ライフサイエンスコーパス: PH

1 PH and eLAP were determined by Doppler echocardiography

2 PH in supracoronary aortic banding+MetS was associated w

3 PH was also associated with STAT3 (signal transducer and

4 PH was identified in 97 (12%) patients; of these, eLAP w

5 PH was induced in male Wistar rats with a single intrape

6 activity, including stable rotors in 4 of 11 PH rats, whereas no significant conduction slowing or ro

7 s: CON-normoxic animals with placebo (n=18); PH-Su/Hx rats+placebo (n=34); PH+Sac/Val (N=24); and PH+

8 pathway in our experimental model of group 2 PH and human patients.

9 sociated with left heart disease, or Group 2 PH, includes heart failure, valvular heart diseases, and

10 due to left heart disease (LHD), or group 2 PH, is the most prevalent form of PH worldwide.

11 sonalized, and timely treatments for Group 2 PH.

12 75 Medicare-eligible veterans with group 2/3 PH by linking national patient-level data from VA and Me

13 ted with PDE5i treatment in VA for group 2/3 PH was prior treatment through Medicare (OR, 6.5 [95% CI

14 ated with prescribing of PDE5i for group 2/3 PH, particularly, to test the hypothesis that veterans p

15 scriptions for PDE5i treatment for group 2/3 PH.

16 lacebo (n=18); PH-Su/Hx rats+placebo (n=34); PH+Sac/Val (N=24); and PH+Val (n=16).

17 th CP (23 S [CP+S] and 22 NS [CP+NS]) and 40 PH individuals (20 S [PH+S] and 20 NS [PH+NS]).

18 surements and Main Results: We identified 49 PH-NF1 cases, characterized by a female/male ratio of 3.

19 ast, unmyristoylated HIV-1 MA, RSV MA, and a PH domain all preferred to interact with free PIP2.

20 ealed that phosphoinositide recognition by a PH domain can be switched through its phosphorylation.

21 otonation to form phosphine carboxylic acid (PH(2) COOH) and functionalization to form esters is show

22 lete deficiency of hepatocyte function after PH.

23 ers temporally spaced at 24 h and 96 h after PH, PVL, and ALPPS.

24 rats+placebo (n=34); PH+Sac/Val (N=24); and PH+Val (n=16).

25 Hyperoxia-induced apoptosis and PH resolved by PND14 and PND70, respectively, in ADM(+/+

26 and the extent of hyperoxia-induced BPD and PH increased in ADM(+/-) mice compared with ADM(+/+) mic

27 d that AM resolves hyperoxia-induced BPD and PH via endothelial nitric oxide synthase (NOS3).

28 d 23 subjects with compensated cirrhosis and PH (hepatic vein pressure gradient [HVPG] >5 mm Hg).

29 1, 2, and 3) in patients with cirrhosis and PH and to prioritize targets and pharmacological therapi

30 on (E2) pathways for F(-) + CH(3)CH(2)Cl and PH(2)(-) + CH(3)CH(2)Cl using the activation strain mode

31 ut mice still displayed miR-210 delivery and PH, thus demonstrating a pathogenic endocrine delivery o

32 Lung injury and development and PH were quantified at different time points.

33 alpha(s) interacted with isolated PRG DH and PH domains and their linker.

34 pport, respiratory support at discharge, and PH therapy.Measurements and Main Results: PA/AO ratio in

35 uted the mechanistic preferences of F(-) and PH(2)(-), i.e., E2 and S(N)2, respectively, to a suppose

36 es correlated with invasive hemodynamics and PH outcome measures (PH-related hospitalization, functio

37 was also upregulated in mice with HFpEF and PH.

38 )C-glycolate in both healthy individuals and PH patients.

39 cant difference in MT levels among CP+NS and PH+S groups (P > 0.05); however, relatively higher level

40 r co-infection were associated with PASP and PH compared to uninfected individuals.

