ライフサイエンスコーパス: PH

1 PH domain binding leads to local clustering of PIP molec

2 PH domains can be grouped by the relative strength of th

3 PH was induced in male rats by SU5416 (25 mg/kg subcutan

4 PH-domain mutants alter subcellular localization and res

5 of primary and secondary phosphines (R(1)R(2)PH, R(2) = H or R(1)) with hydrosilanes (R(3)R(4)R(5)SiH

6 At week 6, PH status was confirmed by echocardiography, and rats we

7 This work identifies a PH domain protein as a regulator of plant metal transpor

8 The crystal structure of a PH-START complex revealed that the START domain binds to

9 wed that supernatants derived from activated PH and not PA-specific clones exhibited robust bacterici

10 of liver tissue showed that at 6 hours after PH, liver XBP1 became bound to a large set of genes impl

11 1 by hepatocytes increased immediately after PH (priming phase of liver regeneration) in control mice

12 G49 administered immediately after PH was also effective at alleviating the pathological ch

13 rkers remained decreased in M+G49 mice after PH, and glucose use was shifted to the pentose phosphate

14 s work we analyzed during regeneration after PH the involvement of P2X4 purinergic receptors, highly

15 During liver regeneration after PH, P2X4 contributes to the complex control of biliary h

16 nts TGF-beta activation and protects against PH development.

17 Although PH- and PA-specific clones expressed similar levels of L

18 H (HR=1.23; 95% CI, 1.12-1.36; P<0.0001) and PH (HR=2.16; 95% CI, 1.96-2.38; P<0.0001) compared with

19 inhibits receptor constitutive activity, and PH domain expression rescues 5-HT6 receptor-operated cAM

20 itor Y-27632 reduced vessel constriction and PH in Pbx-mutant mice.

21 ort high-resolution structures of the DH and PH domains and characterize conformations of the DH-PH u

22 w is to examine the effect of IIP on MFR and PH after at least 12 months of functional loading.

23 er fibrosis (LF), liver microthrombosis, and PH in cirrhotic rats.

24 classified as reference, borderline PH, and PH, respectively.

25 stablished pulmonary vascular remodeling and PH.

26 ate a rodent model of metabolic syndrome and PH-HFpEF, suggesting a potential role of nitrite and met

27 he efficacy of management strategies for any PH type in patients with renal failure is largely unprov

28 tistically significantly less MFR and better PH maintenance in IIP with thick biotype (MFR: MD -0.478

29 e provisionalization had less MFR and better PH than IIP in thin biotype or with delayed restoration.

30 D 0.253, P = 0.384) and significantly better PH maintenance were found in IIP with immediate provisio

31 Similarly, there was better PH maintenance in CIPs, with statistical significance fo

32 One-year mortality was similar between PH-LHD groups.

33 ng for potential confounders, including BNP, PH was found to be associated with HF hospitalization (h

34 Borderline PH is common in patients undergoing RHC and is associate

35 ong whom the prevalence of PH and borderline PH was 62% and 18%, respectively.

36 ortality hazard was increased for borderline PH (HR=1.23; 95% CI, 1.12-1.36; P<0.0001) and PH (HR=2.1

37 a Cox proportional hazards model, borderline PH was associated with increased mortality compared with

38 iated with a higher likelihood of borderline PH compared with reference patients in a logistic regres

39 nown about the natural history of borderline PH.

40 o identify clinical correlates of borderline PH.

41 Hg were classified as reference, borderline PH, and PH, respectively.

42 according to mPAP level and that borderline PH is associated with increased mortality and hospitaliz

43 the hypothesis that patients with borderline PH have decreased survival compared with patients with l

44 In the 70 patients with borderline PH who underwent a repeated RHC, 43 (61%) had developed

45 patients initially diagnosed with borderline PH.

46 taneous binding of multiple PIP molecules by PH domains contributes to high-affinity membrane interac

47 our understanding of membrane recognition by PH domains in vivo.

48 First, categorizing PH according to underlying pathophysiologies, hemodynami

49 ation as a potential treatment for cirrhotic PH.

