ライフサイエンスコーパス: PAH

1 PAH analyses were realized after certain drying times an

2 PAH is the first human disease related to potential TET2

3 PAH photoinduced toxicity, which has been documented in

4 PAH variants were scored using an allelic phenotype valu

5 PAH[4]'s unique properties of a high water/solute permse

6 PAHs analysis was performed using HPLC-FLD/DAD and confi

7 PAHs and dichloromethane co-permeate the membrane into t

8 ; Fontan control = 0.99 +/- 0.21, P = 0.005; PAH = 1.22 +/- 0.27, PAH control = 0.91 +/- 0.12, P = 0.

9 trol = -0.29 +/- 0.23, PAH = -0.27 +/- 0.09, PAH control = -0.25 +/- 0.18, P = 0.91) between groups.

10 l benefit for Hispanic patients with Group 1 PAH in multiple clinical settings.

11 ents with PAH.Methods: Patients with Group 1 PAH were included from two national registries with geno

12 The contents of acrolein, acrylamide and 16 PAHs in the roasted beans were determined; only acrylami

13 The highest sums of 19 PAHs were determined in roasted cocoa beans, cocoa mass

14 Significant differences in total 19 PAHs contents between raw cocoa beans of different varie

15 human lungs of patients with PVOD (n = 19), PAH (n = 20), idiopathic pulmonary fibrosis (n = 13), an

16 1) cm(-1) ; Fontan control = -0.29 +/- 0.23, PAH = -0.27 +/- 0.09, PAH control = -0.25 +/- 0.18, P =

17 99 +/- 0.21, P = 0.005; PAH = 1.22 +/- 0.27, PAH control = 0.91 +/- 0.12, P = 0.02) but similar betwe

18 Concentrations of E(39)PAHs were 1004 ngg(-1) freeze-dried weight (fdw) and 139

19 genic polycyclic aromatic hydrocarbons (E(39)PAHs) in the livers and muscles of three coral-reef fish

20 beans were determined; only acrylamide and 5 PAHs were nevertheless found.

21 l and oil-exposed (24 h, 14.5 mug/L Sigma(50)PAH) juvenile mahi-mahi (27-85 mm) could detect crude oi

22 -1) ml(-1) ; Fontan control = 3.09 +/- 0.58, PAH = 3.63 +/- 1.95; PAH control = 3.98 +/- 0.91, P = 0.

23 Of 758 PAH variants, c.1222C>T (p.Arg408Trp) (22.2%), c.1066-11

24 (average percent difference of -9% across 9 PAHs in 8 soil samples), presenting a compelling argumen

25 ontrol = 3.09 +/- 0.58, PAH = 3.63 +/- 1.95; PAH control = 3.98 +/- 0.91, P = 0.26), and the slopes o

26 ression is ubiquitous and has potential as a PAH biomarker.

27 ive trait loci and summary statistics from a PAH genome-wide association study.Measurements and Main

28 Most of the abundant PAHs identified were low molecular weight (LMW-PAH) (liv

29 idence for KDR being a clinically actionable PAH gene and further support the central role of the vas

30 Four additional PAH cases with rare likely loss-of-function variants in

31 fee origin and brewing operations may affect PAHs content, we thoroughly analysed the literature on e

32 ve dispersion was greater in both Fontan and PAH than controls (Fontan = 1.46 +/- 0.18; Fontan contro

33 cted an association between SMAD5 levels and PAH disease susceptibility (odds ratio, 0.317; 95% confi

34 a consistent critical determinant of PH and PAH in experimental animal models and humans.

35 ude that patients with Fontan physiology and PAH have increased pulmonary perfusion heterogeneity tha

36 tate of mechanistic knowledge linking PM and PAH exposure to mammalian cardiovascular patho-physiolog

37 Concentrations of both fragrances and PAHs rose throughout the considered period, reflecting t

38 chitecture, peptide-appended hybrid[4]arene (PAH[4]), as a new class of artificial water channels.

39 k to the genetic and molecular events behind PAH pathogenesis.

40 se tools, we determined correlations between PAH degradation network data and intermediate metabolite

41 Conversely, biliary PAH concentrations were relatively low for most other sp

42 The highest concentrations of biliary PAH metabolites occurred in Yellowfin Tuna (Thunnus alba

43 n GoM had significantly higher total biliary PAH concentrations than the West Florida Shelf, and coas

44 females burrow, their eggs may bioaccumulate PAHs from contaminated sediments, leading to in ovo expo

45 At both PAH stages changes in RV proteins linked to apoptosis in

46 this innovative methodology to quantify both PAH and HPAH in VGOs for the first time.

