M L Barr

University of Southern California, Los Angeles, CA, United States

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Publications (134)673.44 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Pregnancy after lung transplantation has been described, but pregnancy after living donor lobar lung transplantation (LDLT) has not been reported. The aim of this study was to evaluate outcomes after pregnancy with LDLT and discuss current recommendations regarding pregnancy and lung transplantation. A total of four LDLT patients and five pregnancies were identified, all from our institution. No patient has developed worsening pulmonary function or acute or chronic rejection. The complications of pulmonary hypertension and rejection may be overestimated in this population, and recommendations for preventive sterilization at transplantation or abortion at the time of conception are likely unwarranted and unnecessary.
    Transplantation 08/2014; · 3.78 Impact Factor
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    ABSTRACT: After the first investigational study on the use of extracorporeal photopheresis for the treatment of cutaneous T-cell lymphoma was published in 1983 with its subsequent recognition by the FDA for its refractory forms, the technology has shown significant promise in the treatment of other severe and refractory conditions in a multi-disciplinary setting. Among the major studied conditions are graft versus host disease after allogeneic bone marrow transplantation, systemic sclerosis, solid organ transplant rejection and inflammatory bowel disease. In order to provide recognized expert practical guidelines for the use of this technology for all indications the European Dermatology Forum (EDF) proceeded to address these questions in the hands of the recognized experts within and outside the field of dermatology. This was done using the recognized and approved guidelines of EDF for this task. These guidelines provide at present the most comprehensive available expert recommendations for the use of extracorporeal photopheresis based on the available published literature and expert consensus opinion.
    Journal of the European Academy of Dermatology and Venereology 01/2014; 28 Suppl 1:1-37. · 2.69 Impact Factor
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    ABSTRACT: In light of continued uncertainty regarding postkidney donation medical, psychosocial and socioeconomic outcomes for traditional living donors and especially for donors meeting more relaxed acceptance criteria, a meeting was held in September 2010 to (1) review lim-itations of existing data on outcomes of living kidney donors; (2) assess and define the need for long-term follow-up of living kidney donors; (3) identify the po-tential system requirements, infrastructure and costs of long-term follow-up for living kidney donor out-comes in the United States and (4) explore practical options for future development and funding of United States living kidney donor data collection, metrics and endpoints. Conference participants included prior kid-ney donors, physicians, surgeons, medical ethicists, social scientists, donor coordinators, social workers, independent donor advocates and representatives of payer organizations and the federal government. The findings and recommendations generated at this meet-ing are presented.
    American Journal of Transplantation 12/2011; · 6.19 Impact Factor
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    ABSTRACT: Vascular inflammatory responses are intimately linked with oxidative stress, favoring the development of pre-atherosclerotic lesions. We proposed that oxidized low density lipoprotein (oxLDL) and foam cell infiltrates in the subendothelial layer engendered distinct electrochemical properties that could be measured in terms of the electrochemical impedance spectroscopy (EIS). Concentric bipolar microelectrodes were applied to interrogate EIS of aortas isolated from fat-fed New Zealand White (NZW) rabbits and explants of human aortas. Frequency-dependent EIS measurements were assessed between 10 kHz and 100 kHz, and were significantly elevated in the pre-atherosclerotic lesions in which oxLDL and macrophage infiltrates were prevalent (At 100 kHz: aortic arch lesion=26.7±2.7 kΩ vs. control=15.8±2.4 kΩ; at 10 kHz: lesions=49.2±7.3 kΩ vs. control=27.6±2.7 kΩ, n=10, p<0.001). Similarly, EIS measurements were significantly elevated in the human descending aorta where pre-atherosclerotic lesions or fatty streaks were prominent. EIS measurements remained unchanged in spite of various depths of electrode submersion or orientation of the specimens. Hence, the concentric bipolar microelectrodes provided a reliable means to measure endoluminal electrochemical modifications in regions of pro-inflammatory with high spatial resolution and reproducibility albeit uneven lesion topography and non-uniform current distribution.