50 nd highest for children <9 years of age (Cox PH: 40%, 95% confidence interval: -49, 76; TH: 52%, 95%

51 both models were similarly low overall (Cox PH: 20%, 95% confidence interval: -57, 59; TH: 27%, 95%

52 Cpc-PH bears similarities to pulmonary arterial hypertension

53 Cases reclassified as Cpc-PH based on QRS-gated DPD demonstrated higher pulmonary

54 restimated in PH-LHD, which may classify Cpc-PH patients as isolated postcapillary pulmonary hyperten

55 e-/postcapillary pulmonary hypertension (Cpc-PH) in left heart disease (PH-LHD).

56 An exploratory genetic analysis in Cpc-PH identified genes and biological pathways in the lung

57 Hg; P<0.01) and a greater proportion of Cpc-PH (24% versus 8%; P<0.01) versus the usual practice DPD

58 ines combined post- and precapillary PH (Cpc-PH).

59 to PAH pathophysiology, suggesting that Cpc-PH may be a distinct and highly morbid PH subphenotype.

60 The Cpc-PH subcategory occurs in 12% to 13% of patients with PH

61 postcapillary pulmonary hypertension to Cpc-PH, which is characterized by an adverse hemodynamic pro

62 Whether Cpc-PH is amenable to therapies targeting the pulmonary circ

63 Patients with Cpc-PH have severe PH, with higher diastolic pulmonary press

64 Patients with Cpc-PH were on average 6 years younger, with more severe pul

65 iotype (MFR: MD -0.478, P <0.001; cumulative PH: MD -0.287, P <0.001; MPH: MD -0.288, P <0.001; DPH:

66 ficance for distal PH (DPH) only (cumulative PH: MD -0.396, P = 0.010; DPH: MD -0.765, P <0.001; mesi

67 of parenteral dextrose infusion that delays PH-induced hypoglycemia for 14 hours after surgery was i

68 ghly specific interaction between PLC delta1-PH and PI(4,5)P2, encoded within the conformational prop

69 lta 1 pleckstrin homology domain (PLC delta1-PH), is completely inhibited in the presence of Ca(2+),

70 Overall, 72 of 141 cases demonstrated PH-LHD.

71 rating characteristic analysis for detecting PH patients using age-specific z scores showed an excell

72 All shunted animals developed PH.

73 We (DG, PH, and SP) did a survey of professional stakeholders an

74 ins and characterize conformations of the DH-PH unit in solution.

75 dscapes for the interactions of 12 different PH domains with membranes containing PIP2 or PIP3, allow

76 We discovered PH fecal microbiomes hosted a distinct and more diverse

77 hypertension (Cpc-PH) in left heart disease (PH-LHD).

78 rican Americans with chronic kidney disease, PH, which is likely pulmonary venous hypertension, was a

79 Ps, with statistical significance for distal PH (DPH) only (cumulative PH: MD -0.396, P = 0.010; DPH:

80 arent phosphinidene complex [Zr(Tren(DMBS) )(PH)][K(B15C5)2 ] [Zr3; Zr=P=2.472(2) A].

81 The initial encounter of the Dok7 PH domain is followed by formation of additional interac

82 ith PIP molecules, which stabilizes the Dok7 PH/membrane complex.

83 mined the method's impact on calculated DPD, PH-LHD subclassification, hemodynamic profiles, and mort

84 Second, echocardiographic PH (based on variable definitions) has been reported in

85 In PAH and experimental PH, KCNK3 expression and activity are strongly reduced i

86 ulmonary vascular remodeling in experimental PH.

87 ts of PYR (40 mg/kg per day) in experimental PH.

88 Following PH, G49 treatment increased survival, restored the cytok

89 f 1583 (0.02%) children met the criteria for PH.

90 ctional complexes (AJCs) was responsible for PH in Nestin-Cre/Llgl1(fl/fl) brains.

91 rtical development in vivo is sufficient for PH.

92 Furthermore, PH domains carrying mutations identified in NF1 patients

93 We next generated PH and PA strain-specific Th17 clones and show that P. a

94 re female, 78% had hypertension, and 22% had PH.

95 At the time of LT, 39% of recipients had PH (mPAP >/= 25 mm Hg) and 10.3% had mPAP >/= 35 mm Hg.

96 were associated with greater odds of having PH.

97 ted in both TH and Cox proportional hazards (PH) models.

98 per type 17 (Th17) cells induced by healthy (PH) versus acne (PA) skin-associated P. acnes strains ar

99 facial recession (MFR) and papillary height (PH) loss.

100 wo important agronomic traits, plant height (PH) and heading date (HD).

