The Diabetes Research Program is made up of outstanding researchers, technicians and administrators. Below are people who have made important contributions to the program and are now doing other work:
Lili Lin, MD
Lili received her MD from Fujian Medical University in China. She also holds a master’s degree in Pharmacology from the same institution. As part of her postdoctoral studies in the Diabetes Research Program, Lili participated in various research projects including “Aging and Vulnerability to Ischemia about the Pathways and Rescue” and “RAGE blockade and Type 1 Diabetic Nephropathy Moving to the Clinic”. Her studies also included hindlimb ischemia and atherosclerosis. Lili has returned to China to continue her studies. Her email address is: email@example.com 
1. Xu Y, Toure F, Qu W, Lin L, Song F, Shen X, Rosario R, Garcia J, Schmidt AM, Yan SF. Advanced glycation end product (AGE)-receptor for AGE (RAGE) signaling and up-regulation of Egr-1 in hypoxic macrophages [J]. J Biol Chem, 2010 Jul 23; 285 (30): 23233-40.
2. Lin L, Xu, Y. Study on 124I labeling of Neurotoxin from Naja naja atra and its biodistribution in rat [J]. Strait Pharmaceutical, 2009, 21(5):36-38.
Fatouma Toure, MD, PhD
As a Nephrologist, my postdoctoral training in the Diabetes Research Program was the perfect time for me to discover the fundamental aspect of RAGE implication in the diseases I was seeing in patients. I was lucky to be part of a project exploring the numerous and critical signaling pathways induced by RAGE activation. The focus of my attention was the interaction of RAGE with molecules from the formin family and the implication of this interaction on RAGE-induced redox signaling. The studies were made in vivo and in vitro, and they highlighted key roles for formins in RAGE-mediated effects. I was also associated with projects studying the progression of diabetic glomerulosclerosis and the role of RAGE in this phenomenon.
I am currently working as an Assistant Professor/Hospital Practitioner at Hospital University of Reims and Research Unit CNRS UMR 6237, France. – Fatouma Toure, MD, PhD
1. Touré F, Fritz G, Li Q, Rai V, Daffu G, Zou YS, Rosario R, Ramasamy R, Alberts AS, Yan SF, Schmidt AM.Formin mDia1 Mediates Vascular Remodeling via Integration of Oxidative and Signal Transduction Pathways.Circ Res. 2012 May 11;110(10):1279-93. Epub 2012 Apr 17.
2. Xu Y, Touré F, Qu W, Lin L, Song F, Shen X, Rosario R, Garcia J, Schmidt AM, Yan SF. Advanced glycation end product (AGE)-receptor for AGE (RAGE) signaling and up-regulation of Egr-1 in hypoxic macrophages. J Biol Chem. 2010 Jul 23; 285(30):23233-40.
3. Shang L, Ananthakrishnan R, Li Q, Quadri N, Abdillahi M, Zhu Z, Qu W, Rosario R, Touré F, Yan SF, Schmidt AM, Ramasamy R. RAGE modulates hypoxia/reoxygenation injury in adult murine cardiomyocytes via JNK and GSK-3beta signaling pathways. PLoS One. 2010 Apr 9; 5(4):e10092.
4. Zhang Y, Nuglozeh E, Touré F, Schmidt AM, Vunjak-Novakovic G. Controllable expansion of primary cardiomyocytes by reversible immortalization. Hum Gene Ther. 2009 Dec;20(12):1687-96.
5. Touré F, Zahm JM, Garnotel R, Lambert E, Bonnet N, Schmidt AM, Vitry F, Chanard J, Gillery P, Rieu P. Receptor for advanced glycation end-products (RAGE) modulates neutrophil adhesion and migration on glycoxidated extracellular matrix. Biochem J. 2008 Dec 1;416(2): 255-61.
Yunlu Xu, MD, PhD
Yunlu received her MD and PhD from Fujian Medical University in China. As a Postdoctoral Research Fellow in the Diabetes Research Program, her research projects included AGE-RAGE signaling in hypoxic macrophages. Currently, Yunlu is a Professor in the Department of Pharmacology, College of Pharmacy, Fujian Medical University. She is also an advisor for PhD candidate students. Yunlu lectures medical students in Chinese and English. She has her own research funding and laboratory.
