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854 results on '"Hogaboam, Cory M"'

153. Acute Myocardial Infarction and Pulmonary Diseases Result in Two Different Degradation Profiles of Elastin as Quantified by Two Novel ELISAs

Author

Skjøt-Arkil, Helene, Clausen, Rikke E, Rasmussen, Lars M, Wang, Wanchun, Wang, Yaguo, Zheng, Qinlong, Mickley, Hans, Saaby, Lotte, Diederichsen, Axel C P, Lambrechtsen, Jess, Martinez, Fernando J, Hogaboam, Cory M, Han, Meilan, Larsen, Martin R, Nawrocki, Arkadiusz, Vainer, Ben, Krustrup, Dorrit, Bjørling-Poulsen, Marina, Karsdal, Morten A, Leeming, Diana J, Skjøt-Arkil, Helene, Clausen, Rikke E, Rasmussen, Lars M, Wang, Wanchun, Wang, Yaguo, Zheng, Qinlong, Mickley, Hans, Saaby, Lotte, Diederichsen, Axel C P, Lambrechtsen, Jess, Martinez, Fernando J, Hogaboam, Cory M, Han, Meilan, Larsen, Martin R, Nawrocki, Arkadiusz, Vainer, Ben, Krustrup, Dorrit, Bjørling-Poulsen, Marina, Karsdal, Morten A, and Leeming, Diana J

Abstract

BACKGROUND: Elastin is a signature protein of the arteries and lungs, thus it was hypothesized that elastin is subject to enzymatic degradation during cardiovascular and pulmonary diseases. The aim was to investigate if different fragments of the same protein entail different information associated to two different diseases and if these fragments have the potential of being diagnostic biomarkers.METHODS: Monoclonal antibodies were raised against an identified fragment (the ELM-2 neoepitope) generated at the amino acid position '552 in elastin by matrix metalloproteinase (MMP) -9/-12. A newly identified ELM neoepitope was generated by the same proteases but at amino acid position '441. The distribution of ELM-2 and ELM, in human arterial plaques and fibrotic lung tissues were investigated by immunohistochemistry. A competitive ELISA for ELM-2 was developed. The clinical relevance of the ELM and ELM-2 ELISAs was evaluated in patients with acute myocardial infarction (AMI), no AMI, high coronary calcium, or low coronary calcium. The serological release of ELM-2 in patients with chronic obstructive pulmonary disease (COPD) or idiopathic pulmonary fibrosis (IPF) was compared to controls.RESULTS: ELM and ELM-2 neoepitopes were both localized in diseased carotid arteries and fibrotic lungs. In the cardiovascular cohort, ELM-2 levels were 66% higher in serum from AMI patients compared to patients with no AMI (p<0.01). Levels of ELM were not significantly increased in these patients and no correlation was observed between ELM-2 and ELM. ELM-2 was not elevated in the COPD and IPF patients and was not correlated to ELM. ELM was shown to be correlated with smoking habits (p<0.01).CONCLUSIONS: The ELM-2 neoepitope was related to AMI whereas the ELM neoepitope was related to pulmonary diseases. These results indicate that elastin neoepitopes generated by the same proteases but at different amino acid sites provide different tissue-related information

Published
2013

154. The Toll-like Receptor 3 L412F Polymorphism and Disease Progression in Idiopathic Pulmonary Fibrosis

Author

O’Dwyer, David N., primary, Armstrong, Michelle E., additional, Trujillo, Glenda, additional, Cooke, Gordon, additional, Keane, Michael P., additional, Fallon, Padraic G., additional, Simpson, A. John, additional, Millar, Ann B., additional, McGrath, Emmet E., additional, Whyte, Moira K., additional, Hirani, Nik, additional, Hogaboam, Cory M., additional, and Donnelly, Seamas C., additional

Published
2013
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156. Novel Protective Effects of Stem Cell Factor in a Murine Model of Acute Septic Peritonitis : Dependence on MCP-1

Author

Bone-Larson, Cynthia L., Hogaboam, Cory M., Steinhauser, Matthew L., Oliveira, Sandra H. P., Lukacs, Nicholas W., Strieter, Robert M., and Kunkel, Steven L.