101 ver regeneration after partial hepactectomy (PH).

102 iver regeneration after partial hepatectomy (PH) increases the protein folding burden at the endoplas

103 of treatment with G49, partial hepatectomy (PH) was performed, and all mice were maintained on the s

104 iver regeneration after partial hepatectomy (PH), to initiate growth, protect liver cells, and sustai

105 ction in the incidence of parastomal hernia (PH) after placement of prophylactic synthetic mesh using

106 sembling severe periventricular heterotopia (PH).

107 In HF, PH is associated with global pulmonary vascular remodeli

108 ; PVOD, 31.1), venous %IT (control, 14.0; HF-PH, 24.9; PVOD, 43.9), and IV %IT (control, 10.6; HF-PH,

109 ents with right heart catheterization (30 HF-PH, 14 PVOD), similar associations between the transpulm

110 ; PVOD, 43.9), and IV %IT (control, 10.6; HF-PH, 25.8; PVOD, 50.0) in HF-PH were higher than controls

111 l percent medial thickness (control, 6.9; HF-PH, 11.0; PVOD, 15.0), arterial %IT (control, 4.9; HF-PH

112 PVOD, 15.0), arterial %IT (control, 4.9; HF-PH, 14.9; PVOD, 31.1), venous %IT (control, 14.0; HF-PH,

113 In lung specimens from autopsy (control, HF-PH, and 7 PVOD) or surgery (10 PVOD), quantitative histo

114 PASP (mm Hg) was lower in HF-PH (median, 59 [interquartile range, 50-70]) than in PVO

115 ontrol, 10.6; HF-PH, 25.8; PVOD, 50.0) in HF-PH were higher than controls (P<0.0001 for all) but lowe

116 nd 55 reduced ejection fraction) with PH (HF-PH; pulmonary artery systolic pressure [PASP] >/=40 mm H

117 PASP was slightly higher in patients with HF-PH with right ventricular dysfunction, pulmonary vascula

118 sociated with PH-HFpEF, we developed a 2-hit PH-HFpEF model in rats with multiple features of metabol

119 ptor with neurofibromin Pleckstrin Homology (PH) domain also inhibits receptor constitutive activity,

120 CERT's N-terminal pleckstrin homology (PH) domain targets it to the Golgi by binding to phospha

121 or 594-labeled PLC-beta pleckstrin homology (PH) domain, we demonstrate that the PH domain is the min

122 t that mutations in the pleckstrin homology (PH) domain-containing protein AtPH1 rescue the iron-defi

123 targeting site-2 of the pleckstrin homology (PH) domain.

124 Pleckstrin homology (PH) domains mediate protein-membrane interactions by bin

125 e Dbl-homology (DH) and Pleckstrin-homology (PH) domains of Bcr-Abl p210, which constitute the only s

126 ted fecal microbiomes of Przewalski's horse (PH; Equus ferus przewalskii), the only horses alive toda

127 Peptide hydrolysate (PH) was produced by deep controllable bioconversion of p

128 one nonhydrolyzed, two partially hydrolyzed (PH), four extensively hydrolyzed (EH), and one amino aci

129 idiopathic pulmonary arterial hypertension (PH-Fibs) displayed aerobic glycolysis when cultured unde

130 the primary factor for portal hypertension (PH) development.

131 Portal hypertension (PH) is a major cause of morbidity and mortality in chron

132 c kidney disease and pulmonary hypertension (PH) at disproportionately high rates.

133 Although pulmonary hypertension (PH) contributes significantly to poor outcomes in divers

134 Pulmonary hypertension (PH) exists when mean pulmonary artery pressure (mPAP) is

135 with the severity of pulmonary hypertension (PH) in HF.

136 Pulmonary hypertension (PH) in neonates, infants, children, adolescents, and you

137 prevent experimental pulmonary hypertension (PH) in pre-clinical models.

138 RATIONALE: Pediatric pulmonary hypertension (PH) is a heterogeneous condition with varying natural hi

139 Severe pulmonary hypertension (PH) is considered to negatively affect the outcome after

140 Pulmonary hypertension (PH) is diagnosed by a mean pulmonary arterial pressure (

141 Pulmonary hypertension (PH) is increasingly recognized among patients with kidne

142 is group and whether pulmonary hypertension (PH) reversal can influence LDL-C levels.

