Daniel J Penny

Baylor College of Medicine, Houston, Texas, United States

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Publications (113)418.98 Total impact

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    ABSTRACT: Mathematical modeling at the level of the full cardiovascular system requires the numerical approximation of solutions to a one-dimensional nonlinear hyperbolic system describing flow in a single vessel. This model is often simulated by computationally intensive methods like finite elements and discontinuous Galerkin, while some recent applications require more efficient approaches (e.g. for real-time clinical decision support, phenomena occurring over multiple cardiac cycles, iterative solutions to optimization/inverse problems, and uncertainty quantification). Further, the high speed of pressure waves in blood vessels greatly restricts the time step needed for stability in explicit schemes. We address both cost and stability by presenting an efficient and unconditionally stable method for approximating solutions to diagonal nonlinear hyperbolic systems. Theoretical analysis of the algorithm is given along with a comparison of our method to a discontinuous Galerkin implementation. Lastly, we demonstrate the utility of the proposed method by implementing it on small and large arterial networks of vessels whose elastic and geometrical parameters are physiologically relevant.
    Journal of Computational Physics 08/2015; 294. DOI:10.1016/j.jcp.2015.03.045 · 2.49 Impact Factor
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    Sebastian Acosta, Daniel J. Penny, Craig G. Rusin
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    ABSTRACT: In this article we derive applicable expressions for the macroscopic compliance and resistance of microvascular networks. This work yields a lumped-parameter model to describe the hemodynamics of capillary beds. Our derivation takes into account the multiscale nature of capillary networks, the influence of blood volume and pressure on the effective resistance and compliance, as well as, the nonlinear interdependence between these two properties. As a result, we obtain a simple and useful model to study hypotensive and hypertensive phenomena. We include two implementations of our theory: (i) Pulmonary hypertension where the flow resistance is predicted as a function of pulmonary vascular tone. We derive from first-principles the inverse proportional relation between resistance and compliance of the pulmonary tree, which explains why the RC factor remains nearly constant across a population with increasing severity of pulmonary hypertension. (ii) The critical closing pressure in pulmonary hypotension where the flow rate dramatically decreases due to the partial collapse of the capillary bed. In both cases, the results from our proposed model compare accurately with experimental data. Copyright © 2015. Published by Elsevier Inc.
    Microvascular Research 04/2015; DOI:10.1016/j.mvr.2015.04.009 · 2.43 Impact Factor
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    ABSTRACT: Mathematical modeling at the level of the full cardiovascular system requires the numerical approximation of solutions to a one-dimensional nonlinear hyperbolic system describing flow in a single vessel. This model is often simulated by computationally intensive methods like finite elements and discontinuous Galerkin, while some recent applications require more efficient approaches (e.g. for real-time clinical decision support, phenomena occurring over multiple cardiac cycles, iterative solutions to optimization/inverse problems, and uncertainty quantification). Further, the high speed of pressure waves in blood vessels greatly restricts the time-step needed for stability in explicit schemes. We address both cost and stability by presenting an efficient and unconditionally stable method for approximating solutions to diagonal nonlinear hyperbolic systems. Theoretical analysis of the algorithm is given along with a comparison of our method to a discontinuous Galerkin implementation. Lastly, we demonstrate the utility of the proposed method by implementing it on an arterial network of 64 vessels whose elastic and geometrical parameters are physiologically relevant.
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    ABSTRACT: Pulmonary arterial hypertension (PAH) is a devastating disease characterized by abnormal remodeling of small, peripheral pulmonary arteries. Germline mutations in the bone morphogenetic protein receptor type 2 (BMPR2) gene are a major risk factor for developing PAH. At present, the correlation between the BMPR2 mutation and the patient's prognosis remains controversial despite several investigations. In this study, we explored the functional effects of four BMPR2 mutations to dissect the functional significance of the BMPR2 gene defect. Cellular immunofluorescence assay of four mutants (Tyr67Cys, Thr268fs, Ser863Asn, and Gln433X) revealed that the BMPR2 protein containing Thr268fs, Ser863Asn, or Gln433X exhibited abnormal subcellular localization. The BrdU incorporation and TUNEL assay suggested that any of the BMPR2 mutations Thr268fs, Ser863Asn, or Gln433X could improve endothelial cell apoptosis and decrease cell proliferation. All of the four mutants could inhibit nitric oxide (NO) synthesis in HLMVE cells, and ET-1 levels increased in the cells transfected with mutant Ser863Asn. Our results will improve the understanding of the genotype-phenotype correlations and mechanisms associated with BMPR2 mutations.