41 Whether PH and PH subtypes unmasked by exercise can be used to guide ta

42 plementation prevents BPD-like phenotype and PH in rodents exposed to neonatal hyperoxia.

43 nic hypoxia to induce miR-210 production and PH, miR-210 was undetectable in knockout-knockout mice p

44 In these mice, vascular remodeling and PH severity were significantly reduced.

45 Arf GAP) with SH3 domain, ankyrin repeat and PH domain 1 (ASAP1) establishes a connection between the

46 ding protein-like domain, Ankyrin repeat and PH domain 2) isoform 2 is considered a proto-oncogene, b

47 that Arf-GAP with coil-coil, ANK repeat and PH domain-containing protein 1 (ACAP1) functions as an a

48 raction by employing small molecules such as PH-687 represents a potentially new and effective strate

49 /valsartan (Sac/Val, LCZ696), will attenuate PH and improve RV function by targeting both pulmonary v

50 alveolar and vascular structure, attenuated PH, reduced pulmonary vascular remodeling and improved c

51 The overexpression of the ASAP1 BAR-PH tandem domain in fibroblasts induced the formation of

52 On the other hand, the less basic PH(2)(-) has a weaker stabilizing interaction with CH(3)

53 However, the mechanism behind PH development in HFpEF is poorly understood.

54 e examined to determine associations between PH, with or without elevated left atrial pressure (eLAP)

55 Correlations between PH and PR values were significant with the exceptions of

56 In experiment 2, using an experimental BPD-PH model, rat pups exposed to room air or hyperoxia (85%

57 els in preterm infants predict increased BPD-PH risk and early Klotho supplementation prevents BPD-li

58 to controls, preterm infants with BPD or BPD-PH had decreased cord Klotho levels.

59 rinatal Klotho deficiency contributes to BPD-PH risk and strategies that preserve Klotho levels, may

60 A dimeric ethylene-bridged PH/BH system reduced carbon monoxide to the -CH(2)-O- st

61 t-capillary, or combined pre-/post-capillary PH now guides point-of-care diagnosis, risk stratificati

62 targets in the established phase of chronic PH.

63 A revised approach to classifying PH patients as pre-capillary, isolated post-capillary, o

64 r pulmonary vascular remodeling.Conclusions: PH-NF1 is characterized by a female predominance, a low

65 SPACox requires fitting a Cox PH regression model only once across the genome-wide ana

66 nt genes using Cox proportional hazards (Cox PH) model and product-limit (PL) estimator.

67 pproximation implementation based on the Cox PH regression model), that is applicable for genome-wide

68 knockout mice in WT-knockout pairs developed PH.

69 ize PRG as a novel effector directing its DH/PH catalytic module to gain affinity for Cdc42.

70 ownstream of Galpha(13) Intriguingly, PRG DH/PH also induced filopodia-like cell protrusions and acti

71 effects of expressing shortened RH-RhoGEF DH/PH constructs of p115RhoGEF/ARHGEF1, PDZ-RhoGEF (PRG)/AR

72 fragment of P-Rex1 and interacts with the DH/PH domains in solution.

73 domain to associate with and inhibit the DH/PH module.

74 an autoinhibit activity in context of the DH/PH-DEP1 fragment of P-Rex1 and interacts with the DH/PH

75 activity or solution conformation of the DH/PH-DEP1 fragment, it inhibits binding of the DEP1 domain

76 allosteric inhibitor MK2206 drives distinct PH domain structural changes compared to baseline autoin

77 ssure (PASP) and prevalent echocardiographic PH.

78 itigated chronic hypoxia-induced established PH in vivo, at variable degree.

79 P9 signaling can predispose to or exacerbate PH, providing a possible mechanistic link between PoPH a

80 nostaining of lung tissues from experimental PH models and patients with PAH, analyses of genetic mur

81 d physiological mouse models of experimental PH, HF, and type 1 diabetes that are associated with alt

82 tissue fibrosis associated with experimental PH, HF, and hyperglycemia.

