Cost-Effectiveness of Carbon Emission Abatement Strategies for a Local Multi-Energy System - A Case Study of Chalmers University of Technology Campus

This paper investigates the cost-effectiveness of operation strategies which can be used to abate CO2\ua0emissions in a local multi-energy system. A case study is carried out using data from a real energy system that integrates district heating, district cooling, and electricity networks at Chalmers University of Technology. Operation strategies are developed using a mixed integer linear programming multi-objective optimization model with a short foresight rolling horizon and a year of data. The cost-effectiveness of different strategies is evaluated across different carbon prices. The results provide insights into developing abatement strategies for local multi-energy systems that could be used by utilities, building owners, and authorities. The optimized abatement strategies include: increased usage of biomass boilers, substitution of district heating and absorption chillers with heat pumps, and higher utilization of storage units. The results show that, by utilizing all the strategies, a 20.8% emission reduction can be achieved with a 2.2% cost increase for the campus area. The emission abatement cost of all strategies is 36.6–100.2 (€/tCO2\ua0), which is aligned with estimated carbon prices if the Paris agreement target is to be achieved. It is higher, however, than average European Emission Trading System prices and Sweden’s carbon tax in 2019

Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation

Epithelial cells lining the adult colon do not normally express gastrin-releasing peptide (GRP) or its receptor (GRPR). In contrast, GRP/GRPR can be aberrantly expressed in human colorectal cancer (CRC) including Caco-2 cells. We have previously shown that GRPR activation results in the up-regulation of HP1β, an epigenetic modifier of gene transcription. The aim of this study was to identify the genes whose expression is altered by HP1β subsequent to GRPR activation. We determined HP1β binding positions throughout the genome using chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq). After exposure to GRP, we identified 9,625 genomic positions occupied by HP1β. We performed gene microarray analysis on Caco-2 cells in the absence and presence of a GRPR specific antagonist as well as siRNA to HP1β. The expression of 97 genes was altered subsequent to GRPR antagonism, while the expression of 473 genes was altered by HP1β siRNA exposure. When these data were evaluated in concert with our ChIP-seq findings, 9 genes showed evidence of possible altered expression as a function of GRPR signaling via HP1β. Of these, genomic PCR of immunoprecipitated chromatin demonstrated that GRPR signaling affected the expression of IL1RAPL2, FAM13A, GBE1, PLK3, and SLCO1B3. These findings provide the first evidence by which GRPR aberrantly expressed in CRC might affect tumor progression

Metal mixture modeling evaluation project: 2. Comparison of four modeling approaches

As part of the Metal Mixture Modeling Evaluation (MMME) project, models were developed by the National Institute of Advanced Industrial Science and Technology (Japan), the US Geological Survey (USA), HDR|HydroQual (USA), and the Centre for Ecology and Hydrology (United Kingdom) to address the effects of metal mixtures on biological responses of aquatic organisms. A comparison of the 4 models, as they were presented at the MMME workshop in Brussels, Belgium (May 2012), is provided in the present study. Overall, the models were found to be similar in structure (free ion activities computed by the Windermere humic aqueous model [WHAM]; specific or nonspecific binding of metals/cations in or on the organism; specification of metal potency factors or toxicity response functions to relate metal accumulation to biological response). Major differences in modeling approaches are attributed to various modeling assumptions (e.g., single vs multiple types of binding sites on the organism) and specific calibration strategies that affected the selection of model parameters. The models provided a reasonable description of additive (or nearly additive) toxicity for a number of individual toxicity test results. Less-than-additive toxicity was more difficult to describe with the available models. Because of limitations in the available datasets and the strong interrelationships among the model parameters (binding constants, potency factors, toxicity response parameters), further evaluation of specific model assumptions and calibration strategies is needed

