Browsing by Subject "Energy balance"
Now showing 1 - 5 of 5
Results Per Page
Sort Options
Item Analysis of a novel thermoelectric generator in the built environment(2011-08) Lozano, Adolfo; Webber, Michael E., 1971-; Schmidt, Philip S.This study centered on a novel thermoelectric generator (TEG) integrated into the built environment. Designed by Watts Thermoelectric LLC, the TEG is essentially a novel assembly of thermoelectric modules whose required temperature differential is supplied by hot and cold streams of water flowing through the TEG. Per its recommended operating conditions, the TEG nominally generates 83 Watts of electrical power. In its default configuration in the built environment, solar-thermal energy serves as the TEG’s hot stream source and geothermal energy serves as its cold stream source. Two systems-level, thermodynamic analyses were performed, which were based on the TEG’s upcoming characterization testing, scheduled to occur later in 2011 in Detroit, Michigan. The first analysis considered the TEG coupled with a solar collector system. A numerical model of the coupled system was constructed in order to estimate the system’s annual energetic performance. It was determined numerically that over the course of a sample year, the solar collector system could deliver 39.73 megawatt-hours (MWh) of thermal energy to the TEG. The TEG converted that thermal energy into a net of 266.5 kilowatt-hours of electricity in that year. The second analysis focused on the TEG itself during operation with the purpose of providing a preliminary thermodynamic characterization of the TEG. Using experimental data, this analysis found the TEG’s operating efficiency to be 1.72%. Next, the annual emissions that would be avoided by implementing the zero-emission TEG were considered. The emission factor of Michigan’s electric grid, RFCM, was calculated to be 0.830 tons of carbon dioxide-equivalent (CO2e) per MWh, and with the TEG’s annual energy output, it was concluded that 0.221 tons CO2e would be avoided each year with the TEG. It is important to note that the TEG can be linearly scaled up by including additional modules. Thus, these benefits can be multiplied through the incorporation of more TEG units. Finally, the levelized cost of electricity (LCOE) of the TEG integrated into the built environment with the solar-thermal hot source and passive ground-based cold source was considered. The LCOE of the system was estimated to be approximately $8,404/MWh, which is substantially greater than current generation technologies. Note that this calculation was based on one particular configuration with a particular and narrow set of assumptions, and is not intended to be a general conclusion about TEG systems overall. It was concluded that while solar-thermal energy systems can sustain the TEG, they are capital-intensive and therefore not economically suitable for the TEG given the assumptions of this analysis. In the end, because of the large costs associated with the solar-thermal system, waste heat recovery is proposed as a potentially more cost-effective provider of the TEG’s hot stream source.Item Energy balance and breast cancer : mechanistic studies(2010-05) Nogueira, Leticia Maciel; Hursting, Stephen D.; DeGraffenried, Linda A.; Kline, Kimberly; Otto, Glen; Sanders, Bob G.Obesity is one the few modifiable risk factors for breast cancer. Hence, an evaluation of the metabolic and cancer inhibitory effects of the obesity reversing strategies, calorie restriction (CR) and exercise, is important for breast cancer prevention. Additionally, a better understanding of the mechanisms underlying the effects of these interventions on cancer will provide scientific basis for therapeutic recommendations, and facilitate the identification of therapeutic agents for breast cancer treatment in obese patients. We found that CR is more effective than exercise in reversing the metabolic and cancer enhancing effects of obesity. Even at comparable levels of adiposity, CR effects on insulin resistance, energy balance related hormones levels, and metabolic genes expression in adipose tissue were more profound than those of exercise. The mechanism by which CR influences tumor progression is thought to involve molecules that respond to energy balance changes and control cell growth, such as the insulin-like growth factor-1 (IGF-1) and the mammalian target of rapamycin (mTOR). The mTOR inhibitor rapamycin decreased mammary tumor burden to levels comparable to CR. While established tumors did not display decreased mTOR activity, constitutively active mTOR was capable of overcoming some of the inhibitory effects of CR on tumor cells invasion and migration. Effects of increasing levels of CR on gene expression indicate that 30% and 40% CR, but not 20% CR, induce beneficial metabolic changes in the liver. However, 40% CR also increases apoptosis of hepatic cells which appears to be detrimental for the liver. IGF-1 infusion partially overcame the beneficial effects of CR on expression of tumor-related genes in the mammary fat pad and on mammary tumor growth. Taken together, our data show that CR, but not exercise, is able to reverse the metabolic and tumorigenic effects of obesity. Furthermore, the IGF-1 and mTOR pathways may mediate, at least in part, many of the beneficial effects of CR on metabolism and tumor progression.Item Energy balance effects on microRNA expression in a mouse model of pancreatic cancer(2010-12) Goldberg, Jason