    PLoS ONE 09/2014; 9(9):e106703. DOI:10.1371/journal.pone.0106703 · 3.53 Impact Factor
  • International Journal of Cardiology 08/2014; 177(3). DOI:10.1016/j.ijcard.2014.08.124 · 6.18 Impact Factor
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    ABSTRACT: Objective Patients with inherited long QT syndrome (LQTS) are prone to torsade de pointes and sudden death (SD). Identifying affected individuals is important for SD prevention. This study aimed to determine the cause and genotype-phenotype characteristics of LQTS in a large Omani family. Methods Upon LQTS diagnosis of a 5-year-old girl (proband), targeted mutation screening was performed based on the gene-specific ECG pattern identified in her mother. ECG-guided family genotyping was conducted for identifying additional affected individuals. Results ECGs of the proband demonstrated 2:1 AV block, incomplete right bundle branch block (IRBBB) and markedly prolonged QTc (571-638 ms) with bizarre T waves. Cardiac imaging revealed dilatation of the ascending aorta and pulmonary artery, and left ventricular non-compaction. Her parents were first cousins. Both showed mild QT prolongation, with the mother presenting a LQT2 T wave pattern and the father IRBBB. Targeted KCNH2 screening identified a novel homozygous frameshift mutation p.T1019Pfs × 38 in the proband within 72-hour. Family genotyping uncovered 3 concealed LQT2 and confirmed 11 members showing LQT2 ECG patterns as heterozygous mutation carriers. All heterozygous carriers were asymptomatic, with 71% showing normal to borderline prolonged QTc (458 ± 33 ms, range 409-522 ms). Conclusion p.T1019Pfs × 38, a novel KCNH2 mutation, has been identified in a large LQTS family in Oman. Consanguineous marriages resulted in a homozygous with severe LQTS. ECG-guided phenotyping and genotyping achieved a high efficiency. Genetic testing is essential in identifying concealed LQTS. Further investigation is warranted to determine if there is a causative relationship between homozygous p.T1019Pfs × 38 and cardiovascular anomaly.
    07/2014; 4. DOI:10.1016/j.ijchv.2014.06.001
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    ABSTRACT: Background:The effects of levosimendan(Levo) on injury patterns in the immature brain following cardiopulmonary bypass (CPB) are unknown.Methods:Eighteen 3-4 week-old anesthetised lambs, instrumented with vascular catheters, aortic and right carotid artery flow probes, were allocated to non-CPB, CPB or CPB+Levo groups(each n=6). After 120 mins CPB with 90 mins aortic cross-clamp, CPB animals received dopamine, and CPB+Levo animals both dopamine and Levo, for 4 hrs. All lambs then underwent brain MRI, followed by post-mortem brain perfusion fixation for immunohistochemical studies.Results:In CPB lambs, aortic(P<0.05) and carotid artery(P<0.01) blood flows fell by 29% and 30 % between 2-4 hr after cross clamp removal, but were unchanged in the CPB+levo group. No brain injury was detectable with MRI in either CPB or CPB+Levo lambs. However, on immunohistochemical analysis, white matter astrocyte density of both groups was higher than in non-CPB lambs (P<0.05), while white matter microglial density was higher (P<0.05), but markers of cortical oxidative stress less prevalent in CPB+Levo than CPB lambs.Conclusions:While Levo prevented early post-operative falls in cardiac output and carotid artery blood flow in a lamb model of infant CPB, this was associated with heterogenous neuroglial activation and manifestation of markers of oxidative stress.Pediatric Research (2014); doi:10.1038/pr.2014.51.
