Obesity and Metabolism Research Unit : People & Places

Ph.D., Department of Pharmacology and Toxicology

University of California, Davis

Office:      430 West Health Sciences Dr.

                University of California

                Davis, CA 95616



Phone:    (530) 752-1009

Fax:        (530) 752-5271

Newman Lab

Biography

Dr. John Newman is an avid collaborator with researchers in the WHNRC, the U.S., and abroad who brings expertise in analytical biochemistry, state-of-the-art analytical instrumentation and the use of metabolomics to the WHNRC. Dr. Newman is applying these tools to determine the impact of diet and dietary components on human health, with a special emphasis given to the obesity problem and its complications associated with the high fat “Western” diet.

Dr. Newman is a California native who has received higher education in Colorado and California. He obtained a baccalaureate degree in biochemistry and molecular biology from the University of California Santa Cruz in 1991, worked extensively in the field of environmental analytical chemistry until 1996, obtained a Ph.D. in pharmacology and toxicology from the University of California, Davis in 2002, and worked as a Research Associate at UC Davis until 2005 exploring the biomedical applications of eicosanoid metabolic profiling. He has extensive experience in trace organic quantitative chemistry, data quality assessment and quality control, analytical method development, as well as modest skills in chemical synthesis and technical experience with a range of state-of-the-art analytical instrumentation: NMR spectroscopy (1H, 13C, 15N, 19F); gas and liquid chromatographic systems (GC, GPC/SEC, FPLC, GPLC, UPLC); gel electrophoresis; mass spectroscopy (MALDI-TOF-MS, API-TOF-MS, API-MS, API/MS/MS). He has applied spectroscopic analysis to support structural confirmation of synthetic products, structural elucidation of unknown products, identification of protein modification, and quantitation of both exogenous and endogenous molecules isolated from an array of biological matrices. Dr. Newman has focused these efforts on the development and application of analytical tools to profile a broad range of lipids with important roles in the regulation of inflammation, vascular and renal function, and cellular growth.

Investigations surrounding the endogenous role of the soluble epoxide hydrolase were at the root of these investigations. They have since expanded to encompass products of the major lipid oxygenases including prostanoids and various eicosanoids as well as analogous materials generated for eighteen and twenty-two carbon lipids. These analytical profiling efforts have more recently broadened to investigate other bioactive lipid mediators involved in the regulation of energy balance and body mass, including a suite of endocannabinoids. The role of these regulatory pathways have been explored in inflammation, renal function, vascular regulation and disease, blood pressure regulation and both male and female reproductive physiology. More recently, these tools have been turned on the lipoprotein particle, and subtle structural changes in these particles are beginning to be observed.

During his research career, Dr. Newman has written or supported more than 60 articles in peer-reviewed journals. He has served as a peer reviewer for an array of journals including the American Journal of Clinical Nutrition, the British Journal of Nutrition, the Journal of Chromatography, Archives in Biochemistry and Biophysics, Chemosphere, Proteomics, and Metabolomics. In addition, Dr. Newman is a member in good standing in the Metabolomics Society and the American Chemical Society.

Research Program

Overview:

The Newman laboratory research program is investigating the impact of dietary lipids on process associated with obesity and inflammation, how these effects alter the structure and function of lipoprotein particles, and how these cumulative changes produce coordinated changes in tissue lipid metabolism and signaling. At the heart of this research is an effort to understand whether fine-tuning an individual’s dietary lipid intake can improve body weight and health beyond those recommended to the general population by the U.S. Dietary Guidelines. To achieve these goals, the group combines high information content analytical chemistry with biochemistry, human interventions, as well as cell and molecular biology to investigate the impact of dietary lipid content and composition on PPAR-dependent signaling, inflammatory status, adipocyte growth and differentiation, and changes in systemic eicosanoid and endocannabinoid system tones. These research goals promise to extend and complement the WHNRC’s impact in the area of dietary fats on health outcomes accomplished by previous ARS scientists Drs. Iacono, Nelson, Kelly and Hwang over the past 40 years.

