Cost of saving natural gas through efficiency programs funded by utility customers: 2012–2017

This study estimates the cost of saving a therm of natural gas from energy efficiency programs funded by utility customers during the period 2012 to 2017. Berkeley Lab researchers compiled and analyzed efficiency program data reported by investor-owned utilities and other program administrators in a dozen states representative of the four U.S. Census regions — Arkansas, California, Connecticut, Iowa, Massachusetts, Michigan, Minnesota, New Jersey, New York, Oklahoma, Rhode Island and Utah. Depending on the year, the dataset accounts for about 50 percent to 70 percent of annual national spending on natural gas efficiency programs. The estimated cost of saving natural gas during the study period is $0.40 per therm. The analysis also includes estimates of the program administrator cost of saved energy for three core sectors for natural gas: commercial and industrial, residential, and low-income households. It aggregates these sectors to provide regional and national values. Our metrics include savings-weighted averages, unweighted medians, and interquartile ranges (25th and 75th percentiles) of the levelized program administrator cost of saving gas, in constant 2017 dollars. In addition, the study analyzes cost trends during the study period, finding that average program costs trended downward. The U.S. Department of Energy’s Building Technologies Office supported this work

Applying Non-Energy Impacts from Other Jurisdictions in Cost-Benefit Analyses of Energy Efficiency Programs: Resources for States for Utility Customer-Funded Programs

Avoided energy and capacity costs are the primary yardstick utilities use to determine which energy efficiency programs are cost-effective for their customers. But sometimes "non-energy impacts" — not commonly recognized as directly associated with energy generation, transmission and distribution — represent substantial benefits, such as improving comfort, air quality and public health.Considering whether and how to include non-energy impacts is an important part of cost-benefit analyses for these programs. This report offers practical considerations for deciding which non-energy impacts to include and how to apply values or methods from other jurisdictions.Researchers reviewed studies quantifying non-energy impacts used in 30 states and applied a five-point system to indicate transferability of a value or method from each study for 16 categories of non-energy impacts:Water resource costs and benefitsOther fuels costs and benefitsAvoided environmental compliance costsEnvironmental impactsProductivityHealth and safety Asset valueEnergy and/or capacity price suppression effectsAvoided costs of compliance with Renewable Portfolio Standard requirementsAvoided credit and collection costsAvoided ancillary servicesComfortEconomic development and job impactsPublic health impactsEnergy security impactsIncreased reliabilityThe U.S. Department of Energy’s Building Technologies Office supported this work

Cost of Saving Electricity Through Efficiency Programs Funded by Customers of Publicly Owned Utilities: 2012–2017

This report finds that energy efficiency programs for customers of publicly owned utilities saved electricity at an average cost of 2.4 cents per kilowatt-hour (kWh) from 2012 to 2017. Utilities use such cost performance metrics to assess effectiveness of efficiency program portfolios, determine what programs to offer customers, and, more broadly, ensure electricity system reliability at the most affordable cost as part of electric utility resource adequacy planning and resource procurement processes. The study analyzed efficiency program data reported by 111 program administrators for 219 publicly owned utilities in 14 states — about 90 percent of the municipal utilities and public utility districts that report the data to the Energy Information Administration (EIA). The data represent 88 percent of all spending and 75 percent of all savings that publicly owned utilities reported to EIA in those years. Berkeley Lab used data from several sources, including data provided directly by American Public Power Association members, publicly available annual reports and regional data collections

