68 Heritable PAH and idiopathic PAH BOECs recapitulated the metabolic

69 from patients with idiopathic and heritable PAH and with pulmonary veno-occlusive disease/pulmonary

70 linically as having idiopathic and heritable PAH.

71 al proliferation and glycolysis in heritable PAH BOECs, corrected the dysregulation of glycolytic gen

72 otyped patients with idiopathic or heritable PAH (n=365) from healthy control subjects (n=121) after

73 athic, drug- and toxin-induced, or heritable PAH enrolled in the French pulmonary hypertension regist

74 l cells (BOECs) from patients with heritable PAH caused by mutations in the bone morphogenetic protei

75 which could be attributed to its higher HMW PAH concentration.

76 e the EC plexiform phenotype in severe human PAH.

77 n (PCDD/F), polycyclic aromatic hydrocarbon (PAH) and polychlorinated biphenyl (PCB) emissions.

78 rsulfurated polycyclic aromatic hydrocarbon (PAH) as a next-generation "sulflower." In this novel PAH

79 as a model polycyclic aromatic hydrocarbon (PAH) degrading bacterium.

80 6-8.43) and polycyclic aromatic hydrocarbon (PAH) gradients (0.18-20.68 mg kg(-1)) were collected fro

81 ion between polycyclic aromatic hydrocarbon (PAH) molecule and energetic ion is a subject of interest

82 mployed for polycyclic aromatic hydrocarbon (PAH)-contaminated media, wherein carcinogenic hazards ar

83 afforded a polycyclic aromatic hydrocarbon (PAH)-porphyrin hybrid in 38% yield.

84 afforded a chiral polyaromatic hydrocarbon (PAH) embedding six enantiomerically stable [5]helicene u

85 pollutant-polycyclic aromatic hydrocarbons (PAH).

86 )-priority polycyclic aromatic hydrocarbons (PAHs) adsorbed on LCPM from thermal decomposition of nan

87 s of large polycyclic aromatic hydrocarbons (PAHs) and graphene nanostructures demand methods that ar

88 icle-phase polycyclic aromatic hydrocarbons (PAHs) and n-alkanes, higher fractions of organic carbon

89 Polycyclic aromatic hydrocarbons (PAHs) are hazardous air pollutants formed during incompl

90 Polycyclic aromatic hydrocarbons (PAHs) are widely distributed throughout the atmosphere a

91 rmation of polycyclic aromatic hydrocarbons (PAHs) as detected in carbonaceous meteorites such as in

92 uating the polycyclic aromatic hydrocarbons (PAHs) contamination of commercial vegetable oils and exa

93 evance are polycyclic aromatic hydrocarbons (PAHs) from combustion processes that are associated with

94 occur with polycyclic aromatic hydrocarbons (PAHs) in contaminated soils.

95 to degrade polycyclic aromatic hydrocarbons (PAHs) into less toxic compounds and can be performed in

96 xposure to polycyclic aromatic hydrocarbons (PAHs) it is important to understand the binding mechanis

97 a suite of polycyclic aromatic hydrocarbons (PAHs) on multiwalled carbon nanotubes (MWCNTs) and exfol

98 ounds; and polycyclic aromatic hydrocarbons (PAHs)) were measured with several online devices, and di

99 xposure to polycyclic aromatic hydrocarbons (PAHs), a group of organic chemical contaminants.

100 esticides, polycyclic aromatic hydrocarbons (PAHs), and polybrominated diphenyl ethers (PBDEs) at two

101 BPCAs) and polycyclic aromatic hydrocarbons (PAHs), preserved in aquatic sediments from a suburban an

102 Bs), seven polycyclic aromatic hydrocarbons (PAHs), three chlorinated pesticides, and five metals in

103 (MAHs) or polycyclic aromatic hydrocarbons (PAHs).

104 to degrade polycyclic aromatic hydrocarbons (PAHs).