    Pediatric Research 04/2014; DOI:10.1038/pr.2014.51 · 2.84 Impact Factor
  • 03/2014; 9(1):e154. DOI:10.1016/j.gheart.2014.03.1777
  • 03/2014; 9(1):e66-e67. DOI:10.1016/j.gheart.2014.03.1444
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    ABSTRACT: INTRODUCTION: Heart failure (HF) is a global epidemic with rising human and economic toll, but few medical options. Alterations in cardiac metabolism precede significant contractile failure and provide a target for cure. Bile acids such as cholic acid (CA) regulate tissue metabolism and function in mice, through membrane receptor TGR5. TGR5 is expressed in the hearts of mice and humans, but its significance in myocardial cell biology remains unknown. We speculate a critical role for TGR5 in cardiac metabolic adaptation to stress. We hypothesize that functional activation of TGR5 in the heart by CA attenuates, while genetic deletion of TGR5 in the heart accelerates cardiomyopathy in Transverse Aortic Constriction (TAC) induced heart failure in mice. METHODS: 8 wk old male C57BL6 mice (n=20), fed 0.5% CA supplemented diet (n=10) or chow (n=10) were randomized to TAC (n=7) or sham (n=3). Serial 2DEchocardiograms (2DE) were obtained every 2 wks for 8 wks, after which hearts were analyzed for genes and proteins regulating contractility, hypertrophy and metabolism. Separately, mice born with constitutive absence of TGR5 in their hearts [TGR5del] (n=14) and their littermate controls, were randomized to TAC (n=10) or sham (n=4) and evaluated as before. Statistics: ANOVA (4 groups); Results: Mean(plus or minus)SD; p<0.05 is significant. RESULTS: CA fed mice showed upregulation of cardiac De-iodinase2 (3X), eNOS (2X) and Thyroid receptor (alpha) (2X), known key RNA targets of TGR5 activation. At the end of 8 wks, CA fed mice had a significant attenuation in TAC induced decreases in shortening fractions (%FS: 30(plus or minus)2 vs 19(plus or minus)7) on 2DE and heart weight/tibial length (0.08(plus or minus).004 vs 0.14(plus or minus).02g/mm) compared to chow fed TAC mice. CA fed hearts had a significant attenuation (~ 50%) in (beta)MYHC/ (alpha)MYHC ratio (marker for hypertrophy) and BNP (marker for heart failure) at RNA level post-TAC compared with chow fed TAC mice. Post TAC hearts of CA fed mice had a significant 2 fold increase in Thr32 and Ser256 phosphorylation (inhibition) of FOXO-1, along with 70% downregulation of PDK4, known to regulate glucose oxidation in the heart. Separately, TGR5del mice had higher mortality (70% vs 30%; p=0.03, Mantel-Cox) and significantly decreased %FS (10(plus or minus)5 vs 20(plus or minus)7) 8 wks post TAC compared to littermates. CONCLUSION: CA feeding functionally activates TGR5 in the heart. CA attenuates contractile failure and pathologic hypertrophy in mouse model of HF. CA fed hearts show molecular evidence of enhanced glucose oxidation, a crucial step in cardiac adaptation to stress. Separately, TGR5 deletion in heart accelerates TAC induced cardiomyopathy. Results suggest that TGR5 regulates myocardial adaptive response to stress.
    Hepatology 01/2014; 60((Desai M.S.; Shabier Z.; Coss-Bu J.) Pediatric Critical Care, Baylor College of Medicine, Houston, United States):819A. · 11.19 Impact Factor
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    ABSTRACT: Multi-scale modelling is a promising tool for the study of coronary hemodynamics. A key strength of this approach is that it accounts for microvascular properties and extravascular forces that differ regionally and transmurally, as well as wave propagation effects in the conduit arteries. However, little validation of such models has been reported and no models of the newborn coronary circulation have been described. We therefore validated a multi-scale model of the left coronary circulation using high-fidelity data from nine adult sheep and nine newborn lambs, and investigated whether wave propagation effects are more prominent in adults, whose body size (and hence wave transit distance) is greater. The model consisted of a one-dimensional (1D) network of the major conduit arteries and a lumped parameter model of microvascular beds. Intramyocardial pressure was considered to arise via contraction-related myocyte thickening and transmission of ventricular cavity pressure into the heart wall. 1D network geometry from published human anatomical data was scaled using myocardial weights, while subject-specific aortic pressure/flow and ventricular pressure formed model inputs. Total vascular resistance was determined iteratively from measured mean circumflex coronary flow (CxQ), but no fitting of phasic aspects of the waveform was performed. Excellent agreement was obtained between simulated and measured CxQ waveforms in most cases. Detailed flow waveform analysis did not clearly reveal a greater prominence of wave propagation effects in adults compared with newborns. This multi-scale model is likely to be useful for investigating wave phenomena and phasic aspects of coronary flow in adults and during development.
