Modelling a mixed system of air pollution fee and tradable permits for controlling nitrogen oxide: a case study of Taiwan

A mixed-integer non-linear programming model that minimises the total regulatory costs of controlling nitrogen oxide is used to investigate how a newly proposed permit trading scheme in Taiwan, which incorporates the features of banking and a nonone- to-one trading ratio, may affect firms’ emission reduction strategies and permit trading decisions. Compared to the previous regulation where only an air pollution fee is used, the new regulation that requires a reduction in emissions by 10 per cent from the emission level in the year 2000 for a 5 year period will increase the costs by 77 per cent, which is equivalent to US # 9.87 million. The design of banking and the increasing returns to scale characteristic of pollution control among firms might lead to an uneven reduction in emissions in each year. Setting a lower reservation rate for banking would, however, help maintain a more stable environmental quality without a significant loss to the government in terms of air pollution fee revenue.air pollution fee, banking, mixed-integer non-linear programming, nitrogen oxide, tradable permits, Resource /Energy Economics and Policy,

AN ECONOMIC ANALYSIS OF THE EMISSION REDUCTION MARKET SYSTEM IN CHICAGO

A mixed-integer programming model is used to investigate economic impacts of the permit trading market in Chicago and determine the equilibrium price. Unlike previous studies, the model determines unit pollution abatement cost endogenously depending on firms' technology adoption decisions. A sequential trading process is used to simulate firms' behavior under incomplete information. The results show that average shadow prices, a counterpart of conventional shadow prices in discrete problems, slightly underestimate the equilibrium prices. Moreover, the model predicts an over-supply of permits for the first two trading seasons.mixed-integer programming, ERMS, average shadow price, pollution permit, Environmental Economics and Policy,

EFFICIENCY LOSS AND TRADABLE PERMITS

This research presents a price endogenous mathematical programming model that incorporates the independent, optimizing behavior of individual participants to estimate the possible efficiency loss of a newly developed permit trading market for nitrogen oxides (NOx) control in southern Taiwan. The result shows that when control equipment decisions are indivisible, an efficiency loss may arise due to over-investment. The efficiency loss found here is not because of a bilateral trading process and/or insufficient information for finding trading partners, but it is due to not having full control ability of the installed equipment.Environmental Economics and Policy,

Counting Independent Sets and Colorings on Random Regular Bipartite Graphs

We give a fully polynomial-time approximation scheme (FPTAS) to count the number of independent sets on almost every Delta-regular bipartite graph if Delta >= 53. In the weighted case, for all sufficiently large integers Delta and weight parameters lambda = Omega~ (1/(Delta)), we also obtain an FPTAS on almost every Delta-regular bipartite graph. Our technique is based on the recent work of Jenssen, Keevash and Perkins (SODA, 2019) and we also apply it to confirm an open question raised there: For all q >= 3 and sufficiently large integers Delta=Delta(q), there is an FPTAS to count the number of q-colorings on almost every Delta-regular bipartite graph

Effect of applied DC voltages and temperatures on space charge behaviour of multi-layer oil-paper insulation

In this paper, space charge in a multi-layer oil-paper insulation system was investigated using the pulsed electroacoustic (PEA) technique. A series of measurements had been carried following subjection of the insulation system to different applied voltages and different temperatures. Charge behaviours in the insulation system were analyzed and the influence of temperature on charge dynamics was discussed. The test results shows that homocharge injection takes place under all the test conditions, the applied DC voltage mainly affects the amount of space charge, while the temperature has greater influence on the distribution and mobility of space charge inside oil-paper samples

Impacts of florfenicol on the microbiota landscape and resistome as revealed by metagenomic analysis.

