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Meet Our California Scientists Tony Hugli
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Tony Hugli

Tony HugliTorreyPinesInstituteCA

Adjunct Member
Protein Chemistry		 858.597.3892 - phone
858.597.3804 - fax
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Dr. Hugli’s research focuses on the mechanisms of hemorrhagic shock. This research involves identifying the source of shock- inducing mediators which has been traced to the pancreas and the pancreatic enzymes. We have shown that a host of both bioactive lipids and peptides generated in the ischemic gut can cause enhanced vascular permeability ( i.e. leakage) and lethal shock in rats. This lethal mix of mediators is generated in the gut lumen by the pancreatic enzymes. Simply by flushing this lethal mixture of compounds from the gut with GoLytely and adding an enzyme inhibitor called Futhan to block the pancreatic enzymes from generating more mediators animals experiencing potentially lethal hemorrhagic shock survived. Dr. Hugli acts as a consultant to and collaborator with Dr. Erik Kistler, UCSD Medical Center who continues his studies on the mechanism of shock. Future studies include:

  • Longer term survival studies in animal models to confirm the survival outcome. Commercial interests have been attracted by a patent (#6,534,283) entitled ‘Methods for Treatment and Prevention of Physiologic Shock’
  • Select other enzyme inhibitor candidates that are FDA-approved to test in the animal models or continue using Futhan which has been shown to be effective.
  • Develop preliminary clinical trials to test efficacy of using a combination of intestinal flushing and enzyme inhibition on potentially lethal shock patients.
  • Immediate life-saving application of this new and novel treatment for traumatic hemorrhagic shock by our military.

Dr. Tony E. Hugli received a Bachelor of Science degree in chemistry form Otterbein College in Ohio in 1963. He received a PhD. in biochemistry from Indiana University in 1965 (Thesis: A Crystal-Solution Comparison for Sperm Whale Metmyoglobin) showing for the first time that the crystalline protein structure was an accurate representation of the protein in solution. Dr. Hugli took post-doctorate training in the laboratory of Drs. William H. Stein and Stanford Moore at Rockefeller University (Nobel Laureates in 1973). He began his research career at The Scripps Research Institute in 1972 as assistant member and rose to the rank of full member in the Immunology Department. Dr. Hugli set up the first protein chemistry laboratory at Scripps.

Education

1968 - Doctor of Philosophy (Chemistry), Indiana University, Bloomington, IN

1963 - Bachelor of Science (Chemistry), Otterbein College, Westerville, OH


Positions

2007-Present: Torrey Pines Inst. for Molecular Studies, La Jolla, CA

2004-2007: California Institute of Toxicology, Carlsbad, CA

2000 – 2004: La Jolla Institute for Molecular Medicine, La Jolla, CA

1972 - 2000: Immunology Department, The Scripps Research Institute, La Jolla, CA

1968-1972: Research Associate, Rockefeller University, New York, NY


Professional Affiliations

1972- Present: American Society for Biochemistry and Molecular Biology (ASBMB)

1972 - Present: Federation of American Societies for Experimental Biology

2000-Present: Breakthroughs in Bioscience Committee member

Honors & Awards

  • Outstanding Alumni Award, Otterbein College
  • Professional Editorial Activities
    • Co-founder and Associate Editor of Protein Science (1991-1995)
    • Co-founder of The Protein Society
    • Editor-in-Chief of Immunopharmacology (1999-2001)
    • Co-Editor-in-Chief of International Immunopharmacology (2001-2008)
  • Biotechnology Experience
    • Co-founder of Cell Activation Inc., La Jolla, CA
    • Co-Founder of Hemosaga Diagnostics, San Diego, CA
    • CEO/Presidient of HealthAide, Inc. , Oklahoma City, OK

Selected Publications (10 of 248)