    Annals of Biomedical Engineering 01/2011; 39(1):287-96. · 3.23 Impact Factor
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    ABSTRACT: Fluid shear stress is intimately linked with vascular oxidative stress and atherosclerosis. We posited that atherogenic oscillatory shear stress (OSS) induced mitochondrial superoxide (mtO2•-) production via NADPH oxidase and c-Jun NH(2)-terminal kinase (JNK-1 and JNK-2) signaling. In bovine aortic endothelial cells, OSS (±3 dyn/cm2) induced JNK activation, which peaked at 1 h, accompanied by an increase in fluorescein isothiocyanate-conjugated JNK fluorescent and MitoSOX Red (specific for mtO2•- production) intensities. Pretreatment with apocynin (NADPH oxidase inhibitor) or N-acetyl cysteine (antioxidant) significantly attenuated OSS-induced JNK activation. Apocynin further reduced OSS-mediated dihydroethidium and MitoSOX Red intensities specific for cytosolic O2•- and mtO2•- production, respectively. As a corollary, transfecting bovine aortic endothelial cells with JNK siRNA (siJNK) and pretreating with SP600125 (JNK inhibitor) significantly attenuated OSS-mediated mtO2•- production. Immunohistochemistry on explants of human coronary arteries further revealed prominent phosphorylated JNK staining in OSS-exposed regions. These findings indicate that OSS induces mtO2•- production via NADPH oxidase and JNK activation relevant for vascular oxidative stress.
    Antioxidants & Redox Signaling 10/2010; 15(5):1379-88. · 8.20 Impact Factor
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    ABSTRACT: In infected lungs of the cystic fibrosis (CF) patients, opportunistic pathogens and mutated cystic fibrosis transmembrane conductance regulator protein (CFTR) contribute to chronic airway inflammation that is characterized by neutrophil/macrophage infiltration, cytokine release and ceramide accumulation. We sought to investigate CF lung inflammation in the alveoli. Lung tissue from 14 CF patients and four healthy individuals was analyzed for numbers of effector cells, elastin and collagen concentrations, inflammatory markers and density of Pseudomonas aeruginosa. Additionally, desmosine and isodesmosine concentrations were determined in 52 urine specimens from CF patients to estimate the burden of elastase activities in respiratory secretions. Elastin concentration was significantly decreased and collagen significantly increased in CF alveolar tissues as compared to age-matched, healthy individuals. Elastin split products were significantly increased in urine samples from patients with CF and correlated inversely with age, indicating local tissue remodelling due to elastin degradation by unopposed proteolytic enzymes. Alveolar inflammation was also characterized by a significant cell infiltration of neutrophils, macrophages and T cells, extensive nuclear factor-kappaB and insulin-like growth factor-1 activation in various cell types and increased intercellular adhesion molecule-1 expression, and increased numbers of myofibroblasts. Additionally, ceramide accumulated in type II alveolar epithelial cells, lacking CFTR. P. aeruginosa organisms were rarely present in inflamed alveoli. Chronic inflammation and remodeling is present in alveolar tissues of the CF lung and needs to be addressed by anti-inflammatory therapies.
    Journal of cystic fibrosis: official journal of the European Cystic Fibrosis Society 03/2010; 9(3):217-27. · 3.19 Impact Factor
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    ABSTRACT: Lung transplantation is a complex, high-risk, potentially life-saving therapy for the end-stage lung disease of cystic fibrosis (CF). The decision to pursue transplantation involves comparing the likelihood of survival with and without transplantation as well as assessing the effect of wait-listing and transplantation on the patient's quality of life. Although recent population-based analyses of the US lung allocation system for the CF population have raised controversies about the survival benefits of transplantation, studies from the United Kingdom and Canada have suggested a definite survival advantage for those receiving transplants. In response to these and other controversies, leaders in transplantation and CF met together in Lansdowne, Virginia, to consider the state of the art in lung transplantation for CF in an international context, focusing on advances in surgical technique, measurement of outcomes, use of prognostic criteria, variations in local control over listing, and prioritization among the United States, Canada, the United Kingdom, and The Netherlands, patient adherence before and after transplantation and other issues in the broader context of lung transplantation. Finally, the conference members carefully considered how efforts to improve outcomes for lung transplantation for CF lung disease might best be studied. This Roundtable seeks to communicate the substance of our discussions.
    Proceedings of the American Thoracic Society 12/2009; 6(8):619-33.
