CURRICULUM VITAE TRAVIS W. HEIN, Ph.D. CONTACT INFORMATION
TAMUSCOM Medical Research Building, Room 106E
EDUCATION Postdoctoral Texas A&M University System Health Science Center. Field of Study:Training
Cardiovascular Physiology, Microcirculatory Control. Mentors: Drs. Lih Kuo and
Mariappan Muthuchamy (September 1997-August 1999).
Medical Sciences, Texas A&M University System Health Science Center,College Station, Texas. Major field: Medical Sciences. Mentor: Dr. Lih Kuo. Dissertation Title: “Low-density lipoproteins impair coronary arteriolar function.”(August 1997).
St. Olaf College, Northfield, Minnesota. Major field: Biology. (May 1992).
Onalaska High School, Onalaska, Wisconsin. (May 1988). PROFESSIONAL POSITIONS Current 2003-present Assistant Professor, Department of Surgery, Division of Ophthalmology, Scott &
White Memorial Hospital, College of Medicine, Texas A&M University SystemHealth Science Center, Temple, Texas
Previous
Research Assistant Professor, Department of Medical Physiology, College ofMedicine, Texas A&M University System Health Science Center, CollegeStation, Texas
Assistant Research Scientist, Department of Medical Physiology, College ofMedicine, Texas A&M University System Health Science Center, CollegeStation, Texas
Postdoctoral Research Associate, Department of Medical Physiology, College ofMedicine, Texas A&M University System Health Science Center, CollegeStation, Texas
Graduate Assistant, Department of Medical Physiology, College of Medicine,Texas A&M University System Health Science Center, College Station, Texas
TEACHING RESPONSIBILITIES
2001-present Advanced Cardiovascular Biology I (MPHY 604); Department of Medical
Physiology; Texas A&M University System Health Science Center
Cardiovascular Sciences (MSCI 689); Department of Medical Physiology; TexasA&M University System Health Science Center
RESEARCH INTERESTS ∑ Cellular and molecular mechanisms of adenosine-induced dilation in the microcirculation
∑ Physiology and pathophysiology of coronary and retinal microcirculation
∑ Mechanisms involved in microvascular control of chronic inflammation
∑ Neurogenic regulation of microvascular blood flow
∑ Influence of exercise on coronary microcirculation
∑ Metabolic regulation of microvascular blood flow
∑ Nitric oxide and microvascular function
SOCIETY MEMBERSHIP
1998-present The Microcirculatory Society1998-present American Heart Association, Council on Basic Cardiovascular Sciences2000-present The American Physiological Society2003-present The Association for Research in Vision and Ophthalmology
INVITED PRESENTATIONS-NATIONAL MEETINGS
Presented: “Characterization of adenosine receptor-mediated dilation of porcine coronaryarterioles” at the American Heart Association meeting, 70th Scientific Sessions, Orlando,Florida, November 1997.
Presented: “Low-density lipoproteins impair nitric oxide-related endothelial function incoronary arterioles” at the American Heart Association meeting, 70th Scientific Sessions,Orlando, Florida, November 1997.
Presented: “Ischemia/reperfusion inhibits nitric oxide-mediated dilation in coronaryarterioles by upregulation of arginase” at the American Heart Association meeting, 73rdScientific Sessions, New Orleans, Louisiana, November 2000.
Presented: “Heterogeneous coronary arteriolar dilation to ß -adrenergic receptor activation:
channels” at the American Heart Association meeting, 74th
Scientific Sessions, Anaheim, California, November 2001.
