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Section V: Biomedical Sciences tapley hall, room 119 Francis Eko, presiding.

9:00 REPLACEMENT OF MEMBRANE CHOLESTEROL DURING PHYTOSTEROL SUPPLEMENTATION IN PROSTATE CANCER CELLS**, Wambui S. Wandu*, Godwin O. Ifere and Godwin A. Ananaba, Department of Biological Sciences, Clark Atlanta University, Atlanta, GA 30314. Enhancement of cellular phytosterol levels may improve its chemotherapeutic potential in prostate cancer cells. This is due to the suggestion that phytsoterols may replace membrane cholesterol, which is known to promote cell proliferation. There is little information that supports phytosterol replacement of membrane cholesterol. We therefore hypothesize that cutback of in vitro cholesterol absorption by supplementation of prostate cancer cells with phytosterols may result in membrane cholesterol depletion and increased phytosterol buildup. In vitro cultures of prostate cancer cell lines PC-3 were supplemented with cholesterol and phytsoterol, facilitated by [beta]-cyclodextrin (as vehicle). After 72 h of incubation at 37[degrees]C, the cells were harvested and their membranes isolated by density gradient centrifugation. After extraction of membrane lipids with chloroform /methanol, cholesterol was estimated by a sensitive enzymatic assay. Our results indicate a minimized level of cholesterol in membranes from phytosterol-treated cells. We conclude that phytosterol treatment might diminish membrane cholesterol and contribute to the success of prostate cancer chemotherapy.

9:15 PLASMA INTERLEUKIN-1[beta] CONCENTRATION PREDICTS RISK OF STROKE IN SICKLE CELL DISEASE, Kwaku O. Asare (1), Beatrice E. Gee (1), Jonathan K. Stiles (1), Nana Wilson (1), Adel Driss (1), Alexander Quarshie (1), Robert J. Adams (2), Abdullah Kutlar (3) and Jacqueline M. Hibbert (1), (1) Morehouse School of Medicine, Atlanta, GA, (2) Medical University of South Carolina, Charleston, SC and (3) Medical College of Georgia, Augusta, GA. The pathogenesis of sickle cell disease (HbSS), which has numerous complications including stroke, involves inflammation resulting in alteration of plasma inflammatory protein concentration. We investigated HbSS children with abnormal cerebral blood flow detected by transcranial Doppler ultrasound (TCD) who participated in a multi-center stroke prevention (STOP) study, to determine if plasma inflammatory protein concentration is associated with the risk of developing stroke. Thirty-nine plasma samples from HbSS participants with elevated TCD who had no stroke, HbSS-NS (n=13) or had stroke, HbSS-S (n=13), HbSS steady-state controls (n=7) and controls with normal hemoglobin, HbAA (n=6), were analyzed simultaneously for 27 circulating inflammatory proteins. Logistic regression and receiver operator characteristics (ROC) curve analysis of stroke on plasma inflammatory mediator concentration, adjusted for age and gender, demonstrated that IL-1[beta] was protective against stroke development and was a good predictor of stroke risk. This result demonstrates a strong association of systemic inflammation with stroke risk in HbSS via moderately increased plasma interleukin-1[beta] concentration, which is furthermore associated with a decreased likelihood of stroke in HbSS.

9:30 IL-10 AND TGF-[beta]1 EXPRESSION IN IP-10-/- C57BL/6 MICE WITH EXPERIMENTAL CEREBRAL MALARIA: ROLE OF REGULATORY T CELLS**, Bismark Sarfo* (1), Nana Wilson(1), Danielle Whittaker (2), Vincent Bond (1) and Jonathan Stiles (1), (1) Morehouse School of Medicine and (2) Vanderbilt University, Nashville, TN. Recent reports indicate that C57BL/6 IP-10-/- mice are less susceptible to experimental CM, and also blocking T cells prevent ECM. Regulatory T cells (Tregs) secrete IL-10 and TGF-[beta]l which limit malaria brain inflammation but their role in CM severity is unclear. We hypothesize that enhanced Tregs production in IP-10-/- mice will prevent ECM. Our objective is to compare Tregs (CD4+CD25+Foxp3), IL-10 and TGF-[beta]l in IP-10-/- and IP-10+/+ mice during ECM. Female IP-10-/- and IP-10+/+ mice were injected with P. berghei parasites and uninfected RBC as controls. ECM symptoms were monitored and mice were sacrificed at day 2, 4 and 8 pi. ELISA was performed to determine IL-10 and TGF-[beta]l in plasma and semi-qRT-PCR was performed to evaluate Foxp3 and TGF-[beta]l in brain. IL-10 and TGF-[beta]1 in infected IP-10-/- plasma were significantly upregulated and down regulated, respectively, compared to infected IP-10+/+ at day 2 and 4 pi. Foxp3 mRNA was significantly increased in IP-10-/- brain at day 4 pi compared with IP-10+/+ and controls. Thus P. berghei infection up regulates IL-10 and Foxp3 in plasma and brain respectively in IP-10-/- but not in IP-10+/+ mice and down regulates plasma levels of TGF-[beta]. Ongoing re-stimulation assay will ascertain if CD4+CD25+ or CD4+CD25- T cells is the predominant source of IL-10 during ECM.