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    ABSTRACT: The purpose of this study was to analyze the efficacy and examine the competitive cost of CT-guided tube pericardiostomy in the management of symptomatic postsurgical pericardial effusion. Over a 4-year period, 36 patients with symptomatic pericardial effusion were treated with CT-guided percutaneous placement of an indwelling pericardial catheter, for a total of 39 CT-guided tube pericardiostomy procedures. Thirty-three patients (92%) had undergone major cardiothoracic surgery, and three patients (8%) had undergone minimally invasive procedures. The medical records were retrospectively reviewed for clinical presentation, surgical history, imaging studies performed, procedural details, fluid characterization, and outcome. Charge comparison was performed with the American Medical Association Current Procedural Terminology codes and information acquired from the billing department at our facility. All 39 CT-guided tube pericardiostomy procedures were performed successfully without clinically significant complications. After 33 of the 39 procedures (85%), symptoms did not recur after the catheter was removed. Three of 36 patients (8%) had a recurrence of pericardial effusion. Comparison of procedure charges showed an 89% saving over intraoperative pericardial window procedures and no significant difference compared with ultrasound-guided tube pericardiostomy. Eight patients (21% of procedures) needed pleural drainage procedures, all of which were performed in the CT suite immediately after the tube pericardiostomy procedure. CT-guided tube pericardiostomy is a safe and effective alternative to surgical drainage in the care of patients with clinically significant pericardial effusion after cardiothoracic surgery and has the additional benefit of substantial cost savings.
    American Journal of Roentgenology 10/2009; 193(4):W314-20. · 2.90 Impact Factor
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    ABSTRACT: Extracorporeal photopheresis (ECP) is a leukapheresis-based therapy that uses 8-methoxypsoralen and ultraviolet A irradiation. Used alone or in combination with biological agents, ECP is an established and effective therapy for advanced cutaneous T-cell lymphoma. ECP has also shown promising efficacy in a number of other severe and difficult-to-treat conditions, including systemic sclerosis, graft-versus-host disease, prevention and treatment of rejection in solid organ transplantation, and Crohn disease. Furthermore, the use of ECP in some of these conditions may allow a significant reduction in the use of systemic steroids and other immunosuppressants, reducing long-term morbidity and mortality. The accumulated experience shows ECP to be well tolerated, with no clinically significant side effects. Progress is also being made in the search for understanding of the mechanisms of action of ECP, which will ultimately facilitate improvements in the use of this therapy.
    Journal of the American Academy of Dermatology 09/2009; 61(4):652-65. · 4.91 Impact Factor
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    ABSTRACT: This study investigated the genetic composition and the functional implication of CD44 species expressed by intragraft fibroblasts. An LEW-to-F344 heart transplant model of chronic rejection was used. Intragraft fibroblasts recovered from the chronically rejecting allografts displayed a 4.5-fold increase in expression of CD44 mRNA when compared with that of the fibroblasts isolated from non-rejecting heart allografts (P < 0.01). The intragraft fibroblasts preferentially expressed CD44 variant isoforms containing v1 exon transcript. Automated nucleotide sequence analysis revealed that the majority (90.12%) of the CD44 v1 isoforms expressed by the rejecting graft fibroblasts were encoded by a mutated CD44 mRNA, which contained two point mutations and a codon deletion in the v1 coding region. Histochemistry demonstrated a massive deposition of extracellular HA in the rejecting heart allografts. Hyaluronic acid (HA) was able to promote in vitro fibroblast adhesion, migration in a CD44-dependent manner, and survival in a serum-free culture condition. The study concludes that up-regulation of CD44 v1 isoforms expressed by the intragraft fibroblasts is associated with an increase in the deposition of extracellular HA, the principal ligand for CD44, in the allografts, suggesting that CD44-HA interaction plays an important role in regulating fibroblast recruitment and growth in allografts developing chronic rejection.