83 odds ratio of 16.16 (95% CI, 6.62-39.46) for PH-related hospitalization or escalation of therapy.

84 resents a promising therapeutic approach for PH.

85 veterans' access to specialists critical for PH management, receiving care in 2 systems may increase

86 new promising therapeutic interventions for PH, and could serve as a clinical tool to improve person

87 t-term clinical outcomes, including need for PH therapies for infants with BPD.Methods: A total of 52

88 ypothesis that veterans prescribed PDE5i for PH in the community (through Medicare) will have increas

89 hibition as a novel therapeutic strategy for PH and right heart failure.

90 rently, there are no effective therapies for PH-HFpEF, although a number of candidate drugs are being

91 (ORs) of receiving daily PDE5i treatment for PH in VA using multivariable models with facility-specif

92 We found PH PASMCs had increased glucose uptake and utilization b

93 rt failure with preserved ejection fraction (PH-HFpEF) is a growing public health problem that is inc

94 ival of patients with PH-NF1 from the French PH registry.Measurements and Main Results: We identified

95 conclusion, PASMCs and PAECs collected from PH subjects have significant changes in metabolite uptak

96 vity by suppressing glutamatergic input from PH premotoneurons to HMNs and by directly inhibiting HMN

97 d utilization in human PASMCs and PAECs from PH versus control specimens, and that TGF-beta treatment

98 knockout-knockout pairs were protected from PH, whereas knockout mice in WT-knockout pairs developed

99 e presence of B(C(6)F(5))(3), the frustrated PH/BH Lewis pair reacted with carbon monoxide by reducti

100 Sixty-five participants had PH defined by mPAP of greater than or equal to 25 mm Hg,

101 r equal to 25 mm Hg, and 51 participants had PH defined by PVR of greater than 3 Wood units.

102 rom consecutive patients suspected of having PH who underwent cardiac MRI and right-sided heart cathe

103 data analysis, the Cox proportional hazards (PH) regression model is one of the most used approaches.

104 the Cox model assumes proportional hazards (PH), which is unlikely to hold for each feature.

105 re them with those of periodontally healthy (PH) individuals.

106 mbin and plasmin concentration peak heights (PH) and production rates (PR) were calculated.

107 l procedures, including partial hepatectomy (PH), intraoperative portal vein ligation (PVL), and asso

108 g of human donor and RM primary hepatocytes (PH) ex vivo revealed the majority of PH expressed MHC-E

109 we report that human posterior hippocampus (PH) invigorates exploration while anterior hippocampus (

110 in, ankyrin repeat, and pleckstrin homology (PH) domain 1 (ASAP1) is a multidomain GTPase-activating

111 wed that the PLCepsilon pleckstrin homology (PH) domain and first two EF hands (EF1/2) are required f

112 between its N-terminal pleckstrin homology (PH) domain and kinase domain, which is relieved by C-tai

113 Pleckstrin homology (PH) domain and leucine-rich repeat protein phosphatase 1

114 inding of PIP(3) to the pleckstrin homology (PH) domain of P-Rex1 is required for its activation in c

115 sphorylate Rok near the pleckstrin homology (PH) domain that mediates membrane association.

116 ma membrane through its pleckstrin homology (PH) domain that recognizes phosphatidylinositol 3,4,5-tr

117 2B1 variants lie in the Pleckstrin homology (PH) domain, suggesting that the PH domain is essential f

118 ppressor of Ras 1) is a pleckstrin homology (PH) domain-containing scaffold protein that increases th

119 d that ArfGAP with dual pleckstrin homology (PH) domains 2 (ADAP2), gamma-interferon-inducible lysoso

120 region comprising three pleckstrin homology (PH) domains interacts with the N-terminal region compris

121 nstrate that binding of pleckstrin homology (PH) domains to phosphatidylinositol 4-phosphate (PI4P) i

122 lytic Dbl-homology (DH)/pleckstrin-homology (PH) regions, which triggers downstream signals.

