Glenn D. Prestwich

University of Utah, Salt Lake City, Utah, United States

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Publications (638)2862.01 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Cathelicidin (LL-37) is an endogenous innate immune peptide that is elevated in patients with chronic rhinosinusitis (CRS). The role of LL-37 in olfactory epithelium (OE) inflammation remains unknown. We hypothesized that: (1) LL-37 topically delivered would elicit profound OE inflammation; and (2) LL-37 induced inflammation is associated with increased infiltration of neutrophils and mast cells. Methods: To test our hypothesis we challenged C57BL/6 mice intranasally with increasing concentrations of LL-37. At 24 hours tissues were examined histologically and scored for inflammatory cell infiltrate, edema, and secretory hyperplasia. In separate experiments, fluorescently conjugated LL-37 was instilled and tissues were examined at 0.5 and 24 hours. To test our last hypothesis, we performed tissue myeloperoxidase (MPO) assays for neutrophil activity and immunohistochemistry for tryptase to determine the mean number of mast cells per mm(2) . Results: LL-37 caused increased inflammatory cell infiltrate, edema, and secretory cell hyperplasia of the sinonasal mucosa, with higher LL-37 concentrations yielding significantly more inflammatory changes (p < 0.01). Fluorescent LL-37 demonstrated global sinonasal epithelial binding and tissue distribution. Further, higher concentrations of LL-37 led to significantly greater MPO levels with dose-dependent increases in mast cell infiltration (p < 0.01). Conclusion: LL-37 has dramatic inflammatory effects in the OE mucosa that is dose-dependent. The observed inflammatory changes in the olfactory mucosa were associated with the infiltration of both neutrophils and mast cells. Our biologic model represents a new model to further investigate the role of LL-37 in OE inflammation.
    International Forum of Allergy and Rhinology 09/2015; DOI:10.1002/alr.21634 · 2.37 Impact Factor
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    ABSTRACT: While approximately 30 % US adults are suffer from moderate to severe form of periodontitis, the available treatment options are far too limited. This chronic disease occurs due to a disruption of homeostasis between the microorganisms residing in the oral cavity and the host immune system. GM-0111 is a modified glycosaminoglycan and it has demonstrated anti-inflammatory effects on various inflammatory diesease models molecular targets and possibly offer alternative therapeutic choices for treating periodontitis. We investigated whether GM-0111, a modified GAG, could block molecular events important for the development of periodontitis and the resulting bone loss. First, we tested GM-0111 on RANKL-induced osteoclast formation and bone resorption in cultured mouse pre-osteoclasts. Next, we tested whether GM-0111 could block proinflammatory TLR2 and TLR4 signaling pathways in mouse macrophage RAW 264.7 cells and heterologously expressed HEK293 cells. Lastly, we investigated the antibacterial effects of GM-0111 on Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans. GM-0111 blocked RANKL-induced osteoclast formation even at 300 ng/mL and it also reduced the resulting bone resorption. The antiosteoclastic effects of GM-0111 were independent of RANKL to RANK signaling. We also found that GM-0111 selectively targets TLR2 (IC50 of 1–10 ng/mL) than TLR4 (IC50[100 lg/mL). By blocking TLR-mediated inflammatory pathways and inhibiting key process leading bone loss, we suggest that GM-0111 can provide a therapeutic potential to treat periodontitis.
    12th World Congress on Inflammation, Boston, MA; 08/2015
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    ABSTRACT: Acute Lung Injury (ALI) is a life-threatening, diffuse heterogeneous lung injury characterized by acute onset, pulmonary edema and respiratory failure. Lipopolysaccharide (LPS) is a common cause of both direct and indirect lung injury and when administered to a mouse induces a lung phenotype exhibiting some of the clinical characteristics of human ALI. Here, we report that LPS inhalation in mice results in increased bronchoalveolar lavage fluid (BALF) levels of Autotaxin (ATX, Enpp2), a lysophospholipase D largely responsible for the conversion of lysophosphatidylcholine (LPC) to lysophosphatidic acid (LPA) in biological fluids and chronically inflamed sites. In agreement, gradual increases were also detected in BALF LPA levels, following inflammation and pulmonary edema. However, genetic or pharmacologic targeting of ATX had minor effects in ALI severity, suggesting no major involvement of the ATX/LPA axis in acute inflammation. Moreover, systemic, chronic exposure to increased ATX/LPA levels was shown to predispose to and/or to promote acute inflammation and ALI unlike chronic inflammatory pathophysiological situations, further suggesting a differential involvement of the ATX/LPA axis in acute versus chronic pulmonary inflammation.
