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Dr. Tony E. Hugli

Direct Phone: (858) ***-****       

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Torrey Pines Institute for Molecular Studies

11350 SW Village Parkway

Port Saint Lucie, Florida 34987

United States

Company Description

Torrey Pines Institute for Molecular Studies offers employment opportunities in Port St. Lucie, Florida and San Diego, California. The research environment at the Institute is one that fosters learning, training, development, and mentoring. We value the d ... more

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Background Information

Employment History

Scientific Director

California Technical Research Institute

Education

Bachelor of Science degree

chemistry form

Web References (41 Total References)


Contact

www.tpims.org [cached]

Tony Hugli


Tony Hugli

www.tpims.org [cached]

Tony Hugli

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Tony Hugli
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Tony Hugli
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Tony Hugli
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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.
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Dr. Tony E. Hugli received a Bachelor of Science degree in chemistry form
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Dr. Hugli took post-doctorate training in the laboratory of Drs.
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Inventors: Hugli, T.E., Stoughton, R.B. 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. 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. 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. his 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:


The Protein Society: The home for the international protein science community

www.proteinsociety.org [cached]

Tony Hugli, Torrey Pines Institute for Molecular Studies Executive Council


Tony Hugli

www.tpims.org [cached]

Tony Hugli

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Tony Hugli
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Tony Hugli
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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.
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Dr. Tony E. Hugli received a Bachelor of Science degree in chemistry form
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Dr. Hugli took post-doctorate training in the laboratory of Drs.
...
Inventors: Hugli, T.E., Stoughton, R.B. 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. 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. 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. his 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:


TPIMS Scientists - Tony Hugli

www.tpims.org [cached]

