B.S., Gannon University Ph.D., University of Minnesota Post-Doctoral, Harvard Medical School
Research Interests Dr. Beitz's laboratory has several lines of ongoing research. One of the current projects focuses on identifying factors secreted by tumors that cause cancer pain in animals and humans (the neurochemical and molecular basis of cancer pain). His laboratory has been involved with developing several animal models of cancer pain. We are also interested in the mechanisms underlying tumor metastasis focusing on bone metastasis and metastasis of pancreatic tumors. Microperfusion studies are underway to identify the substances secreted by tumors. Once the substances are identified tumor cells are transfected with siRNA constructs to knockdown these substances in order to determine the role they play in tumor-induced pain and/or tumor metastasis. A second major research project in the lab focuses on investigating the basis for gender differences observed in certain pain syndromes. A number of pain syndromes are more common in females than males and this project attempts to elucidate the mechanisms responsible for these sex differences. We are also investigating the mechanisms that underlie the development of pain in a mouse model of multiple sclerosis. Finally, work is being done to determine the neural mechanisms responsible for acupuncture’s analgesic and anti-inflammatory effects.
Selected Publications
(For a comprehensive list of Dr. Beitz's recent publications, refer to PubMed, a service provided by the National Library of Medicine.)
Pacharinsak, C and Beitz, A.J. (2008) Animal Models of Cancer Pain (review). Comparative Medicine 58:220-233.
Lynch, JL, Gallus, NJ, Ericson ME, Beitz AJ (2008) Analysis of nociception, sex and peripheral nerve innervation in the TMEV animal model of multiple sclerosis. Pain 136 (3):293-304.
Lynch, JL, Alley, JF, Wellman L, Beitz AJ (2008) Decreased spinal cord opioid receptor expression and antinociception in a TMEV mouse model of multiple sclerosis. Brain Research 1191:180-91.
Kim HW, Uh DK, Yoon SY, Roh DH, Kwon YB, Han HJ, Lee HJ, Beitz AJ, Lee JH. (2008) Low-frequency electroacupuncture suppresses carrageenan-induced paw inflammation in mice via sympathetic post-ganglionic neurons, while high-frequency EA suppression is mediated by the sympathoadrenal medullary axis. Brain Res. Bull. 75:698-705.
Kim, H-W, Roh, D-H, Yoon, S-Y, Kwon, Y-B, Han, H-J, Kim, K-W, Beitz, A.J. and Lee, J-H. (2008) Activation of spinal sigma-1 receptor enhances NMDA-induced pain via PKC and PKA-dependent phosphorylations of the NMDA receptor NR 1 subunit in mice. British Journal of Pharmacology 154(5):1125-1134.
Schreiber KL, Beitz AJ, Wilcox GL (2008) Activation of spinal microglia in a murine model of peripheral inflammation-induced, long-lasting contralateral allodynia. Neurosci Lett. 440(1):63-67.
Roh DH, Kim HW, Yoon SY, Seo HS, Kwon YB, Han HJ, Beitz AJ, Lee JH (2008) Intrathecal Clonidine Suppresses Phosphorylation of the NMDA Receptor NR1 Subunit in Spinal Dorsal Horn Neurons of Rats with Neuropathic Pain. Anesthesia and Analgesia 107:693-700.
Pacharinsak, C., Khasabov, S.G., Beitz, A.J., Simone, DA (2008) NK-1 Receptors in the Rostral Ventromedial Medulla (RVM) Contribute to Hyperalgesia Produced by Intraplantar Injection of Capsaicin. Pain (in Press)
Khasabova JA, Stucky CL, Harding-Rose C, Eikmeier L, Beitz, AJ, Coicou LG, Hanson AE, Simone DA, Seybold VS. (2007) Chemical interactions between fibrosarcoma cancer cells and sensory neurons contribute to cancer pain. J. Neuroscience 27(38):10289-10298.
Vit, J.P., Ohara, P.T., Tien, D., Fike, J., Eikmeier, L., Beitz, A., Wilcox, G., Jasmin, L. (2006) The analgesic effect of low dose radiation in a mouse model of bone metastasis is associated with a decreased inflammatory response in the spinal cord. Pain 120(1-2):188-201.
Current Funding:
1. NIH/NCI (R01-CA84233), Title: Cancer Pain: Nerve/Tumor Interactions; Beitz, Principal Investigator; $1,831,189 (total costs 09/07-07/12), project period12/01/1999 – 07/31/2012.