Subjects
Cell Nucleus, STAT3 Transcription Factor, Stem Cell Factor, Tumor Necrosis Factor-alpha, Mice, Inbred Strains, Punctures, Peritonitis, Interleukin-10, DNA-Binding Proteins, Mice, Liver, embryonic structures, Acute Disease, Trans-Activators, Animals, Female, Mast Cells, Therapeutic Irrigation, Cecum, Ligation, Chemokine CCL2, Regular Articles
Abstract

Mast cells participate in the host response during sepsis and have been shown to have a protective effect in a murine model of acute septic peritonitis and multi-organ failure initiated by cecal ligation and puncture (CLP). Stem cell factor (SCF) is a hematopoietic cytokine important in mast cell proliferation and activation. In the present study, we examined the protective effects of a single intraperitoneal injection of SCF given 2 hours before CLP surgery in mice. Four days after the CLP surgery, SCF pretreatment significantly improved mouse survival from 29 to 56% and mast cells were absolutely required for this effect. Immunoneutralization studies revealed that the SCF-stimulated release of monocyte chemoattractant protein-1 (MCP-1) into the septic peritoneal cavity contributed to the protective effect of SCF in this model. One potential cellular source of MCP-1 was the SCF-activated mast cell. In addition, SCF pretreatment significantly augmented circulating levels of SCF and the immunomodulatory cytokine interleukin-10 in septic mice, in part because the SCF pretreatment seemed to promote the release of both mediators from the liver. Additional hepatic effects of SCF treatment included an accelerated expression of hepatic levels of signal transducer and activator of transcription-3 (STAT-3) in CLP mice pretreated with SCF. Taken together, the findings from the present study demonstrate that the intraperitoneal delivery of SCF has a major protective effect in a murine model of CLP.

Published
2000

157. CC chemokine receptor 4 modulates Toll-like receptor 9-mediated innate immunity and signaling

Author

Immunology Program, Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA, Ishii, Makoto, Hogaboam, Cory M., Joshi, Amrita, Ito, Toshihiro, Fong, Daniel J., Immunology Program, Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA, Ishii, Makoto, Hogaboam, Cory M., Joshi, Amrita, Ito, Toshihiro, and Fong, Daniel J.

Abstract

The present study addressed the modulatory role of CC chemokine receptor 4 (CCR4) in Toll-like receptor (TLR) 9-mediated innate immunity and explored the underlying molecular mechanisms. Our results demonstrated that CCR4-deficient mice were resistant to both septic peritonitis induced by cecal ligation and puncture (CLP) and CpG DNA/D-galactosamine-induced shock. In bone marrow-derived macrophages (BMMφ) from CLP-treated CCR4-deficient mice, TLR9-mediated pathways of MAPK/AP-1, PI3K/Akt, and IκB kinase (IKK)/NF-κB were impaired compared to wild-type (WT) cells. While TLR9 expression was not altered, the intensity of internalized CpG DNA was increased in CCR4-deficient macrophages when compared to WT macrophages. Pharmacological inhibitor studies revealed that impaired activation of JNK, PI3K/Akt, and/or IKK/NF-κB could be responsible for decreased proinflammatory cytokine expression in CCR4-deficient macrophages. Interestingly, the CCR4-deficient BMMφ exhibited an alternatively activated (M2) phenotype and the impaired TLR9-mediated signal transduction responses in CCR4-deficient cells were similar to the signaling responses observed in WT BMMφ skewed to an alternatively activated phenotype. These results indicate that macrophages deficient in CCR4 impart a regulatory influence on TLR9-mediated innate immunity.

Published
2008

158. IL-13 Immunotoxin Accelerates Resolution of Lung Pathological Changes Triggered by Silica Particles in Mice

Author

Ferreira, Tatiana Paula T., primary, de Arantes, Ana Carolina S., additional, do Nascimento, Caio Victor M. F., additional, Olsen, Priscilla C., additional, Trentin, Patrícia G., additional, Rocco, Patricia R. M., additional, Hogaboam, Cory M., additional, Puri, Raj K., additional, Martins, Marco Aurélio, additional, and Silva, Patrícia Machado Rodrigues e, additional

Published
2013
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159. Cytokine Induced Phenotypic and Epigenetic Signatures Are Key to Establishing Specific Macrophage Phenotypes