123 tein [ArfGAP] with dual pleckstrin homology [PH] domains 1) has been suggested to control dendrite br

124 ulation and transcriptional targets in human PH and the therapeutic potential of isoform-selective en

125 Primary hyperoxalurias (PH) are inborn errors of glyoxylate metabolism character

126 Portal hypertension (PH) is the main driver of cirrhosis decompensation, the

127 e therapies ameliorates portal hypertension (PH); however, it remains unclear whether a decrease in h

128 However, persistent pulmonary hypertension (PH) after PEA remains a major determinant of poor progno

129 dysplasia (BPD) and pulmonary hypertension (PH) after preterm birth.

130 e pathophysiology of pulmonary hypertension (PH) and heart failure (HF) includes fibrogenic remodelin

131 Pulmonary hypertension (PH) associated with left heart disease, or Group 2 PH, i

132 Rationale: Pulmonary hypertension (PH) associated with neurofibromatosis type 1 (NF1) is a

133 Pulmonary hypertension (PH) due to left heart disease (LHD), or group 2 PH, is t

134 the manifestation of pulmonary hypertension (PH) has advanced considerably over the past decade.

135 dysplasia (BPD) and pulmonary hypertension (PH) have accelerated lung aging and poor long-term outco

136 sia (BPD)-associated pulmonary hypertension (PH) have increased morbidity and mortality.

137 apeutic strategy for pulmonary hypertension (PH) in experimental models of PH.

138 Pulmonary hypertension (PH) is a common clinical condition associated with morbi

139 Pulmonary hypertension (PH) is a feature of a variety of diseases and continues

140 Rationale: Pulmonary hypertension (PH) is a life-threatening cardiopulmonary disorder in wh

141 Pulmonary hypertension (PH) is an independent risk factor for adverse clinical o

142 sia (BPD)-associated pulmonary hypertension (PH) is an infantile lung disease characterized by aberra

143 Pulmonary hypertension (PH) is characterized by pulmonary artery remodeling that

144 Chronic pulmonary hypertension (PH) is characterized by the accumulation of persistently

145 Pulmonary hypertension (PH) is frequently reported in patients with advanced chr

146 ) for groups 2 and 3 pulmonary hypertension (PH) is rising nationally, despite guidelines recommendin

147 s (HCV) may increase pulmonary hypertension (PH) risk among people living with HIV (PLWH).

148 iven murine model of pulmonary hypertension (PH) that generates robust and diffuse occlusive neointim

149 have been linked to pulmonary hypertension (PH), a deadly vascular disease with poorly defined molec

150 to the pathology of pulmonary hypertension (PH), but changes in substrate uptake and how substrates

151 requently present in pulmonary hypertension (PH), can be quantified using eccentricity index (EI).

152 In pulmonary hypertension (PH), microRNA-210 (miR-210) in pulmonary endothelial cel

153 lected phenotypes of pulmonary hypertension (PH), we used the Bayesian rare-variant association metho

154 e pathophysiology of pulmonary hypertension (PH).

155 thologic features of pulmonary hypertension (PH).

156 ote severe occlusive pulmonary hypertension (PH).

157 nary vasculature and pulmonary hypertension (PH).

158 an important role in pulmonary hypertension (PH).

159 improve experimental pulmonary hypertension (PH).

160 osis associated with pulmonary hypertension (PH).

161 inant of outcomes in pulmonary hypertension (PH).

162 Fhit(-/-) mice had exaggerated hypoxic PH and failed to recover in normoxia.

163 es in the initiation of experimental hypoxic PH and can serve as a prognostic biomarker of outcome in

164 es in the initiation of experimental hypoxic PH and demonstrates complement signaling as a critical d

165 In experimental hypoxic PH, proinflammatory and pro-proliferative responses were

166 rom lung tissues of patients with idiopathic PH.