    Journal of Biochemistry 09/2008; 144(5):571-80. · 3.07 Impact Factor
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    ABSTRACT: Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr –/– Smpd1 +/– mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis. The genetic disorder cystic fibrosis, which affects approximately 80,000 individuals in Europe and North America, is caused by mutations in the CFTR gene 1–3 . Chronic microbial lung infections, most commonly caused by the opportunistic bacterial pathogen P. aeruginosa, lower the life expectancy of people with cystic fibrosis owing to excessive lung tissue remodeling and destruction 4 . How mutation or absence of CFTR, which is primarily expressed in ciliated and submucosal gland epithelial cells of the respiratory tract 5,6 , promotes pulmonary infec-tions, is still incompletely understood. Several studies support the notion that cystic fibrosis cells and respiratory tissues have a proin-flammatory status, which may facilitate bacterial lung colonization and infection 7–10 . Here we investigated the role of sphingolipids in the pathogenesis of cystic fibrosis. CFTR belongs to the ATP-binding cassette transporter family, which has been previously shown to be involved in lipid transport 11,12 . Furthermore, studies indicate that defective CFTR leads to higher pH levels in intracellular organelles 13,14 , which might be important for the regulation of the cellular sphingolipid metabolism by enzymes with activity peaks at acidic pH values. Because sphingo-lipids are crucially involved in the regulation of cell survival 15,16 ,
    Nature Medicine 03/2008; 14(4):382. · 22.86 Impact Factor
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    [Show abstract] [Hide abstract]
    ABSTRACT: Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr –/– Smpd1 +/– mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis. The genetic disorder cystic fibrosis, which affects approximately 80,000 individuals in Europe and North America, is caused by mutations in the CFTR gene 1–3 . Chronic microbial lung infections, most commonly caused by the opportunistic bacterial pathogen P. aeruginosa, lower the life expectancy of people with cystic fibrosis owing to excessive lung tissue remodeling and destruction 4 . How mutation or absence of CFTR, which is primarily expressed in ciliated and submucosal gland epithelial cells of the respiratory tract 5,6 , promotes pulmonary infec-tions, is still incompletely understood. Several studies support the notion that cystic fibrosis cells and respiratory tissues have a proin-flammatory status, which may facilitate bacterial lung colonization and infection 7–10 . Here we investigated the role of sphingolipids in the pathogenesis of cystic fibrosis. CFTR belongs to the ATP-binding cassette transporter family, which has been previously shown to be involved in lipid transport 11,12 . Furthermore, studies indicate that defective CFTR leads to higher pH levels in intracellular organelles 13,14 , which might be important for the regulation of the cellular sphingolipid metabolism by enzymes with activity peaks at acidic pH values. Because sphingo-lipids are crucially involved in the regulation of cell survival 15,16 ,
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    [Show abstract] [Hide abstract]
    ABSTRACT: Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr- /- Smpd1+/- mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis.
    Nature Medicine 03/2008; 14(4):382-391. · 22.86 Impact Factor
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    ABSTRACT: Characteristics of and survival estimates for recipients of lung retransplantation in the modern era are unknown. To compare lung retransplant patients in the modern era with historical retransplant patients, to compare retransplant patients with initial transplant patients in the modern era, and to determine the predictors of the risk of death after lung retransplantation. We performed a retrospective cohort study of patients who underwent lung retransplantation between January 2001 and May 2006 in the United States (modern retransplant cohort). The characteristics and survival of this cohort were compared with those of patients who underwent first lung retransplantation between January 1990 and December 2000 (historical retransplant cohort) and patients who underwent initial lung transplantation between January 2001 and May 2006 (modern initial transplant cohort). Modern retransplant recipients (n = 205) had a lower risk of death compared with that of the historical retransplant cohort (n = 184) (hazard ratio, 0.7; 95% confidence interval, 0.5-0.9; P = 0.006). However, modern retransplant recipients had a higher risk of death than that of patients who underwent initial lung transplantation (n = 5,657) (hazard ratio, 1.3; 95% confidence interval, 1.2-1.5; P = 0.001), which appeared to be explained by a higher prevalence of certain comorbidities. Retransplantation at less than 30 days after the initial transplant procedure was associated with worse survival. Outcomes after lung retransplantation have improved; however, retransplantation continues to pose an increased risk of death compared with the initial transplant procedure. Retransplantation early after the initial transplant poses a particularly high mortality risk.