105 ntercalation into polyaromatic hydrocarbons (PAHs) has been studied intensely after reports of superc

106 teraction of poly(allylamine) hydrochloride (PAH) and its monomeric precursor allylamine hydrochlorid

107 the gene encoding phenylalanine hydroxylase (PAH), and a small proportion (2%) exhibit tetrahydrobiop

108 ne model of pulmonary arterial hypertension (PAH) are described.

109 tients with pulmonary arterial hypertension (PAH) at rest.

110 survival in pulmonary arterial hypertension (PAH) at the time of diagnosis.

111 its role in pulmonary arterial hypertension (PAH) has not been determined.

112 -associated pulmonary arterial hypertension (PAH) in BPD mouse models, which, conversely, is worsened

113 teration in pulmonary arterial hypertension (PAH) in which apelin signaling is downregulated, and to

114 Pulmonary arterial hypertension (PAH) is a rare cardiopulmonary disorder that affects chi

115 Pulmonary arterial hypertension (PAH) is an obstructive disease of the precapillary pulmo

116 RATIONALE: Pulmonary arterial hypertension (PAH) is an obstructive vasculopathy characterized by exc

117 Pulmonary arterial hypertension (PAH) is characterized by abnormal growth and enhanced gl

118 r pediatric pulmonary arterial hypertension (PAH) is hampered by lack of pediatric clinical trials.

119 culature in pulmonary arterial hypertension (PAH) is primarily provided by autopsy or tissue specimen

120 eficial for pulmonary arterial hypertension (PAH) remains to be explored.

121 modeling in pulmonary arterial hypertension (PAH) that is hereditary, idiopathic, or associated with

122 tients with pulmonary arterial hypertension (PAH), but the mechanisms by which these mutations impact

123 rategies in pulmonary arterial hypertension (PAH).

124 ildren with pulmonary arterial hypertension (PAH).

125 h heritable pulmonary arterial hypertension (PAH).

126 f angina in pulmonary arterial hypertension (PAH).

127 Heritable PAH and idiopathic PAH BOECs recapitulated the metabolic abnormalities obse

128 complexes from 16 hereditary and idiopathic PAH versus 12 control lungs.

129 as more accurate in patients with idiopathic PAH at 3 years (sensitivity, 89 [95% CI, 65-84]; specifi

130 2 (BMPR2) gene and patients with idiopathic PAH to determine mechanisms underlying abnormal endothel

131 othelial cells from patients with idiopathic PAH, confirming a switch from oxidative phosphorylation

132 represents a new promising target to improve PAH.

133 In PAH patients lower LDL-C significantly predicted death (

134 In PAH RV samples, alpha-7 nicotinic acetylcholine receptor

135 In PAH, elevated miRs (notably miR-138) down-regulate MCU d

136 ately 8% in controls and approximately 6% in PAH patients during expiration compared to inspiration,

137 metabolic and proliferative abnormalities in PAH ECs via PTPB1 and PKM1/PKM2.

138 assessed whether LDL-C levels are altered in PAH patients, if they are associated with survival in th

139 ne the safety and efficacy of anastrozole in PAH.

140 out to identify specific target antigens in PAH lung immune complexes as a starting point toward res

141 rgetic shifts and associated consequences in PAH-resistant killifish by integrating genomic, physiolo

142 d Kv1.5 protein expression were decreased in PAH smooth muscle cells (primary culture).

143 w studies that address health disparities in PAH.

144 scussing the impact of health disparities in PAH.

145 f cardiopulmonary remodeling and function in PAH in rats.

146 r the first time that HDAC6 is implicated in PAH development and represents a new promising target to

147 essure caused by arterial waves increased in PAH patients compared to controls.

148 ydroxylase domain activity were increased in PAH smooth muscle cells.

149 riate treatment target than cardiac index in PAH.

150 ble approach for therapeutic intervention in PAH.

151 of human endogenous retrovirus K (HERV-K) in PAH versus control lungs (n=4).

152 rial compliance, after initial management in PAH.

153 ransmitter deficiencies without mutations in PAH or BH4 metabolism disorder-related genes.

