Combined Heat and Power for Saving Energy and Carbon in Residential Buildings

ABSTRACT Combined Heat and Power (CHP) systems can simultaneously deliver thermal and electric (or mechanical) energy services and thus use fuel very efficiently. Today's smallscale CHP systems already provide heat, cooling and electricity at nearly twice the fuel efficiency of separate heat and power based on power remote plants, electric chilling, and onsite hot water and space heating. In this paper, we have refined and extended our earlier methodology used in assessments of small-scale CHP for commercial buildings, to homes. Recent U.S. and European technology, policy and market developments make the adoption of such "microCHP" technologies by 2010 more likely. Solid oxide and proton exchange membrane fuel cells, reciprocating gas engines and stirling engines are currently being tested for residential applications. The second part of the paper compares gas fired microCHP systems with traditional gas fired furnaces and water heaters for typical single family homes in New England where high electricity costs, net metering and high thermal-to-electric ratios make microCHP more attractive. Our model provides 1) the allowable turn key cost premium, $1,444 for a 4-year payback and an assumed$100 additional annual maintained cost, and the 2) carbon reductions, 29% or 0.8 Mt c (metric tons of carbon equivalent). 1 The complete study with additional market segments, scenarios and uncertainty analysis will be available at http://gwu.edu/~deppe/chp.htm or can be requested at [email protected]. Background/Motivatio

Estrogen protects neuronal cells from amyloid beta-induced apoptosis via regulation of mitochondrial proteins and function

BACKGROUND: Neurodegeneration in Alzheimer's disease is associated with increased apoptosis and parallels increased levels of amyloid beta, which can induce neuronal apoptosis. Estrogen exposure prior to neurotoxic insult of hippocampal neurons promotes neuronal defence and survival against neurodegenerative insults including amyloid beta. Although all underlying molecular mechanisms of amyloid beta neurotoxicity remain undetermined, mitochondrial dysfunction, including altered calcium homeostasis and Bcl-2 expression, are involved in neurodegenerative vulnerability. RESULTS: In this study, we investigated the mechanism of 17β-estradiol-induced prevention of amyloid beta-induced apoptosis of rat hippocampal neuronal cultures. Estradiol treatment prior to amyloid beta exposure significantly reduced the number of apoptotic neurons and the associated rise in resting intracellular calcium levels. Amyloid beta exposure provoked down regulation of a key antiapoptotic protein, Bcl-2, and resulted in mitochondrial translocation of Bax, a protein known to promote cell death, and subsequent release of cytochrome c. E(2 )pretreatment inhibited the amyloid beta-induced decrease in Bcl-2 expression, translocation of Bax to the mitochondria and subsequent release of cytochrome c. Further implicating the mitochondria as a target of estradiol action, in vivo estradiol treatment enhanced the respiratory function of whole brain mitochondria. In addition, estradiol pretreatment protected isolated mitochondria against calcium-induced loss of respiratory function. CONCLUSION: Therefore, we propose that estradiol pretreatment protects against amyloid beta neurotoxicity by limiting mitochondrial dysfunction via activation of antiapoptotic mechanisms

Combined Heat and Power for Saving Energy and Carbon in Residential Buildings

This report is the description of saving carbon in residences using the microCHP