Her email address is: firstname.lastname@example.org 
1. Huang C, Chang JS, Xu Y, Li Q, Zou YS, Yan SF. Reduction of PKCbetaII activity in smooth muscle cells attenuates acute arterial injury. Atherosclerosis. 2010 Sep; 212(1):123-30.
2. Xu Y, Toure F, Qu W, Lin L, Song F, Shen X, Rosario R, Garcia J, Schmidt AM, Yan SF. Advanced glycation end product (AGE)-receptor for AGE (RAGE) signaling and up-regulation of Egr-1 in hypoxic macrophages. J Biol Chem. 2010 Jul 23; 285(30):23233-40.
Srinivasan Vedantham, PhD
As a postdoctoral fellow in the Diabetes Research Program my main research focus was to understand the role of Aldose Reductase (AR) in causing early atherosclerosis diabetes and to delineate the mechanisms by which they do so. Important findings have been made in understanding how polyol pathway affects NAD+ synthesis and sirtuin activity in early atherosclerotic events.
I am currently working as a scientist at the Madras Diabetes Research Foundation, Chennai, India, leading a program in Growth & Development in Metabolism. My present research focus is on understanding how maternal blood and food-derived Advanced Glycation End-Products (AGEs) predispose to diabetes and other chronic metabolic diseases in infants and young children. Additionally I am also interested in understanding developmental programming of obesity and metabolic syndrome during the life course.
My email address is: email@example.com 
1. Vedantham S, Ananthakrishnan R, Schmidt AM, Ramasamy R. Aldose Reductase, Oxidative Stress and Diabetic Cardiovascular Complications. Cardiovasc Hematol Agents Med Chem. 2012 May 21. [Epub ahead of print]
2. Zeng S, Zhang QY, Huang J, Vedantham S, Rosario R, Ananthakrishnan R, Yan SF, Ramasamy R, DeMatteo RP, Emond JC, Friedman RA, Schmidt AM. Opposing roles of RAGE and Myd88 signaling in extensive liver resection. FASEB J. 2012 Feb;26(2):882-93. Epub 2011 Nov 10.
3. Vedantham S, Noh H, Ananthakrishnan R, Son N, Hallam K, Hu Y, Yu S, Shen X, Rosario R, Lu Y, Ravindranath T, Drosatos K, Huggins LA, Schmidt AM, Goldberg IJ, Ramasamy R. Human aldose reductase expression accelerates atherosclerosis in diabetic apolipoprotein E-/- mice. Arterioscler Thromb Vasc Biol. 2011 Aug;31(8):1805-13. Epub 2011 Jun 2.
4. Hallam KM, Li Q, Ananthakrishnan R, Kalea A, Zou YS, Vedantham S, Schmidt AM, Yan SF, Ramasamy R. Aldose reductase and AGE-RAGE pathways: central roles in the pathogenesis of vascular dysfunction in aging rats. Aging Cell. 2010 Oct;9(5):776-84. doi: 10.1111/j.1474-9726.2010.00606.x. Epub 2010 Aug 15.
Zhou Chen, MD, PhD
As a postdoc, I was lucky to participate in an aging project. The project involved the use of primary cultured endothelial cells isolated from young and aged rats for vitro studies. Young and aged wild type and RAGE knockout mice were also used for in vivo studies. As a member of the Diabetes Research Program, we found that RAGE modulates expression of proinflammatory and procoagulant genes in response to aging and hypoxia stresses.
My new position is Associate Professor of Pharmacology at Fujian Medical University in China. In addition to my lecturing duties, I will continue to focus on Geriatrics and the diseases related to aging.
My email address is: firstname.lastname@example.org 
Lingjie Wang, MD, PhD
As a cardiologist, the postdoctoral fellow training in the Diabetes Research Program was a crucial step in my academic career. My primary project was to address the mechanisms by which RAGE blockade protects hearts from high fat diet induced functional and metabolic changes. Specifically, it revealed the impact of RAGE blockade on cardiac mitochondrial biogenesis in HFD-induced obesity mice or high fatty acid treated cardiomyocytes.
I was lucky to be part of a project establishing the impact of aldose reductase pathway on mitochondrial function and mitochondrial biogenesis in acute and chronic diabetic hearts. The aim was to investigate the potential mechanisms by which aging and diabetes increase vulnerability of hearts to ischemia-reperfusion injury. I also participated in studies that resulted in demonstrating cardio-protection afforded by the carbon monoxide form of PEGylated hemoglobin (SANGUINATE™) in diabetic and non-diabetic mice models of myocardial infarction.
