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K Kaur, AK Sharma, PK Singal Institute of Cardiovascular Sciences and Department of Physiology, St Boniface Research Centre, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba TNF- is one of the key cytokines in the pathogenesis of heart failure. The mechanism by which inflammatory cytokine, TNF- produces heart dysfunction is not yet clear. TNF- has been suggested to mediate some of its effects by modifying the antioxidant reserve of the heart. OBJECTIVE: The study investigated the effects of TNF- on the oxidative stress and antioxidant enzymes in adult rat cardiac myocytes. METHODS: Adult rat cardiac myocytes were exposed to TNF- 120 ng mL ; for 4 hrs. Myocytes were analyzed for oxidative stress as well as for different antioxidant enzymes. Effects of H2O2, a positive control, were also studied. RESULTS: TNF- caused a dose dependent increase in the generation of hydroxyl radicals OH ; , lipid peroxides and a decrease in redox ratio. TNF- also caused a dose dependent increase. Glutathione peroxidase protein and activity were significantly decreased at 20 ng mL, however, its mRNA was increased at this concentration. MnSOD protein levels and mRNA levels were decreased both at 10 and 20 ng mL. There was no change in Cu ZnSOD. Catalase CAT ; protein levels were decreased both at 10 and 20 ng mL, whereas CAT mRNA was decreased only at 20 ng mL. H2O2 caused a significant increase in production of OH, lipid peroxides and a decrease in redox ratio. H2O2 caused a significant decrease in the protein and mRNA levels of all the four antioxidant enzymes. CONCLUSION: These results suggest that TNF- increases oxidative stress in cardiac myocytes by effecting both the ROS generation and their detoxification. Supported by CIHR, for instance, drug interaction singulair.

WINTERGREEN RESEARCH, INC. Figure 2-13 Amgen's Product Sales Figure 2-14 Amgen's Total Product Sales Continued, Dollars, 2003 Figure 2-15 Amgen's Total International Product Sales, Dollars Figure 2-16 Amgen's Total U.S. Product Sales, Dollars Table 2-17 Amgen's Regional Product Sales Figure 2-18 AstraZeneca Net Sales, Dollars, 2004 Figure 2-19 AstraZeneca Net Sales, Dollars, 2003 Table 2-20 AstraZeneca Product Sales Full Year Figure 2-21 AstraZeneca Net Sales, Dollars, 1st Quarter, 2005 Table 2-22 AstraZeneca Product Sales, 1st Quarter Figure 2-23 AstraZeneca Geographic Product Sales, Segments Percents, 2004 Figure 2-24 AstraZeneca Geographic Product Sales, Segments Percents, 2003 Table 2-25 AstraZeneca Geographic Sales Full Year Figure 2-26 Genentech's Total Revenue, Dollars Figure 2-27 Genentech Total Product Sales, Dollars Table 2-28 Genentech Figure 2-29 Genentech Total Product Sales, Dollars, 2004 Table 2-30 Genentech Oncology Product Sales Figure 2-31 Genentech Net Foreign Revenues, Segment Percents, 2004 Figure 2-32 Genentech Net Foreign Revenues, Segment Percents, 2004 Table 2-33 Genentech Net Foreign Revenues Figure 2-34 Bristol-Myers Squibb's Worldwide Net Sales, Dollars, 2004 Table 2-35 Bristol-Myers Squibb's Product Sales Figure 2-36 Bristol-Myers Squibb's U.S. Net Sales, Dollars, 2004 Table 2-37 Bristol-Myers Squibb's U.S. Net Sales Figure 2-38 Millennium's Total Revenues, Dollars and tobradex.

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While singulair can be part of an overall strategy for eib, singulair is not indicated for eib and should not be used by itself for the treatment and management of this condition. Using data from the 2003 Minnesota Adult Tobacco Survey, Table 1 provides demographic data on the current and former smokers, the subject of this report. Never smokers are included to provide a comparison group. Among each of the three groups, slightly more than half live in the Twin Cities sevencounty metropolitan area, reflecting the distribution of the Minnesota population. A greater percentage of men are current and former smokers than are women. Among never smokers, however, 55 percent are women. Never, former, and current smokers differ primarily on age, education, and marital status. Never smokers are, on average, 10.0 years younger than former smokers and 4.2 years older than current smokers. Never smokers 42% ; are much more likely to have a college degree than former smokers 35% ; and current smokers 19% ; . Two-thirds 66% ; of never smokers, nearly three-quarters 72% ; of former smokers, and only about half 49% ; of current smokers are married, a difference that in part reflects the average age of the groups. In the 1999 Adult Tobacco Prevalence Survey, the demographic characteristics among the three groups were similar to the 2003 profile and triamterene and singulair, for instance, child singulair.