154 table disorders were diagnosed (mutations in PAH, CBS, MTHFR, CYP27A1, and HIBCH), and in 1 family, 2

155 Metabolic profiles in PAH are strongly related to survival and should be consi

156 ial compliance may also predict prognosis in PAH.

157 Sixty-two metabolites were prognostic in PAH, with 36 of 62 independent of established prognostic

158 a 72% reduction in PM2.5, a 78% reduction in PAH levels, and significant reductions in water-soluble

159 A treatment on cardiopulmonary remodeling in PAH was investigated in the monocrotaline rat model.

160 ioenergetic processes are under selection in PAH-adapted fish from the most contaminated ER site and

161 tributing to PAH, and support its testing in PAH treatment in patients.

162 ries and a response to targeted treatment in PAH.

163 eceptor agonist may be of therapeutic use in PAH in humans.

164 hods demonstrated appropriate performance in PAHs analysis even at low contamination levels.

165 We explain increased PAH desorption after addition of toluene by competitive

166 at toluene could additionally have increased PAH mobility within the soil matrix.

167 Samples were analyzed for 17 individual PAHs through extraction with dichloromethane and gas chr

168 d vasodilation in SUGEN-5416/hypoxia-induced PAH rats than oral, intravenous, or intratracheal plain

169 ntation at first follow-up RHC after initial PAH treatment.

170 chemistry of alkali metal intercalation into PAHs differs from that into fullerenes and graphite, in

171 ely 80%, while bioavailability of the larger PAHs was reduced by less than 50%.

172 ective at reducing bioavailability of linear PAHs by approximately 70%, but had little impact on angu

173 EF data for many PAHs from the eucalypt forest fire were comparable with

174 hrene were consistently the highest measured PAHs.

175 a next-generation "sulflower." In this novel PAH, disulfide units establish an all-sulfur periphery a

176 employed for human health risk assessment of PAH mixtures.

177 regulated, and to demonstrate attenuation of PAH severity with exogenous administration of ELA in a r

178 2 (BMPR2) are the commonest genetic cause of PAH, whereas biallelic mutations in the eukaryotic trans

179 metabolite profiling to compare extracts of PAH-contaminated soil from a former manufactured-gas pla

180 This unique murine model of PAH-like plexiform/obliterative arteriopathy induced via

181 , and fibrosis in the experimental models of PAH and lung fibrosis.

182 contributing factors in the pathogenesis of PAH in patients with caveolin-1 c.474delA mutation.

183 cal role in the hyperglycolytic phenotype of PAH endothelial cells.

184 process, the presence and quantification of PAH in the corn grains was investigated.

185 he pulmonary arteries as a paramount sign of PAH, we hypothesized that the ascending aorta will prese

186 ative to oral sildenafil in the treatment of PAH.

187 el therapeutic approach for the treatment of PAH.

188 found to be adequate for routine analysis of PAHs in the vegetable oils evaluated.

189 but could not degrade alkanes or the bulk of PAHs.

190 Highest concentrations of PAHs and PCBs were found close to densely populated and

191 ctic circle, we found that concentrations of PAHs increased from south to north most likely related t

192 -throughput screening (HTS) in vitro data of PAHs to predict health risks associated with coarse and

193 stent with faster atmospheric degradation of PAHs.

194 Emissions of PAHs are found to be sensitive to differences in combust

195 ssays with and without the pre-extraction of PAHs from PM.

196 irst time provides the restricted factors of PAHs and heavy metal acropetal translocation by maize wh

197 e cannot be responsible for the formation of PAHs in extreme environments.

198 ibility and thereby exposure and mobility of PAHs.

199 physics because of the complex reactivity of PAHs with strong reducing agents at high temperature.

200 The translocation of PAHs in maize tissues has positive relationship with log

201 KA;1) and that this repression is reliant on PAH.

202 One PAH antigen linked to immunity and inflammation was purs

203 aromatic hydrocarbons ( summation operator13 PAHs) were determined from the subtropical forest fire (

204 Several other PAH topologies are also reported.

205 A literature review indicated that diesel p-PAH emission factors varied widely by engine technology,

206 experiments have been conducted to measure p-PAH emissions.