I am currently working as a physician of Cardiology at Ruijin Hospital of Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China.
My e-mail address is email@example.com .
1. Ananthakrishnan R, Li Q, O'Shea KM, Quadri N, Wang L, Abuchowski A, Schmidt AM, Ramasamy R. Carbon monoxide form of PEGylated hemoglobin protects myocardium against ischemia/reperfusion injury in diabetic and normal mice. Artif Cells Nanomed Biotechnol. 2013 Jan 23. [Epub ahead of print]
2. Lin L, Wang YN, Sun WH, Liu ZH, Zhang Q, P LJ, Yang K, Wang LJ, Zhu ZB, Meng H, Yang P, Du R, Chen QJ, Wang LS, Yu H, Shen WF. 2D-DIGE of Coronary Restenosis Tissues in Minipigs: Increased AFABP induces ROS-Mediated Growth and Migration in SMCs. Arteriosclerosis, Thrombosis, and Vascular Biology. 2013, In press.
Judyta Juranek, DVM, PhD
As a postdoctoral fellow in the Diabetes Research Program, I worked on deciphering the role of the Receptor for Advanced Glycation End-Products (RAGE) and its most prominent ligands in the pathogenesis of diabetic peripheral neuropathy. Studies showed that in normoglycemia peripheral neuronal RAGE contributes to effective axonal regeneration prompted by acute crush injury; while in diabetes, intact peripheral nerve studies showed that RAGE signaling is a deteriorating factor.
In the present study I hypothesized that in diabetes, peripheral nervous system RAGE contributes to progressive neuropathy and that upon superimposed acute injury, RAGE-dependent neuronal dysfunction would worsen, thereby attenuating neurite outgrowth and further suppressing effective axonal regeneration and re-innervation of target tissues. The findings of the study, published in Diabetes (Juranek et al, 2013) provide evidence that RAGE suppresses effective axonal regeneration in diabetic peripheral nerve after acute injury.
Throughout this project, I have had the opportunity to advance my laboratory skills as well as evolve as a mentor to undergraduate students. In addition to my laboratory and mentoring tasks I have also acted as a head of a microscopy unit in my laboratory and have been responsible for training laboratory members in microscopy techniques, image capturing and signal quantification.
My future plans include continuing my efforts to further deepen my knowledge of the pathogenesis of neurodegenerative disorders. I will investigate new treatments by actively engaging in collaboration with my fellow researchers and aim to create joint multilevel projects.
My email address is firstname.lastname@example.org .
1. Juranek JK, Mukherjee K, Siddiqui T, Kaplan B, Li JY, Ahnert-Hilger G, Jahn R, Calka J. Active Zone protein expression changes at key stages of cerebellar cortex neurogenesis in the rat. Acta Histochemica 2013 Feb 20. (Epub. ahead of print)
2. Juranek JK, Geddis MS, Song F, Zhang J, Garcia J, Rosario R, Yan SF, Brannagan TH, Schmidt AM. RAGE deficiency improves post-injury sciatic nerve regeneration in type 1 diabetic mice. Diabetes 2013 62(3):931-43.
3. Wojtkiewicz J, Juranek JK, Kowalski I, Bladowski M, Calka J, Majewski M. Immunohistochemical characterization of superior cervical ganglion neurons supplying porcine parotid salivary gland. Neurosci Lett. 2011 500 (1): 57-62. (Equal authorship)
4. Juranek JK, Aleshin A, Rattigan E, Johnson L, Qu W, Song F, Ananthakrishnan R, Quadri N, Yan SD, Ramasamy R, Schmidt AM, Geddis M. Morphological Changes and Immunohistochemical Expression of RAGE and its Ligands in the Sciatic Nerve of Hyperglycemic Pig (Sus Scrofa). Biochemistry Insights 2010 (3): 47-59.
5. Juranek J, Mukherjee K (2009) Piccolo and Bassoon. Encyclopedia of Neuroscience, Elsevier, p. 707-711.
6. Brunk I, Blex C, Sanchis-Segura C, Sternberg J, Perreau-Lenz S, Bilbao A, Hörtnagl H, Baron J, Juranek J, Laube G, Birnbaumer L, Spanagel R, Ahnert-Hilger G. Deletion of Go2α abolishes cocaine-induced behavioral sensitization by disturbing the striatal dopamine system. The FASEB Journal 2008 22: 3736-3746.