Specific Research Areas

Do lipoprotein particles deliver bioactive lipids to peripheral tissues? A central hypothesis being tested in the laboratory is that lipoprotein particles transport bioactive signaling lipids to peripheral tissues, influencing homeostatic set points, and that this process is influenced by dietary lipid compositions. With the exception of small free fatty acid and lyso-phosphotide pools associated with albumin, plasma lipids are esterified within lipoproteins, where apolipoproteins facilitate systemic lipid trafficking. Moreover, the dietary saturated/monounsaturated/polyunsaturated fatty acid balance has significant impacts on the structure and function of lipoprotein particles and lipid trafficking, with consequences on vascular health. For instance, high omega-3 fatty acid consumption can have both anti-inflammatory and anti-hypertriglyceridemic cardioprotective effects. In obese animals, high n3 LC-PUFA diets can also reduce weight and hypothalamic drivers of hunger, while increasing anorexigenic adipokine production, and improve central sensitivity to these adipokines. While LpL-mediated lipolysis dominates VLDL clearance, whole particle uptake of VLDL₁ accounts for 20-30% of clearance in normolipidemic humans, and dominates LDL and HDL clearance. Moreover, fish oil feeding increases adipose expression of the oxo-LDL receptor CD36 through the PPAR-γ dependent mechanisms. Since cell growth and differentiation is influenced by PUFA metabolites, including eicosanoids and endocannabinoids produced within cells, delivery of these agents preformed to cells could have profound effects on cellular homeostasis. Our earlier studies have shown that obesity increases concentrations of oxygenated lipids esterified into lipoprotein particles, that these lipids are released by lipoprotein lipase, and their release is associated with a postprandial inflammatory response in the vascular endothelium. In addition, we have seen that n3 LC-PUFA supplementation significantly alters the profiles of circulating oxygenated PUFAs. Current efforts in the laboratory are designed to evaluate the ramifications of these altered lipoprotein structures on the function of exposed cellular systems including vascular and adipose cell types.

Does variance in LC-PUFA biosynthesis influence the efficacy of dietary fish oil? Dietary PUFAs in the United States are rich in linoleic (LA; 18:2n6) and alpha-linolenic (ALA; 18:3n3) acids, essential fatty acid precursors to the long chain (i.e. ≥ twenty carbon) n6 and n3 PUFAs (LC-PUFAs). LC-PUFA biosynthesis greatly outweighs their dietary intake in most individuals, but these rates vary, being influenced by lipid consumption, gender, and genetic polymorphisms. How LC-PUFA biosynthetic efficiency impacts the beneficial effects of n3 LC-PUFA consumption is not known, but responses to fish oil feeding also vary. We hypothesize that those individuals with reduced LC PUFA biosynthetic capacity may be more sensitive to the therapeutic effects of a high fish oil diet and are testing this hypothesis with both retrospective and prospective studies. To approach these questions, we are investigating product:substrate ratios of metabolic intermediates as indices of LC-PUFA biosynthesis in human, focusing on markers of elongase activity (i.e. 22:5n3/20:5n3 + 22:6n6/20:4n6) in red blood cell phospholipids. We have found that these markers increase as the LC‑PUFA n6/n3 ratio increases (n=768; p<0.0001), findings consistent with reports that high n6 PUFA diets inhibit the conversion of 18:3n3 to 20:5n3. However, on inspection of other product:substrate ratios, apparent differences in LC‑PUFA handling are seen. In particular, the variance in elongase (ELO) activity increases as the n6:n3 ratio increases. Also, the frequency distributions of the LC-PUFA n6/n3, LC‑ELO index and a delta-5 desaturase (D5D) index are all bimodal yet unique. Current efforts in the lab are focused on understanding the interactions between these metabolic phenotypes and individual responses to fish oil interventions.

Selected Publications & Patent Applications

1.            Psychogios, N., D.D. Hau, J. Peng, A.C. Guo,R. Mandal, S. Bouatra, I. Sinelnikov, R. Krishnamurthy, R. Eisner, B. Gautam, N. Young, J. Xia, C. Knox, E. Dong, P. Huang, J. McManus, T.L. Pedersen, F. Bamforth, R. Greiner, B. McManus, J.W. Newman, D.S. Wishart. 2011. The human serum metabolome. PLOS One. 6(2):e16857.