  1. Kistler, Erik B., Hugli, T.E. , Schmid-Schoenbein, Geert W.  The pancreas as a source of cardiovascular cell activating factors. Microcirculation (2000) 7, 183-192
  2. Schmid-Schoenbein, Geert W., Kistler, Erik B., Hugli, Tony E.  Mechanisms for cell activation and its consequences for biorheology and microcirculation: Multi-organ failure in shock. Biorheology (2001) 38, 185-201
  3. Kistler, Erik, Lefer, A., Hugli, TE, Schoenbein, GW  Plasma activation during splenic arterial occlusion shock. Shock (2000) 14, 30-34.
  4. Kramp, William J., Waldo, Steve, Schmid-Schoenbein, Geert W., Hoyt, David, Coimbra, Raul, Hugli, Tony E. Characterization of two classes of pancreatic shock factors: Functional differences exhibited by hydrophilic and hydrophobic shock factors.  Shock (2003) 20, 356-362.
  5. Geert W. Schmid-Schoenbein and Tony E. Hugli  A new hypothesis for microvascular inflammation in shock and multiorgan failure: Self-digestion by pancreatic enzymes. Microcirculation (2005) 12, 71-82.
  6. Pfeifer, P.H., Brems, JJ, Brunson, M, Hugli, TE.  Plasma C3a and C4a levels in liver transplant recipients: a longitudinal study. Immunopharmacology (2000), 46, 163-174
  7. Jagels, MA, Hugli, TE.  Mixed effects of TGF-beta on human airway epithelial-cell chemokine responses  Immunopharmacology (2000) 48, 17-26
  8. Tsuji, RF, Kawikova, I, Ramabhadran, R, Akahira-Azuma M., Taub, D, Hugli, TE, Gerard, C, Askenase, PW. Early local generation of C5a initiates the elicitation of contact sensitivity by leading to early T cell recruitment. J. Immunol. (2000) 165, 1588-1598.
  9. Hayashi, J, Salomon, DR, Hugli, TE. Elevated kallikrein activity in plasma from stable liver transplant recipients. Int. immunopharm. (2002) 2, 1667-1680.
  10. Doucet, JJ, Hoyt, DB, Coimbra, R. Schmid-Schonbein, GW, Junger, WG, Wolf, PL, Loomis, WH, Hugli, TE. Inhibition of enteral enzymes by enterclysis with Nafamostat reduces neutrophil activation and transfusion requirements following hemorrhagic shock. Trauma (2004) 56, 501-512.

Patents

  1. Methods for assessing complement activation. U.S. Patent No. 6,297,024. Issued October 2, 2001.   Inventors:  Hugli, T.E., Stoughton, R.B.
  2. Substrates for assessing mannan-binding protein-associated serine protease activity and methods using the substarates. U.S. Patent No. 6,235,494. Issued May 22, 2001.   Inventors:  Hugli, T.E.
  3. Antibodies to human C5a receptor. U.S. Patent No. 5,480,974. Issued January 2, 1996.   Inventors:  Morgan, E.L., Ember, J.A., Hugli, T.E.
  4. Synthetic peptides. U.S. Patent No. 4,438,029. Issued March 20, 1984.  Inventors:  Erickson, B.W., Hugli, T.E.

·Dr. Hugli’s research focuses on the mechanisms of hemorrhagic shock. This research involves identifying the source of shock- inducing mediators which has been traced to the pancreas and the pancreatic enzymes. We have shown that a host of both bioactive lipids and peptides generated in the ischemic gut can cause enhanced vascular permeability ( i.e. leakage) and lethal shock in rats and pigs. This lethal mix of mediators is generated in the gut lumen by the pancreatic enzymes. Simply by flushing this lethal mixture of compounds from the gut with GoLytely and adding an enzyme inhibitor called Futhan to block the pancreatic enzymes from generating more mediators animals experiencing potentially lethal hemorrhagic shock survived. Dr. Hugli acts as a consultant to and collaborator with Dr. Erik Kistler, UCSD Medical Center who continues his studies on the mechanism of shock. Future studies include:

· Longer term survival studies in a pig model to confirm the survival outcome. Commercial interests have been attracted by a patent (#6,534,283) entitled ‘Methods for Treatment and Prevention of Physiologic Shock’

· Select other enzyme inhibitor candidates that are FDA-approved to test in the animal models or continue using Futhan which has been shown to be effective.

· Develop preliminary clinical trials to test efficacy of using a combination of intestinal flushing and enzyme inhibition on potentially lethal shock patients.

· Immediate life-saving application of this new and novel treatment for traumatic hemorrhagic shock by our military.