    American Journal of Respiratory and Critical Care Medicine 02/2008; 177(1):114-20. · 11.04 Impact Factor
  • The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 02/2008; 27(1):138. · 3.54 Impact Factor
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    ABSTRACT: Urgent heart transplant candidates classified as United Network for Organ Sharing status 1B who require continuous infusions of inotropic agents for hemodynamic stability often have hemodynamic, electrical, or multisystem decompensation. This multicenter trial will study both traditional safety and efficacy parameters and the physiologic mechanisms of benefit of the addition to conventional therapy of nesiritide, a recombinant analog of brain-type natriuretic peptide, in this population. TMAC is a prospective, randomized, parallel, multicenter, double-blind, placebo-controlled study in patients awaiting heart transplantation who meet United Network for Organ Sharing status 1B criteria (N = 120) and receive continuous dobutamine or milrinone through a double-lumen central catheter for at least 3 consecutive days before randomization. Patients will receive standard care and continuous intravenous inotrope therapy plus a 28-day continuous infusion of nesiritide or placebo. There will be up to 6 months of follow-up. Primary efficacy end point will be days alive after treatment without renal, hemodynamic, or electrical worsening at completion. Secondary analyses will evaluate effects on hemodynamics, echocardiographic parameters, endogenous brain-type natriuretic peptide levels, modification of diet in renal disease-calculated glomerular filtration rate, and all-cause and cardiovascular mortality. Two mechanistic substudies will evaluate the effect on iohexol-determined glomerular filtration rate and assess changes in lung mechanics. This investigation will provide key data for clinical profiles of heart transplant candidates bound to inotropic support. It will investigate the efficacy and safety (especially renal) of nesiritide and provide mechanistic insight into benefits of its use for the relief of breathlessness.
    American heart journal 07/2007; 153(6):932-40. · 4.65 Impact Factor
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    ABSTRACT: CXCL11 is thought to play a critical role in allograft rejection. To clarify the role of CXCL11 in the rat transplantation model, we cloned CXCL11 cDNA from rat liver tissue and used it to study CXCL11 structure, function and expression. The rat CXCL11 gene encodes a protein of 100 amino acids and spans approximately a 2.8 kb DNA segment containing 4 exons in the protein coding region. Tissue distribution of rat CXCL11 was analyzed by quantitative RT-PCR and showed that rat CXCL11 mRNA is expressed in various tissues and, in particular, at high levels in the spleen and lymph nodes. COS-1 cells were transfected with a plasmid vector encoding rat CXCL11 and used to study CXCL11 effects on cell migration and internalization of CXCR3, the CXCL11 receptor. The recombinant CXCL11 showed chemotactic properties and induced CXCR3 internalization in CD4(+) T cells. Expression of CXCL11 mRNA also was measured in rat acute (ACI to LEW) and chronic (LEW to F344) heart transplant rejection models. CXCL11 mRNA expression in allografts increased in both models, compared with controls, and was primarily observed in infiltrating macrophages and donor endothelial cells. These results indicate that, like the other CXCR3 chemokines, rat CXCL11 seems to have a role in the homing of CD4(+) T cells in both acute and chronic rejection models of heart allotransplantation.