Dr. Hugli | Tony Hugli

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Dr. Hugli | Tony Hugli
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Tony Hugli Adjunct Member Protein Chemistry
858.597.3982 - phone 858.597.3804 - fax
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Kistler, EB, Hugli, TE, Schmid-Schoenbein GW. The Pancreas as a Source of Cardiovascular Cell Activation Factors. Microcirculation 2000; 7: 183-192. Schmid-Schoenbein, GW, Kistler, EB, Hugli, TE. Mechanisms for Cell Activation and its Consequences for Biorheology and Microcirculation: Multi-organ Failure in Shock. Biorheology 2001; 38: 185-201. Fitzal, F, Kistler, EB, Mitsuoka, H., Hugli, TE, Schmid-Schoenbein, GW. A New Hypothesis for the Origin of Shock: Self-Digestion of the Ischemic Intestine by Pancreatic Enzymes. Progress in Inflammation 2005, in press. (a review) Schmid-Schoenbein, GW and Hugli, TE. Analysis of Trigger Mechanisms for Inflammation in Cardiovascular Diseases: Application to Shock and Multi-Organ Failure. Microcirculation 2005, in press. (a review) Kramp, WJ, Waldo, S., Schmid-Schoenbein, GW, Hoyt, D., Coimbra, R, Hugli, TE. Characterization of Two Classes of Pancreatic Shock Factors: Differences Exhibited by Hydrophilic and Hydrophobic Shock Factors. Shock 2003; 20: 356-362. Doucet, JJ, Hoyt, DB, Coimbra, R., Schmid-Schoenbein, GW, Junger, WG, Wolf, PL, Loomis, WH, Hugli, TE. Inhibition of Enteral Enzymes by Enteroclysis with Nafamostat Reduces Neutrophil Activation and Transfusion Requirements Following Hemorrhagic Shock. Trauma 2004; 56: 501-512.
Publications
Acosta, J.A., Hoyt, D.B., Schmid-Schoenbein, G.W., Hugli, T.E., Anjaria, D.J., Frankel.
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Abe, M., Hama, H., Shirakusa, T., Iwasaki, A., Ono, N., Kimura, N., Hugli, T., Okada, N., Katsuragi, T., Okada, H. Contribution of anaphylatoxins to allergic inflamation in human lungs. Microbiol. Immunol. 49:981-986, 2005. Schmid-Shoenbein, G.W., Hugli, T.E. A new hypothesis for microvascular inflammation in shock and multiorgan failure: self-digestion by pancreatic enzymes. Microcirculation 12:71-82, 2005.
Kramp, W.J., Waldo, S., Schmid-Schoenbein, G.W., Hoyt, D., Coimbra, R., Hugli, T.E. Characterization of two classes of pancreatic shock factors: functional differences exhibited by hydrophilic and hydrophobic shock factors. Shock 20: 356-362, 2003.
Hayashi, J., Salomon, D.R., Hugli, T.E. Elevated kallikrein activity in plasma from stable liver transplant recipients.
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Jagels, M.A., Daffern, P.J., Hugli, T.E. C3a and C5a enhance granulocyte adhesion to endothelial and epithelial cell monolayers: Epithelial and endothelial priming is required for C3a-induced eosinophil adhesion.
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Jagels, M.A., Hugli, T.E. Mixed effects of TGF-b on human airway epithelial-cell chemokine responses.
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Kistler, E.B., Hugli, T.E., Schmid-Shoenbein, G.W.
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Kistler, E.B., Lefer, A.M., Hugli, T.E., Schmid-Schoenbein, G.W. Plasma activation during splanchnic arterial occlusion shock.
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Kodani, M., Sakata, N., Takano, Y., Kamiya, H., Katsuragi, T., Hugli, T.E., Abe, M. Intratracheal administration of anaphylatoxin C5a potentiates: Antigen-induced pulmonary reactions through the prolonged production of cysteinyl-leukotrienes.
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Pfeifer, P.H., Brems, J.J., Brunson, M., Hugli, T.E. Plasma C3a and C4a levels in liver transplant recipients: A longitudinal study.
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Tsuji, R.F., Kawikova, I., Ramabhadran, R., Akahira-Azuma, M., Taub, D., Hugli, T.E., Gerard, C., Askenase, P.W. Early local generation of C5a initiates the elicitation of contact sensitivity by leading to early T cell recruitment.
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Askenase, P.W., Kawikova, I., Paliwal, V., Akahira-Azuma, M., Gerard, C., Hugli, T.E., Tsuji R. A new paradigm of T-cell allergy: Requirement for the B-1 cell subset.
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Chao, T.-H., Ember, J.A., Wang, M., Bayon, Y., Hugli, T.E., Ye, R.D. Role of the second extracellular loop of human C3a receptor in agonist binding and receptor function.
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Daffern, P.J., Jagels, M.A., Hugli, T.E. Multiple Epithelial Cell-Derived Factors Enhance Neutrophil Survival: Regulation by Glucocorticoids and TNF-a. AJRCMB 21: 259-267, 1999. Daffern, P.J., Jagels, M.A., Saad, J.J., Fischer, W., Hugli, T.E. Upper and lower airway epithelial cells support eosinophil survival in vitro through production of GM-CSF: Regulation by glucocorticoids and TNF-a. Allergy Asthma Proc. 20:243-253, 1999. Daffern, P.J., Muilenberg, D., Hugli, T.E., Stevenson, D.D. Urinary excretion of leukotriene E4 excretion during aspirin challenge with severity of respiratory responses.