Author

Kittan, Nicolai A., primary, Allen, Ronald M., additional, Dhaliwal, Abhay, additional, Cavassani, Karen A., additional, Schaller, Matthew, additional, Gallagher, Katherine A., additional, Carson, William F., additional, Mukherjee, Sumanta, additional, Grembecka, Jolanta, additional, Cierpicki, Tomasz, additional, Jarai, Gabor, additional, Westwick, John, additional, Kunkel, Steven L., additional, and Hogaboam, Cory M., additional

Published
2013
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160. Animal Models of Fibrotic Lung Disease

Author

B. Moore, Bethany, primary, Lawson, William E., additional, Oury, Tim D., additional, Sisson, Thomas H., additional, Raghavendran, Krishnan, additional, and Hogaboam, Cory M., additional

Published
2013
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161. Acute Myocardial Infarction and Pulmonary Diseases Result in Two Different Degradation Profiles of Elastin as Quantified by Two Novel ELISAs

Author

Skjøt-Arkil, Helene, primary, Clausen, Rikke E., additional, Rasmussen, Lars M., additional, Wang, Wanchun, additional, Wang, Yaguo, additional, Zheng, Qinlong, additional, Mickley, Hans, additional, Saaby, Lotte, additional, Diederichsen, Axel C. P., additional, Lambrechtsen, Jess, additional, Martinez, Fernando J., additional, Hogaboam, Cory M., additional, Han, MeiLan, additional, Larsen, Martin R., additional, Nawrocki, Arkadiusz, additional, Vainer, Ben, additional, Krustrup, Dorrit, additional, Bjørling-Poulsen, Marina, additional, Karsdal, Morten A., additional, and Leeming, Diana J., additional

Published
2013
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162. Toll Like Receptor 3 Plays a Critical Role in the Progression and Severity of Acetaminophen-Induced Hepatotoxicity

Author

Cavassani, Karen A., primary, Moreira, Ana Paula, additional, Habiel, David, additional, Ito, Toshihiro, additional, Coelho, Ana Lucia, additional, Allen, Ron M., additional, Hu, Bin, additional, Raphelson, Janna, additional, Carson, William F., additional, Schaller, Matthew A., additional, Lukacs, Nicholas W., additional, Omary, M. Bishr, additional, Hogaboam, Cory M., additional, and Kunkel, Steven L., additional

Published
2013
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163. Surrogate Antibodies That Specifically Bind and Neutralize CCL17 But Not CCL22

Author

Santulli-Marotto, Sandra, primary, Fisher, Jamie, additional, Petley, Theodore, additional, Boakye, Ken, additional, Panavas, Tadas, additional, Luongo, Jennifer, additional, Kavalkovich, Karl, additional, Rycyzyn, Michael, additional, Wu, Bingyuan, additional, Gutshall, Lester, additional, Coelho, Ana, additional, Hogaboam, Cory M., additional, and Ryan, Mary, additional

Published
2013
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165. Bleomycin Induces Molecular Changes Directly Relevant to Idiopathic Pulmonary Fibrosis: A Model for “Active” Disease

Author

Peng, Ruoqi, primary, Sridhar, Sriram, additional, Tyagi, Gaurav, additional, Phillips, Jonathan E., additional, Garrido, Rosario, additional, Harris, Paul, additional, Burns, Lisa, additional, Renteria, Lorena, additional, Woods, John, additional, Chen, Leena, additional, Allard, John, additional, Ravindran, Palanikumar, additional, Bitter, Hans, additional, Liang, Zhenmin, additional, Hogaboam, Cory M., additional, Kitson, Chris, additional, Budd, David C., additional, Fine, Jay S., additional, Bauer, Carla MT., additional, and Stevenson, Christopher S., additional

Published
2013
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166. The chemokine receptor CCR6 is an important component of the innate immune response

Author

Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA, Immunobiology Center, Mount Sinai School of Medicine, New York, NY, USA, Wen, Haitao, Hogaboam, Cory M., Lukacs, Nicholas W., Cook, Donald N., Lira, Sergio A., Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA, Immunobiology Center, Mount Sinai School of Medicine, New York, NY, USA, Wen, Haitao, Hogaboam, Cory M., Lukacs, Nicholas W., Cook, Donald N., and Lira, Sergio A.