Trans-Neptunian objects and Centaurs at thermal wavelengths

The thermal emission of transneptunian objects (TNO) and Centaurs has been observed at mid- and far-infrared wavelengths - with the biggest contributions coming from the Spitzer and Herschel space observatories-, and the brightest ones also at sub-millimeter and millimeter wavelengths. These measurements allowed to determine the sizes and albedos for almost 180 objects, and densities for about 25 multiple systems. The derived very low thermal inertias show evidence for a decrease at large heliocentric distances and for high-albedo objects, which indicates porous and low-conductivity surfaces. The radio emissivity was found to be low ($\epsilon_r$=0.70$\pm$0.13) with possible spectral variations in a few cases. The general increase of density with object size points to different formation locations or times. The mean albedos increase from about 5-6% (Centaurs, Scattered-Disk Objects) to 15% for the Detached objects, with distinct cumulative albedo distributions for hot and cold classicals. The color-albedo separation in our sample is evidence for a compositional discontinuity in the young Solar System. The median albedo of the sample (excluding dwarf planets and the Haumea family) is 0.08, the albedo of Haumea family members is close to 0.5, best explained by the presence of water ice. The existing thermal measurements remain a treasure trove at times where the far-infrared regime is observationally not accessible.Comment: Review chapter in "The Trans-Neptunian Solar System" (D. Prialnik, M.A. Barucci and L. Young, eds.), accepted for publication in January 2019, 3 Tables, 2 Figures, 27 Page

Social Class

Discussion of class structure in fifth-century Athens, historical constitution of theater audiences, and the changes in the comic representation of class antagonism from Aristophanes to Menander

Thermodynamic stability, unfolding kinetics, and aggregation of the N-terminal actin-binding domains of utrophin and dystrophin.

Muscular dystrophy (MD) is the most common genetic lethal disorder in children. Mutations in dystrophin trigger the most common form of MD, Duchenne, and its allelic variant Becker MD. Utrophin is the closest homologue and has been shown to compensate for the loss of dystrophin in human disease animal models. However, the structural and functional similarities and differences between utrophin and dystrophin are less understood. Both proteins interact with actin through their N-terminal actin-binding domain (N-ABD). In this study, we examined the thermodynamic stability and aggregation of utrophin N-ABD and compared with that of dystrophin. Our results show that utrophin N-ABD has spectroscopic properties similar to dystrophin N-ABD. However, utrophin N-ABD has decreased denaturant and thermal stability, unfolds faster, and is correspondingly more susceptible to proteolysis, which might account for its decreased in vivo half-life compared to dystrophin. In addition, utrophin N-ABD aggregates to a lesser extent compared with dystrophin N-ABD, contrary to the general behavior of proteins in which decreased stability enhances protein aggregation. Despite these differences in stability and aggregation, both proteins exhibit deleterious effects of mutations. When utrophin N-ABD mutations analogous in position to the dystrophin disease-causing mutations were generated, they behaved similarly to dystrophin mutants in terms of decreased stability and the formation of cross-β aggregates, indicating a possible role for utrophin mutations in disease mechanisms

Angiotensin-2 receptors (AT1-R and AT2-R), new prognostic factors for renal clear-cell carcinoma?

International audienceBackground: The growth factor Angiotensin-2 signals through Angiotensin receptor type 1 (AT1-R) in a broad range of cell types and tumours and through the type-2 receptor (AT2-R) in a more restricted group of cell types. Although numerous forms of cancer have been shown to overexpress AT1-R, expression of AT1-R and AT2-R by human renal clear-cell carcinoma (RCCC) is not well understood. In this study, the expression of both angiotensin receptors was quantified in a retrospective series of RCCC and correlated with prognostic factors.Methods: Angiotensin receptor type 1 and AT2-R expressions were quantified on tumour tissues by immunohistochemistry (IHC), western blot and quantitative reverse transcriptase PCR (qRT–PCR). IHC results were correlated to Fuhrman's grade and patient progression-free survival (PFS).Results: A total of 84 RCCC were analysed. By IHC, AT1-R and AT2-R were expressed to a greater level in high-grade tumours (AT1-R: P<0.001, AT2-R: P<0.001). Univariate analysis showed a correlation between PFS and AT1-R or AT2-R expression (P=0.001). By multivariate analysis, only AT2-R expression correlated with PFS (HR 1.021, P=0.006) and cancer stage (P<0.001). By western blot, AT1-R and AT1-R were also found to be overexpressed in higher Fuhrman's grade (P<0.01 and P=0.001 respectively). By qRT–PCR, AT1-R but not AT2-R mRNA were downregulated (P=0.001 and P=0.118, respectively).Conclusion: Our results show that AT1-R and AT2-R proteins are overexpressed in the most aggressive forms of RCCC and that AT2-R expression correlates with PFS. AT1-R or AT2-R blockage could, therefore, offer novel directions for anti-RCCC therapy