2.            Stephensen, C.B., P. Armstrong, J.W. Newman, T.L. Pedersen, J. Legault, G. Schuster, D. Kelley, S. Vikman, J. Hartiala,H. Allayee. 2011. ALOX5 gene variants affect eicosanoid production and response to fish oil supplementation. J. Lipid Res. Feb 4. [Epub ahead of print]

3.            Hartiala, J., D. Li, D.V. Conti, S. Vikman, Y. Patel, W.H.W. Tang, M-L. Brennan, J.W. Newman, C.B. Stephensen, P. Armstrong, S.L. Hazen, H. Allayee. 2011. Genetic contribution of the leukotriene pathway to coronary artery disease.   Hum. Genet. DOI 10.1007/s00439-011-0963-3

4.            Gertow, K., E. Nobili, L. Folkersen, J.W. Newman, T.L. Pedersen, G. Paulsson-Berne, U. Hedin, J. Swedenborg, H. Kühn, C.E. Wheelock, G.K. Hansson, J.Z. Haeggström, A. Gabrielsen. 2011. Expression of 12- and 15-lipoxygenase mRNAs in human carotid atherosclerotic lesions: associations with cerebrovascular symptoms. Atherosclerosis. Accepted Jan, 2011. Epub Feb 2011.

5.            Bendsen, N.T., E. Chabanova, H.S. Thomsen, T.M. Larsen, J.W. Newman, S. Stender, J. Dyerberg, S.B. Haugaard, A. Astrup. 2011. Trans fatty acids adversely affect blood lipids but not intra-abdominal and liver fat deposition in overweight postmenopausal women. Nutr. Diab. 1: e4;

6.            Fiehn O., W.T. Garvey, J.W. Newman, K.H. Lok, C.L. Hoppel, S.H. Adams. 2010. The plasma metabolome of obese african-american type 2 diabetic and non-diabetic women: unique metabolite and amino acid signatures reflective of diabetes status and associated with markers of metabolic homeostasis. PloS One. 5(12):e15234.

7.            Stumbo, P., R. Weiss, J.W. Newman, J.A. Pennington. K.L. Tucker, P.L. Wiesenfield, A-K. Illner, D.M. Klurfeld, J. Kaput. 2010. Web-enabled and improved software tools and data are needed to measure nutrient intakes and physical activity for personalized health research. J. Nutr. E pub. Oct 27,2010. doi: 10.3945/jn.110.128371.

8.            Van Erk, M.J., S. Wopereis, C. Rubingh, T. van Vliet, E. Verheij, N.H.P. Cnubben, T. L. Pedersen, J.W. Newman, A.K.Smilde, J. van der Greef, H.F.J. Hendriks, B. van Ommen. 2010. Insight in modulation of inflammation in response to diclofenac intervention: a human intervention study. BMC Medical Genomics. 3(5).

9.            Shearer, G.C.,J.W. Newman. 2009. Impact of circulating esterified eicosanoids and other oxylipins on endothelial function. Curr. Atheroscler. Rep. 11(6):403-10.

10.        Shearer, G.C.,W.S. Harris, T.L. Pedersen, J.W. Newman. 2010. Detection of omega-3 oxylipins in human plasma and response to treatment with omega-3 acid ethyl esters. J. Lipid Res. 51(8): 2074-81. [EPub Aug, 2009].

11.    Adams, S.H., C.L. Hoppel, K. Lok, L. Zhao, S. Wong, P.E. Minkler, D.H. Hwang,J.W Newman, W.T. Garvey. 2009. Plasma acylcarnitine profiles suggest incomplete fatty acid β-oxidation and altered TCA cycle activity in type 2 diabetes. J. Nutr. 139(6):1073-81.

12.        Paulino, G., C.B. de la Serre, T. Knotts, P. Oort, J.W. Newman, S. Adams, H. Raybould. 2009. Increased expression of receptors for orexigenic factors in nodose ganglion of diet-induced obese rats. Am J Physiol Endocrinol Metab 296:898-903, 2009. First published Feb 3, 2009.

13.        Shearer, G.C, J.W. Newman. 2008. Lipoprotein lipase liberates esterified oxylipins from very low-density lipoproteins. Prostaglandins Leukot. Essent. Fatty Acids. 79(6):215–22.

14.    Wang, L., R. Gill, T.L. Pedersen, J.W. Newman, J.C. Rutledge. 2009. Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized free fatty acids that induce endothelial cell inflammation. J. Lipid Res. 50(2):204-13 [EPub Sept, 2008].