143 metabolic theory of pulmonary hypertension (PH) suggests that cellular and mitochondrial metabolic d

144 ue for assessment of pulmonary hypertension (PH) with studies to date exclusively performed in adults

145 transition leads to pulmonary hypertension (PH), a major cause of newborn mortality associated with

146 adverse outcomes in pulmonary hypertension (PH).

147 ding fibroblasts, in pulmonary hypertension (PH).

148 most common cause of pulmonary hypertension (PH).

149 ion, in experimental pulmonary hypertension (PH).

150 the pathogenesis of pulmonary hypertension (PH).

151 emammillary (PM) and posterior hypothalamic (PH) populations.

152 rapeutic targeting of macrophages in hypoxic PH and potentially other inflammatory lung diseases.

153 thogenesis of vascular remodeling in hypoxic PH involves an early compartment-independent activation

154 In PH, miR-124, through the alternative splicing factor PTB

155 Recent advancements in PH-targeted therapies and interventional-surgical proced

156 Fourth, recent advances in PH treatment in the general population focus on World He

157 sponsible for these metabolic alterations in PH-Fibs remain unknown.

158 nd between mesenchymal inflammatory cells in PH.

159 RA function was impaired in PH patients versus controls (P<0.001).

160 thermore, normalizing the PKM2/PKM1 ratio in PH-Fibs by miR-124 overexpression or PTBP1 knockdown rev

161 We detected an increased PKM2/PKM1 ratio in PH-Fibs compared with normal subjects.

162 fect of inflammation and oxidative stress in PH and provides insight for new therapies.

163 provement in quality of life and survival in PH/PHVD.

164 We hypothesized that in PH-Fibs microRNA-124 (miR-124) regulates PTBP1 (polypyri

165 Chronic PYR treatment in PH rats normalized the cardiovascular autonomic function

166 lated in usual practice is underestimated in PH-LHD, which may classify Cpc-PH patients as isolated p

167 asts from calves with severe hypoxia-induced PH and humans with idiopathic pulmonary arterial hyperte

168 nary vascular disease than patients with Ipc-PH, despite similar comorbidities and prevalence, severi

169 In this study we show that isolated PH and START domains interact with each other.

170 s of the full-length protein compared to its PH domain.

171 ith PI(3,4)P2 on the plasma membrane via its PH domain.

172 ia transcription factors (Pbx) led to lethal PH in mice shortly after birth.

173 orbidity patterns captured most of the major PH subtypes with known pathological basis defined by the

174 sed in synchrony after the late Golgi marker PH(OSBP) .

175 P = 0.010; DPH: MD -0.765, P <0.001; mesial PH [MPH]: MD -0.285, P = 0.256).

176 minogen activator inhibitor-1, and mitigated PH and pulmonary vascular remodeling in monocrotaline-tr

177 t Cpc-PH may be a distinct and highly morbid PH subphenotype.

178 hosphinidiide complex [{U(Tren(TIPS) )}2 (mu-PH)] (3).

179 y be a more effective treatment for neonatal PH.

180 broadly, our findings indicate that neonatal PH can result from perturbation of multiple pathways and

181 The posterior hypothalamic nucleus (PH) stimulates autonomic stress responses.

182 g-intrinsic, herniation-independent cause of PH in CDH.

183 Precise classification of PH subtypes is, therefore, crucial for individualizing c

184 quired and sufficient for the development of PH in Schistosoma-exposed mice.

185 The diagnosis of PH due to left heart disease relies on a clinical probab

186 The effect of PH reversal on LDL-C levels was assessed in 34 patients

187 emical analyses and live cortical imaging of PH formation revealed that disruption of apical junction

188 Induction of PH-Tau triggered neuronal death (60% in CA3), astrocytos

189 frequency, causes, and optimal management of PH in kidney transplant candidates and recipients.

190 optimizing the assessment and management of PH in kidney transplant candidates and recipients.

191 We seek to study the manifestations of PH in children and to assess the feasibility of applying

192 Third, although measures of PH have been associated with adverse patient and graft o

193 r volume in an experimental porcine model of PH because of aorto-pulmonary shunt using cardiac magnet

194 his study, we used a hypoxic murine model of PH in combination with FACS to quantify and isolate lung

195 and our understanding of the pathobiology of PH in HF.