    PLoS ONE 07/2015; 10(7). DOI:10.1371/journal.pone.0133619 · 3.23 Impact Factor
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    ABSTRACT: Publication only meeting abstract.
    2015 ASCO Annual Meeting; 05/2015
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    Anna I Astashkina · Brenda K Mann · Glenn D Prestwich · David W Grainger
    Biomaterials 01/2015; 38:108. DOI:10.1016/j.biomaterials.2014.10.072 · 8.56 Impact Factor
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    Glenn D Prestwich · Kevin E Healy
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    ABSTRACT: Regenerative medicine is now coming of age. Many attempts at cell therapy have failed to show significant efficacy, and the umbrella term 'stem cell therapy' is perceived in some quarters as hype or just expensive and unnecessary medical tourism. Here we present a short editorial in three parts. First, we examine the importance of using a semisynthetic extracellular matrix (ECM) mimetic, or sECM, to deliver and retain therapeutic cells at the site of administration. Second, we describe one approach in which biophysical and biochemical properties are tailored to each tissue type, which we call "design for optimal functionality." Third, we describe an alternative approach to sECM design and implementation, called "design for simplicity," in which a deconstructed, minimalist sECM is employed and biology is allowed to perform the customization in situ. We opine that an sECM, whether minimal or instructive, is an essential contributor to improve the outcomes of cell-based therapies.
    Expert Opinion on Biological Therapy 01/2015; 15(1):3-7. DOI:10.1517/14712598.2015.975200 · 3.74 Impact Factor
  • Glenn D. Prestwich · Brenda K. Mann
    Translational Regenerative Medicine, 01/2015: pages 185-195; , ISBN: 9780124103962
  • Barbara Wirostko · Brenda K Mann · David L Williams · Glenn D Prestwich
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    ABSTRACT: Significance: Hyaluronic acid (HA, or hyaluronan) is a ubiquitous naturally occurring polysaccharide that plays a role in virtually all tissues in vertebrate organisms. HA-based hydrogels have wound-healing properties, support cell delivery, and can deliver drugs locally. Recent Advances: A few HA hydrogels can be customized for composition, physical form, and biomechanical properties. No clinically approved HA hydrogel allows for in vivo crosslinking on administration, has a tunable gelation time to meet wound-healing needs, or enables drug delivery. Recently, a thiolated carboxymethyl HA (CMHA-S) was developed to produce crosslinked hydrogels, sponges, and thin films. CMHA-S can be crosslinked with a thiol-reactive crosslinker or by oxidative disulfide bond formation to form hydrogels. By controlled crosslinking, the shape and form of this material can be manipulated. These hydrogels can be subsequently lyophilized to form sponges or air-dried to form thin films. CMHA-S films, liquids, and gels have been shown to be effective in vivo for treating various injuries and wounds in the eye in veterinary use, and are in clinical development for human use. Critical Issues: Better clinical therapies are needed to treat ophthalmic injuries. Corneal wounds can be treated using this HA-based crosslinked hydrogel. CMHA-S biomaterials can help heal ocular surface defects, can be formed into a film to deliver drugs for local ocular drug delivery, and could deliver autologous limbal stem cells to treat extreme ocular surface damage associated with limbal stem cell deficiencies. Future Directions: This CMHA-S hydrogel increases the options that could be available for improved ocular wound care, healing, and regenerative medicine.