7. Calka J, Zasadowski A, Juranek J. Some aspects of green tea curative effects. Bromat. Chem. Toksykol. 2008 1: 5-14.
8. Calka J, Juranek J, Wasowicz K, Kaleczyc J, Lakomy M. Distribution and morphology of ChAT- and VAChT – immunoreactive neurons in the tuberal hypothalamus of the pig. Med. Wet. 2007 63(4): 412-415.
9. Juranek J, Calka J, Lakomy M. Synaptic active zone proteins as coordinators of nervous system neurotransmission. Humanistyka i przyrodoznastwo 2007 13: 273 – 280.
10. Juranek J, Mukherjee K, Rickmann M, Martens H, Calka J, Sudhof T, Jahn R. Differential expression of active zone proteins in neuromuscular junctions suggests functional diversification. Eur. J. Neurosci. 2006 24(11): 3043-3052.
11. Wisniewska M, Madany J, Pomianowski A, Juranek J. Obesity in carnivores. Pol. J. Vet. Sci. 2005 8: 329-335. Review.
12. Kaleczyc J, Juranek J, J.Calka, Lakomy M. Immunohistochemical characterization of porcine ciliary ganglion. Pol. J. Vet. Sci. 2005 8(1): 65-72.
Vivek Rai, PhD
Dr. Rai was born in Allahabad, India and received his Ph.D. from Jawaharlal Nehru University (JNU), New Delhi, India. He joined Dr. Ann Marie Schmidt's laboratory as a Postdoctoral Research Scientist in 2008 at Columbia University Medical Center and later at the Diabetes Research Program, NYU Langone Medical Center. His research focused on two areas: the study of the RAGE ligands family of molecules and how they regulate RAGE signaling and the analysis of the mechanisms by which RAGE mediates diabetic complications.
Dr. Rai is currently working as a Principal Investigator at Institute of Life Sciences (ILS), Bhubaneswar, India; a leading institute specializing in infectious diseases. He is the recipient of two prestigious 2012-13 awards: the Ramanujan award and the Ramalingaswami Fellowship which is primarily given to selected Indian scientists working overseas. His present research focus is on understanding the molecular mechanisms and signaling events associated with vascular immunology in pathogenesis.
Dr. Rai’s email address is email@example.com .
1. Reverdatto S, Rai V, Xue J, Burz D, Schmidt AM, Shekhtman A. Combinatorial Library of Improved Peptide Aptamers, CLIPs to inhibit RAGE signal transduction in mammalian cells. PLOS ONE. 2013, 10.1371/journal.pone.0065180.
2. Rai V, Toure F, Chitayat S, Pei R, Li Q, Rosario R, Zhu Z, Song F, Ramasamy R, Chazin W, Schmidt AM. Lysophosphatidic acid targets vascular and oncogenic pathways via RAGE signaling. J. Exp. Med. 2012, 209(13):2339-50.
3. Touré F, Fritz G, Li Q, Rai V, Daffu G, Zou YS, Rosario R, Ramasamy R, Alberts AS, Yan SF, Schmidt AM. Formin mDia1 mediates vascular remodeling via integration of oxidative and signal transduction pathways. Circulation Research, 2012 110(10):1279-93.
4. Rai V, Maldonado AY, Burz DS, Reverdatto S, Schmidt AM, Shekhtman A. Signal Transduction in Receptor for Advanced Glycation End Products (RAGE): solution structure of C-Terminal RAGE (ctRAGE) and its binding to mDia1. J Biol Chem. 2012; 287(7):5133-44.
5. Ma W, Rai V, Hudson BI, Song F, Schmidt AM, Barile GR. RAGE binds C1q and enhances C1q-mediated phagocytosis. Cell Immunol. 2012; 274(1-2):72-82.