47 hase PAHs were more abundant than soot-bound PAHs in the engine cylinder.

48 cross-coupling of sterically hindered bulky PAHs.

49 hanism for the formation of radical cationic PAHs in dopant-assisted DBDI.

50 ir target genes are elevated in pre-clinical PAH, idiopathic PAH and heritable PAH with missense p.H2

51 The food safety parameters and contaminants (PAH, 3-MCPD ester, 2-MCPD ester, glycidyl ester and trac

52 with PAH (n = 6) and healthy older controls (PAH control) using proton magnetic resonance imaging.

53 >1), while all chlorinated paraffins (CPs), PAHs, and phthalates underwent a trophic dilution (TMF <

54 Levels of both PM and the total in-cylinder PAHs decreased following a peak at 10 CAD ATDC but subse

55 The in-cylinder PAHs included 2- to 6-ring PAHs; however, 6-ring PAHs we

56 Demographics, PAH clinical subtypes, comorbidities, and medications we

57 Measurable concentrations of fire-derived PAH compounds, namely, phenanthrene, pyrene, benzo( e)py

58 osures in firefighters susceptible to dermal PAH absorption when using personal protective equipment.

59 Tet2-knockout mice spontaneously developed PAH, adverse pulmonary vascular remodeling, and inflamma

60 Diagnostic PAH adduct ions were formed at either M + 45 ([M + CH(2)

61 A model of 25 RNAs distinguished PAH with 87% accuracy (area under the curve 95% confiden

62 ecognition studies of peripherally NBN-doped PAHs to form H-bonded DD.AA- and ADDA.DAAD-type complexe

63 In RV during early PAH, especially proteins associated with myocardial stru

64 In early PAH LV myocardium proteins that may be linked to an incr

65 on of pulmonary artery pressure in the early PAH group (27.00 +/- 4.93 mmHg) and severe elevation in

66 A helically twisted, fully BNB-embedded PAH 11 was prepared by combining 2 with a dibrominated m

67 genotypically sexed individuals to evaluate PAH exposure, general and oxidative stress, estrogenic a

68 on the abundance and composition of exhaust PAH.

69 Although familial PAH most often has an autosomal-dominant pattern of inhe

70 cue patients with HIV-X4 variants from fatal PAH.

71 For all fish, PAHs originated mostly from petroleum and combustion sou

72 hat provides rapid, quantitative results for PAH isomer measurements in soil samples.

73 p53-based vasculoregenerative therapies for PAH by extending the therapeutic focus to PAEC dysfuncti

74 y was developed and applied to a set of four PAHs to demonstrate a possible solution to this challeng

75 AC proved to be better in reducing C(free) PAHs than biochar, though for 2- and 3-ring PAHs, the di

76 ed neuronal network differentiated PVOD from PAH samples with a sensitivity of 100% and a specificity

77 Furthermore, PAH size distributions proximal and distal to the crater

78 ntaining polycyclic aromatic hydrocarbons (H-PAHs) with alkyl and aryl substitution are demonstrated.

79 Three H-PAHs, including heteroatom-containing rubicenes (H-rubic

80 e-clinical PAH, idiopathic PAH and heritable PAH with missense p.H288Y KLF2 mutation.

81 sed amounts of platelet-associated histones (PAHs), which appear to be correlated with the type of in

82 tential agents in the pathophysiology of HIV-PAH.

83 plays a key role in the pathogenesis of HIV-PAH.

84 t significantly more persons living with HIV-PAH harbor HIV-X4 variants.

85 l exhaust, the model accurately predicts HMW PAH concentrations with R(2) = 0.976 and overestimates L

86 with R(2) = 0.988 for LMW and 0.998 for HMW PAHs.

87 f arteries in lung tissue samples from human PAH and control patients were investigated using matrix-

88 orms are significantly dysregulated in human PAH.

89 s a prognostic biomarker of outcome in human PAH.Methods: We used immunostaining of lung tissues from

90 KLF2 signalling is a common feature of human PAH and highlights the potential therapeutic role of KLF

91 hologies and physiological measures of human PAH.

92 e show that polycyclic aromatic hydrocarbon (PAH) chromophores that are linked between two five-membe

93 for biliary polycyclic aromatic hydrocarbon (PAH) concentrations.