196 he heterogeneous etiology/pathophysiology of PH in the young, and particularly on PHVD associated wit

197 AT values with scores <-2 were predictive of PH.

198 and 86% white) among whom the prevalence of PH and borderline PH was 62% and 18%, respectively.

199 tion is crucial given the high prevalence of PH and difficulties in the surgical repair of PH.

200 lic function, we report a high prevalence of PH.

201 Prevention of PH formation is crucial given the high prevalence of PH

202 H and difficulties in the surgical repair of PH.

203 Reversal of PH increases LDL-C levels.

204 ary vascular remodeling, but the severity of PH correlates most strongly with venous and small IV int

205 cluding TNF, are associated with severity of PH.

206 main in our understanding of the spectrum of PH in children.

207 inhibition reversed the glycolytic status of PH-Fibs, decreased their cell proliferation, and attenua

208 The QRS-gated DPD reclassifies a subset of PH-LHD patients from isolated postcapillary pulmonary hy

209 PAAT values of PH patients negatively correlated (rho=-0.497) with pulm

210 One PH formula and the EH formula containing casein componen

211 ssed similar levels of LL-37 and DEFB4, only PH-specific clones secreted molecules sufficient to kill

212 Overall, PH was documented in 117 (39%) of 300 transplant recipie

213 with lower mPAP and frequently develop overt PH and to identify clinical correlates of borderline PH.

214 a repeated RHC, 43 (61%) had developed overt PH, with a median increase in mPAP of 5 mm Hg (interquar

215 secondary outcome was the diagnosis of overt PH in patients initially diagnosed with borderline PH.

216 nificant comorbidities, progression to overt PH, and decreased survival.

217 Pediatric PH patients exhibit LV diastolic dysfunction most consis

218 to evaluate (1) the RA function in pediatric PH patients compared with controls, (2) compare the RA d

219 rties are significantly altered in pediatric PH patients.

220 e emerged as outcome predictors in pediatric PH.

221 (reservoir, conduit, and pump) in pediatric PH.

222 lated from calves and humans with severe PH (PH-Fibs) and from normal subjects.

223 It comprises 1D periodic PH3-PH-PH2-PH-PH3 oligomers.

224 It comprises 1D periodic PH3-PH-PH2-PH-PH3 oligomers.

225 We show that the phosphatase PH domain leucine-rich repeat protein phosphatase (PHLPP

226 y using patch clamp recording, GFP-PLCdelta1-PH imaging and co-localization techniques.

227 1,4,5-trisphosphate biosensor GFP-PLCdelta1-PH was reduced by STIM1 shRNA and absent in TRPC1(-/-) c

228 e show that the main producers of IL-22 post-PH are conventional natural killer cells and innate lymp

229 nerate the liver epithelial compartment post-PH.

230 Postcapillary PH is associated with a decreased survival in proportion

231 Postcapillary PH is generally associated with a diastolic pulmonary pr

232 Postcapillary PH with elevated vascular gradients and pulmonary vascul

233 mean PAP and mean PAWP defines postcapillary PH.

234 life expectancy than isolated postcapillary PH.

235 n of criteria defines isolated postcapillary PH.

236 and inflammation play a role in potentiating PH and pro-inflammatory cytokines, including TNF, are as

237 ance defines combined post- and precapillary PH (Cpc-PH).

238 s with NASH and particularly those requiring PH.

239 e six 3' --> 5' exonucleases (RNase T, RNase PH, RNase D, RNase BN, RNase II and polynucleotide phosp

240 structural and energetic basis of selective PH-PIP interactions is central to understanding many cel

241 tor of 1-year mortality than baseline severe PH.

242 Patients with Cpc-PH have severe PH, with higher diastolic pulmonary pressure gradient, t

243 The persistence of severe PH after transcatheter aortic valve replacement is a str

244 and, in a larger extent, a persistent severe PH after 1 month (HR, 2.4 [1.5-2.8]; P=0.004), independe

245 isolated from calves and humans with severe PH (PH-Fibs) and from normal subjects.

246 METHODS AND Sixty-six PH patients (mean age 7.9+/-4.7 years) were compared wit

247 tly reduced compared to the wild-type strain PH-1, while 10 Group 2 mutants grew normally.

248 PPIs with the expression of nuclear-targeted PH domains, which inhibits recruitment of Ataxia telangi

249 2), a terminal thorium(IV)-phosphinidene (Th=PH), a parent dithorium(IV)-phosphinidiide (Th-P(H)-Th)

250 t PA strains induce higher IL-17 levels than PH strains.

