Densified biomass can cost-effectively mitigate greenhouse gas emissions and address energy security in thermal applications.

Regional supplies of biomass are currently being evaluated as feedstocks in energy applications to meet renewable portfolio (RPS) and low carbon fuel standards. We investigate the life cycle greenhouse gas (GHG) emissions and associated abatement costs resulting from using densified switchgrass for thermal and electrical energy. In contrast to the large and positive abatement costs for using biomass in electricity generation ($149/Mg CO(2)e) due to the low cost of coal and high feedstock and power plant operation costs, abatement costs for replacing fuel oil with biomass in thermal applications are large and negative (-$52 to -$92/Mg CO(2)e), resulting in cost savings. Replacing fuel oil with biomass in thermal applications results in least cost reductions compared to replacing coal in electricity generation, an alternative that has gained attention due to RPS legislation and the centralized production model most often considered in U.S. policy. Our estimates indicate a more than doubling of liquid fuel displacement when switchgrass is substituted for fuel oil as opposed to gasoline, suggesting that, in certain U.S. locations, such as the northeast, densified biomass would help to significantly decarbonize energy supply with regionally sourced feedstock, while also reducing imported oil. On the basis of supply projections from the recently released Billion Ton Report, there will be enough sustainably harvested biomass available in the northeast by 2022 to offset the entirety of heating oil demand in the same region. This will save NE consumers between $2.3 and $3.9 billion annually. Diverting the same resource to electricity generation would cost the region $7.7 billion per year. While there is great need for finding low carbon substitutes for coal power and liquid transportation fuels in the U.S., we argue that in certain regions it makes cost- (and GHG mitigation-) effective sense to phase out liquid heating fuels with locally produced biomass first.

Efficacy of vitamin E, phosphatidyl choline, and pyruvate on buffering neuronal degeneration and oxidative stress in cultured cortical neurons and in central nervous tissue of apolipoprotein E-deficient mice.

Oxidative stress is a pivotal factor in neuronal degeneration. However, vitamin E was only marginally effective in clinical trials. We examined whether or not a mixture of vitamin E (as alpha-tocopherol), sodium pyruvate and phosphatidyl choline (PC), a mixture that promotes wound healing in non-neuronal systems, would provide neuroprotection beyond that observed with vitamin E alone. Combined treatment with these agents improved survival and neuritic spouting of murine embryonic cortical neurons in culture, and provided neuroprotection against oxidative damage following treatment with hydrogen peroxide. Dietary treatment with these three agents also compensated for the diminished oxidative buffering capacity of brains of apolipoprotein E-deficient mice, while vitamin E alone failed to do so. These data underscore the possibility that critical nutritional deficiencies may modulate the impact of genetic compromise on neurodegeneration.

Vitamin E deficiency does not induce compensatory antioxidant increases in central nervous system tissue of apolipoprotein E-deficient mice.

Compensatory upregulation in endogenous antioxidants has been shown to accompany certain genetic and dietary deficiencies that promote oxidative stress, including that related to Alzheimer's disease. We compared antioxidant levels in brain tissue of normal and transgenic mice lacking apolipoprotein E following dietary deprivation of vitamin E or folate. As described previously, ApoE-deficient mice displayed increased levels of the endogenous antioxidant glutathione as compared to normal mice, and increased these levels further following folate deprivation. By contrast, glutathione was depleted following vitamin E deprivation in brain tissue of normal and ApoE-deficient mice. TBAR analyses confirmed increased oxidative damage following vitamin E deprivation. However, combined deprivation of folate and vitamin E resulted in levels of glutathione intermediate between those observed following deprivation of either agent, indicating that the lack of compensatory increase in glutathione following vitamin E deprivation was not due to overt neurotoxicity. Similar results were observed for total antioxidant levels in brain tissue. The differential response to vitamin E and folate deprivation is consistent with the possibility that specific differences in oxidative damage may result from deficiencies in either of these agents. The lack of a compensatory response to vitamin E deprivation highlights the importance of dietary vitamin E in prevention of chronic neurodegeneration.