Asher; Lashinger, Laura M.; Hursting, Stephen D.Pancreatic cancer is the fourth leading cause of cancer death in the United States, with a five-year survival rate under 5%. Given the disease’s deadliness, increasing our understanding of the molecular nature of the pancreatic cancer is key to developing more effective preventive measures and treatments. Dietary energy restriction (DER) has been shown to have potent anticancer effects in pancreatic cancer, but the mechanism of action has yet to be completely elucidated. Here we investigate the potential of altered microRNA expression as a mechanism by which DER exerts its anticancer effect. Using the Exiqon microRNA Array, we identified several microRNAs of interest for further study. This includes microRNA (mir) 669c, a known regulator of glutathione-S transferases (linked to carcinogen metabolism and oxidative stress) that increases with age. To our knowledge, this is the first exploration of the effects of DER (which is known to suppress oxidative stress and other processes associated with aging and cancer) on microRNA expression. These findings may provide the initial steps towards identifying novel targets for pancreatic cancer prevention or treatment.Item Energy balance modulation and pancreatic tumor growth : the role of NF-kB(2012-12) Hays, Drew; Hursting, Stephen D.Obesity is a known risk factor for many types of cancer including pancreatic. Calorie restriction (CR), an anti-obesity diet regimen, has potent anticancer effects that may be mediated through its ability to reduce serum metabolic hormones and protumorigenic cytokines such as insulin-like growth factor (IGF)-1. IGF-1 is a metabolic hormone responsive to nutrient status that activates the inflammatory, cancer-related pathway, nuclear factor (NF)-[kappa]B. For this report, we tested the hypothesis that CR, via regulation of IGF-1, inhibits pancreatic tumor cell growth through modulation of NF-kB activation and protumorigenic gene expression. Male athymic nude mice were randomized to either a control diet consumed ad libitum (n=15) or a 30% CR diet (n=15) for 17 weeks, at which time, mice were injected with human pancreatic cancer cells (MiaPaca) and tumor growth was monitored for 6 weeks. Translocation of p65, a regulatory element of NF-[kappa]B, and expression of its downstream gene targets were analyzed in excised tumors. CR mice weighed less, (p<0.05), and had smaller tumors (p=0.022) relative to controls. Tumors from CR mice, relative to controls, demonstrated significant decreases in NF-[kappa]B downstream genes CCND1, RELA, Survivin, VEGF, and XIAP. These findings parallel our previous studies in pancreatic tumors from mouse origin, and suggest that the inhibitory effects of CR on MiaPaca pancreatic tumor growth are associated with decreased NF-kB activation.Item Energy balance, inflammation, and tumor progression : the role of NF-[kappa]B(2011-05) Harvey, Alison Elise; Hursting, Stephen D.; Kline, Kimberly; Sanders, Bob; Otto, Glen; Fischer, SusanObesity is an established risk and progression factor for many types of cancer, including pancreatic and colon cancer, and is characterized by abnormal metabolic hormone production and a chronic low-grade state of inflammation. However, the links between obesity, hormones, inflammation and tumorigenesis in colon and pancreatic tissue are poorly understood. Calorie restriction (CR), an anti-obesity dietary regimen with potent anticancer effects, reduces serum metabolic hormones and protumorigenic cytokines. Insulin-like growth factor (IGF)-1 is a metabolic hormone that activates NF-[kappa]B, a key regulator of inflammation. NF-[kappa]B is a transcription factor that mediates transcription of many cancer- and inflammation-related genes and is upregulated in both colon and pancreatic cancer. We hypothesized that CR inhibits colon and pancreatic tumor cell growth through modulation of hormone-stimulated NF-[kappa]B activation and protumorigenic gene expression. To test this hypothesis, we used CR and ad libitum feeding to generate a lean and overweight (control) phenotype, respectively; in C57BL/6 mice transplanted with MC38 colon cancer cells or Panc 02 pancreatic cancer cells, and analyzed the effect of diet on circulating hormone levels, markers of inflammation, and tumor growth. We also investigated the in vitro effects of IGF-1 on NF-[kappa]B activation and downstream protumorigenic gene expression in MC38 and Panc 02 cells. CR, relative to control diet, reduced body weight, circulating IGF-1 levels, and transplanted MC38 and Panc 02 tumor growth, as well as protumorigenic gene expression in the MC38 and Panc 02 tumor microenvironment. IGF-1 increased cell viability, NF-[kappa]B nuclear translocation and DNA binding, transcriptional activation, and downstream gene expression of inflammation and other protumorigenic genes in MC38 colon cancer cells and Panc 02 pancreatic cancer cells in vitro. Knockdown studies of NF-[kappa]B in Panc 02 cells using si-RNA established that the IGF-1-induced increase in protumorigenic gene expression is mediated, at least partially, through an NF-[kappa]B-dependent mechanism. In conclusion, these findings in models of pancreatic and colon cancer help clarify the links between obesity, IGF-1, NF-[kappa]B-mediated inflammation, and cancer. This work provides the underpinnings for several new molecular targets and strategies to test in model systems and translational studies for preventing or controlling obesity-related cancer.