251 In this study, we demonstrated that PH domain leucine-rich repeat protein phosphatase (PHLPP

252 porter localization, providing evidence that PH domain proteins may be effectors of PI3P for protein

253 In livers of mice, we found that PH induces expression of XBP1, and that this activity re

254 ney transplantation, pilot data suggest that PH may improve with successful transplantation.

255 of a serine-rich motif immediately after the PH domain decreases both PtdIns(4)P binding and ceramide

256 This down-regulation requires both the PH and START domains, suggesting a possible inhibitory i

257 further report that mutations disrupting the PH-START interaction increase both PtdIns(4)P-binding af

258 total of 31 QTSs associated with either the PH or the HD.

259 to 45.63% and from 37.53% to 55.96% for the PH and HD, respectively.

260 Hence, the PH domain, but not the DH domain, plays an important rol

261 Moreover, the PH appears to be uniquely situated to have a role in str

262 ding site and unique peripheral sites of the PH domain, the Arf GTPase and, unexpectedly, the Sec7 do

263 the complexities of the interactions of the PH domains with PIP molecules in membranes.

264 esses, yet the molecular complexities of the PH-PIP interactions are largely unknown.

265 Detailed analysis of the PH/PIP interactions reveal both a canonical and an atypi

266 nt distributions of cationic residues on the PH domain, were observed, involving PIP interactions at

267 TSP-1 blockade also prevents the PH in a second model, chronic hypoxia.

268 omology (PH) domain, we demonstrate that the PH domain is the minimal Gbetagamma binding region in PL

269 revealed that the START domain binds to the PH domain at the same site for PtdIns(4)P-binding, sugge

270 vergent stress-activated limbic input to the PH, emanating predominantly from the prefrontal cortex,

271 localization to the plasma membrane via the PH domain and implicate this mechanism in the inhibition

272 nine nucleotide exchange factor, whereas the PH domain binds to various phosphatidylinositol-phosphat

273 phenylquinolin-2(1H)-one interacted with the PH domain of Akt, apparently inducing a conformation tha

274 tes with PtdIns(4)P for association with the PH domain.

275 Within the PH population, four individuals were born in captivity i

276 This PH domain surface is not solvent-exposed in crystal stru

277 This PH phenotype can be rescued with interventions at variou

278 Alternatively, reaction of [U(Tren(TIPS) )(PH)][Na(12C4)2 ] (5, 12C4=12-crown-4 ether) with [U{N(CH

279 ed, and the hepatic regenerative response to PH was compared between dextrose-treated and control mic

280 and beta-lactoglobulin were found in the two PH formulas and casein components in one of the EH formu

281 Mice underwent PH or sham surgeries.

282 djusting for relevant confounding variables, PH was independently associated with higher risk for dea

283 ovine hypertensive pulmonary arterial walls (PH-Fibs) that exhibit constitutive reprogramming of glyc

284 We used Cox models to assess whether PH (PASP>35 mm Hg) was associated with higher rates of H

285 Little is known whether PH heightens the risk of heart failure (HF) admission or

286 treatment of children and young adults with PH.

287 comorbidities significantly associated with PH compared with the general population of children with

288 itrite in metabolic syndrome associated with PH-HFpEF, we developed a 2-hit PH-HFpEF model in rats wi

289 re found to be significantly associated with PH.

290 approaches toward the care of children with PH have been limited by the lack of consensus guidelines

291 ted abnormal PAAT values in 54 children with PH.

292 d 1 day to 18 years) and in 54 children with PH.

293 ndations regarding the care of children with PH.

294 erved and 55 reduced ejection fraction) with PH (HF-PH; pulmonary artery systolic pressure [PASP] >/=

295 or protein, phosphotyrosine interacting with PH domain and leucine zipper 1 (APPL1) signaling endosom

296 tegory occurs in 12% to 13% of patients with PH due to left heart disease.

297 0[2.8-4.9]mmol/l, p = 0.01) in patients with PH reversal but remained unchanged in other patients (2.

298 cirrhotic bile duct ligated (BDL) rats with PH were treated with Infliximab (IFX, a monoclonal antib

299 Within PH-LHD, the QRS-gated DPD yielded higher calculated DPD

300 h the general population of children without PH.