    11/2014; 3(11):708-716. DOI:10.1089/wound.2014.0572
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    ABSTRACT: Autotaxin (ATX) is an enzyme discovered in the conditioned medium of cultured melanoma cells and identified as a protein that strongly stimulates motility. This unique ectonucleotide pyrophosphatase and phosphodiesterase facilitates the removal of a choline headgroup from lysophosphatidylcholine (LPC) to yield lysophosphatidic acid (LPA), which is a potent lipid stimulator of tumorigenesis. Thus, ATX has received renewed attention because it has a prominent role in malignant progression with significant translational potential. Specifically, we sought to develop active site-targeted irreversible inhibitors as anti-cancer agents. Herein we describe the synthesis and biological activity of an LPC-mimetic electrophilic affinity label that targets the active site of ATX, which has a critical threonine residue that acts as a nucleophile in the lysophospholipase D reaction to liberate choline. We synthesized a set of quaternary ammonium derivative-containing vinyl sulfone analogs of LPC that function as irreversible inhibitors of ATX and inactivate the enzyme. The analogs were tested in cell viability assays using multiple cancer cell lines. The IC50 values ranged from 6.74 to 0.39μM, consistent with a Ki of 3.50μM for inhibition of ATX by the C16H33 vinyl sulfone analog CVS-16 (10b). A phenyl vinyl sulfone control compound, PVS-16, lacking the choline-like quaternary ammonium mimicking head group moiety, had little effect on cell viability and did not inhibit ATX. Most importantly, CVS-16 (10b) significantly inhibited melanoma progression in an in vivo tumor model by preventing angiogenesis. Taken together, this suggests that CVS-16 (10b) is a potent and irreversible ATX inhibitor with significant biological activity both in vitro and in vivo. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Cancer Research 10/2014; 74(19 Supplement):2672-2672. DOI:10.1158/1538-7445.AM2014-2672 · 9.33 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):3965-3965. DOI:10.1158/1538-7445.AM2014-3965 · 9.33 Impact Factor
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    ABSTRACT: Ewing sarcoma is a malignant pediatric bone and soft tissue tumor. Although the 5-year survival rate of localized disease approaches 75%, the prognosis of metastatic and/or therapy-resistant disease remains dismal despite the wide use of aggressive therapeutic strategies. We previously reported that high expression of glutathione S-transferase M4 (GSTM4) in primary tumors correlates with poor patient outcomes. GSTM4 is required for oncogenic transformation and mediates resistance to chemotherapeutic drugs in Ewing sarcoma cells. Here, we performed RNA-sequencing analyses of Ewing sarcoma cells and combined our results with publicly-available datasets to demonstrate that GSTM4 is a major GST specifically expressed in Ewing sarcoma. Pharmacological inhibition of GSTM4 activity using a pan GST inhibitor, 6-(7-nitro-2,1,3-benzoxadiazol-4-ylthio) hexanol (NBDHEX), significantly limited cellular proliferation and oncogenic transformation of Ewing sarcoma cells. Moreover, combined use of NBDHEX and etoposide synergistically increased cytotoxicity, suggesting a role for GSTM4 as an inhibitor of apoptosis. Mechanistic studies revealed that GSTM4 limits apoptosis owing to its ability to interact with Apoptosis Signal-regulating Kinase 1 (ASK1) and inhibit signaling via the c-Jun N-terminal Kinase axis. To exploit our observation that GSTM4 expression is specifically up-regulated in Ewing sarcoma, we tested the effect of a GSTM4-activated anti-cancer agent, O2-(2,4-dinitrophenyl) 1-[(4-ethoxycarbonyl)piperazin-1-yl]diazen-1-ium-1,2-diolate or JS-K, on tumor growth and survival. We found that JS-K robustly decreased Ewing sarcoma cell viability and xenograft tumor growth, and improved overall survival of xenograft mice. Our data suggest that GSTM4 is a novel therapeutic target for the treatment of high GSTM4-expressing Ewing sarcoma. Strategies that combine standard chemotherapy with agents that inhibit GSTM4, or that are activated by GSTM4, or that block GSTM4/ASK1 interaction
    Frontiers in Pediatrics 08/2014; 2:83. DOI:10.3389/fped.2014.00083
  • Aixia Han · Xiaohui Liu · Glenn D. Prestwich · Ling Zang
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    ABSTRACT: A new water-soluble fluorescent perylene sensor was synthesized and compared to the previous non-aqueous sensors. The new sensor, MSI-1-9, exhibits sensitive and selective detection of mercuric ion (Hg2+) directly in aqueous solution through fluorescence quenching. The detection was not affected by the coexistence of other common divalent metal ions. MSI-1-9 possesses the necessary criteria for use in affordable, real-time measurement of Hg2+ in environmental water samples, permitting its incorporation into a portable mercury detection kit.