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Fischer, W.H., Jagels, M.A., Hugli, T.E. Regulation of IL-6 synthesis in human peripheral blood mononuclear cells by C3a and C3adesArg. J. Immunology 162:453-459, 1999. Fukuoka, Y., Ember, J.A., Hugli, T.E. Ligand binding sites on guinea pig C3aR: Point- and deletion mutations in the large extracellular loop and vicinity. Biochem. Biophysic. Res. Commun. 263:357-360, 1999. Jagels, M.A., Daffern, P.J., Zuraw, B.L., Hugli, T.E. Mechanisms and regulation of PMN and eosinophil adherence to human airway epithelial cells. Am. J. Respir. Cell. Mol. Biol. 21:418-427, 1999. Pfiefer, P.H., Kawahara, M.S., Hugli, T.E. Possible Mechanism for in vitro complement activation in blood and plasma samples: Futhan/EDTA controls in vitro complement activation. Clinical Chem. 45(8 Pt 1):1190-1199, 1999. Sun, J., Ember, J.A., Chao, Ta.-H., Fukuoka, Y., Ye, R.D., Hugli, T.E. Identification of ligand effector binding sites in transmembrane regions of the human G-protein-coupled C3a receptor.
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Carney, D.F., Jagels, M.A., Hugli, T.E., Sands, H., Rubin, H. Effect of serine proteinase inhibitors on neutrophil function: alpha-1-proteinase inhibitor, antichymotrypsin, and a recombinant hybrid mutant of antichymotrypsin (LEX32) modulate neutrophil adhesion interactions.
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Ember, J.A., Jagels, M.A., Hugli, T.E. Characterization of complement activation factors: (anaphylatoxins) and their biological responses.
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Fukuoka, Y., Ember, J.A., Hugli, T.E. Cloning and characterization of rat C3a receptor: Differential expression of rat C3a and C5a receptors by LPS stimulation. Biochem. Biophysic. Res. Commun. 242:663-668, 1998. Fukuoka, Y., Ember, J.A., Hugli, T.E. Molecular cloning of two isoforms of the guinea pig C3a anaphylatoxin receptor: Alternative splicing at the large extracellular loop. J. Immunol. 161:2977-2984, 1998. Fukuoka, Y., Ember, J.A., Yasui, A., Hugli, T.E. Cloning and characterization of the guinea pig C5a anaphylatoxin receptor: Interspecies diversity among the C5a receptors. Int. Immunol. 10:275-283, 1998. Hetland, G., Pfeifer, P.H., Hugli, T.E. Processing of C5a by human polymorpho-nuclear leukocytes. J. Leukocyte Biology. 63 :456-462, 1998. Mainwaring, R.D., Lamberti, J.J., Hugli, T.E. Complement and cytokine activation following modified fontan procedure.
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Nakashima, K., Sakurada, T., Imayama, S., Masukawa, S., Ember, J.A., Hugli, T.E., Abe, M. A case of episodic angioedema associated with blood eosinophilia: upregulated C5a receptor expression on eosinophils.
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Akatsu, H., Miwa, T., Sakurada, C., Fukuoka, Y., Ember, J.A., Yamamoto, T., Hugli, T.E., Okada, H. cDNA cloning and characterization of rat C5a anaphylatoxin receptor.
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Ames, R.S., Tornetta, M.A., Foley, J.J., Hugli, T.E., Sarau, H.M. Evidence that the receptor for C4a is distinct from the C3a receptor.
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Ember, J.A., Hugli, T.E. Complement factors and their receptors. In: Special Issue on Complement and Disease. Ed(s). Würzner R, Hugli TE., Amsterdam: Elsevier (Introduction: 38:1, 1997) 38: 3-15, 1997. Fischer, W.H., Hugli, T.E. Regulation of B cell functions by C3a and C3adesArg: Suppression of TNF-alpha, IL-6, and the polyclonal immune response. J. Immunol. 159 (9) 4279-4286, 1997. Hsu, M.H., Ember, J.A., Wang, M., Prossnitz, E.R., Hugli, T.E., Ye, R.D. Cloning and functional characterization of the mouse C3a anaphylatoxin receptor gene.
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Mulligan, M.S., Schmid, E., Till, G.O., Hugli, T.E., Friedl, H.P., Roth, R.A., Ward, P.A. C5a-dependent upregulation in vivo of lung vascular P-selectin.
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Pfeifer, P.H., Hugli, T.E., Davie, E.W., Fujikawa, K. Complement activation in EDTA blood/plasma samples may be caused by coagulation proteases.
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S., Friedl, H.P., Warner, R.L., Mulligan, M.S., Hugli, T.E., Till, G.O., Ward, P.A. Requirements for C5a in dermal and lung vascular injury following thermal trauma to rat skin.
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Schmid, E., Warner, R.L., Crouch L.D., Friedl, H.P., Till, G.O., Hugli, T.E., Ward, P.A. Neutrophil chemotactic activity and C5a following systemic activation of complement in rats.
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Tanaka, F., Dannenberg Jr., A.M., Higuchi, K., Nakamura, M., Pula, P.J., Hugli, T.E., DiScipio, R.G., Wagner, J.L.

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