15.        Sanchez-Mejia, R.S., J.W. Newman, S. Toh, G-Q. Yu, Y. Zhou, K. Scearce-Levie, I.H. Cheng, L. Gan, J.J. Palop, J.V. Bonventre, L. Mucke. 2008. Phospholipase A2 reduction ameliorates cognitive deficits in mouse model of Alzheimer’s disease. Nat Neurosci. 11(11):1311-8.

16.        Kim, S.I., C.B. Andaya, J.W. Newman, S.S. Goyal, T.H. Tai. 2008. Isolation and characterization of a low phytic acid rice mutant reveals a mutation in the rice orthologue of maize MIK. Theor. Appl. Genet. 117(8):1291-301.

17.        Athirakul, K., J. A. Bradbury, J.P. Graves, L.M. DeGraff, J. Ma, Y. Zhao, J.F. Couse, R. Quigley, D.R. Harder, X. Zhao, J.D. Imig, T.L. Pedersen, J.W. Newman, B.D. Hammock, A.J. Conley, K.S. Korach, T.M. Coffman, D.C. Zeldin. 2008. Increased blood pressure in mice lacking cytochrome P450 2J5. FASEB. 22(12):4096-108 [EPub. Aug 2008].

18.        Olearczyk, J.J., J.E. Quigley, B.C. Mitchell, T. Yamamoto, I-H. Kim, J.W. Newman, A. Luria, B.D. Hammock, J.D. Imig. 2009. Administration of a substituted adamantly-urea inhibitor of the soluble epoxide hydrolase protects the kidney from damage in hypertensive Goto-Kakizaki rats. Clin. Sci. (Lond). 116:61-70 [EPub May 7, 2008].

19.        Morisseau, C., J.W. Newman, C.E. Wheelock, T. Hill, D. Morin, A.R. Buckpitt, B.D. Hammock. 2008. Development of metabolically stable inhibitors of mammalian microsomal epoxide hydrolase. Chem. Res. Toxicol. 21(4):951-7.

20.        Driesbach, A., J.C. Rice, S. Japa, J.W. Newman, A. Sigel, R.S. Gill, A.E. Hess, B.D. Hammock, J.J.L. Lertora, L.L. Hamm. 2008. Salt loading increases urinary excretion of linoleic acid diols and triols in healthy human subjects. Hypertension. 51:755-761.

21.        Wheelock, C.E., J. Forshed, S. Goto, B.D. Hammock, J.W. Newman. 2008. Effects of pyridine exposure upon structural lipid metabolism in Swiss Webster mice. Chem. Res. Toxicol. 21(3):583-90.

22.        Vogel, C.F.A., W. Li, J.W. Newman, B.D. Hammock, J. Tuscano, F. Matsumura. 2007. Pathogenesis of Ah-Receptor mediated development of lymphoma is associated with increased Cyclooxygense-2 expression. Am J Pathol. 171(5):1538-48.

23.        Newman, J.W., B.D. Hammock, G.A. Kaysen, G.C. Shearer. 2007. Proteinuria increases oxylipid concentrations in VLDL and HDL, but not LDL particles in the rat. J. Lipid Res. 48(8):1792-800.

24.        Wheelock, C.E., S. Goto, B.D. Hammock, J.W. Newman. 2007. Clofibrate-induced changes in the liver, heart, brain and white adipose lipid metabolome of Swiss-Webster mice. Metabolomics. 3(2):137-145.

25.    Luria, A., S.M. Weldon, A.K. Kabcenell, R.H. Ingraham, D. Matera, R. Gill, C. Morisseau, J.W. Newman , B.D. Hammock. 2007. Compensatory mechanism for homeostatic blood pressure regulation in Ephx2 gene disrupted mice. J Biol Chem. 282(5):2891-2898.

26.        Morisseau, C., J.W. Newman, H.-J. Tsai, P.A. Beacker, B.D. Hammock. 2006. Peptidyl-urea based inhibitors of soluble epoxide hydrolases. Bioorg Med Chem Lett. 16:5439-5444.

27.        Seubert, J.M., C.J. Sinal, J.P. Graves, L.M. DeGraff, C.R. Lee, K.B. Goralski, M.A. Carey, A.H. Luria, J.W. Newman, B.D. Hammock, H. Roberts, H.A. Rockman, E. Murphy, D.C. Zeldin. 2006. Role of soluble epoxide hydrolase in post-ischemic recovery of heart contractile function. Circ Res. 99(4):442-450.