167 ately define those with clinically important PH.

168 ed pulmonary vascular remodeling and improve PH due to LHD.

169 r, the true requirement for myeloid cells in PH development has not been demonstrated, and a specific

170 ibe a platform for RNA-mediated crosstalk in PH, providing an impetus for developing blood-based miR-

171 c profiles, there may be some disparities in PH development.

172 hese failures is that processes important in PH development may not be good treatment targets in the

173 lar measures were significantly increased in PH compared with controls.

174 positive cell proliferation and migration in PH.

175 stimulates SMC accumulation to distal PAs in PH remains unclear.

176 Although proinflammatory processes in PH and pulmonary arterial hypertension (PAH) are the foc

177 measure for endogenous oxalate production in PH patients and not applicable in those with kidney fail

178 ostsystolic septal flattening, often seen in PH.

179 Although it is axiomatic that in PH due to heart failure the increase in pulmonary pressu

180 a generalized pseudo-R2 index that includes PH, PO, crossing hazards and crossing odds models as spe

181 had greater odds of comorbidities, including PH (adjusted odds ratio [aOR]: 193.8; 95% confidence int

182 from mice with chronic hypoxia (CH)-induced PH.

183 ation and cell proliferation, and CH-induced PH in mice.

184 .6 KO or FK506 treatment enhances CH-induced PH, while S107 (a specific stabilizer of RyR2/FKBP12.6 c

185 MC) and in vivo (rat chronic hypoxia-induced PH and zebrafish angiogenesis).

186 Fucoidan attenuated chronic hypoxia-induced PH in mice, reducing pulmonary vascular remodeling and r

187 e determined that, in murine hypoxia-induced PH, Ly6C(lo) nonclassical monocytes are recruited to sma

188 ption factor Twist1 mediates hypoxia-induced PH.

189 tase (SOD3) protects against hypoxia-induced PH.

190 s expressing HBV Ags recognized HBV-infected PH from both human donor and RM.

191 that the phosphorylation of Grp1 induces its PH domain to recognize instead phosphatidylinositol 4-ph

192 vasive hemodynamics and PH outcome measures (PH-related hospitalization, functional class, medical th

193 r enhance the investigation of the metabolic PH derangements, provides a tool to accurately assess th

194 prove mPAP and PVR prediction in noninvasive PH evaluation.Supplemental material is available for thi

195 nd 40 PH individuals (20 S [PH+S] and 20 NS [PH+NS]).

196 on of the EC clones caused arterio-occlusive PH in rats exposed to chronic hypoxia.

197 xploits hitherto unknown Michael addition of PH-containing compounds (diphenylphosphine oxide, diisop

198 ter hypoxia exposure, prior to appearance of PH, and may contribute to the early pathogenesis of this

199 ements alone in characterizing the burden of PH in individuals with dyspnea.

200 However, the causes of PH are heterogeneous, and patient prognosis may vary by

201 While the systemic character of PH and right-sided heart failure is often neglected or u

202 The main consequence of PH is right-sided heart failure which causes a complex c

203 nderstanding of the systemic consequences of PH and right-sided heart failure on multiple organ syste

204 vant therapeutic molecules in the context of PH.

205 ime resulted in a new clinical definition of PH that is evidenced-based, is inclusive of mPAP >20 mm

206 fied as a consistent critical determinant of PH and PAH in experimental animal models and humans.

207 monocytes contributes to the development of PH, mice lacking expression of hypoxia-inducible factor-

208 omote vascular remodeling and development of PH.

209 sive methods for monitoring the evolution of PH.

210 or group 2 PH, is the most prevalent form of PH worldwide.

211 ocytes (PH) ex vivo revealed the majority of PH expressed MHC-E but not MHC class II.