    AJP Heart and Circulatory Physiology 12/2013; 306(4). DOI:10.1152/ajpheart.00603.2013 · 4.01 Impact Factor
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    ABSTRACT: Triggers and exacerbants of cirrhotic cardiomyopathy (CC) are poorly understood, limiting treatment options in patients with chronic liver diseases. Liver transplantation alone reverses some features of CC, but the physiology behind this effect has never been studied. We aimed to determine whether reversal of liver injury and fibrosis in mouse affects cardiac parameters. The second aim was to determine whether cardiomyopathy can be induced by specifically increasing systemic bile acid (BA) levels. 6-8 week old male C57BL6J mice were fed either chow (n=5) or 3, 5-diethoxycarbonyl-1, 4-dihydroxychollidine (DDC) (n=10) for 3 weeks. At the end of 3 weeks, half the mice in the DDC fed group were randomized to chow (the reversed [REV] group). Serial ECHOs and electrocardiographic analysis was conducted weekly for 6 weeks followed by liver tissue and serum studies. Hearts were analyzed for key components of function and cell signaling. Cardiac physiologic and molecular parameters were similarly analyzed in Abcb11(-/-) mice (n=5/grp) fed 0.5% cholic acid supplemented diet for 1 week. Mice in the REV group showed normalization of biochemical markers of liver injury with resolution of electrocardiographic and ECHO aberrations. Catecholamine resistance seen in DDC group resolved in the REV group. Cardiac recovery was accompanied by normalization of cardiac troponin-T2 as well as resolution of cardiac stress response at RNA level. Cardiovascular physiologic and molecular parameters correlated with degree of cholanemia. Cardiomyopathy was reproduced in cholanemic BA fed Abcb11(-/-) mice. Cardiomyopathy resolves with resolution of liver injury, is associated with cholanemia, and can be induced by BA feeding. This article is protected by copyright. All rights reserved.
    Liver international: official journal of the International Association for the Study of the Liver 12/2013; 35(4). DOI:10.1111/liv.12438 · 4.41 Impact Factor
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    ABSTRACT: Most studies have not demonstrated improved survival after prenatal diagnosis of critical congenital heart disease, including hypoplastic left heart syndrome (HLHS). However, the effect of delivery near a cardiac surgical center (CSC), the recommended action after prenatal diagnosis, on HLHS mortality has been poorly investigated. Using Texas Birth Defects Registry data, 1999-2007, which monitored >3.4 million births, we investigated the association between distance (calculated driving time) from birth center to CSC and neonatal mortality in 463 infants with HLHS. Infants with extracardiac birth defects or genetic disorders were excluded. The associations between prenatal diagnosis, CSC HLHS volume, and mortality were also examined. Neonatal mortality in infants born <10 minutes from a CSC was 21.0%, 10-90 minutes 25.2%, and >90 minutes 39.6% (p for trend <0.001). Prenatal diagnosis alone was not associated with improved survival (p=0.14). In multivariable analysis, birth >90 minutes from a CSC remained associated with increased mortality, OR 2.03 (95%CI 1.19-3.45), compared to <10 minutes. In subanalysis, birth >90 minutes from a CSC was associated with higher pre-transport mortality (OR 6.69, 95%CI 2.52-17.74) and birth 10-90 minutes with higher pre-surgical mortality (OR 4.45, 95%CI 1.17-17.00). Higher surgical mortality was associated with lower CSC HLHS volume (OR per 10 patients 0.88, 95%CI 0.84-0.91). Infants with HLHS born far from a CSC have increased neonatal mortality, and most of this mortality is pre-surgical. Efforts to improve prenatal diagnosis of HLHS and subsequent delivery near a large volume CSC may significantly improve neonatal HLHS survival.