Dynamical compactification from de Sitter space

We show that D-dimensional de Sitter space is unstable to the nucleation of non-singular geometries containing spacetime regions with different numbers of macroscopic dimensions, leading to a dynamical mechanism of compactification. These and other solutions to Einstein gravity with flux and a cosmological constant are constructed by performing a dimensional reduction under the assumption of q-dimensional spherical symmetry in the full D-dimensional geometry. In addition to the familiar black holes, black branes, and compactification solutions we identify a number of new geometries, some of which are completely non-singular. The dynamical compactification mechanism populates lower-dimensional vacua very differently from false vacuum eternal inflation, which occurs entirely within the context of four-dimensions. We outline the phenomenology of the nucleation rates, finding that the dimensionality of the vacuum plays a key role and that among vacua of the same dimensionality, the rate is highest for smaller values of the cosmological constant. We consider the cosmological constant problem and propose a novel model of slow-roll inflation that is triggered by the compactification process.Comment: Revtex. 41 pages with 24 embedded figures. Minor corrections and added reference

Entropy-Area Relations in Field Theory

We consider the contribution to the entropy from fields in the background of a curved time-independent metric. To account for the curvature of space, we postulate a position-dependent UV cutoff. We argue that a UV cutoff on energy naturally implies an IR cutoff on distance. With this procedure, we calculate the scalar contribution in a background anti-de Sitter space, the exterior of a black hole, and de Sitter space. In all cases, we find results that can be simply interpreted in terms of local energy and proper volume, yielding insight into the apparent reduced dimensionality of systems with gravity.Comment: 20 pages, 1 figur

Arrhythmogenic Calmodulin Mutations Disrupt Intracellular Cardiomyocyte Ca\u3csup\u3e2+\u3c/sup\u3e Regulation by Distinct Mechanisms

BACKGROUND: Calmodulin (CaM) mutations have been identified recently in subjects with congenital long QT syndrome (LQTS) or catecholaminergic polymorphic ventricular tachycardia (CPVT), but the mechanisms responsible for these divergent arrhythmia-susceptibility syndromes in this context are unknown. We tested the hypothesis that LQTS-associated CaM mutants disrupt Ca2+ homeostasis in developing cardiomyocytes possibly by affecting either late Na current or Ca2+-dependent inactivation of L-type Ca2+ current. METHODS AND RESULTS: We coexpressed CaM mutants with the human cardiac Na channel (NaV1.5) in tsA201 cells, and we used mammalian fetal ventricular cardiomyocytes to investigate LQTS- and CPVT-associated CaM mutations (LQTS- and CPVT-CaM). LQTS-CaM mutants do not consistently affect L-type Na current in heterologous cells or native cardiomyocytes, suggesting that the Na channel does not contribute to LQTS pathogenesis in the context of CaM mutations. LQTS-CaM mutants (D96V, D130G, F142L) impaired Ca2+-dependent inactivation, whereas the CPVT-CaM mutant N54I had no effect on Ca2+-dependent inactivation. LQTS-CaM mutants led to loss of Ca2+-transient entrainment with the rank order from greatest to least effect: CaM-D130G~CaM-D96V\u3e\u3eCaM-F142L. This rank order follows measured Ca2+-CaM affinities for wild-type and mutant CaM. Acute isoproterenol restored entrainment for CaM-130G and CaM-D96V but caused irreversible cytosolic Ca2+ overload for cells expressing a CPVT-CaM mutant. CONCLUSIONS: CaM mutations associated with LQTS may not affect L-type Na+ current but may evoke defective Ca2+-dependent inactivation of L-type Ca2+ current

Unification and the Hierarchy from AdS5

In AdS5, the coupling for bulk gauge bosons runs logarithmically, not as a power law. For this reason, one can preserve perturbative unification of couplings. Depending on the cutoff, this can occur at a high scale. We discuss subtleties in the calculation and present a regularization scheme motivated by the holographic correspondence. We find that generically, as in the standard model, the couplings almost unify. For specific choices of the cutoff and number of scalar multiplets, there is good agreement between the measured couplings and the assumption of high scale unification.Comment: 5 pages, 2 figure

Localized Gravity in String Theory

We propose a string realization of the AdS4 brane in AdS5 that is known to localize gravity. Our theory is M D5 branes in the near horizon geometry of N D3 branes, where M and N are appropriately tuned.Comment: 4 pages, Revtex, a typo corrected and references adde