    Sensors and Actuators B Chemical 07/2014; 198:274–277. DOI:10.1016/j.snb.2014.03.033 · 4.10 Impact Factor
  • Richard Koehn · Brenda Mann · Sarah Atzet · Glenn Prestwich
    Veterinary Surgery 01/2014; 43(2). DOI:10.1111/j.1532-950X.2014.12106.x · 1.04 Impact Factor
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    ABSTRACT: Autotaxin (ATX), an autocrine motility factor that is highly upregulated in metastatic cancer, is a lysophospholipase D enzyme that produces the lipid second messenger lysophosphatidic acid (LPA) from lysophosphatidylcholine (LPC). Dysregulation of the lysolipid signaling pathway is central to the pathophysiology of numerous cancers, idiopathic pulmonary fibrosis, rheumatoid arthritis, and other inflammatory diseases. Consequently, the ATX/LPA pathway has emerged as an important source of biomarkers and therapeutic targets. Herein we describe development and validation of a fluorogenic analog of LPC (AR-2) that enables visualization of ATX activity in vivo. AR-2 exhibits minimal fluorescence until it is activated by ATX, which substantially increases fluorescence in the near-infrared (NIR) region, the optimal spectral window for in vivo imaging. In mice with orthotopic ATX-expressing breast cancer tumors, ATX activated AR-2 fluorescence. Administration of AR-2 to tumor-bearing mice showed high fluorescence in the tumor and low fluorescence in most healthy tissues with tumor fluorescence correlated with ATX levels. Pretreatment of mice with an ATX inhibitor selectively decreased fluorescence in the tumor. Together these data suggest that fluorescence directly correlates with ATX activity and its tissue expression. The data show that AR-2 is a non-invasive and selective tool that enables visualization and quantitation of ATX-expressing tumors and monitoring ATX activity in vivo.
    PLoS ONE 11/2013; 8(11):e79065. DOI:10.1371/journal.pone.0079065 · 3.23 Impact Factor
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    ABSTRACT: Interstitial cystitis (IC), often referred to in combination with painful bladder syndrome, is a chronic inflammatory disease of the bladder. Current therapies primarily focus on replenishing urothelial glycosaminoglycan (GAG) layer using GAG analogs and managing pain with supportive therapies. However, the elusive etiology of IC and the lack of animal models to study the disease have been major hurdles developing more effective therapeutics. Previously, we showed an increased urinary concentration of antimicrobial peptide LL-37 in spina bifida patients and used LL-37 to develop a mouse model of cystitis that mimics important clinical findings of IC. Here we investigate (1) the molecular mechanism of LL-37 induced cystitis in cultured human urothelial cells and in mice, (2) the protective effects of GM-0111, a modified GAG, within the context of this mechanism, (3) the physiological and molecular markers that correlate with the severity of the inflammation, and (4) the protective effects of several GAGs using these biomarkers in our LL-37 induced cystitis model. We find that LL-37 quickly induces release of ATP and apoptosis in the urothelium. These changes can be inhibited by a chemically-modified GAG, GM-0111. Furthermore, we also find that GAG analogs provide varying degrees of protection against LL-37 challenge in mice. These findings suggest that GM-0111 and possibly GAG molecules prevent the development of cystitis by blocking the apoptosis and the concurrent release of ATP from the urothelium.
    PLoS ONE 10/2013; 8(10):e77854. DOI:10.1371/journal.pone.0077854 · 3.23 Impact Factor
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    ABSTRACT: Changes in tissue and organ stiffness occur during development and are frequently symptoms of disease. Many cell types respond to the stiffness of substrates and neighboring cells in vitro and most cell types increase adherent area on stiffer substrates that are coated with ligands for integrins or cadherins. In vivo cells engage their extracellular matrix (ECM) by multiple mechanosensitive adhesion complexes and other surface receptors that potentially modify the mechanical signals transduced at the cell/ECM interface. Here we show that hyaluronic acid (also called hyaluronan or HA), a soft polymeric glycosaminoglycan matrix component prominent in embryonic tissue and upregulated during multiple pathologic states, augments or overrides mechanical signaling by some classes of integrins to produce a cellular phenotype otherwise observed only on very rigid substrates. The spread morphology of cells on soft HA-fibronectin coated substrates, characterized by formation of large actin bundles resembling stress fibers and large focal adhesions resembles that of cells on rigid substrates, but is activated by different signals and does not require or cause activation of the transcriptional regulator YAP. The fact that HA production is tightly regulated during development and injury and frequently upregulated in cancers characterized by uncontrolled growth and cell movement suggests that the interaction of signaling between HA receptors and specific integrins might be an important element in mechanical control of development and homeostasis.