212 r understanding the initiating mechanisms of PH and testing biologically relevant therapeutic molecul

213 ole of miR-200b in the nitrofen rat model of PH and CDH and evaluate its use as an in vivo prenatal t

214 as well as RV hypertrophy in a rat model of PH and may be appropriate for treatment of pulmonary hyp

215 of adeno-associated virus in mouse models of PH.

216 hypertension (PH) in experimental models of PH.

217 To describe characteristics and outcomes of PH-NF1.Methods: We reported the clinical, functional, ra

218 road regulatory roles in the pathogenesis of PH via the direct binding to messenger RNA transcripts f

219 e, play a direct role in the pathogenesis of PH.

220 ntal and pivotal role in the pathogenesis of PH.

221 ht the mechanisms and clinical phenotypes of PH in HFpEF and HFrEF.

222 Therefore, the mechanistic preference of PH(2)(-) is steered to the S(N)2 reaction channel (less-

223 c EI of 1.16 best identified the presence of PH, whereas a maximal EI of 1.42 and 1.94 best identifie

224 3,4)P(2,) which regulates the recruitment of PH domain-containing scaffolds such as lamellipodin to i

225 le traits in addition to targeted therapy of PH and underlying causes.

226 potentially beneficial for the treatment of PH.

227 t whether IGF-1 treatment can prevent BPD or PH is unknown.Objectives: To evaluate whether postnatal

228 t input from neurons in the parahypoglossal (PH) region to the HMNs is critical for MoXII respiratory

229 performed at 2 institutions in 78 pediatric PH patients during cardiac catheterization and in 78 mat

230 ardiography to identify and follow pediatric PH patients, especially in the absence of methods to qua

231 ) was an independent predictor of persistent PH (odds ratio per 10%, 0.40 [95% CI, 0.23-0.69]; P=0.00

232 ortant role in the development of persistent PH and survival after PEA.

233 sclosed that R(up) <66% predicted persistent PH after PEA, whereas R(up) <60% identified patients wit

234 cantly increased in patients with persistent PH and nonsurvivors.

235 ated with idiopathic interstitial pneumonia (PH-IIP).

236 rophic" for oligohaline (OH) and polyhaline (PH) salinity zones, and from "hypertrophic" to "eutrophi

237 tic banding+MetS rats developed precapillary PH, as measured by both echocardiography and right/left

238 t catheterization showed severe precapillary PH with a mean pulmonary artery pressure of 45 (10) mm H

239 on between HIV/HCV coinfection and prevalent PH.

240 peptide 3) improves lung growth and prevents PH in two antenatal models of BPD induced by intraamniot

241 ulmonary vascular endothelial cells promotes PH, offering fundamental insight into the systemic physi

242 ulmonary vascular endothelial cells promotes PH.

243 between the IN region (aa 27-93) and the RA-PH module.

244 assessment could augment decisions regarding PH therapies.Objectives: We hypothesized that neonatal c

245 that the Ly6C(lo) monocyte lineage regulates PH through complement, phagocytosis, Ag presentation, an

246 es remained significant after excluding rest PH (n = 146, hazard ratio: 1.75; 95% confidence interval

247 Enzastaurin reversed PH in the Sugen5416/hypoxia/normoxia rat model, by impro

248 mall molecules that interact with the P-Rex1 PH domain and block binding of and activation by PIP(3)

249 the dehydrogenation of phosphine-boranes, RR'PH.BH(3), using a CAAC, which behaves as a stoichiometri

250 22 NS [CP+NS]) and 40 PH individuals (20 S [PH+S] and 20 NS [PH+NS]).

251 occlusive pulmonary arteriopathy and severe PH.

252 tients with compensated cirrhosis and severe PH; an effect upon portal venous inflow is likely, and c

253 4.05] mm Hg; P = 0.003) in those with severe PH: 4/12 had a >=20% decrease, 8/12 had a >=10% decrease

254 patients who resolved clinically significant PH (CSPH) were protected from hepatic decompensation.