Presented: “Elevated intraocular pressure inhibits endothelium-dependent nitric oxide-mediated dilation of retinal arterioles: role of superoxide” at the Association for Researchin Vision and Ophthalmology annual meeting, Fort Lauderdale, Florida, April 2004. HONORS AND AWARDS
Graduated cum laude, St. Olaf College, Northfield, Minnesota
Research Award, 3rd Place, Seventh Annual Graduate Research Symposium andPoster Competition, Texas A&M Health Science Center, College Station, TX
August Krogh Young Investigator Award, Microcirculatory Society
Scientist Development Grant, American Heart Association National Center
Cardiovascular Section New Investigator Award, American Physiological Society
Organized and Chaired Featured Topic at Experimental Biology Meeting forAmerican Physiological Society Cardiovascular Section
COMMITTEES AND SERVICES
Treasurer, Graduate Student Organization, College of Medicine, Texas A&MUniversity
Membership Committee, The Microcirculatory Society
2003-present Abstract grader, American Heart Association, Annual Scientific Session2004
Editorial Board of American Journal of Physiology: Heart & CirculatoryPhysiologyJOURNAL REVIEWER American Journal of Physiology: Heart and Circulatory PhysiologyInvestigative Ophthalmology and Visual ScienceJournal of Applied PhysiologyJournal of Vascular ResearchCirculation ResearchGRANT REVIEWS
Merit Review, Endocrinology Review Board, Department of Veterans Affairs’Medical Research Service, VA Medical Center (February)
Research Peer Review Committee, American Heart Association Western ReviewConsortium
CURRENT-PENDING GRANT/FUNDING SUPPORT Current: 2002-2006
AHA National- Scientist Development GrantConducted Dilation of Coronary Arterioles and Role of Inward RectifierPotassium ChannelsRole: Principal Investigator
2002-present Characterization of vasoregulatory mechanisms in the retinal microcirculation
(Ophthalmic Vascular Research Program)Sponsor: Scott & White Research FoundationRole: Co-Investigator
Pending: 2004-2009
NIH RO1 EY016221-01Mechanisms of retinal arteriolar dilation to adenosineRole: Principal Investigator
STUDENTS/POSTDOCTORATES/COLLEAGUES-TRAINED/MENTORED
Cuihua Zhang, M.D., Ph.D, postdoctorate, 9/97-8/2003- Cardiovascular physiology andmicrocirculatory control. Current position: Assistant Professor, Louisiana State UniversityHealth Center
Wei Wang, M.D., postdoctorate, Texas A&M University System Health Science Center -Cardiovascular physiology. 9/99-present
Erion Qamirani, graduate student, Texas A&M University System Health Science Center -C-reactive protein and coronary arteriolar function, 9/02-present
Robert H. Rosa, Jr., M.D., Associate Professor of Ophthalmology, Chief, Section ofOphthalmic Pathology, Scott & White Eye Institute, Texas A&M University SystemHeatlh Science Center- Trained in isolated retinal microvessel techniques, 11/02-present
Andrew Bossen, medical student, Texas A&M University System Health Science Center -Development of animal model for elevated intraocular pressure, 11/03
Habib Razavi, postdoctorate, Texas A&M University System Health Science Center -Conducted vasodilation and coronary arteriolar function, 11/03-present
Zhaoxu Yuan, postdoctoral fellow, Scott & White Memorial Hospital- Vascular regulation in retinal microcirculation, 11/03-present GRADUATE STUDENT COMMITTEE
Erion Qamirani, Texas A&M University System Health Science Center, 6/03-present
RESEARCH PUBLICATIONS A. Peer-Reviewed Publications
Hein TW, Kuo L. LDLs impair vasomotor function of the coronary microcirculation: roleof superoxide anions. Circ Res. 83:404-414, 1998.
Liao JC, Hein TW, Vaughn MW, Huang K-T, Kuo L. Intravascular flow decreaseserythrocyte consumption of nitric oxide. Proc Natl Acad Sci USA. 96:8757 8761, 1999.
Hein TW, Kuo L. cAMP-independent dilation of coronary arterioles to adenosine: role ofnitric oxide, G proteins, and K
channels. Circ Res. 85:634-642, 1999.
Hein TW, Belardinelli L, Kuo L. Adenosine A receptors mediate coronary microvascular
dilation to adenosine: role of nitric oxide and ATP-sensitive potassium channels. JPharmacol Exp Ther. 291:655-664, 1999.
Hein TW, Liao J, Kuo L. Oxidized LDL specifically impairs endothelium dependent, NO-mediated dilation of coronary arterioles. Am J Physiol. 278:H175-H183, 2000.
Zhang C, Hein TW, Kuo L. Transmural difference in coronary arteriolar dilation toadenosine: effect of luminal pressure and K
channels. Am J Physiol. 279:H2612-H2619,
Hein TW, Wang W, Zoghi B, Muthuchamy M, Kuo L. Functional and molecularcharacterization of receptor subtypes mediating microvascular dilation to adenosine. J MolCell Cardiol. 33:271-282, 2001.