28.        Lee, C.R. K.E. North, M.S. Bray, M. Fornage, J.M. Seubert, J.W. Newman, B.D. Hammock, D.J. Couper, G. Heiss, D.C. Zeldin. 2006. Genetic variation in soluble epoxide hydrolase (EPHX2) and risk of coronary heart disease: an Atherosclerosis Risk in Communities (ARIC) study. Human Molec Genetics. 15(10):1640-1649.

29.        Kelley, D.S.,G.L. Bartolini, J.W. Newman, M. Vemuri, B.E. Mackey. 2006. Fatty acid composition of liver, adipose tissue, spleen, and heart of mice fed diets containing t10,c12-, and c9,t11-conjugated linoleic acid. Prostaglandins Leukot Essent Fatty Acids. 74(5):331-338.

30.        Davis, B.B., C. Morisseau, T. Pedersen, J.W. Newman, B.D. Hammock, R.H. Weiss. 2006. Attenuation of vascular smooth muscle cell proliferation by 1-cyclohexyl-3-dodecyl urea is independent of soluble epoxide hydrolase inhibition. J Pharmacol Exp Ther. 316(2):815-821.

31.        Dorrance, A.M., N. Rupp, D.M. Pollock, J.W. Newman, B.D. Hammock, J.D. Imig. 2005. An epoxide hydrolase inhibitor, 12-(3-adamantan-1-yl-ureido) dodecanoic Acid (AUDA), reduces ischemic cerebral infarct size in stroke-prone spontaneously hypertensive rats. J Cardiovasc Pharmacol. 46(6):842-846.

32.        Imig, JD., X. Zhao, C.Z. Zaharis, J.J. Olearczyk, D.M. Pollock, J.W. Newman, I-H. Kim, T. Watanabe, B.D. Hammock. 2005. An orally active epoxide hydrolase inhibitor lowers blood pressure and provides renal protection in salt-sensitive hypertension. Hypertension. 46(4): 975-81.

33.        Tran, K.L., P.A. Aronov, H. Tanaka, J.W. Newman, B.D. Hammock, C. Morisseau. 2005. Lipid sulfates and sulfonates are allosteric competitive inhibitors of the N-terminal phosphatase activity of the mammalian soluble epoxide hydrolase. Biochemistry. 44(36): 12179-87.

34.        Schmelzer, K., L. Kubala, J. Eiserich, J.W. Newman, B.D. Hammock. 2005. Soluble epoxide hydrolase is a therapeutic target for acute inflammation. PNAS. 102(28):9772-77.

35.        Shearer, G.C., J.W. Newman, B.D. Hammock, G.A. Kaysen. 2005. The graded effects of proteinuria on HDL structure in nephrotic rats. J Am Soc Nephrol. 16:1309-19.

36.        Newman, J.W., C. Morisseau, B.D. Hammock. 2005. Epoxide hydrolases: Their role and interactions with lipid metabolism. Prog Lipid Res. 44:1-51.

37.        Newman J.W., Stok J.E., Vidal J.D., Corbin C.J., Huang Q., Hammock B.D., Conley AJ. 2004. Cytochrome p450-dependent lipid metabolism in preovulatory follicles. Endocrinology 145:5097-105.

38.        Seubert, J., B. Yang, A. Bradbury, J. Graves, L. Miller, S. Gabel, R. Gooch, J. Foley, J. Newman, L. Mao, H.A. Rockman, B.D. Hammock, E. Murphy, D.C. Zeldin. 2004. Enhanced postischemic functional recovery in CYP2J2 transgenic hearts involves mitochondrial ATP-sensitive K⁺ channels and p42/p44 MAPK pathway. Circ Res 95:506-14.

39.        Dey, A., R.S. Williams, D.M. Pollock, D.W. Stepp, J.W. Newman, B.D. Hammock, J.D. Imig. 2004. Altered kidney CYP2C and cyclooxygenase-2 levels are associated with obesity-related albuminuria. Obes Res 12:1278-89.

40.        Zhao, X., T. Yammamoto, J.W. Newman, I-H. Kim, T. Watanabe, B.D. Hammock, J. Stewart, J.S. Pollock, D.M. Pollock, J.D. Imig. 2004. Soluble epoxide hydrolase inhibition protects the kidney from hypertension-induced damage. J Am Soc Nephrol. 15:1244-1253.