94 oatom-doped polycyclic aromatic hydrocarbon (PAH) isosteres, which expose BN mimics of the amidic NH

95 is is that polynuclear aromatic hydrocarbon (PAH) molecules are the dominant component of soot, with

96 Polycyclic aromatic hydrocarbons (PAHs) are a diverse group of environmental contaminants

97 Polycyclic aromatic hydrocarbons (PAHs) are common atmospheric pollutants and known to cau

98 Polycyclic aromatic hydrocarbons (PAHs) are considered to be potentially genotoxic and car

99 Polycyclic aromatic hydrocarbons (PAHs) are potentially carcinogenic pollutants emitted by

100 Polycyclic aromatic hydrocarbons (PAHs) are routinely screened for in soils, where quantit

101 ducts, and polycyclic aromatic hydrocarbons (PAHs) as combustion and industrial markers, across the o

102 lar weight polycyclic aromatic hydrocarbons (PAHs) as key mediators of cardiotoxicity.

103 inetics of polycyclic aromatic hydrocarbons (PAHs) during drying of olive pomace.

104 cifically, polycyclic aromatic hydrocarbons (PAHs) found in ultrafine PM have been linked to cardiova

105 Levels of polycyclic aromatic hydrocarbons (PAHs) in cocoa beans of several varieties originating fr

106 exposed to polycyclic aromatic hydrocarbons (PAHs) in marine sediments as the result of oil spills.

107 ristics of polycyclic aromatic hydrocarbons (PAHs) in the Chicxulub crater sediments and at two deep

108 species of polycyclic aromatic hydrocarbons (PAHs) including naphthalene (NAP) and the known carcinog

109 on of four polycyclic aromatic hydrocarbons (PAHs) over a 2.2 s separation window using a poly(dimeth

110 Polycyclic aromatic hydrocarbons (PAHs) present in crude oil are known to impair visual de

111 nthesis of polycyclic aromatic hydrocarbons (PAHs) solely proceeds at elevated temperatures.

112 mprised of polycyclic aromatic hydrocarbons (PAHs) that are a mixture of single-core (island) and mul

113 helicenes-polycyclic aromatic hydrocarbons (PAHs) that are distinct via the linear, zigzag, and orth

114 Polycyclic aromatic hydrocarbons (PAHs) with six and seven rings were synthesized via dire

115 s (PBDEs), polycyclic aromatic hydrocarbons (PAHs), phthalates, insecticides, pyrethroids, and N,N-di

116 cizers and polycyclic aromatic hydrocarbons (PAHs).

117 lamide and polycyclic aromatic hydrocarbons (PAHs).

118 tionalized polycyclic aromatic hydrocarbons (PAHs).

119 ds such as polycyclic aromatic hydrocarbons (PAHs).

120 small amounts of polyaromatic hydrocarbons (PAHs) into water from the built environment.

121 prefunctionalized polyaromatic hydrocarbons (PAHs).

122 y variants in the phenylalanine hydroxylase (PAH) gene, is the most common autosomal-recessive Mendel

123 ents, as in pulmonary arterial hypertension (PAH) and pulmonary veno-occlusive disease (PVOD), respec

124 tients with pulmonary arterial hypertension (PAH) and two groups of controls using a proton magnetic

125 d heritable pulmonary arterial hypertension (PAH) are rare but comprise a genetically heterogeneous p

126 s in PH and pulmonary arterial hypertension (PAH) are the focus of extensive investigation, the initi

127 tients with pulmonary arterial hypertension (PAH) have been found to harbor rare mutations in disease

128 Pulmonary arterial hypertension (PAH) is a disease characterized by progressive loss and

129 Pulmonary arterial hypertension (PAH) is a fatal disease characterized by profound vascul

130 Pulmonary arterial hypertension (PAH) is a lethal vasculopathy.

131 Rationale: Pulmonary arterial hypertension (PAH) is a life-shortening condition.

132 Pulmonary arterial hypertension (PAH) is a rare and deadly disease affecting roughly 15-6

133 Pulmonary arterial hypertension (PAH) is a rare, fatal, and incurable disorder.

134 Pulmonary arterial hypertension (PAH) is a rare, progressive disorder typified by occlusi

135 Pulmonary arterial hypertension (PAH) is a severe disorder of lung vasculature that cause

136 Pulmonary Arterial Hypertension (PAH) is overrepresented in People Living with Human Immu

137 In pulmonary arterial hypertension (PAH), endothelial dysfunction and obliterative vascular

138 Another is pulmonary arterial hypertension (PAH), where gravitational gradients may be reduced secon

139 response to pulmonary arterial hypertension (PAH)-approved drugs, and transplant-free survival of pat

140 ess this in pulmonary arterial hypertension (PAH).