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Could penetrate into the tablet core via these channels to cross the hydrophobic EC membrane. Water uptake caused the expansion of the disintegrating agent within the tablet core, resulting in a gradual build-up of pressure within the coated tablets. Once the inside pressure exceeded the critical disrupted value that the coating layer resisted most, the coating layer would be ruptured and release drug in a manner of burst, thus forming the delay effect of drug release from the coated tablets. Taken together, the formation of micro-channels was the first crucial step, and the critical disrupted pressure governed by the coating layer and the expansibility of the disintegrating agent were the key factors for time-dependent controlled release[15]. The release profiles of the DS coated tablets at 7.5% coating level were not affected by the pH values of media Figure 2 ; . This was reasonably expected, since the channeling agent PEG 400 was pH-insensitive and formation of the micro-channels was not affected by pH. The effects of the coating level on the lag time of DS release from the coated tablets were tested, indicating that the coating level played a significant role in controlling the lag time of release. To increase the coating level would extend the lag time of DS release from the coated tablets Figure 1 ; . There were two possible mechanisms contributing to this phenomenon. For one thing, since the hydrophobic EC membrane was relatively impermeable to water molecules, substantial effect on the rate of the water molecules diffusion and water uptake, was exerted by the number, size, length and tortuosity of the aqueous micro-channels in the coating layer. The coating level and thickness of the coating layer certainly determined the rate of water uptake, by controlling the formation rate and physical characteristics of the aqueous channels. To be evident, the increase of the coating level would elicit the longer and more tortuous aqueous micro-channels, severely impairing the rate of water uptake. Alternatively, the thicker coating layer developed the higher critical resistant pressure to be surpassed for disrupting the coating membrane, required the greater water uptake to gradually build up inside pressure by the disintegrating agent's expansion and prolonged the lag time of drug release from the coated tablets[16]. The mean in vivo lag time of the DS absorption from coated tablets was significantly longer than that from enteric tablets, being 5.80 h vs 2.80 h Figure 7 and Table 2 ; . The results were in accordance with the in vitro lag time of DS release from two formulations, and the lag time of DS release from test tablets was nearly 2 h longer than that from the enteric tablets Figure 3 ; . Furthermore, the in vivo absorption kinetics of the time-dependent DS coated tablets was assessed by the typical Wagner-Nelson method. The absorption percentage in vivo versus time profile was analogous to the cumulative release percentage in vitro versus time profile, which validated the in vitro dissolution conditions and verified the utility of the timedependent CDDS Figure 8 ; . The good correlation coefficient r 0.95 ; between in vivo absorption and in vitro release percentages, further confirmed this conclusion. To our knowledge, there exists a pH gradient along the GI tract, a fact that pH in the stomach is approximately 1.5 in the fasted state, ranges roughly from 5.0 to 7.0 in the small intestine, and from 6.0 to 7.2 in the colon[1]. The pH values at the end of ileum and in the colon are notably higher than the upper GI tract, therefore providing the rationale for developing pH-dependent CDDS. In addition, a novel dosage form, pellets, is the multiple units' drug delivery system, and it is superior to the conventional preparation, such as tablets, for the following reasons. The pellets appear to be less influenced by the physiologic factors, such as the gastric emptying, intestinal transit, than tablets. Moreover, the pellets could be widely and evenly distributed in the GI tract surfaces, which increase the drug-tract contact surface and thus improve bioavailability.

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References: 1 ; Klimesch W. EEG alpha and theta oscillations reflect cognitive and memory performance : a review and analysis. Brain Resaerch Reviews, 1999, 29 : 169-195 2 ; Montangero J. How can we define the sequential organization of dreams? Percept Mot Skills, 1991, 73: 1059-1073. Research supported by Fond National Suisse: N1114-061508.00 300.D Thoughts and Hallucinations in NREM and REM Sleep Across the Night Fosse R, Stickgold R, Hobson JA Harvard Medical Shool.
ET-05. RETARGETING OF ADENOVIRAL VECTOR FOR GENE THERAPY IN GLIOBLASTOMA MULTIFORME Jason Chua, 1 Weijun Wang, 2, 4 and Thomas C. Chen2, 3, 4; 1Keck School of Medicine, Departments of 2Neurosurgery and 3Pathology, and 4USC Center for Brain Tumor Research, University of Southern California, Los Angeles, CA, USA The average life span of a patient with glioblastoma multiforme GBM ; is currently 12 to 15 months after diagnosis, despite improvements in surgery, radiation, and chemotherapy. Because there is such an urgent need for novel treatment methods, adenovirus-mediated gene therapy has recently undergone clinical trials in treating patients with GBM, but results have been less promising than originally hoped. It has been shown that the human Cocksackie and Adenovirus Receptor hCAR ; plays a key role in viral attachment, and that more malignant glioma cell lines have reduced or no expression of hCAR. The goal of this project was to determine whether retargeting by using adenovirus conjugated to the basic fibroblast growth factor FGF2-Fab' ; ligand to the fibroblast growth factor receptor FGFR ; , which is expressed strongly on all GBM cell types, could increase adenoviral infectivity in tumorigenic cell lines. Using GBM cell line U-118 no hCAR ; , at MOI of 100 pfu ml, we found that up to 85% transduction efficiency can be achieved with the help of FGF2-Fab' compared to only 5% without FGF2-Fab' conjugation, using green fluorescent protein GFP ; as a detection marker. In contrast, the transduction efficiency in U-87 GBM cell line high hCAR ; was greater than 90% using Ad-GFP alone and was not significantly improved in the presence of FGF2-Fab'. Furthermore, when using an intracranial in vivo model in mice, we found a similarly significant increase in U-118 transduction 80% ; when exposed to retargeted adenovirus, compared to adenovirus alone, where the transduction rate was 5%. Transduction efficiency was 85% in the U-87 glioma cells in vivo and slightly increased to 90% with FGF2-Fab'. No significant GFP expression was found in the normal brain. These results demonstrate that retargeting of adenovirus to FGFR allows for efficient glioma cell transduction independent of hCAR and integrin status, which could greatly improve the efficacy of adenovirus-mediated gene therapy.

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