41.       DuTeaux, S.B., J.W. Newman, C. Morisseau, E.A. Fairbairn, K. Jelks, B.D. Hammock, M.G. Miller. 2004. Epoxide hydrolases in the rat epididymis: Possible roles in xenobiotic metabolism and endogenous fatty acid metabolism. Toxicol Sci. 78: 187-195.

42.        Sather, P.J., J.W. Newman, M.G. Ikonomou. 2003. Congener based Aroclor quantification and speciation techniques – A comparison of the strengths, weaknesses, and proper use of two alternative approaches. Environ Toxicol Chem. 37: 5678-5686.

43.    Vishwanathan, S., B.D. Hammock, J.W. Newman, P. Meerarani, M. Toborek, B.Hennig. 2003. Involvement of CYP 2C9 in mediating the proinflammatory effects of linoleic acid in vascular endothelial cells. J Am Coll Nutr. 22(6):502-510.

44.        Koivunen, M.E., C. Morisseau, J.W. Newman, W.R. Horwath, B.D. Hammock. 2003. Purification and characterization of a methylene urea-hydrolyzing enzyme from Rhizobium radiobacter (Agrobacterium tumefaciens). Soil Biol Biochem. 35: 1433-1442.

45.        Watanabe, T., C. Morisseau, J.W. Newman, B.D. Hammock. 2003. In vitro metabolism of the mammalian soluble epoxide hydrolase inhibitor 1-cyclohexyl-3-dodecyl-urea. Drug Metab Dispos. 31(7): 846-853.

46.        Newman, J.W., C. Morisseau, T.R. Harris, B.D. Hammock. 2003. The soluble epoxide hydrolase encoded by EPXH2 is a bifunctional enzyme with novel lipid phosphate phosphatase activity. Proc Nat Acad Sci USA. 100(4):1558-63.

47.        Newman, J.W., T. Watanabe, B.D. Hammock. 2002. The simultaneous quantification of cytochrome P450 dependent linoleate and arachidonate metabolites in urine by high-performance liquid chromatography - tandem mass spectroscopy. J Lipid Res. 43:1563-1578.

48.        Wheelock, C.E., T.A. Baumgartner, J.W. Newman, M.F. Wolfe, R.S. Tjeerdema. 2002. Effect of nutritional state on Hsp60 levels in the rotifer Brachionus plicatilis following toxicant exposure. Aquatic Toxicol. 61(1-2):89-93.

49.        Morisseau, C., M.H. Goodrow, J.W. Newman, C.E. Wheelock, D.L. Dowdy, B.D. Hammock. 2002. Structural refinement of urea based soluble epoxide hydrolase inhibitors. Biochem Pharmacol. 63(9):1599-1608.

50.        Watkins, S.M., B.D. Hammock, J.W. Newman, J.B. German. 2001. Individual metabolism should guide agriculture toward foods for improved health and nutrition. Am J Clin Nutr. 74(3):283-6.

51.        Newman, J.W., and B.D. Hammock. 2001. Optimized thiol derivatizing reagent for the mass spectral analysis of disubstituted epoxy fatty acids. J Chromatogr A. 925(1-2):223-40.

52.        Hunt, J.W., B.S. Anderson, B.M. Phillips, J. Newman, R.S. Tjeerdema, R. Fairey, H.M. Puckett, M. Stephenson, R.W. Smith, C.J. Wilson, and K.M. Taberski. 2001. Evaluation and use of sediment toxicity reference sites for statistical comparisons in regional assessments. Environ Toxicol Chem. 20(6):1266-1275.

53.        Morisseau, C., J.W. Newman, D.L. Dowdy, M.H. Goodrow and B.D. Hammock. 2001. Inhibition of microsomal epoxide hydrolases by ureas, amides and amines. Chem Res Toxicol. 14:409-415.

54.        Slim, R., B.D. Hammock, M. Toborek, L.W. Robertson, J.W. Newman, C.H.P. Morisseau, B.A. Watkins,V. Saraswathi, and B. Hennig. 2001. The role of methyl-linoleic acid epoxide and diol metabolites in the amplified toxicity of linoleic acid and polychlorinated biphenyls to vascular endothelial cells. Toxicol Appl Pharmacol. 171(3):184-193.