Abstract

In our initial studies we found that naÏve CCR6-deficient (CCR6 –/– ) C57BL/6 mice possessed significantly lower number of both F4/80 + macrophages and dendritic cells (DC), but higher number of B cells in the peritoneal cavity, as compared to naÏve wild type (WT) controls. Furthermore, peritoneal macrophages isolated from CCR6 –/– mice expressed significantly lower levels of inflammatory cytokines and nitric oxide following lipopolysaccharide (LPS)stimulation, as compared to WT macrophages. In a severe experimental peritonitis model induced by cecal ligation and puncture (CLP), CCR6 –/– mice were protected when compared with WT controls. At 24 h following the induction of peritonitis, CCR6 –/– mice exhibited significantly lower levels of inflammatory cytokines/chemokines in both the peritoneal cavity and blood. Interestingly, DC recruitment into the peritoneal cavity was impaired in CCR6 –/– mice during the evolution of CLP-induced peritonitis. Peritoneal macrophages isolated from surviving CCR6 –/– mice 3 days after CLP-induced peritonitis exhibited an enhanced LPS response compared with similarly treated WT peritoneal macrophages. These data illustrate that CCR6 deficiency alters the innate response via attenuating the hyperactive local and systemic inflammatory response during CLP-induced peritonitis.

Published
2007

167. IL-18 modulates chronic fungal asthma in a murine model; putative involvement of Toll-like receptor-2

Author

Department of Pathology, University of Michigan Medical School, 1301 Catherine Road, Ann Arbor MI, 48109-0602, USA, Fax: ++1 734 764 2397, e-mail: hogaboam@med.umich.edu, US, Ann Arbor, Hogaboam, Cory M., Blease, K., Kunkel, Steven L., Department of Pathology, University of Michigan Medical School, 1301 Catherine Road, Ann Arbor MI, 48109-0602, USA, Fax: ++1 734 764 2397, e-mail: hogaboam@med.umich.edu, US, Ann Arbor, Hogaboam, Cory M., Blease, K., and Kunkel, Steven L.

Abstract

Fungus-induced asthmatic disease is characterized by persistent airway hyperreactivity and remodeling.?? Objective and design: To determine the role of IL-18 in the allergic airway response to Aspergillus fumigatus conidia in a murine model of A. fumigatus -induced asthma.?? Methods: A. fumigatus -sensitized mice were depleted of IL-18 using a polyclonal anti-IL-18 antibody for 3 days after a conidia challenge.?? Results: Airway hyperresponsiveness and eosinophil numbers were significantly elevated 3-30 days after conidia challenge compared to the normal serum-treated group. Histological evidence showed retention of A. fumigatus conidia, airway remodeling, subepithelial fibrosis, and increased collagen deposition in the lungs of IL-18-depleted mice at day 30 after the conidia challenge. Prolonged retention of conidia in IL-18 depleted A. fumigatus -sensitized mice was associated with decreased Toll-like receptor-2 (TLR-2) expression compared with the control group.?? Conclusions: IL-18 modulates the innate immune response against A. fumigatus conidia and prevents the development of severe fungus-induced asthmatic disease.

Published
2006

168. III. Chemokines and other mediators, 8. Chemokines and their receptors in cell-mediated immune responses in the lung

Author

Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109, Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109 ; Department of Pathology, University of Michigan Medical School, Med Sci I, Rm 5214, 1301 Catherine Rd., Ann Arbor, MI 48109, Department of Pathology, Veteran Affairs Medical Center, Ann Arbor, Michigan 48105, Matsukawa, Akihiro, Lukacs, Nicholas W., Hogaboam, Cory M., Chensue, Stephen W., Kunkel, Steven L., Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109, Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109 ; Department of Pathology, University of Michigan Medical School, Med Sci I, Rm 5214, 1301 Catherine Rd., Ann Arbor, MI 48109, Department of Pathology, Veteran Affairs Medical Center, Ann Arbor, Michigan 48105, Matsukawa, Akihiro, Lukacs, Nicholas W., Hogaboam, Cory M., Chensue, Stephen W., and Kunkel, Steven L.

