Abstract

Animal modeling and the reproducibility of the model are important aspects in obtaining potentially clinically as well as biologically relevant information. Thus, the first goal of the Animal Models Core is to provide a well-controlled and consistent source of tissue, blood and plasma samples from animals subjected to the various models proposed in this grant to the Project leaders. The second goal is to promote the integration of the results obtained in the various projects with each other as well as to reduce costs and limit the number of animals required to carry out the proposed studies. By centralizing the expertise and equipment required to carry out the various trauma-hemorrhagic shock (T/HS) and trauma-sham-shock (T/SS) models in one location, the consistency of the results obtained will be increased, while the overall costs and number of animals used will be significantly reduced. Also by creating an animal registry, the results observed in specific animal tested in the different projects can be integrated with each other to form a more complete physiologic picture.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Specialized Center (P50)
Project #
5P50GM069790-05
Application #
8116419
Study Section
Special Emphasis Panel (ZGM1)
Project Start
Project End
Budget Start
2010-06-01
Budget End
2011-05-31
Support Year
5
Fiscal Year
2010
Total Cost
$361,959
Indirect Cost

  Institution

Name
University of Medicine & Dentistry of NJ
Department
Type
DUNS #
623946217
City
Newark
State
NJ
Country
United States
Zip Code
07107

  Publications

Reino, Diego C; Palange, David; Feketeova, Elenora et al. (2012) Activation of toll-like receptor 4 is necessary for trauma hemorrhagic shock-induced gut injury and polymorphonuclear neutrophil priming. Shock 38:107-14
Sheth, Sharvil U; Palange, David; Xu, Da-Zhong et al. (2011) Testosterone depletion or blockade in male rats protects against trauma hemorrhagic shock-induced distant organ injury by limiting gut injury and subsequent production of biologically active mesenteric lymph. J Trauma 71:1652-8
Reino, Diego C; Pisarenko, Vadim; Palange, David et al. (2011) Trauma hemorrhagic shock-induced lung injury involves a gut-lymph-induced TLR4 pathway in mice. PLoS One 6:e14829
Kannan, Kolenkode B; Colorado, Iriana; Reino, Diego et al. (2011) Hypoxia-inducible factor plays a gut-injurious role in intestinal ischemia reperfusion injury. Am J Physiol Gastrointest Liver Physiol 300:G853-61
Condon, Michael; Senthil, Maheswari; Xu, Da-Zhong et al. (2011) Intravenous injection of mesenteric lymph produced during hemorrhagic shock decreases RBC deformability in the rat. J Trauma 70:489-95
Qin, Yong; Prescott, Lauriston M; Deitch, Edwin A et al. (2011) Heparin use in a rat hemorrhagic shock model induces biologic activity in mesenteric lymph separate from shock. Shock 35:411-21
Sharpe, Susan M; Qin, Xiaofa; Lu, Qi et al. (2010) Loss of the intestinal mucus layer in the normal rat causes gut injury but not toxic mesenteric lymph nor lung injury. Shock 34:475-81
Doucet, Danielle; Badami, Chirag; Palange, David et al. (2010) Estrogen receptor hormone agonists limit trauma hemorrhage shock-induced gut and lung injury in rats. PLoS One 5:e9421
Doucet, Danielle R; Bonitz, R Paul; Feinman, Rena et al. (2010) Estrogenic hormone modulation abrogates changes in red blood cell deformability and neutrophil activation in trauma hemorrhagic shock. J Trauma 68:35-41
Mohr, Alicia M; Lavery, Robert F; Sifri, Ziad C et al. (2010) Gender differences in glucose variability after severe trauma. Am Surg 76:896-902

Showing the most recent 10 out of 23 publications