    Biomaterials 10/2013; 35(1). DOI:10.1016/j.biomaterials.2013.09.066 · 8.56 Impact Factor
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    ABSTRACT: Rationale: Bioactive lipid mediators, derived from membrane lipid precursors, are released into the airway and airspace where they bind high affinity cognate receptors and may mediate asthma pathogenesis. Lysophosphatidic acid (LPA), a bioactive lipid mediator generated by the enzymatic activity of extracellular autotaxin (ATX), binds LPA receptors resulting in an array of biological actions on cell proliferation, migration, survival, differentiation and motility, and therefore could mediate asthma pathogenesis. Objectives: To define a role for the ATX-LPA pathway in human asthma pathogenesis and a murine model of allergic lung inflammation. Methods: We investigated the profiles of LPA molecular species and the level of ATX exoenzyme in BAL fluids of human asthmatics subjected to sub-segmental broncho-provocation with allergen. We interrogated the role of the ATX-LPA pathway in allergic lung inflammation using a murine allergic asthma model in ATX-LPA pathway-specific genetically modified mice. Measurements and Main Results: Sub-segmental broncho-provocation with allergen in mild asthmatics resulted in a remarkable increase in BAL fluid levels of LPA enriched in polyunsaturated 22:5 and 22:6 fatty acids in association with increased concentrations of ATX protein. Using a triple allergen mouse asthma model, we showed that ATX over-expressing transgenic mice had a more severe asthmatic phenotype, whereas blocking ATX activity and knockdown of the LPA2 receptor in mice produced a marked attenuation of Th2 cytokines and allergic lung inflammation. Conclusions: The ATX-LPA pathway plays a critical role in the pathogenesis of asthma. These preclinical data indicate that targeting the ATX-LPA pathway could be an effective anti-asthma treatment strategy.
    American Journal of Respiratory and Critical Care Medicine 09/2013; 188(8). DOI:10.1164/rccm.201306-1014OC · 13.00 Impact Factor
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    ABSTRACT: Chondroitin sulfate (CS) proteoglycans (CSPGs) are known to be primary inhibitors of neuronal regeneration at scar sites. However, a variety of CSPGs are also involved in neuronal growth and guidance at other physiological stages. Sulfation patterns of CS chains influence their interactions with various growth factors in the central nervous system (CNS), thus influencing neuronal growth, inhibition and pathfinding. This report demonstrates the use of differentially sulfated CS chains for neuronal navigation. Surface-immobilized patterns of CS glycosaminoglycan chains were used to determine neuronal preference towards specific sulfations of five CS variants: CS-A, CS-B (dermatan sulfate), CS-C, CS-D and CS-E. Neurons preferred CS-A, CS-B and CS-E and avoided CS-C containing lanes. In addition, significant alignment of neurites was observed using underlying lanes containing CS-A, CS-B and CS-E chains. In order to utilize differential preference of neurons towards the CS variants, a binary combinations of CS chains were created by backfilling a neuro-preferred CS variant between the microcontact printed lanes of CS-C stripes, which are avoided by neurons. The neuronal outgrowth results demonstrate for the first time that a combination of sulfation variants of CS chains without any protein component of CSPG is sufficient for directing neuronal outgrowth. Biomaterials with surface immobilized GAG chains could find numerous applications as bridging devices for tackling CNS injuries where directional growth of neurons is critical for recovery.
    Journal of the American Chemical Society 08/2013; 135(36):13488. DOI:10.1021/ja4056728 · 12.11 Impact Factor
  • Cancer Research 08/2013; 73(8 Supplement):3918-3918. DOI:10.1158/1538-7445.AM2013-3918 · 9.33 Impact Factor
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    ABSTRACT: To elucidate pathways in bladder inflammation, we employed our physiologically relevant LL-37 induced cystitis model. Based on inflammatory studies involving other organ systems implicating the receptor for advanced glycation end-products (RAGE), we first hypothesized that RAGE is critically involved in LL-37 induced cystitis. We further hypothesized a common RAGE ligand - high mobility group box 1 (HMGB1) is up-regulated in bladders challenged with LL-37. Finally, we hypothesized NF-κB dependent inflammatory genes are activated in LL-37 induced cystitis. Testing our first hypothesis, C57Bl/6 mice were challenged with either saline (control) or 320 μM of LL-37 intravesically for 1 hr. After 12 or 24 hours, tissues were examined with immunohistochemistry (IHC) for RAGE, and both mRNA and protein isolation for respective qRT-PCR and Western Blot analysis. Our second hypothesis was tested by employing HMGB1 IHC. Testing our final hypothesis, qRT-PCR was performed investigating five genes: TNFα, IL-6, IL-1β, GM-CSF, COX-2. In control and LL-37 challenged tissues, IHC for RAGE revealed similar qualitative expression. Evaluation with qRT-PCR and Western Blot for RAGE revealed diminished expression at the mRNA and protein level within LL-37 challenged bladders. IHC for HMGB1 revealed a moderate qualitative increase within LL-37 challenged tissues. Finally, with the exception of TNF α, all NF- κB dependent inflammatory genes yielded substantial up-regulation. We have employed our LL-37 induced cystitis model to gain insight towards a possible mechanistic pathway involved in bladder inflammation. This work provides data for future studies involving the inflammatory ligand HMGB1, RAGE, and receptor pathways that activate NF-κB.