Zhang C, Hein TW, Wang W, Chang C-I, Kuo L. Constitutive expression of arginase incoronary microvascular endothelial cells counteracts nitric oxide-mediated vasodilatory
1 0 . 1 0 9 6 / f j . 0 0 - 0 6 8 1 f j e
(http://www.fasebj.org/cgi/doi/10.1096/fj.00-0681fje); FASEB J. 15:1264-1266, 2001.
Kuo L, Hein TW. Functional and molecular evidence of adenosine A receptor in
coronary arteriolar dilation to adenosine. Drug Dev Res. 52:350-356, 2001.
10. Hein TW, Platts SH, Waitkus-Edwards KR, Kuo L, Mousa SA, Meininger GA. Integrin-
binding peptides containing RGD produce coronary arteriolar dilation via cyclooxygenaseactivation. Am J Physiol. 281: H2378-H2384, 2001.
11. Rivers R, Hein TW, Zhang C, Kuo L. Activation of barium-sensitive inward rectifier
potassium channels mediates remote dilation of coronary arterioles. Circulation. 104:1749-1753, 2001.
12. Huang K-T, Han TH, Hyduke DR, Vaughn MW, Van Herle, Hein TW, Zhang C, Kuo L,
Liao JC. Modulation of nitric oxide bioavailability by erythrocytes. Proc Natl Acad SciUSA. 98:11771-11776, 2001.
13. Gamperl AK, Hein TW, Kuo L, Cason, BA. Isoflurane-induced dilation of porcine
coronary microvessels is endothelium dependent and inhibited by glibenclamide. Anesthesiology. 96:1465-1471, 2002.
14. Zhang C, Hein TW, Wang W, Kuo L. Divergent roles of angiotensin II AT and AT
receptors in modulating coronary microvascular function. Circ Res. 92:322-329, 2003.
15. Hein TW, Zhang C, Wang W, Chang C-I, Thengchaisri N, Kuo L. Ischemia-reperfusion
selectively impairs nitric oxide-mediated dilation in coronary arterioles: counteracting roleof arginase. FASEB J. (October 16, 2003) 10.1096/fj.03-0115fje
(http://www.fasebj.org/cgi/doi/10.1096/fj.03-0115fje); FASEB J. 17:2328-2330, 2003.
16. Hein TW, Zhang C, Wang W, Kuo L. Transmural difference in coronary arteriolar dilation
to ß-adrenergic receptor activation: role of ß -adrenergic receptors and K
17. Zhang C, Hein TW, Wang W, Kuo L. Tumor necrosis factor-induced production of
superoxide inhibits endothelium-dependent NO-mediated dilation of coronary arterioles:role of ceramide signaling and xanthine oxidase. Submitted to Circ Res., 2004.
18. Zhang C, Hein TW, Wang W, Miller MW, Fossum T, Humphrey JD, Kuo L. Hypertension
impairs nitric oxide-mediated dilation of coronary arterioles by upregulation of vasculararginase. Submitted to Hypertension, 2004.
19. Qamirani E, Wu X, Davis MJ, Kuo L, Hein TW. Differential effects of C-reactive protein
on coronary arteriolar function. Submitted to Circulation, 2004.
20. Hein TW, Wang W, Rosa RH Jr, Kuo L. Requisite roles of A receptors and K
in retinal arteriolar dilation to adenosine. Submitted to Invest Ophthalmol Vis Sci., 2004. B. Book Chapters 1. Kuo L, Hein TW. Mechanism of shear stress-induced coronary microvascular dilation. In:
Sensors and Sensing in Biology and Engineering, edited by FG Barth, JAC Humphrey, andTW Secomb. Springer-Verlag Wien, New York, 2003. C. Conference Chapters 1.
Thengchaisri N, Hein TW, Zhang C, Wang W, Kuo L. Upregulation of endothelial arginaseby oxidative stress impairs NO-mediated vasodilation. Proceedings of the 7th WorldCongress for Microcirculation, 579-584, Monduzai Editore, NelserBo-Bologna, Italy,2001. D. Abstracts
Schmiege LM, Liao JC, Ghosheh SA, Hein TW, Miller SM, Kuo L. Effects of endotoxinand low-density lipoprotein on the L-arginine transport of endothelial cells. Microcirculation. 2:94, 1995.