141 tients with pulmonary arterial hypertension (PAH).

142 e to severe pulmonary arterial hypertension (PAH).

143 f rats with pulmonary arterial hypertension (PAH).

144 origins of pulmonary arterial hypertension (PAH).

145 ferences in pulmonary arterial hypertension (PAH).Objectives: Determine effects of race/ethnicity and

146 are elevated in pre-clinical PAH, idiopathic PAH and heritable PAH with missense p.H288Y KLF2 mutatio

147 jects (n = 120) and patients with idiopathic PAH (n = 260).Measurements and Main Results: We identifi

148 ns occur in <25% of patients with idiopathic PAH and are rare in PAH associated with connective tissu

149 cimens derived from patients with idiopathic PAH.

150 and BMP10 levels in patients with idiopathic PAH.Methods: Missense BMP9 mutant proteins were expresse

151 nd long-term survival (P = 4.66 x 10(-6)) in PAH.

152 ima would represent a significant advance in PAH treatment; however, our understanding of the cellula

153 ppel-like factor 2 (KLF2) are compromised in PAH.

154 extensive remodeling at active enhancers in PAH PAECs and identify hundreds of differentially active

155 network and predict that primed enhancers in PAH PAECs are activated by the differentially active TFs

156 troduction to the major systemic findings in PAH and the evidence that supports a common mechanistic

157 To identify missing heritability in PAH we integrated deep phenotyping with whole-genome seq

158 hereby filling in the gaps of information in PAH degradation pathways.

159 ast 6 years, additional pathways involved in PAH susceptibility have been described through the ident

160 control subjects, BMP10 levels were lower in PAH females.

161 ion contribute to systemic manifestations in PAH.

162 ic role of KLF2-regulated exosomal miRNAs in PAH and other diseases associated with vascular remodell

163 critical determinant of clinical outcome in PAH.

164 a prognostic factor for clinical outcome in PAH.Conclusions: This study establishes immunoglobulin-d

165 cells and attenuates disease progression in PAH mice.

166 patients with idiopathic PAH and are rare in PAH associated with connective tissue diseases.

167 elopment of pulmonary vascular remodeling in PAH rats.

168 bably reflects the effects of remodelling in PAH and possibly in Fontan physiology.

169 is probably reflects vascular remodelling in PAH and possibly in Fontan physiology.

170 tegies to enhance BMP9 or BMP10 signaling in PAH.

171 ion of cardiac MRI in risk stratification in PAH.

172 genetic ancestry to differential survival in PAH.

173 The role of TET2 in PAH is unknown.

174 ted deleterious germline variants in TET2 in PAH patients of European ancestry (9/1832) compared with

175 discuss the knowledge and recent advances in PAHs formation during roasting.

176 of specific MS/MS transitions for individual PAH isomers.

177 dominant component of soot, with individual PAH molecules forming ordered stacks that agglomerate in

178 the known levels of toxicity for individual PAHs, a toxic unit approach for characterizing mixtures,

179 with idiopathic, heritable, and drug-induced PAH and 72 age- and sex-matched healthy volunteers.

180 cle over the course of monocrotaline-induced PAH to delineate potential therapeutic targets for the t

181 at different stages of monocrotaline-induced PAH.

182 use in the treatment of arrythmia, inhibited PAH-associated pulmonary vascular remodeling.

183 ee is an extensively consumed drink, and its PAHs contamination is not only ascribed to environmental

184 f total contamination were noted, with light PAHs being predominant and the sum of 4 heavy and marker

185 ions with R(2) = 0.976 and overestimates LMW PAHs.

186 Hs identified were low molecular weight (LMW-PAH) (liver > muscle) with 2-3 aromatic ring.

187 redominant and the sum of 4 heavy and marker PAHs much lower than the maximum legal limit.

188 The members PAH, RST, TAFH, NCBD, and HHD are found in large protein

189 In PAECs from BMPR2 mutant PAH patients, pharmacological induction of p53 and PPARg

190 s of aza-polycyclic aromatic hydrocarbons (N-PAHs) from readily available aryl ketones and alkynes ha

191 utral directing group for the formation of N-PAHs via isoquinoline.

192 Nitrated PAHs (NPAHs) are formed in combustion activities and by

193 rowth Factor Receptor 2 (VEGFR2), as a novel PAH candidate gene.

