petent Balb/c mice, showing that these effects did not involve anti- tumor T lymphocyte responses.Ongoing studies seek to evaluate the molecular targets of sympathetic signaling in micrometastases, and define the role of inflammation and innate immune responses in mediating these effects. doi:10.1016/j.bbi.2009.06.119 115. Multiple stress-related mechanisms mediate in vivo sup- pression of IL-12 serum levels in rats L. Sominsky,S.Shemer,M. Benish,S. Ben-Eliyahu Tel Aviv University, Neuroimmunology Research Unit, Dept.of Psychol- ogy,Tel Aviv,Israel IL-12 is the major Th1 differentiation factor,and a potent pro- inflammatory/pro-CMI-Th1 cytokine.Stress is believed to perturb Th1 status, but the evidence is mostly based on in vitro induced pro- duction (IVIP) studies that are affected by sample cellular composi- tion, and employ adjuvant stimulation in an artificialmilieu. Here we studied serum IL-12 levels in rats following different stress par- adigms,in vivo stress hormone administration, and employment of specific blockers.Simultaneously,IL-12 IVIP was studied. Results: Corticosterone (1 mg/kg/h), epinephrine (0.02 mg/kg/h), and prosta- glandin (0.03 mg/kg/h) administered in a slow-release preparation and at physiologically relevant doses, each reduced baseline IL-12 serum levels (300 pg/ml) by up to 3-fold at 5 and 10 h after admin- istration. No circadian IL-12 rhythm was evident. Social confronta- tion (12 h), 2 cm water stress (10 h), and surgery (laparotomy), reduced baseline levels by approximately 2-fold; reduction follow- ing surgery was noticeable at 2 h, significant at 6 h,maximized at 12–24 h,and began dissipating at 48 h. IVIP mimicked only a small portion of these effects.We are currently attempting to abolish stress- and surgery-induced serum IL-12 reduction by simulta- neously employing blockers for corticosterone, prostaglandin,and beta-adrenoceptors, as the solitary use of any blocker was ineffec- tive. Conclusions: The stress- and surgery-induced decrease in serum IL-12 levels is a robust and multi-factorial phenomenon in rats, sug- gesting its biologicalsignificance.The ex-vivo induced production approach seems to reflect different aspects of the cytokine system. doi:10.1016/j.bbi.2009.06.120 116. Curcumin inhibits tumor growth and angiogenesis in ovar- ian carcinoma by targeting the nuclear factor- j B pathway A.K. Sood a , Y.G. Lin a , G. Armaiz-Pena a , S.K.Lutgendorf b , B.B.Aggarwal a a UT M.D. Anderson Cancer Center, P.O. Box 301439, Unit 1362, Houston, TX 77230,United States b University of Iowa, United States Curcumin, a component of turmeric, has been shown to suppress inflammation and angiogenesis largely by inhibiting the transcrip- tion factor NF- j B. This study evaluates the effects of curcumin on ovarian cancer growth using an orthotopic murine model of ovarian cancer. In vitro and in vivo experiments of curcumin with and with- out docetaxel were done using human ovarian cancer cell lines SKO- V3ip1,HeyA8,and HeyA8-MDR in athymic mice. NF- j B modulation was ascertained using EMSA. Evaluation of angiogenic cytokines, cel- lular proliferation (PCNA), angiogenesis (CD31), and apoptosis (TUN- EL) was done using immunohistochemical analyses. Curcumin inhibited inducible NF- j B activation and suppressed proliferation in vitro. In vivo experiments revealed that500 mg/kg orally was the optimal dose needed to suppress NF- j B and STAT-3 activation. In the SKOV3ip1 and HeyA8 in vivo models, curcumin alone resulted in 49% (P = 0.08)and 55% (P = 0.01)reductions in mean tumor growth compared with controls,and combineation with docetaxel elicited 96% (P < 0.001) and 77% reductions compared with controls. Curcumin based therapy was effective even in the HeyA8-MDR mod- el. In SKOV3ip1 and HeyA8 tumors, curcumin alone and with doce- taxel decreased both proliferation (P < 0.001)and microvessel density (P < 0.001)and increased tumor cell apoptosis (P < 0.05). Based on significant efficacy in preclinicalmodels,curcumin may be an attractive therapeutic strategy for cancer patients. doi:10.1016/j.bbi.2009.06.121 117. Could COX-2 inhibitors and beta-blockers improve postop- erative survival rates in cancer patients? L. Sorski,A. Glasner,E. Rosenne,M. Benish,B. Levi,A. Hoffman, S. Ben-Eliyahu Tel Aviv university, Tel Aviv 69978, Israel We have previously reported that blocking excess release of cat- echolamines and prostaglandins in the perioperative context pre- vented NK suppression and promotion of experimental metastasis. By using tumor models of greater clinical relevance, and employing clinically applicable drugs, we herein aim at estimating the biologi- cal and clinical significance of this approach. Methods: CT26 colon carcinoma cells were inoculated into the he- patic portal vein of operated BALB/C mice, and liver metastases were counted 19 days later. B16F10.9-melanoma orLewis-lung-carci- noma cells were implanted subcutaneously into C57B/6j mice foot- pads, developing tumor were surgically removed when reaching 100–150l l, and recurrence-free survival rates were assessed there- after. The beta-blocker,propranolol, the COX2 inhibitor, etodolac, both drugs, or vehicle, was administered once before tumor inocula- tion/excision. Results:Each drug and their combination similarly decreased number of liver CT26 metastases. Only the drugs combination, but neither drug alone, doubled survival rates in each of the two sponta- neous metastasesmodels. To estimate drugs’ efficacy we also compared and combined them with established BRMs (poly I-C and IL-12). The drugs treatment was at least as effective as immuno- stimulation,which did not further enhance survival rates. Conclusion:Propranolol and etodolac administration reduced metastasesand improved recurrence-free survivalrates in mice undergoing tumor excision. Such approach could be applied in most cancer patients undergoing primary tumor resection with minimal risk and low cost,and may improve survival rates. doi:10.1016/j.bbi.2009.06.122 118. Effects of voluntary exercise on acute stress responses in white adipose tissue K.J. Speaker,B.N.Greenwood,M. Fleshner University of Colorado, Integrative Physiology, 1725 Pleasant St., Clare Small 114/UCB 354, Boulder,CO 80309, United States White adipose tissue (WAT) is an active endocrine organ which synthesizes a variety of proteins including numerous inflammatory Abstracts / Brain, Behavior,and Immunity 23 (2009) S25–S64 S57