Hein TW, Kuo L. Oxidized-LDL impairs endothelium-dependent nitric oxide-mediateddilation of coronary arterioles. Microcirculation. 3:89,1996.
Hein TW, Kuo L. Oxidized low-density lipoprotein impairs nitric oxide-mediated dilationof coronary arterioles. Circulation. 94: I-426, 1996.
Hein TW, Kuo L. Native low-density lipoprotein impairs endothelium-dependent and nitricoxide-mediated dilation in porcine coronary arterioles. Microcirculation. 4:171, 1997.
Hein TW, Gamperl AK, Kuo L, Cason BA. Isoflurane-induced dilation of porcine coronaryarterioles is inhibited by glyburide. Anesthesiology. 87:3, 1997.
Hein TW, Kuo L. Characterization of adenosine receptor-mediated dilation of porcinecoronary arterioles. Circulation. 96:I114, 1997.
Hein TW, Kuo L. Oxidized LDL specifically impairs nitric oxide-mediated dilation ofcoronary arterioles. Circulation. 96:I316, 1997.
Hein TW, Kuo L. Low-density lipoproteins impair nitric oxide-related endothelial functionin coronary arterioles. Circulation. 96:I447, 1997.
Hein TW, Kuo L. Differential effect of oxidized low-density lipoprotein on nitric oxide-and potassium channel-mediated dilation of coronary arterioles. FASEB J. 12:A239, 1998.
10. Hein TW, Kuo L. cAMP-independent dilation of coronary arterioles to adenosine: role of
channels. FASEB J. 12:A13, 1998.
11. Zhang C, Hein TW, Kuo L. Intraluminal pressure influences K
coronary arteriolar dilation. Circulation. 98:I139, 1998.
channel-mediated coronary arteriolar dilation to adenosine is
independent of cAMP. Circulation. 98:I139, 1998.
13. Hein TW, Kuo L. cAMP-independent dilation of coronary arterioles to isoproterenol: role
channels. Circulation. 98:I139, 1998.
14. Hein TW, Ma Y, Muthuchamy M, Kuo L. Functional and molecular studies of adenosine
channels in the coronary microcirculation. Circulation. 98:I139, 1998.
15. Hein T, Muthuchamy M, Kuo L. Mechanism of coronary arteriolar dilation to adenosine.
16. Meininger GA, Waitkus KR, Hein TW, Kuo L, Davis GE. Regulation of vasomotor
function by integrins. J. Vasc. Res. 36:424, 1999.
17. Zhang C, Hein T, Kuo L. Regulation of nitric oxide-mediated dilation by arginase in
coronary arterioles. FASEB J. 14:A29, 2000.
18. Kuo L, Hein T, Wang W, Zoghi B, Muthuchamy M. Functional and molecular evidence of
adenosine A receptor in coronary arteriolar dilation to adenosine. Drug Develop. Res.
19. Hein TW, Zhang C, Wang W, Kuo L. Ischemia/reperfusion inhibits nitric oxide-mediated
dilation in of arterioles by upregulation of arginase. Circulation. 102:II229, 2000.
20. Zhang C, Hein TW, Kuo L. Angiotensin II AT receptor mediates potentiation of coronary
arteriolar constriction to phenylephrine. FASEB J. 15:A51, 2001.
21. Hein TW, Zhang C, Wang W, Kuo L. Upregulation of arginase in coronary
microcirculation by ischemia/reperfusion inhibits nitric oxide-mediated vasodilation. FASEB J. 15:A462, 2001.
22. Gaffin R, Boswell N, Hein T, Kuo L, Muthuchamy M. Impaired adenosine-induced
dilation in coronary arteries from transgenic mouse hearts expressing a familialhypertrophic cardiomyopathy mutation. FASEB J. 15:A765, 2001.
23. Rivers R, Zhang C, Hein TW, Kuo L. Conducted remote dilations of isolated coronary
arterioles require activation of barium-sensitive inward rectifier potassium channels. Circulation. 104:II32, 2001.
24. Hein TW, Zhang C, Kuo L. Heterogeneous coronary arteriolar dilation to ß -adrenergic
receptor activation: role of nitric oxide and K
channels. Circulation. 104:II138, 2001.
25. Zhang C, Hein TW, Kuo L. Activation of angiotensin II AT1 receptor inhibits
endothelium-dependent nitric oxide-mediated dilation of coronary arterioles: role ofsuperoxide anion. Circulation. 104:II174, 2001.