6. Xue J*, Rai V*, Singer D, Chabierski S, Xie J, Reverdatto S, Burz DS, Schmidt AM, Hoffmann R, Shekhtman A. Advanced glycation end product recognition by the receptor for AGEs. Structure 2011; 19(5):722-32. (*Joint first author)
7. Bu DX*, Rai V*, Shen X, Rosario R, Lu Y, D'Agati V, Yan SF, Friedman RA, Nuglozeh E, Schmidt AM. Activation of the ROCK1 branch of the transforming growth factor- βPathway contributes to RAGE-dependent acceleration of atherosclerosis in diabetic ApoE null mice. Circulation Research. 2010; 106(6):1040-51. (*Joint First Author)
8. Reiniger N, Lau K, McCalla D, Eby B, Cheng B, Lu Y, Qu W, Quadri N, Ananthakrishnan R, Furmansky M, Rosario R, Song F, Rai V, Weinberg A, Friedman R, Ramasamy R, D'Agati V, Schmidt AM. Deletion of the receptor for advanced glycation endproducts reduces glomerulosclerosis and preserves renal function in the diabetic OVE26 mouse. Diabetes. 2010; 59(8):2043-54.
Mariane Abdillahi, PhD
During my research studies at the Diabetes Research Program, I investigated the signal transduction mechanisms by which the aldose reductase (AR) pathway contributes to the vulnerability of the myocardium to ischemic challenge. I worked to elucidate whether AR pathway mediated ischemia-reperfusion (I/R) injury is linked to changes in GSK3 beta phosphorylation and to autophagy.
Studies have provided contrasting conclusions on whether induction of autophagy is protective during I/R. Therefore, my goal was to determine whether increased flux via AR influences autophagy induction during I/R injury. These research efforts were published in the American Journal of Physiology: Heart and Circulatory Physiology and shred insight into the mechanisms via which AR modulates changes in GSK3 beta phosphorylation and highlighted potential therapeutic targets for myocardial infarction.
I am currently continuing my research training at Columbia University. I am working to understand the role of triglycerides in metabolism and the pathogenesis of diabetic vascular disease. My long term goal is to employ my scientific training and communication skills to pursue a career in science policy with the aim of understanding how scientific research drives recommendations and implementation for public policies.
My email address is: firstname.lastname@example.org .
1. Abdillahi M, Ananthakrishnan R, Vedantham S, Shang L, Zhu Z, Rosario R, Zirpoli H, Gabbay K, Ramasamy R, Cardiac glycogen synthase kinase-3β phosphorylation is altered in human aldose reductase expressing mice during ischemia-reperfusion. Am J Physiol Heart Circ Physiol. 2012 Aug 1; 303(3):H297-308. doi: 10.1152/ajpheart.00999.2011. Epub 2012 Jun 1.
2. Shang L, Ananthakrishnan R, Li Q, Quadri N, Abdillahi M, Zhu Z, Qu W, Rosario R, Touré F, Yan SF, Schmidt AM, Ramasamy R. Rage modulates hypoxia/reoxygenation injury in adult murine cardiomyocytes via JNK and GSK 3 beta signaling pathways. PLoS One. 2010 Apr 9; 5(4):e10092. doi: 10.1371/journal.pone.0010092.
3. Geliebter A, Iching L, Abdillahi M, Jones J. Satiety following intake of potatoes and other carbohydrate test meals. Ann Nutr Metab. 2012 Dec 4; 62(1):37-43.
4. Book Chapter: Mariane Abdillahi & Ravichandran Ramasamy. Aldose Reductase and Diabetic Cardiovascular Disease in Diabetic Cardiomyopathy: Biochemical and Molecular Mechanisms. (In press)
Devi Thiagarajan, PhD
As a postdoctoral fellow in the Diabetes Research Program, my main focus was to understand the role of Aldose Reductase (AR) in mediating secondary complications in the heart and to underpinning the mechanisms related to it. My contribution was in delineating the epigenetic mechanisms associated with increased polyol pathway and how it results in ectopic lipid accumulation in the heart.
I am currently working as a research associate at University of Southern California, Los Angeles. My present work involves understanding the epigenetic events leading to increased susceptibility of the aging population to cancer. I am also interested in understanding the epigenetic mechanisms related to aging.
1. Vedantham S, Thiagarajan D, Ananthakrishnan R, Wang L, Rosario R, Zou YS, Goldberg I, Yan SF, Schmidt AM, Ramasamy R. Aldose reductase drives hyperacetylation of Egr-1 in hyperglycemia and consequent upregulation of proinflammatory and prothrombotic signals. Diabetes. 2014 Feb; 63(2):761-74.