194 timate both absolute concentrations and NPAH/PAH ratios at observational sites.

195 ired abnormalities of TET2 occur in 0.39% of PAH cases.

196 relate with age and was decreased in >86% of PAH patients.

197 The remodelled pulmonary arteries of PAH patients harboured CD117(+) ECs.

198 al biomonitoring tools for the assessment of PAH toxicity and induced biological alterations in the f

199 provides the most comprehensive baselines of PAH exposure in fishes ever conducted for a large marine

200 Despite a potential benefit of PAH treatment, prognosis remains poor, and double-lung t

201 uscle cells (PASMCs), a major contributor of PAH pathobiology, and identified cyclin-dependent kinase

202 erlying heart remodelling over the course of PAH are still insufficiently understood.

203 ted hemodynamic and histological evidence of PAH in hematopoietic Tet2-knockout mice.

204 ormation was comprised with the formation of PAH compounds through the drying process.

205 evolution of temperature on the formation of PAH compounds.

206 r understanding of the molecular genetics of PAH.

207 The levels of PAH or phthalate metabolites were not significantly corr

208 identify the ion at m/z 885.6 as a marker of PAH in human lung tissue.

209 However, the underlying mechanism of PAH-induced toxicity to the visual system of fish is not

210 complex and dynamic competing mechanisms of PAH formation, growth and oxidation in the gas phase, an

211 of genetic heterogeneity support a model of PAH as a Mendelian disorder with complex disease feature

212 In two experimental models of PAH (i.e., monocrotaline and Su5416/hypoxia treated rats

213 vascular endothelium in the pathobiology of PAH.

214 kin-1beta blockade resulted in regression of PAH.

215 ion, and model validation to define a set of PAH-associated RNAs and a single summarizing RNA model s

216 .Conclusions: A whole-blood RNA signature of PAH, which includes RNAs relevant to disease pathogenesi

217 Treatment of PAH rats with dofetilide, an Kv11.1 channel blocker appr

218 therapeutic advancements in the treatment of PAH.

219 enhancers in disease-relevant cell types of PAH.

220 subsequently used for the direct analyses of PAHs in real soils where CP-MIMS-LEI/CI was shown to be

221 quantify the presence and concentrations of PAHs with lower molecular weight (LMW, 126 < MW < 202) a

222 ould contribute to the daily human intake of PAHs.

223 in combustion activities and by nitration of PAHs in the atmosphere and may be equally or more toxic,

224 risk assessment concluded the probability of PAHs intake via fish consumption was considerable in thi

225 s to tailor the organizational properties of PAHs.

226 following the release of large quantities of PAHs into the marine environment from point oil spills (

227 gument for direct, quantitative screening of PAHs in soils by CP-MIMS-LEI/CI, particularly given the

228 predicting the location of reactive sites on PAHs (i.e., the carbon where atmospheric oxidants attack

229 These patients had no mutations in other PAH-related genes.

230 ew technique that yields the single-particle PAH composition along with both positive and negative in

231 In-cylinder results showed that gas-phase PAHs were more abundant than soot-bound PAHs in the engi

232 ion potentiates the toxicity of photodynamic PAHs (often leading to mortality).

233 es result in lower PM yields however, the PM PAH content increases significantly.

234 HIV-gp120 that predict tropism also predict PAH.

235 of fossil diesel with the 16 US-EPA priority PAH species identified and quantified.

236 including altered DNA methylation, promotes PAH.

237 s clear evidence for the presence of radical PAH in the particulate samples.

238 Forty patients received PAH-approved drugs with a significant improvement in fun

239 Until recently, PAH was seen as a disease restricted to the pulmonary ci

240 tream of dysfunctional BMPR2 to rehabilitate PAH PAECs, regenerate pulmonary microvessels, and revers

241 Once released, PAHs deposit in soil and water bodies where they are sub

242 fixed limits have yet been set for residual PAHs in coffee, the present review intends to summarise

243 PAHs than biochar, though for 2- and 3-ring PAHs, the differences in AC and biochar performances wer

244 included 2- to 6-ring PAHs; however, 6-ring PAHs were not observed in the soot samples collected fro

245 rmances were smaller than those for 4-6-ring PAHs.

246 The in-cylinder PAHs included 2- to 6-ring PAHs; however, 6-ring PAHs were not observed in the soot

247 s afforded various fused six- and seven-ring PAHs, all in good yields and with fluorescent properties

248 The contents of three-ring PAHs, namely fluorene, phenanthrene and anthracene, in d

249 tic hydrocarbons with less than seven rings (PAHs) naturally contained in vacuum gas oils (VGOs) act

250 n were susceptible to developing more severe PAH.