    Advances in Bioscience and Biotechnology 08/2013; 4(8B):1-8. DOI:10.4236/abb.2013.48A2001

Publication Stats

25k Citations
2,862.01 Total Impact Points


  • 1993–2015
    • University of Utah
      • • Department of Medicinal Chemistry
      • • Department of BioEngineering
      • • Department of Chemistry
      Salt Lake City, Utah, United States
    • The Ohio State University
      Columbus, Ohio, United States
    • Johns Hopkins Medicine
      • Department of Neuroscience
      Baltimore, MD, United States
  • 2012
    • Biomedical Sciences Research Center Alexander Fleming
      • Institute of Immunology
      Vári, Attiki, Greece
  • 2005–2011
    • Salt Lake City Community College
      Salt Lake City, Utah, United States
  • 1996–2010
    • Simon Fraser University
      • Department of Chemistry
      Burnaby, British Columbia, Canada
    • Memorial Sloan-Kettering Cancer Center
      New York City, New York, United States
  • 1979–2010
    • State University of New York
      New York City, New York, United States
  • 1978–2010
    • Stony Brook University
      • • Department of Chemistry
      • • Department of Biochemistry and Cell Biology
      Stony Brook, New York, United States
  • 2006
    • University of Denver
      Denver, Colorado, United States
  • 2003–2005
    • Echelon Biosciences Incorporated
      Salt Lake City, Utah, United States
    • Rice University
      • Department of Biochemistry and Cell Biology
      Houston, Texas, United States
  • 2004
    • Icahn School of Medicine at Mount Sinai
      Manhattan, New York, United States
  • 2002
    • Oregon State University
      Corvallis, Oregon, United States
    • University of Oxford
      • Department of Biochemistry
      Oxford, ENG, United Kingdom
  • 1999
    • University of Alabama at Birmingham
      • Division of Molecular and Cellular Pathology
      Birmingham, Alabama, United States
  • 1978–1999
    • Cornell University
      • Department of Chemistry and Chemical Biology
      Итак, New York, United States
  • 1997
    • Yamagata University
      Ямагата, Yamagata, Japan
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 1995
    • Stony Brook University Hospital
      Stony Brook, New York, United States
    • Albert Einstein College of Medicine
      • Department of Molecular Pharmacology
      New York, New York, United States
    • York University
      • Department of Biology
      Toronto, Ontario, Canada
  • 1985–1995
    • University of California, Davis
      • Department of Environmental Toxicology
      Davis, California, United States
  • 1994
    • University of Nebraska at Lincoln
      • Department of Chemistry
      Lincoln, Nebraska, United States
  • 1992
    • Hohenheim University
      • Institute of Physiology
      Stuttgart, Baden-Württemberg, Germany
  • 1991
    • Johns Hopkins University
      Baltimore, Maryland, United States
  • 1981–1991
    • CUNY Graduate Center
      New York, New York, United States
  • 1990
    • Semmelweis University
      • Department of Medical Microbiology
      Budapeŝto, Budapest, Hungary
  • 1982
    • University of North Carolina at Chapel Hill
      • Department of Chemistry
      North Carolina, United States
  • 1980
    • University of Malaya
      • Department of Chemistry
      Kuala Lumpor, Kuala Lumpur, Malaysia
  • 1976–1977
    • Columbia University
      • Department of Chemistry
      New York, New York, United States
  • 1975–1977
    • icipe – International Centre of Insect Physiology and Ecology
      Nairoba, Nairobi Area, Kenya