Abstract

Chemokines constitute a large family of chemotactic cytokines that belong to a super-gene family of 8-10 kDa proteins. The chemokines are considered to be primarily beneficial in host defense against invading pathogens. However, the reactions induced by chemokines can be occasionally excessive, resulting in a harmful response to the host. Recent studies in chemokine biology have elucidated that chemokines are involved in the initiation, development, and maintenance of numbers of diseases including lung diseases. In addition to its chemotactic activity, evidence suggests that chemokines can modify the outcome of the cell-mediated immune responses by altering the Th1/Th2 cytokine profile. Chemokines are also capable of dictating the direction of specific immune responses. Chemokine action is mediated by a large super-family of G-protein coupled receptors, and the receptors are preferentially expressed on Th1/Th2 cells. Certain chemokine receptors are constitutively expressed in immune surveying cells such as dendritic cells and naive T cells. The corresponding chemokines are present in normal lymphoid tissues, suggesting a role of chemokines/receptors in cell homing and cell-cell communication in lymphoid tissue that can be an initial step for immune recognition. Thus, comprehension of the chemokine biology in immune responses appears to be fundamental for understanding the pathogenesis of T cell-mediated immune responses. The following review will highlight the current insight into the role of chemokines and their receptors in the cell-mediated immune response, with a special focus on lung diseases. Microsc. Res. Tech. 53:298-306, 2001. © 2001 Wiley-Liss, Inc.

Published
2006

174. Genomic And Phenotypic Characterization Of Fibroblasts From Normal As Well As Stable And Rapidly Progressing Idiopathic Pulmonary Fibrosis (IPF) Patients

Author

Kitson, Christopher, primary, Coelho, Ana Lucia, additional, Sridhar, Sriram, additional, Tang, Xiaoyan, additional, Deguzman, Jeremy, additional, Jung, Jimmy, additional, Allard, John, additional, Bitter, Hans, additional, Martinez, Fernando J., additional, Fuentes, Maria, additional, Hogaboam, Cory M., additional, DeMartino, Julie, additional, and Budd, David, additional

Published
2012
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176. Erratum: Amelioration of sepsis by inhibiting sialidase-mediated disruption of the CD24-SiglecG interaction

Author

Chen, Guo-Yun, primary, Chen, Xi, additional, King, Samantha, additional, Cavassani, Karen A, additional, Cheng, Jiansong, additional, Zheng, Xincheng, additional, Cao, Hongzhi, additional, Yu, Hai, additional, Qu, Jingyao, additional, Fang, Dexing, additional, Wu, Wei, additional, Bai, Xue-Feng, additional, Liu, Jin-Qing, additional, Woodiga, Shireen A, additional, Chen, Chong, additional, Sun, Lei, additional, Hogaboam, Cory M, additional, Kunkel, Steven L, additional, Zheng, Pan, additional, and Liu, Yang, additional

Published
2012
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177. Repeated Exposure to Aspergillus fumigatus Conidia Results in CD4 + T Cell-Dependent and -Independent Pulmonary Arterial Remodeling in a Mixed Th1/Th2/Th17 Microenvironment That Requires Interleukin-4 (IL-4) and IL-10

Author

Shreiner, Andrew B., primary, Murdock, Benjamin J., additional, Sadighi Akha, Amir A., additional, Falkowski, Nicole R., additional, Christensen, Paul J., additional, White, Eric S., additional, Hogaboam, Cory M., additional, and Huffnagle, Gary B., additional

Published
2012
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181. A Micro RNA Processing Defect in Rapidly Progressing Idiopathic Pulmonary Fibrosis

Author

Oak, Sameer R., primary, Murray, Lynne, additional, Herath, Athula, additional, Sleeman, Matthew, additional, Anderson, Ian, additional, Joshi, Amrita D., additional, Coelho, Ana Lucia, additional, Flaherty, Kevin R., additional, Toews, Galen B., additional, Knight, Darryl, additional, Martinez, Fernando J., additional, and Hogaboam, Cory M., additional

Published
2011
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185. High-Throughput Plasma Biomarker Analysis In Ipf Reveals An Extracellular Matrix Remodeling Signature

Author

White, Eric S., primary, Cornett, Ashley M., additional, Cheng, Ling, additional, Dreffs, Alyssa A., additional, Yan, Mei, additional, Sagana, Rommel L., additional, Booth, Adam J., additional, Moore, Bethany B., additional, Lama, Vibha N., additional, Hogaboam, Cory M., additional, Schmidt, Shelley L., additional, Toews, Galen B., additional, Flaherty, Kevin R., additional, Martinez, Fernando J., additional, and Kurtis, Jonathan D., additional