207 ficant correlation (R(2) 0.85) between the p-PAH and black carbon emissions was identified with a mas

208 By assessing real traffic conditions, the p-PAH emission factors on freeways were lower than on loca

209 ticulate polycyclic aromatic hydrocarbons (p-PAHs) emitted from diesel vehicles are of concern becaus

210 re real-world emission factors of priority p-PAHs for diesel vehicles representative of an array of e

211 e's capability to reveal the single-particle PAH-distribution in aerosols (mixing state) and its assi

212 concentrations of total suspended particles, PAHs, PCBs, PCNs, and PBDEs, were typically observed in

213 Pediatric PAH patients have increased apparent ascending aortic st

214 ul endpoint for clinical trials in pediatric PAH, although its clinical utility and prognostic value

215 d impacts systemic hemodynamics in pediatric PAH.

216 ption of PHOSPHATIDIC ACID PHOSPHOHYDROLASE (PAH) activity in Arabidopsis thaliana stimulates biosynt

217 pean Union (EU) for the sum of four priority PAHs (PAH4) in processed cereal-based foods, sensitive a

218 Although inflammation promotes PAH, the mechanisms by which inflammation and BMPR-II dy

219 the same soil with only desorption-resistant PAHs present.

220 approximately 60-fold higher EFs for 3-ring PAHs from the former.

221 The 3-ring PAHs were most likely to be taken up by maize roots wher

222 en up by maize roots whereas 2- and 4-6 ring PAHs had the lower likelihood.

223 stribution in soils indicated that 2-3 rings PAHs with low octanol-water partition coefficient (log K

224 is downregulated in human disease and rodent PAH models, and exogenous peptide can reduce the severit

225 nes in the rat SUGEN-hypoxia model of severe PAH, characterized by reduced BMPR2 expression and endot

226 Some PAH metabolites showed consistent positive associations

227 SSc-PAH patients showed significant thickening of Intima Med

228 y thrombus formation was found in 19% of SSc-PAH patients.

229 iotic molecules such as nitrogen substituted PAHs (NPAHs), which represent the missing link between n

230 d haemodynamic response to previous targeted PAH treatment was associated with a significantly greate

231 and potencies of a small number of targeted PAHs results in values that are surprisingly close to th

232 the Registry to Evaluate Early and Long-Term PAH Disease Management score, the Pulmonary Hypertension

233 substantial influence of acidification than PAH pollution on bacteria driven ecological processes.

234 These results demonstrate that PAH-porphyrin hybrids are easily accessible, and this st

235 edox-controlled reducing agent to access the PAH dianions, and so enables the determination of their

236 a generally negative correlation between the PAH concentration in cuticles and the epicuticular wax c

237 on and ionization method delivering both the PAH-profile and the inorganic composition from the same,

238 of urinary PAH metabolites, depending on the PAH metabolite (p < 0.0001).

239 al PASMCs, MCUC inhibition recapitulates the PAH phenotype.

240 carried by each adsorbate, we find that the PAH is associated with only 70% of the positive charges

241 urvival using 12 variables or less while the PAH-degrading activity of strain LH128 in soils that sho

242 molecular layers, and thus interact with the PAH anion pi systems.

243 After extracting the PAHs of the matrix, the material was subjected to analys

244 rial calcium uptake protein 1, is central to PAH's pathogenesis.

245 nce mitochondrial dynamics and contribute to PAH's cancer-like phenotype.

246 MF on key molecular pathways contributing to PAH, and support its testing in PAH treatment in patient

247 ss the contribution of health disparities to PAH.

248 utaMouse mice were subchronically exposed to PAH mixtures (p.o.), and mutagenic potency (MP) values w

249 y and inflammation was pursued and a link to PAH pathophysiology was investigated by next-generation

250 and elevated cytokines have been related to PAH pathogenesis but without a clear understanding of ho

251 ty of GN-adsorbed PAHs was more sensitive to PAH morphology than MWCNTs.