Comprehensive Analysis of HLA-A, HLA-B, HLA-C, HLA-DRB1, and HLA-DQB1 Loci and Squamous Cell Cervical Cancer Risk

Variation in human major histocompatibility genes may influence the risk of squamous cell cervical cancer (SCC) by altering the efficiency of the T-cell–mediated immune response to human papillomavirus (HPV) antigens. We used high-resolution methods to genotype human leukocyte antigen (HLA) class I (A, B, and Cw) and class II (DRB1 and DQB1) loci in 544 women with SCC and 542 controls. Recognizing that HLA molecules are codominantly expressed, we focused on co-occurring alleles. Among 137 allele combinations present at >5% in the case or control groups, 36 were significantly associated with SCC risk. All but one of the 30 combinations that increased risk included DQB1*0301, and 23 included subsets of A*0201-B*4402-Cw*0501-DRB1*0401-DQB1*0301. Another combination, B*4402-DRB1*1101-DQB1*0301, conferred a strong risk of SCC (odds ratio, 10.0; 95% confidence interval, 3.0–33.3). Among the six combinations that conferred a decreased risk of SCC, four included Cw*0701 or DQB1*02. Most multilocus results were similar for SCC that contained HPV16; a notable exception was A*0101-B*0801-Cw*0701-DRB1*0301-DQB1*0201 and its subsets, which were associated with HPV16-positive SCC (odds ratio, 0.5; 95% confidence interval, 0.3–0.9). The main multilocus associations were replicated in studies of cervical adenocarcinoma and vulvar cancer. These data confirm that T helper and cytotoxic T-cell responses are both important cofactors with HPV in cervical cancer etiology and indicate that co-occurring HLA alleles across loci seem to be more important than individual alleles. Thus, certain co-occurring alleles may be markers of disease risk that have clinical value as biomarkers for targeted screening or development of new therapies

Cervical and Vulvar Cancer Risk in Relation to the Joint Effects of Cigarette Smoking and Genetic Variation in Interleukin 2.

Cigarette smoking is an established cofactor to human papillomavirus (HPV) in the development of cervical and vulvar squamous cell carcinoma (SCC), and may influence risk through an immunosuppressive pathway. Genetic variation in interleukin 2 (IL2), associated in some studies with the inhibition of HPV-targeted immunity, may modify the effect of smoking on the risk of HPV-related anogenital cancers. We conducted a population-based case-only study to measure the departure from a multiplicative joint effect of cigarette smoking and IL2 variation on cervical and vulvar SCC. Genotyping of the four IL2 tagSNPs (rs2069762, rs2069763, rs2069777, and rs2069778) was done in 399 cervical and 486 vulvar SCC cases who had been interviewed regarding their smoking history. Compared with cases carrying the rs2069762 TT genotype, we observed significant departures from multiplicativity for smoking and carriership of the TG or GG genotypes in vulvar SCC risk [interaction odds ratio (IOR), 1.67; 95% confidence interval (CI), 1.16-2.41]. Carriership of one of three diplotypes, together with cigarette smoking, was associated with either a supramultiplicative (TGCT/GGCC; IOR, 2.09; 95% CI, 0.98-4.46) or submultiplicative (TTCC/TGTC; IOR, 0.37; 95% CI, 0.16-0.85 or TGCT/TGCC; IOR, 0.37; 95% CI, 0.15-0.87) joint effect in vulvar cancer risk. For cervical SCC, departure from multiplicativity was observed for smokers homozygous for the rs2069763 variant allele (TT versus GG or GT genotypes; IOR, 1.87; 95% CI, 1.00-3.48), and for carriership of the TTCC/TTCC diplotype (IOR, 2.08; 95% CI, 1.01-4.30). These results suggest that cervical and vulvar SCC risk among cigarette smokers is modified by genetic variation in IL2. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1790-9)