Published
2011
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187. Amelioration of sepsis by inhibiting sialidase-mediated disruption of the CD24-SiglecG interaction

Author

Chen, Guo-Yun, primary, Chen, Xi, additional, King, Samantha, additional, Cavassani, Karen A, additional, Cheng, Jiansong, additional, Zheng, Xincheng, additional, Cao, Hongzhi, additional, Yu, Hai, additional, Qu, Jingyao, additional, Fang, Dexing, additional, Wu, Wei, additional, Bai, Xue-Feng, additional, Liu, Jin-Qing, additional, Woodiga, Shireen A, additional, Chen, Chong, additional, Sun, Lei, additional, Hogaboam, Cory M, additional, Kunkel, Steven L, additional, Zheng, Pan, additional, and Liu, Yang, additional

Published
2011
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188. TGF-beta driven lung fibrosis is macrophage dependent and blocked by Serum amyloid P

Author

Murray, Lynne A., primary, Chen, Qingsheng, additional, Kramer, Michael S., additional, Hesson, David P., additional, Argentieri, Rochelle L., additional, Peng, Xueyang, additional, Gulati, Mridu, additional, Homer, Robert J., additional, Russell, Thomas, additional, van Rooijen, Nico, additional, Elias, Jack A., additional, Hogaboam, Cory M., additional, and Herzog, Erica L., additional

Published
2011
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189. Triggering Receptor Expressed on Myeloid cells-1 (TREM-1) Modulates Immune Responses to Aspergillus fumigatus During Fungal Asthma in Mice

Author

Buckland, Karen F., primary, Ramaprakash, Hemanth, additional, Murray, Lynne A., additional, Carpenter, Kristin J., additional, Choi, Esther S., additional, Kunkel, Steven L., additional, Lukacs, Nicholas W., additional, Xing, Zhou, additional, Aoki, Naoko, additional, Hartl, Dominik, additional, and Hogaboam, Cory M., additional

Published
2011
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190. TLR9 Differentiates Rapidly from Slowly Progressing Forms of Idiopathic Pulmonary Fibrosis

Author

Trujillo, Glenda, primary, Meneghin, Alessia, additional, Flaherty, Kevin R., additional, Sholl, Lynette M., additional, Myers, Jeffrey L., additional, Kazerooni, Ella A., additional, Gross, Barry H., additional, Oak, Sameer R., additional, Coelho, Ana Lucia, additional, Evanoff, Holly, additional, Day, Elizabeth, additional, Toews, Galen B., additional, Joshi, Amrita D., additional, Schaller, Matthew A., additional, Waters, Beatrice, additional, Jarai, Gabor, additional, Westwick, John, additional, Kunkel, Steven L., additional, Martinez, Fernando J., additional, and Hogaboam, Cory M., additional

Published
2010
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195. Delta-Like 4 Differentially Regulates Murine CD4+ T Cell Expansion via BMI1

Author

Schaller, Matthew A., primary, Logue, Hannah, additional, Mukherjee, Sumanta, additional, Lindell, Dennis M., additional, Coelho, Ana Lucia, additional, Lincoln, Pamela, additional, Carson, William F., additional, Ito, Toshihiro, additional, Cavassani, Karen A., additional, Chensue, Stephen W., additional, Hogaboam, Cory M., additional, Lukacs, Nicholas W., additional, and Kunkel, Steven L., additional

Published
2010
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196. The antifibrotic effects of plasminogen activation occur via prostaglandin E2 synthesis in humans and mice

Author

Bauman, Kristy A., primary, Wettlaufer, Scott H., additional, Okunishi, Katsuhide, additional, Vannella, Kevin M., additional, Stoolman, Joshua S., additional, Huang, Steven K., additional, Courey, Anthony J., additional, White, Eric S., additional, Hogaboam, Cory M., additional, Simon, Richard H., additional, Toews, Galen B., additional, Sisson, Thomas H., additional, Moore, Bethany B., additional, and Peters-Golden, Marc, additional

Published
2010
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