    Circulation 10/2013; 129(3). DOI:10.1161/CIRCULATIONAHA.113.003711 · 14.95 Impact Factor
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    ABSTRACT: The purpose of this study was to describe patient characteristics and outcomes of heart failure (HF)-related intensive care unit (ICU) hospitalizations in children with cardiomyopathy (CM). A query of the Pediatric Health Information System database, a large administrative and billing database of 43 tertiary children's hospitals, was performed. A total of 17,309 HF-related ICU hospitalizations from 2005 to 2010 of 14,985 children ≤18 years old were analyzed. Of those, 2,058 (12%) hospitalizations for CM-HF in 1,599 (11%) children were identified. Classification into CM subtypes was not possible owing to database limitations. The number of yearly CM-HF hospitalizations significantly increased during the study period (P = .036). Overall mortality was 11%, and cardiac transplantation occurred in 20% of hospitalizations. Mechanical circulatory support (MCS) was used in 261 (13%) of hospitalizations. Renal failure, MCS, respiratory failure, sepsis, and vasoactive medications were associated with mortality on multivariable analysis. Significant comorbidities associated with these hospitalizations included arrhythmias in 42%, renal failure in 13%, cerebrovascular disease in 6%, and hepatic impairment in 5%. HF-related ICU hospitalizations in children with cardiomyopathy are increasing. These children are at high risk for poor outcomes with an in-hospital mortality of 11%.
    Journal of cardiac failure 10/2013; 19(10):672-677. DOI:10.1016/j.cardfail.2013.08.006 · 3.07 Impact Factor
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    ABSTRACT: Malouf syndrome is a rare congenital disorder involving the heart, genitalia, skin and skeletal characteristics. In the present study, we report on the sporadic case of a young female with dilated cardiomyopathy, hypergonadotropic hypogonadism, a small chin, bilateral blepharoptosis, marfanoid elongated fingers and hypothyroidism. Malouf syndrome may be caused by heterozygous mutations in the lamin A/C (LMNA) gene. Genetic analyses and autopsy were performed. In spite of the patient's features, sequence analysis of the coding region of the LMNA gene including exon‑intron boundaries identified only one benign polymorphism: homozygous silent variant 1698C>T (H566). There is a possibility that the sequence analysis may have not detected intronic mutations or mutations in portions of the 5'- and 3'-untranslated regions, which would confirm the clinical diagnosis.
    Molecular Medicine Reports 09/2013; 8(5). DOI:10.3892/mmr.2013.1669 · 1.48 Impact Factor
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    ABSTRACT: Mutations in FBN1 cause a range of overlapping but distinct conditions including Marfan syndrome (MFS), Weill-Marchesani syndrome (WMS), familial thoracic aortic aneurysms/dissections (FTAAD), acromicric dysplasia (AD), and geleophysic dysplasia (GD). Two forms of acromelic dysplasia, AD and GD, characterized by short stature, brachydactyly, reduced joint mobility, and characteristic facies, result from heterozygous missense mutations occurring in exons 41 and 42 of FBN1; missense mutations in these exons have not been reported to cause MFS or other syndromes. Here we report on probands with MFS and WMS who have heterozygous FBN1 missense mutations in exons 41 and 42, respectively. The proband with WMS has ectopia lentis, short stature, thickened pinnae, tight skin, striae atrophicae, reduced extension of the elbows, contractures of the fingers and toes, and brachydactyly and has a missense mutation in exon 42 of FBN1 (c.5242T>C; p.C1748R). He also experienced a previously unreported complication of WMS, an acute thoracic aortic dissection. The second proband displays classic characteristics of MFS, including ectopia lentis, skeletal features, and aortic root dilatation, and has a missense mutation in exon 41 of FBN1 (c.5084G>A; p.C1695Y). These phenotypes provide evidence that missense mutations in exons 41 and 42 of FBN1 lead to MFS and WMS in addition to AD and GD and also suggest that all individuals with pathogenic FBN1 mutations in these exons should be assessed for thoracic aortic disease and ectopia lentis. Further studies are necessary to elucidate the factors responsible for the different phenotypes associated with missense mutations in these exons of FBN1. © 2013 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part A 09/2013; 161(9). DOI:10.1002/ajmg.a.36044 · 2.05 Impact Factor
  • Moreshwar S Desai, Daniel J Penny
    Heart (British Cardiac Society) 08/2013; 99(22). DOI:10.1136/heartjnl-2013-304546 · 6.02 Impact Factor
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    ABSTRACT: We validated a multi-scale model of a left-dominant coronary circulation using high fidelity pressure and flow data acquired in adult sheep and newborn lambs. The model incorporated a one-dimensional representation of the major left conduit coronary arteries, allowing for the study of wave propagation effects. The coronary microvasculature was represented by regional instances of a lumped parameter model consisting of three transmural layers, each with two serial compartments accounting for compliance, resistance and intramyocardial pressure effects. Model inputs comprised measured aortic pressure/flow and ventricular pressure. Minimal data fitting was employed, with only measured mean coronary flow used to iteratively adjust total coronary resistance. The model was adapted to different heart sizes via allometric scaling. Excellent agreement was observed between model and experimental flow waveforms in the proximal circumflex artery, both in terms of the degree of systolic flow impediment and transient waveform features. The proposed multi-scale modelling approach is likely to be useful for studying phasic features of the coronary flow waveform, including coronary waves in different coronary anatomies and throughout development.