26. Fogarty JA, Hein TW, Zhang C, Parker JL, Kuo L. Adenosine-stimulated production of
nitric oxide in porcine collateral-dependent coronary arterioles is enhanced by exercisetraining. Circulation. 104:II175, 2001.
27. Fogarty JA, Hein TW, Zhang C, Kuo L, Parker JL. Exercise training enhances basal and
VEGF-stimulated nitric oxide production in porcine collateral-dependent coronaryarterioles. Circulation. 104:II265, 2001.
28. Thengchaisri N, Wang W, Chang C, Hein TW, Kuo L. Hydrogen peroxide specifically
impairs endothelium-dependent nitric oxide-mediated dilation of coronary arterioles: roleof arginase. Circulation. 104:II286, 2001.
29. Zhang C, Hein TW, Kuo L. Stimulation of a - and ß -adrenergic receptors by
norepinephrine elicits endothelium-dependent nitric oxide-mediated dilation of coronaryarterioles. FASEB J. 16:A125, 2002.
30. Han TH, Huang KT, Hyduke DR, Vaughn MW, van Herle H, Hein TW, Zhang C, Kuo L,
Liao. Modulation of nitric oxide bioavailability by erythrocytes. FASEB J. 16:A913, 2002.
31. Zhang C, Hein TW, Wang W, Kuo L. Tumor necrosis factor-induced production of
superoxide inhibits endothelium-dependent NO-mediated dilation of coronary arterioles:role of ceramide signaling and xanthine oxidase. FASEB J. 17:A138, 2003.
32. Zhang C, Hein TW, Wang W, Miller MW, Fossum T, Humphrey JD, Kuo L. Hypertension
impairs NO-mediated dilation of coronary arterioles by upregulation of endothelialarginase. FASEB J. 17:A504, 2003.
33. Hein TW, Wang W, Rosa RH, Kuo L. Requisite roles of A receptors and K
in retinal arteriolar dilation to adenosine. Invest Ophthalmol Vis Sci. 2003;44:E-Abstract327.
34. Rosa RH, Hein TW, Kuo L. Activation of a -adrenergic receptors by brimonidine evokes
nitric oxide-mediated dilation of retinal microvessels. Invest Ophthalmol Vis Sci. 2003;44:E-Abstract 958.
35. Zhang C, Hein TW, Wang W, Kuo L. Tumor necrosis factor-alpha-induced activation of
JNK impairs nitric oxide-mediated dilation of coronary arterioles. Circulation. 108:IV-79,2003.
36. Wang W, Zhang C, Hein TW, Kuo L. Oxidized low-density lipoprotein impairs nitric
oxide-mediated dilation of coronary arterioles via upregulation of endothelial arginase. Circulation. 108:IV-99, 2003.
37. Qamirani E, Hein TW, Kuo L. C-Reactive protein dilates coronary arterioles via barium-
sensitive inward rectifier potassium channels. Circulation. 108:IV-226, 2003.
38. Qamirani E, Wang W, Kuo L, Hein TW. C-Reactive protein inhibits endothelium-
dependent nitric oxide-mediated dilation in coronary arterioles: roles of superoxide andvascular NADPH oxidase. FASEB J. 18:A622, 2004.
39. Shipley R, Hein TW, Kuo L. Acidosis enhances vasodilation of coronary arterioles to
channels. FASEB J. 18:A250, 2004.
40. Hein TW, Bossen A, Yuan J, Rosa RH Jr, Kuo L. Elevated intraocular pressure inhibits
endothelium-dependent nitric oxide-mediated dilation of retinal arterioles: role ofsuperoxide anion. Invest Ophthalmol Vis Sci. 2004;45:E-Abstract 2337.
41. Rosa RH, Hein TW, Kuo L. Retinal autoregulation: The myogenic response in retinal
arterioles. Invest Ophthalmol Vis Sci. 2004;45:E-Abstract 2335.
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THE NEWSLETTER Datchet Health Centre JUNE 2012 Patient Participation Group Editor’s note Last March, in my first newsletter, I said that comments or questions will be welcomed if left, in writing, at Reception. Although there have been none, I have been asked if letters to the editor, intended for publication, are acceptable. My reply is “Of course”, provided that my decisio