255 binding may occur through PIP3/PIP2-specific PH domains or nonspecific ionic interactions involving b

256 The effect of Klotho on lung structure, PH and cardiac function was assessed.

257 4 best identified half-systemic and systemic PH, respectively.

258 Now we show that PH domains occur in all Dictyostelium myosin 1s and that

259 The PH domain of Cnk1 bound with greater affinity to PtdIns(

260 The PH-TEC homology (PHTH) domain within the TEC family of t

261 rity of the abstracted beta-proton along the PH(2)(-)-induced E2 pathway while claiming that "...no c

262 t is known that the interactions between the PH domain and kinase domain (KD) are important for maint

263 ependently bound to a protein containing the PH domain and a 17-amino acid-long interdomain linker im

264 Next, we propose R2 measures for the PH and PO models that can be interpreted in terms of exp

265 Prentice model that includes methods for the PH and proportional odds (PO) models as special cases.

266 es rich in PtdIns, suggesting a role for the PH domain in the biological activity of Cnk1.

267 rential reinforcement representations in the PH and AH.

268 fy a role for a dynamic short segment in the PH domain that appears to regulate autoinhibition and PD

269 on error signals are early and phasic in the PH tail, global value maximum signals are delayed and su

270 linker or the C-terminal alpha-helix of the PH domain decreased [2-17]ARF1 binding and GAP activity.

271 Our results indicate that tilt of the PH domain drives deformation and fragmentation of the ol

272 s to characterize structural features of the PH domain in its autoinhibited and activated states.

273 y N-terminal to the first beta-strand of the PH domain.

274 ion depends on the length/flexibility of the PH-kinase linker.

275 in homology (PH) domain, suggesting that the PH domain is essential for SH2B1's function.

276 These results suggest that the PH domain of P-Rex1 is a tractable drug target and that

277 that reduced ARF1 N-terminal binding to the PH domain also reduced the effect of ASAP1 on cellular a

278 mpound PHT-7.3 that bound selectively to the PH domain of Cnk1, preventing plasma membrane colocaliza

279 howed more similar expression pattern to the PH than the PVL at the early phase of the regeneration.

280 , mutation of the BH site located within the PH domains of PIP3-specific Myo1D and Myo1F completely e

281 ositions near the beta3/beta4 loops of their PH domains.

282 re not capable of dimerization through their PH-TH modules.

283 rial hypertension and chronic thromboembolic PH: as part of an adaptive response to prevent cardiomyo

284 1a) and Ar(F)-P=CPh(2) (1b), along with TMOP-PH(2) (3a) have been characterized by X-ray crystallogra

285 antly higher in the CP groups as compared to PH groups (P < 0.05).

286 n and FKBP12.6/RyR2 dissociation, leading to PH.

287 ialysis vintage, and kidney transplantation, PH was associated with twice the 5-year mortality (hazar

288 of HIF isoforms and their impact in various PH subtypes, as well as the elaborate conditional and ce

289 Whether PH and PH subtypes unmasked by exercise can be used to g

290 The mortality risk associated with PH among patients with advanced chronic kidney disease a

291 d PA/AO ratio and MR-EI were associated with PH therapy during hospitalization and at discharge.Concl

292 One hundred and twenty-five children with PH (8 years [3-12 years]) underwent 3-dimensional echoca

293 By either definition, participants with PH had higher PAenh/WLenh ratio and lower WLenh and DAen

294 Patients with PH had lower SV/ESV compared with controls (0.88+/-0.18

295 Patients with PH in the absence of eLAP are at high risk of death and

296 t of hepatic decompensation in patients with PH who achieved SVR to IFN-free therapy.

297 y also aid decision-making for patients with PH-LHD or otherwise unexplained dyspnea.

298 nd transplant-free survival of patients with PH-NF1 from the French PH registry.Measurements and Main

299 nagement strategies including treatment with PH therapies.

300 etween subjects with CpcPH and those without PH.