2. Suri D, Veenit V, Sarkar A, Thiagarajan D, Kumar A, Nestler EJ, Galande S, Vaidya VA. Early stress evokes age-dependent biphasic changes in hippocampal neurogenesis, BDNF expression, and cognition. Biol Psychiatry. 2013 Apr 1; 73(7):658-66.
3. Thiagarajan D, Dev RR, Khosla S. The DNA methyltranferase Dnmt2 participates in RNA processing during cellular stress. Epigenetics. 2011 Jan; 6(1):103-13.
4. Sowpati DT, Thiagarajan D, Sharma S, Sultana H, John R, Surani A, Mishra RK, Khosla S. An intronic DNA sequence within the mouse Neuronatin gene exhibits biochemical characteristics of an ICR and acts as a transcriptional activator in Drosophila. Mech Dev. 2008 Nov-Dec; 125(11-12):963-73.
Karen O'Shea, PhD
As a postdoctoral fellow, the goal of my research was to investigate underlying signaling mechanisms in cardiomyocytes in response to ischemia/reperfusion injury. Previous studies by our laboratory have revealed a central role for the receptor for advanced glycation end-products (RAGE) in ischemia/reperfusion by contributing to subsequent oxidative stress and mitochondrial dysfunction. The RAGE cytoplasmic domain interacts with diaphanous-1 (mDia1), a member of the formin family, and an effector of Rho GTPases. With the other members of the Diabetes Research Program, I examined the role of RAGE and mDia1 signaling in mediating myocardial ischemia/reperfusion injury.
I am currently working as a Senior Scientist at Myologica, a contract research organization specializing in neuromuscular function and muscle phenotyping. My goal is to apply the laboratory skills I have acquired as a postdoctoral fellow to being a successful scientist at this company.
My email address is: email@example.com 
1. Daffu G, del Pozo CH, O'Shea KM, Ananthakrishnan R, Ramasamy R, Schmidt AM. Radical roles for RAGE in the pathogenesis of oxidative stress in cardiovascular diseases and beyond. Int J Mol Sci. 2013 Oct 1;14(10):19891-910. doi: 10.3390/ijms141019891. Review.
2. Ananthakrishnan R, Li Q, O'Shea KM, Quadri N, Wang L, Abuchowski A, Schmidt AM, Ramasamy R. Carbon monoxide form of PEGylated hemoglobin protects myocardium against ischemia/reperfusion injury in diabetic and normal mice. Artif Cells Nanomed Biotechnol. 2013 Dec;41(6):428-36. doi: 10.3109/21691401.2012.762370. Epub 2013 Jan 23.
3. Abel ED, O'Shea KM, Ramasamy R. Insulin resistance: metabolic mechanisms and consequences in the heart. Arterioscler Thromb Vasc Biol. 2012 Sep;32(9):2068-76. doi: 10.1161/ATVBAHA.111.241984.Review.
4. Papanicolaou KN, Khairallah RJ, Ngoh G, Chikando A, Luptak I, O’Shea KM, Riley DD, Lugus JJ, Colucci WS, Lederer WJ, Stanley WC, and Walsh K. Mitofusin-2 maintains mitochondrial structure and contributes to stress-induced permeability transition in cardiac myocytes. Mol Cell Biol 2011 31:1309-28.
5. Hecker PA, O’Shea KM, Galvao TF, Brown BH, and Stanley WC. Role of adiponectin in the development of high-fat diet-induced metabolic abnormalities in mice. Horm Metab Res 2011 43:100-5.
6. O'Shea KM, Chess DJ, Khairallah RJ, Hecker P, Lei B, Walsh K, Des Rosiers C, and Stanley WC. ω-3 polyunsaturated fatty acids prevent pressure overload-induced ventricular dilation and decrease in mitochondrial enzymes despite no change in adiponectin. Lipids Health Dis 2010 9:95.
7. Khairallah RJ, O’Shea KM, Brown BH, Khanna N, Des Rosiers C, and Stanley WC. Treatment with docosahexaenoic acid, but not eicosapentaenoic acid, delays Ca2+-induced mitochondrial permeability transition in normal and hypertrophied myocardium. J Pharmacol Exp Ther 2010 335:155-162.