252 ke lesions in pulmonary arteries, similar to PAH patients.

253 r PCBs during flaming was faster compared to PAHs, while levoglucosan concentrations increased.

254 These data suggest that exposure to PAHs may cause systemic changes during pregnancy that co

255 most sensitive one activated by exposure to PAHs.

256 ne of the major sources of human exposure to PAHs.

257 estimating cumulative exposure of humans to PAHs.

258 The practice of treating PAH patients with oral or intravenous sildenafil suffers

259 the formation of even the simplest tricyclic PAHs like anthracene and phenanthrene are still elusive.

260 Urinary PAH metabolites were highly detectable (>88%) in the stu

261 of the variation in fold changes of urinary PAH metabolites (p < 0.002).

262 ases in average post-event levels of urinary PAH metabolites, depending on the PAH metabolite (p < 0.

263 medium contamination level and the vertical PAHs distribution in soils indicated that 2-3 rings PAHs

264 the accessibility of higher molecular weight PAHs (log Kow > 6) was affected.

265 sights into the cancer risks associated with PAH-contaminated soils and places bioremediation outcome

266 d estimated the cancer risks associated with PAH-contaminated soils.

267 m and cause vascular changes associated with PAH.

268 VM CPM was lower in children with PAH (n = 29) than in controls (n = 60; 647 vs. 921; P <

269 signs of apparent stiffness in children with PAH and that this effect may be because of mechanical in

270 Children with PAH had significantly increased pulse wave velocity in t

271 Children with PAH spent less time in moderate and vigorous PA (13 vs.

272 PA is markedly decreased in children with PAH.

273 cohort of patients diagnosed clinically with PAH.

274 valence of LMCA compression in patients with PAH and angina is high.

275 All patients with PAH and angina or angina-like symptoms attending the cen

276 lated pulmonary artery (PA) in patients with PAH and angina or angina-like symptoms, determine the us

277 gest that CTCA is indicated in patients with PAH and angina or angina-like symptoms.

278 PASMCs were isolated from patients with PAH and healthy control subjects and assessed for expres

279 ded that LDL-C level is low in patients with PAH and is associated with an increased risk of death.

280 ificantly reduced E2 levels in patients with PAH but had no effect on TAPSE.

281 ndothelial cells isolated from patients with PAH demonstrate downregulation of miR-124, leading to th

282 metabolites also discriminated patients with PAH from disease control subjects (symptomatic patients

283 tment, and clinical outcome of patients with PAH has not been systematically investigated.

284 RV (n=11) and lungs (n=7) from patients with PAH undergoing heart/lung transplantation and compared w

285 Consecutive patients with PAH undergoing MRI were identified from the ASPIRE (Asse

286 rolled trial of anastrozole in patients with PAH who received background therapy at two centers.

287 Patients with PAH with biallelic EIF2AK4 mutations had a shorter survi

288 Patients with PAH with lower RV ejection fraction (<41%) had a signifi

289 phy of the chest compared with patients with PAH without EIF2AK4 mutations.

290 t ventricular (RV) function in patients with PAH, and the potential therapeutic effects of pyridostig

291 ypothesis that, in PASMCs from patients with PAH, decreases in HIF-1alpha expression and activity und

292 In PASMCs derived from patients with PAH, HIF-1alpha expression is decreased, and MLCK activi

293 ypothesized that in BOECs from patients with PAH, the downregulation of microRNA-124 (miR-124), deter

294 ascular tone-were increased in patients with PAH.

295 accuracy in the evaluation of patients with PAH.

296 nastrozole may be warranted in patients with PAH.

297 ertensive control patients and patients with PAH.

298 n fraction was assessed in 112 patients with PAH.

299 ality of care of vulnerable populations with PAH.

300 Thickening Area compared to patients without PAH (27 +/- 5.8% vs. 21 +/- 1.4%, p = 0.024).