    Conference proceedings: ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Conference 07/2013; 2013:3857-3860. DOI:10.1109/EMBC.2013.6610386
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    ABSTRACT: Objective: Barth syndrome is an X-linked recessive disorder characterized by dilated cardiomyopathy, neutropenia, 3-methylglutaconic aciduria, abnormal mitochondria, variably expressed skeletal myopathy, and growth delay. The disorder is caused by mutations in the tafazzin (TAZ/G4.5) gene located on Xq28. We report a novel exonic splicing mutation in the TAZ gene in a patient with atypical Barth syndrome. Patient & Methods: The 4-month-old proband presented with respiratory distress, neutropenia, and dilated cardiomyopathy with reduced ejection fraction of 10%. No 3-methylglutaconic aciduria was detected on repeated urine organic acid analyses. Family history indicated that his maternal uncle died of endocardial fibroelastosis and dilated cardiomyopathy at 26 months. TAZ DNA sequencing, mRNA analysis, and cardiolipin analysis were performed. Results: A novel nucleotide substitution c.553A>G in exon 7 of the TAZ gene was identified in the proband, predicting an amino acid substitution p.Met185Val. However, this mutation created a new splice donor signal within exon 7 causing mis-splicing of the message, producing two messages that only differ in the presence/absence of exon 5; these retain intron 6 and have only 11 bases of exon 7. Cardiolipin analysis confirmed the loss of tafazzin activity. The proband's mother, maternal aunt, and grandmother carry the same mutation. Conclusions: The identification of a TAZ gene mutation, mRNA analysis, and monolysocardiolipin/cardiolipin ratio determination were important for the diagnosis and genetic counseling in this family with atypical Barth syndrome that was not found to be associated with 3-methylglutaconic aciduria.
    04/2013; DOI:10.1007/8904_2013_228
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    Yuxin Fan, Hu Wang, Daniel Penny
    Journal of the American College of Cardiology 03/2013; 61(10):E1296. DOI:10.1016/S0735-1097(13)61296-6 · 15.34 Impact Factor

Publication Stats

1k Citations
418.98 Total Impact Points

Institutions

  • 2010–2014
    • Baylor College of Medicine
      • • Section of Cardiology
      • • Department of Pediatrics
      Houston, Texas, United States
  • 2012–2013
    • Texas Children's Hospital
      Houston, Texas, United States
  • 2006–2013
    • Murdoch Childrens Research Institute
      • Research Group for Heart Research
      Melbourne, Victoria, Australia
  • 2006–2012
    • University of Melbourne
      • Department of Paediatrics
      Melbourne, Victoria, Australia
  • 2003–2012
    • The Royal Children's Hospital
      • Department of Cardiology
      Melbourne, Victoria, Australia
    • University College London
      • Institute of Neurology
      London, ENG, United Kingdom
  • 2011
    • Starship Children's Hospital
      Окленд, Auckland, New Zealand
  • 2008
    • University of Vic
      Vic, Catalonia, Spain
  • 2000–2003
    • Great Ormond Street Hospital for Children NHS Foundation Trust
      • • Department of Cardiology
      • • Cardiac Intensive Care Unit (CICU)
      • • Department of Cardiothoracic Surgery
      London, ENG, United Kingdom
    • Hospital Universitario de Maracaibo
      Maracaibo, Estado Zulia, Venezuela
  • 2002
    • Monash University (Australia)
      • Department of Medicine
      Melbourne, Victoria, Australia
  • 2001
    • Royal Brompton and Harefield NHS Foundation Trust
      Harefield, England, United Kingdom