Alvin J. Beitz

e-mail: beitz001@umn.edu

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.

Schiller, KA, Zillhardt, MR, Alley J, Borjesson DL, Beitz, AJ, Mauro, LJ. (2009) Secretion of MCP-1 and other paracrine factors in a novel tumor-bone co-culture model. BMC Cancer 9:45. PMID: 19192289

Roh DH, Yoon SY, Seo HS, Kang SY, Han HJ, Beitz AJ, Lee JH. (2010) Intrathecal injection of carbenoxolone, a gap junction decoupler, attenuates the induction of below-level neuropathic pain after spinal cord injury in rats. Exp Neurol. 224(1):123-32. PMID: 20226782

Roh DH, Yoon SY, Seo HS, Kang SY, Moon JY, Song S, Beitz AJ, Lee JH. (2010) Sigma-1 receptor-induced increase in murine spinal NR1 phosphorylation is mediated by the PKC-alpha and epsilon, but not the PKC-zeta isoforms. Neurosci Lett. 477(2):95-9. PMID: 20600171.

Seo HS, Roh DH, Kwon SG, Yoon SY, Kang SY, Moon JY, Choi SR, Beitz AJ, Lee JH. (2011) Acidic pH facilitates peripheral αβmeATP-mediated nociception in rats: differential roles of P2X, P2Y, ASIC and TRPV1 receptors in ATP-induced mechanical allodynia and thermal hyperalgesia. Neuropharmacology. 60(4):580-6.  PMID: 21172361

Roh DH, Choi SR, Yoon SY, Kang SY, Moon JY, Kwon SG, Han HJ, Beitz AJ, Lee JH. (2011) Spinal nNOS activation mediates sigma-1 receptor-induced mechanical and thermal hypersensitivity in mice: involvement of PKC-dependent NR1 phosphorylation. Br J Pharmacol. 2011 Mar 10. doi: 10.1111/j.1476-5381.2011.01316.x. [Epub ahead of print]] PMID: 21391983

Wacnik, PW, Pacharinsak, C, Beitz, AJ (2011) Animal Models of Cancer Pain. In Chao Ma and Jun-Ming Zhang (eds.), Animal Models of Pain, Neuromethods, vol. 49, 117-145; Springer.

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. 

2. NIH (R01HD052074), Title: GABAergic Dysfunction in Autism. Fatemi, Principal Investigator,; Beitz, Coinvestigator.. $1,511,395 (total costs) Project period: 08/15/2007 –    05/31/2012.

3. NIH; Neuroscience Training Program, Beitz, Trainer, (T. Ebner, P.I.), $70,000/yr, 7/1/09-6/30/13.

4. NIH (NIDA) Psychoneuroimmunology Training Program, Beitz, Coinvestigator (T. Molitor, P.I.), $2,939,585, 7/1/09-6/30/12.

5. NIH (NIDA) Psychoneuroimmunology Training Program, Beitz, Coinvestigator (T. Molitor, P.I.), $2,939,585, 7/1/06-6/30/09.

6. NIH; Neuroscience Training Program, Beitz, Trainer, (T. Ebner, P.I.), $70,000/yr, 7/1/04-6/30/08.