    Molecular and Cellular Biochemistry 03/2007; 296(1-2):1-9. · 2.33 Impact Factor
  • The Journal of Heart and Lung Transplantation 02/2007; 26(2). · 5.11 Impact Factor
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    ABSTRACT: Hemodynamics, specifically, fluid shear stress, modulates the focal nature of atherogenesis. Superoxide anion (O2(-.)) reacts with nitric oxide (.NO) at a rapid diffusion-limited rate to form peroxynitrite (O2(-.) + .NO-->ONOO(-)). Immunohistostaining of human coronary arterial bifurcations or curvatures, where OSS develops, revealed the presence of nitrotyrosine staining, a fingerprint of peroxynitrite; whereas in straight segments, where PSS occurs, nitrotyrosine was absent. We examined vascular nitrative stress in models of oscillatory (OSS) and pulsatile shear stress (PSS). Bovine aortic endothelial cells (BAEC) were exposed to fluid shear stress that simulates arterial blood flow: (1) PSS at a mean shear stress (tau(ave)) of 23 dyn cm(-2) and a temporal gradient (partial differential(tau)/partial differential(t)) at 71 dyn cm(-2) s(-1), and (2) OSS at tau(ave) = 0.02 dyn cm(- 2) and partial differential(tau)/partial differential(t) = +/- 3.0 dyn cm(-2) s(-1) at a frequency of 1 Hz. OSS significantly up-regulated one of the NADPH oxidase subunits (NOx4) expression accompanied with an increase in O2(-.) production. In contrast, PSS up-regulated eNOS expression accompanied with .NO production (total NO(2)(-) and NO(3)(-)). To demonstrate that O2(-.) and .NO are implicated in ONOO(-) formation, we added low-density lipoprotein cholesterol (LDL) to the medium in which BAEC were exposed to the above flow conditions. The medium was analyzed for LDL apo-B-100 nitrotyrosine by liquid chromatography electrospray ionization tandem mass spectrometry (LC/ESI/MS/MS). OSS induced higher levels of 3-nitrotyrosine, dityrosine, and o-hydroxyphenylalanine compared with PSS. In the presence of ONOO(-), specific apo-B-100 tyrosine residues underwent nitration in the alpha and beta helices: alpha-1 (Tyr(144)), alpha-2 (Tyr(2524)), beta-2 (Tyr(3295)), alpha-3 (Tyr(4116)), and beta-2 (Tyr(4211)). Hence, the characteristics of shear stress in the arterial bifurcations influenced the relative production of O2(-.) and .NO with an implication for ONOO(-) formation as evidenced by LDL protein nitration.
    Free Radical Biology and Medicine 02/2007; 42(4):519-29. · 5.27 Impact Factor
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    ABSTRACT: Solid organ transplantation is accepted as a standard lifesaving therapy for end-stage organ failure in children. This article reviews trends in pediatric transplantation from 1996 to 2005 using OPTN data analyzed by the Scientific Registry of Transplant Recipients. Over this period, children have contributed significantly to the donor pool, and although the number of pediatric donors has fallen from 1062 to 900, this still accounts for 12% of all deceased donors. In 2005, 2% of 89,884 candidates listed for transplantation were less than 18 years old; in 2005, 1955 children, or 7% of 28,105 recipients, received a transplant. Improvement in waiting list mortality is documented for most organs, but pretransplant mortality, especially among the youngest children, remains a concern. Posttransplant survival for both patients and allografts similarly has shown improvement throughout the period; in most cases, survival is as good as or better than that seen in adults. Examination of immunosuppressive practices shows an increasing tendency across organs toward tacrolimus-based regimens. In addition, use of induction immunotherapy in the form of anti-lymphocyte antibody preparations, especially the interleukin-2 receptor antagonists, has increased steadily. Despite documented advances in care and outcomes for children undergoing transplantation, several considerations remain that require attention as we attempt to optimize transplant management.
    American Journal of Transplantation 01/2007; 7(5 Pt 2):1339-58. · 6.19 Impact Factor

Publication Stats

4k Citations
673.44 Total Impact Points

Institutions

  • 1993–2009
    • University of Southern California
      • • Department of Radiology
      • • Department of Cardiothoracic Surgery
      • • Department of Surgery
      Los Angeles, CA, United States
  • 2008
    • University of Duisburg-Essen
      • Arbeitsgruppe Molekularbiologie I
      Duisburg, North Rhine-Westphalia, Germany
  • 1990–2008
    • Columbia University
      • • Department of Medicine
      • • College of Physicians and Surgeons
      • • Department of Surgery
      New York City, NY, United States
  • 2007
    • Keck School of Medicine USC
      Los Angeles, California, United States
  • 1999–2007
    • University of California, Los Angeles
      • Division of Cardiothoracic Surgery
      Los Angeles, California, United States
  • 1998–2006
    • Children's Hospital Los Angeles
      • • Division of Cardiothoracic Surgery
      • • Department of Surgery
      Los Angeles, California, United States
    • Wolfson Childrens Hospital
      Jacksonville, Florida, United States
  • 2004
    • University of Maryland Medical Center
      Baltimore, Maryland, United States
  • 2003
    • University of Colorado
      Denver, Colorado, United States
  • 1990–1995
    • New York Presbyterian Hospital
      New York City, New York, United States