8. Khairallah RJ, Sparagna GC, Khanna N, O’Shea KM, Hecker PA, Des Rosiers C, Fiskum G, and Stanley WC. Dietary supplementation with docosahexaenoic acid, but not eicosapentanoic acid, profoundly remodels cardiac mitochondrial phospholipid fatty acid composition and prevents permeability transition. Biochim Biophys Acta 2010 1797:1555-1562.
9. O’Shea KM, Chess DJ, Khairallah RJ, Rastogi S, Hecker PA, Sabbah HN, Walsh K, and Stanley WC. Adiponectin plays a permissive role for structural and metabolic remodeling in mice subjected to pressure overload. Am J Physiol Heart Circ Physiol 2010 298:H1639-45.
10. Chess DJ, Khairallah RJ, O’Shea KM, Xu W, and Stanley WC. Dietary fat-induced adiposity elevates leptin, prevents down regulation of mitochondrial oxidative enzymes, and does not worsen cardiac dysfunction in response to pressure overload. Am J Physiol Heart Circ Physiol 2009 297:H1585-93.
11. O’Shea KM, Khairallah RJ, Sparagna GC, Xu W, Hecker PA, Robillard-Frayne I, Des Rosiers C, Kristian T, Murphy RC, Fiskum G, and Stanley WC. Dietary ω-3 fatty acids alter cardiac mitochondrial phospholipid composition and delay Ca2+-induced permeability transition. J Mol Cell Cardiol 2009 47:819-27.
12. Shah KB, Duda MK, O’Shea KM, Sparagna GC, Chess DJ, Khairallah RJ, Frayne-Robillard I, Xu W, Murphy RC, Des Rosiers C, and Stanley WC. High fat intake alters cardiac phospholipid composition and prevents cardioprotection with fish oil during pressure overload. Hypertension 2009 54:605-11.
13. Duda MK, O’Shea KM, and Stanley WC. Omega-3 polyunsaturated fatty acid supplementation for the treatment of heart failure: mechanisms and clinical potential. Cardiovasc Res 2009 84:33-41.
14. Duda MK, O'Shea KM, Tintinu A, Xu W, Khairallah RJ, Barrows BR, Chess DJ, Azimzadeh AM, Harris WS, Sharov VG, Sabbah HN, and Stanley WC. Fish oil, but not flaxseed oil, decreases inflammation and prevents pressure overload-induced cardiac dysfunction. Cardiovasc Res 2009 81:319-27.
15. Chess DJ, Xu W, Khairallah R, O'Shea KM, Kop WJ, Azimzadeh AM, and Stanley WC. The antioxidant tempol attenuates pressure overload-induced cardiac hypertrophy and contractile dysfunction in mice fed a high-fructose diet. Am J Physiol Heart Circ Physiol 2008 295:H2223-30.
16. Lei B, Chess DJ, Keung W, O'Shea KM, Lopaschuk GD, and Stanley WC. Transient activation of p38 MAP kinase and up-regulation of Pim-1 kinase in cardiac hypertrophy despite no activation of AMPK. J Mol Cell Cardiol 2008 45:404-10.
17. Duda MK, O’Shea KM, Lei B, Barrows BR, Azimzadeh A, McElfresh TE, Hoit BD, Kop WJ, and Stanley WC. Low carbohydrate/high fat diet attenuates pressure overload induced ventricular remodeling and dysfunction. J Card Fail 2008; 14:327-35.
18. Duda MK, O'Shea KM, Barrows BR, Lei B, Azimzadeh A, McElfresh TE, Hoit BD, and Stanley WC. Dietary supplementation with ω-3 polyunsaturated fatty acids increases plasma adiponectin and prevents ventricular remodeling and dysfunction with pressure overload. Cardiovasc Res 2007;76:303-310.
19. King KL, Young ME, Kerner J, Huang H, O’Shea KM, Alexson SEH, Hoppel CL, and Stanley WC. Diabetes and activation of peroxisome proliferator activated receptor α selectively up-regulate mitochondrial thioesterase I activity and protein expression in the heart. J Lipid Res 2007;48:1511-1517.
20. Sharma N, Okere IC, Duda MK, Chess DJ, O'Shea KM, and Stanley WC. Potential impact of carbohydrate and fat intake on pathological left ventricular hypertrophy. Cardiovasc Res 2007;73:257-268.