9:45 PCGEM1 MEDIATES CHOLESTEROL ASSUALTS ON PROSTATE CELLS BY INITIATING THE ATTENUATION OF P53 EXPRESSION, Godwin O. Ifere*, Sylvia Wandu, Angela Campbell, Nehemiah Diala, Lucky Nwankwo and Godwin A. Ananaba, Department of Biological Sciences, Clark Atlanta University, Atlanta, GA 30314. Over-expression of the novel prostate-specific proto-oncogene, PCGEM1 is reputed to mediate aggressive prostate tumorigenesis, thus suggesting that it favors prostate cell division. The exact mechanism by which this non-coding RNA gene stimulates hysterical cell division is not yet understood. Since cell growth involves uncoupling of blockades across checkpoints, we hypothesize that PCGEM1 may stimulate cell division by triggering the passage for instance, through the G1 checkpoint. We therefore investigated PCGEM1 effects on the expression of p53, a pro-apoptotic gene, and on the production of D-type cyclins and the retinoblastoma (RB) gene product. Our results show that over-expressed PCGEM1 mediates cell progression by regulating cylin production and substantial enrichment of sub-mitotic cell populations. Elucidation of the checkpoint proteins amenable to over-expressed PCGEM1 may enable their scrutiny as potential anticancer therapeutic targets in prostate cancers that show elevated PCGEM1.

10:00 Section business meeting

10:30 EX-VIVO PULSED IL-10 DEFICIENT DENDRITIC CELLS INFLUENCE THE PRODUCTION OF IMMUNE MODULATORS OF PROSTATE CANCER, Godwin Ananaba* (1), Lucky Nwankwo (1), Kereen Gordon (1), Godwin Ifere (1), Angela Campbell(1), Francis Eko (2), Qing He(2/3), Eno Ekong (2) and Joseph Igietseme (2/3), (1) Clark Atlanta University, (2) Morehouse School of Medicine and (3) Centers for Disease Copntrol and Prevention, Atlanta, GA. Cancer cells evade the immune system by eliciting the production of immuno-suppressive factors such as IL-10, VEGF, PGE2 and TGF-[beta]. Abnormal differentiation of dendritic cells gives rise to accumulation of immature DCs with dysregulated expression of costimulatory molecules. Our goal is to elucidate the role of IL-10 deficiency on the ability of dendritic cells to regulate immune response against prostate cancer. We investigated the hypothesis that ex-vivo pulsing of DCs overcomes the suppressive effects of immature DCs, accumulation of Tregs and nonresponsiveness of antigen-specific T cells to cancer. A combination of genomic and proteomic methods were used to assess the transcription al and translational activities of chemokines and cytokines expressed by prostate cancer associated antigen (PCAA)-pulsed DCs. The results show that IFN-[gamma], IP-10 are reduced in prostate cancer cells compared to immortalized normal prostate epithelial cells. Also, PCAA pulsed DCs enhanced the expression of IFN-[gamma], MIP-1[alpha]/[beta], and IP-10 and CXCR3. These results suggest that the expression of cytokines and chemokines could be used as prognostic markers for prostate cancer progression. The efficacy of an anti-prostate cancer vaccine will depend on its ability to inhibit the recruitment of functional immunosuppressive molecules.

10:45 THE BACTERIAL GHOST PLATFORM AS A NOVEL STRATEGY FOR VACCINE AND DRUG DELIVERY, Francis O. Eko* (1), Eno Ekong (1), Qing He (2), Godwin Ananaba (1) and Joseph U. Igietseme (1.3), (1) Morehouse School of Medicine, Atlanta, GA 30310, (2) Clark Atlanta University, Atlanta, GA 30310 and (3) National Center for Infectious Diseases (CDC), Atlanta GA 30333. The bacterial ghost system is a novel vaccine and drug delivery system endowed with intrinsic adjuvant properties as well as carrier and targeting functions. Bacterial ghosts are non-living Gram-negative bacterial cells devoid of cytoplasmic contents that retain the morphological characteristics and structural integrity of their living counterparts. They are produced by the controlled expression of PhiX174 protein E and have a high capacity to simultaneously carry and present multiple antigens to the immune system. They are stable at room temperature as lyophilized preparations, have no 'cold chain' or refrigeration requirements and provide a simple method for packaging various antigens for effective delivery. In addition to being effective adjuvants, ghosts are an efficient vaccine and drug delivery system. Thus, bacterial ghosts represent a novel approach for drug delivery and offer an exceptional opportunity to develop multiple or combination vaccines.
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Publication:Georgia Journal of Science
Article Type:Calendar
Geographic Code:1U5GA
Date:Mar 22, 2009
Previous Article:Section IV: Physics, Mathematics, Computer Science.
Next Article:Section VI: philosophy and history of science science center, room 238 vivian rogers-price, presiding.

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