55.        Anderson, B.S., J.W. Hunt, B.M. Phillips, R. Fairey, H.M. Puckett, M. Stephenson, K. Taberski, J. Newman, R.S. Tjeerdema. 2001. Influence of sample manipulation on contaminant flux and toxicity at the sediment-water interface. Mar Environ Res. April, 2001. 51(3):191-211.

56.        Newman, J.W., D.L. Denton, C. Morisseau, C.S. Koger, C.E. Wheelock, D.E. Hinton and B.D. Hammock. 2001. Evaluation of fish models of soluble epoxide hydrolase inhibition. Environ Health Persp. 109(1):61-66.

57.        Yu, Z., F. Xu, L.M. Huse, C. Morisseau, A.J. Draper, J.W. Newman, C. Parker, L. Graham, M.M. Engler, B.D. Hammock, D.C. Zeldin and D.L. Kroetz. 2000. Soluble epoxide hydrolase regulates hydrolysis of vasoactive epoxyeicosatrienoic acids. Circ Res. 87(11):992-998.

58.        Morisseau, C., J.K. Beetham, F. Pinot, S. Debernard, J.W. Newman and B.D. Hammock. 2000. Cress and potato soluble epoxide hydrolases: Purification, biochemical characterization, and comparison to mammalian enzymes. Arch. Biochem. Biophys. 378(2):321-332.

59.        Greene, J.F., J.W. Newman, K.C. Williamson, and B.D. Hammock. 2000. Toxicity of epoxy fatty acids and related compounds to cells expressing human soluble epoxide hydrolase. Chem Res Toxicol. 13(4):217-226.

60.        Greene, J.F., K.C. Williamson, J.W. Newman, C. Morisseau, and B.D. Hammock. 2000. Metabolism of monoepoxides of methyl linoleate: bioactivation and detoxification. Arch Biochem Biophys. 376(2):420-432.

61.        Newman, J.W., J.S. Becker, G. Blondina, and R.S. Tjeerdema. 1998. Quantitation of Aroclors using congener specific results. Environ Toxicol Chem. 17(11):2159-2167.

62.        Morisseau, C., G. Du, J.W. Newman, and B. D. Hammock. 1998. Mechanism of mammalian soluble epoxide hydrolase inhibition by chalcone oxide derivatives. Arch Biochem Biophys. 356(2):214-228.

63.        Fairey R., C. Roberts, M. Jacobi, S. Lamerdin , R. Clark , J. Downing, E. Long, J. Hunt, B. Anderson, J. Newman, R. Tjeerdema, M. Stephenson, and C. Wilson. 1998. Assessment of sediment toxicity and chemical concentrations in the San Diego Bay Region, California, USA. Environ Toxicol Chem. 17(8):1570-1581. ://000075130900019

64.        Anderson, B.S., J.W. Hunt, B.M. Phillips, S. Tudor, R. Fairey, J. Newman, H.M. Puckett, M. Stephenson, E.R. Long, R.S. Tjeerdema. 1998. Comparison of marine sediment toxicity test protocols for the amphipod Rhepoxynius abronius and the polychaete worm Nereis (Neanthes) arenaceodentata. Environ Toxicol Chem. 17(5):859-866.

65.        Fairey R., K. Taberski , S. Lamerdin , E. Johnson , R.P. Clark , J.W. Downing, J. Newman and M. Petreas. 1997. Organochlorines and other environmental contaminants in muscle tissue of sportfish collected from San Francisco Bay. Mar Pollut Bull. 34: 1058-1071.

66.        Beckmen, K.B., L.J. Lowenstine, J. Newman, J. Hill, K. Hanni, and J. Gerber. 1997. Clinical and pathological characterization of northern elephant seal skin disease. J Wildlife Dis. 33(3):438-449.

67.        Hunter, C. L., M.D. Stephenson, R.S. Tjeerdema, D.G. Crosby, G.S. Ichikawa, J.D. Goetzl, K.M. Paulson, D.B. Crane, M. Martin, and J.W. Newman. 1995. Contaminants in oysters in Kaneohe Bay, Hawaii. Mar Pollut Bull. 30: 646-654.

68.        Newman, J.W., J. Vedder, W.M. Jarman, and R.R. Chang. 1994. A method for the determination of environmental contaminants in living marine mammals using microscale samples of blubber and blood. Chemosphere 28: 1795-1805.

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