251 olymerization), the photo-oxidation of small PAHs isolated from a low-boiling petroleum distillation

252 During end-stage PAH an increase in proteins associated with apoptosis, f

253 mmHg) and severe elevation in the end-stage PAH group (50.50 +/- 11.56 mmHg).

254 During end-stage PAH significant changes in RV proteins abundance related

255 and 2-NPYR are found in regions with strong PAH emissions, but because of continued secondary format

256 anged at 0.02-0.07 ng mL(-1) for all studied PAHs.

257 studies reveal that the Bu(3)Sn-substituted PAHs are moderately fluorescent, and their protodestanny

258 can Registry to Evaluate Early and Long-Term PAH Disease Management) risk score calculator (REVEAL 2.

259 xperiments and simulations demonstrated that PAH[4]s can form, through lateral diffusion, clusters in

260 Quantitative transport studies revealed that PAH[4]s can transport >10(9) water molecules per second

261 tected at 150 degrees C which indicates that PAHs was transferred from dried shells to roasted cocoa

262 This analysis revealed that PAHs of 239-838 Da, containing few oxygenated species, c

263 ET2, we used a cohort of 2572 cases from the PAH Biobank.

264 se of continued secondary formation from the PAH precursors, these two NPAHs are predicted to be spre

265 lthough advances in the understanding of the PAH pathobiology have been seen in recent years, molecul

266 inally lead to a better understanding of the PAH pathology and highlights the vital role IMS can play

267 Here we show that the PAH composition of soot can be exactly determined and sp

268 study, of which 1,148 were recruited to the PAH domain.

269 The PAHs content in whole cocoa bean roasting was detected e

270 applied to access the content safety of the PAHs studied in a variety of commercial food and beverag

271 tack), and hence the chemoselectivity of the PAHs.

272 ies, and subsequent charge exchange with the PAHs, is proposed as the principal ionization mechanism

273 D5 expression may increase susceptibility to PAH.

274 ng DWH, more recent increases in exposure to PAHs in some species suggest a complex interaction betwe

275 roasting temperature of 160 degrees C led to PAHs formation, though not the heavy ones.

276 deas that molecular mass growth processes to PAHs transpire at elevated temperatures.

277 Total PAH fomration rate constants (k) increased with the dryi

278 Kinetics of the total PAH formation was comprised with the formation of PAH co

279 rare and common genetic variants underlying PAH susceptibility and disease progression.

280 KDR were independently identified in the US PAH Biobank cohort with similar phenotypic characteristi

281 ysfunction and to DNA damage associated with PAH progression.

282 that supports a common mechanistic link with PAH pathophysiology.

283 on-making.Methods: Consecutive patients with PAH (n = 438) undergoing cardiac MRI were identified fro

284 trols (Fontan control, n = 5), patients with PAH (n = 6) and healthy older controls (PAH control) usi

285 there is growing evidence that patients with PAH also exhibit systemic vascular dysfunction, as evide

286 using 1832 unrelated European patients with PAH and 7509 non-Finnish European subjects from the Geno

287 levels did not differ between patients with PAH and control subjects, BMP10 levels were lower in PAH

288 differential RNA expression in patients with PAH compared with control subjects.

289 A subset of patients with PAH had markedly reduced plasma levels of BMP9 and BMP10

290 nts with Fontan physiology and patients with PAH have increased pulmonary perfusion heterogeneity tha

291 I can be used to risk stratify patients with PAH using a threshold approach.

292 npatient-specific mortality in patients with PAH were also calculated for race/ethnic groups from an

293 Patients with PAH who carried these mutations exhibited reduced plasma

294 s and activity were assayed in patients with PAH with GDF2 variants and in control subjects.

295 rom experimental PH models and patients with PAH, analyses of genetic murine models lacking specific

296 rker risk panel from plasma of patients with PAH, we demonstrated that complement signaling can serve

297 tations in their management of patients with PAH.

298 rker risk panel from plasma of patients with PAH.Measurements and Main Results: Pulmonary perivascula

299 nd disease outcomes in diverse patients with PAH.Methods: Patients with Group 1 PAH were included fro

300 ated pulmonary hypertension and in rats with PAH, Kv11.1 channels were expressed in both the large an

301 s is critical due to varying toxicity within PAH isomer classes.