BACKGROUND:Drug-resistant fish pathogens can cause significant economic loss to fish farmers. Since 2012, florfenicol has become an approved drug for treating both septicemia and columnaris diseases in freshwater fish. Due to the limited drug options available for aquaculture, the impact of the therapeutical florfenicol treatment on the microbiota landscape as well as the resistome present in the aquaculture farm environment needs to be evaluated. RESULTS:Time-series metagenomic analyses were conducted to the aquatic microbiota present in the tank-based catfish production systems, in which catfish received standard therapeutic 10-day florfenicol treatment following the federal veterinary regulations. Results showed that the florfenicol treatment shifted the structure of the microbiota and reduced the biodiversity of it by acting as a strong stressor. Planctomycetes, Chloroflexi, and 13 other phyla were susceptible to the florfenicol treatment and their abundance was inhibited by the treatment. In contrast, the abundance of several bacteria belonging to the Proteobacteria, Bacteroidetes, Actinobacteria, and Verrucomicrobia phyla increased. These bacteria with increased abundance either harbor florfenicol-resistant genes (FRGs) or had beneficial mutations. The florfenicol treatment promoted the proliferation of florfenicol-resistant genes. The copy number of phenicol-specific resistance genes as well as multiple classes of antibiotic-resistant genes (ARGs) exhibited strong correlations across different genetic exchange communities (p < 0.05), indicating the horizontal transfer of florfenicol-resistant genes among these bacterial species or genera. Florfenicol treatment also induced mutation-driven resistance. Significant changes in single-nucleotide polymorphism (SNP) allele frequencies were observed in membrane transporters, genes involved in recombination, and in genes with primary functions of a resistance phenotype. CONCLUSIONS:The therapeutical level of florfenicol treatment significantly altered the microbiome and resistome present in catfish tanks. Both intra-population and inter-population horizontal ARG transfer was observed, with the intra-population transfer being more common. The oxazolidinone/phenicol-resistant gene optrA was the most prevalent transferred ARG. In addition to horizontal gene transfer, bacteria could also acquire florfenicol resistance by regulating the innate efflux systems via mutations. The observations made by this study are of great importance for guiding the strategic use of florfenicol, thus preventing the formation, persistence, and spreading of florfenicol-resistant bacteria and resistance genes in aquaculture

Variational equalities of entropy in nonuniformly hyperbolic systems

In this paper we prove that for an ergodic hyperbolic measure $\omega$ of a $C^{1+\alpha}$ diffeomorphism $f$ on a Riemannian manifold $M$, there is an $\omega$-full measured set $\widetilde{\Lambda}$ such that for every invariant probability $\mu\in \mathcal{M}_{inv}(\widetilde{\Lambda},f)$, the metric entropy of $\mu$ is equal to the topological entropy of saturated set $G_{\mu}$ consisting of generic points of $\mu$: $$h_\mu(f)=h_{\top}(f,G_{\mu}).$$ Moreover, for every nonempty, compact and connected subset $K$ of $\mathcal{M}_{inv}(\widetilde{\Lambda},f)$ with the same hyperbolic rate, we compute the topological entropy of saturated set $G_K$ of $K$ by the following equality: $$\inf\{h_\mu(f)\mid \mu\in K\}=h_{\top}(f,G_K).$$ In particular these results can be applied (i) to the nonuniformy hyperbolic diffeomorphisms described by Katok, (ii) to the robustly transitive partially hyperbolic diffeomorphisms described by ~Ma{\~{n}}{\'{e}}, (iii) to the robustly transitive non-partially hyperbolic diffeomorphisms described by Bonatti-Viana. In all these cases $\mathcal{M}_{inv}(\widetilde{\Lambda},f)$ contains an open subset of $\mathcal{M}_{erg}(M,f)$.Comment: Transactions of the American Mathematical Society, to appear,see http://www.ams.org/journals/tran/0000-000-00/S0002-9947-2016-06780-X

ROS regulation of axonal mitochondrial transport

Mitochondria perform critical functions including aerobic ATP production and calcium (Ca2+) homeostasis, but are also a major source of reactive oxygen species (ROS) production. To maintain cellular function and survival in neurons, mitochondria are transported along axons, and accumulate in regions with high demand for their functions. Oxidative stress and abnormal mitochondrial axonal transport are associated with neurodegenerative disorders. However, we know little about the connection between these two. Using primaryDrosophila neuronal cell culture and the third instar larval nervous system as in vitro and in vivo models, respectively, we studied mitochondrial transport under oxidative stress conditions. In vitro, hydrogen peroxide (H2O2) diminished the percentage of moving mitochondria, the mitochondrial length and inner membrane potential. In vivo, ROS inhibited specifically mitochondrial axonal transport, primarily due to reduced flux and velocity, but did not affect transport of other organelles. In addition to excess ROS, down-regulation of Nox or Duox expression, which reduces endogenous ROS levels, mitochondrial transport was impaired. To understand the mechanisms underlying these effects, we examined Ca2+ levels and the JNK (c-Jun N-terminal Kinase) pathway, which have been shown to regulate mitochondrial transport and general fast axonal transport, respectively. We found that elevated ROS increased Ca 2+levels, and that the Ca2+ chelator EGTA rescued ROS-induced defects in mitochondrial transport. In addition, activation of the JNK pathway reduced mitochondrial flux and velocities, while JNK knockdown partially rescued ROS-induced defects in the anterograde direction. We conclude that ROS have the capacity to regulate mitochondrial traffic, and that Ca 2+ and JNK signaling play roles in mediating these effects