388 research outputs found
Induced Technological Change: Exploring its Implications for the Economics of Atmospheric Stabilization: Synthesis Report from the Innovation Modeling Comparison Project
This paper summarizes results from ten global economy-energy-environment models implementing mechanisms of endogenous technological change (ETC). Climate policy goals represented as different CO2 stabilization levels are imposed, and the contribution of induced technological change (ITC) to meeting the goals is assessed. Findings indicate that climate policy induces additional technological change, in some models substantially. Its effect is a reduction of abatement costs in all participating models. The majority of models calculate abatement costs below 1 percent of present value aggregate gross world product for the period 2000-2100. The models predict different dynamics for rising carbon costs, with some showing a decline in carbon costs towards the end of the century. There are a number of reasons for differences in results between models; however four major drivers of differences are identified. First, the extent of the necessary CO2 reduction which depends mainly on predicted baseline emissions, determines how much a model is challenged to comply with climate policy. Second, when climate policy can offset market distortions, some models show that not costs but benefits accrue from climate policy. Third, assumptions about long-term investment behavior, e.g. foresight of actors and number of available investment options, exert a major influence. Finally, whether and how options for carbon-free energy are implemented (backstop and end-of-the-pipe technologies) strongly affects both the mitigation strategy and the abatement costs
The unequal burden of human-wildlife conflict
The costs of human-wildlife conflict are measurably more impactful in areas of the developing world where the loss of cattle can mean the entire livelihood of a family being erased.Human-wildlife conflict is one of the most pressing sustainable development challenges globally. This is particularly the case where ecologically and economically important wildlife impact the livelihoods of humans. Large carnivores are one such group and their co-occurrence with low-income rural communities often results in real or perceived livestock losses that place increased costs on already impoverished households. Here we show the disparities associated with the vulnerability to conflict arising from large carnivores on cattle (Bos taurus) globally. Across the distribution of 18 large carnivores, we find that the economic vulnerability to predation losses (as measured by impacts to annual per capita income) is between two and eight times higher for households in transitioning and developing economies when compared to developed ones. This potential burden is exacerbated further in developing economies because cattle keepers in these areas produce on average 31% less cattle meat per animal than in developed economies. In the lowest-income areas, our estimates suggest that the loss of a single cow or bull equates to nearly a year and a half of lost calories consumed by a child. Finally, our results show that 82% of carnivore range falls outside protected areas, and five threatened carnivores have over one third of their range located in the most economically sensitive conflict areas. This unequal burden of human-carnivore conflict sheds light on the importance of grappling with multiple and conflicting sustainable development goals: protecting life on land and eliminating poverty and hunger
Fiscal Federalism and Foreign Transfers: Does Inter-Jurisdictional Competition Increase Foreign Aid Effectiveness?
Validating anthropogenic threat maps as a tool for assessing river ecological integrity in Andean-Amazon basins
Fiscal Decentralization and Regional Disparity: Evidence from Cross-Section and Panel Data
Contact allergy to thiurams: multifactorial analysis of clinical surveillance data collected by the IVDK network
Theory and Applications of X-ray Standing Waves in Real Crystals
Theoretical aspects of x-ray standing wave method for investigation of the
real structure of crystals are considered in this review paper. Starting from
the general approach of the secondary radiation yield from deformed crystals
this theory is applied to different concreat cases. Various models of deformed
crystals like: bicrystal model, multilayer model, crystals with extended
deformation field are considered in detailes. Peculiarities of x-ray standing
wave behavior in different scattering geometries (Bragg, Laue) are analysed in
detailes. New possibilities to solve the phase problem with x-ray standing wave
method are discussed in the review. General theoretical approaches are
illustrated with a big number of experimental results.Comment: 101 pages, 43 figures, 3 table
Cytotoxic CD8+ T cell-neuron interactions: perforin-dependent electrical silencing precedes but is not causally linked to neuronal cell death
Cytotoxic CD8(+) T cells are considered important effector cells contributing to neuronal damage in inflammatory and degenerative CNS disorders. Using time-lapse video microscopy and two-photon imaging in combination with whole-cell patch-clamp recordings, we here show that major histocompatibility class I (MHC I)-restricted neuronal antigen presentation and T cell receptor specificity determine CD8(+) T-cell locomotion and neuronal damage in culture and hippocampal brain slices. Two separate functional consequences result from a direct cell-cell contact between antigen-presenting neurons and antigen-specific CD8(+) T cells. (1) An immediate impairment of electrical signaling in single neurons and neuronal networks occurs as a result of massive shunting of the membrane capacitance after insertion of channel-forming perforin (and probably activation of other transmembrane conductances), which is paralleled by an increase of intracellular Ca(2+) levels (within <10 min). (2) Antigen-dependent neuronal apoptosis may occur independently of perforin and members of the granzyme B cluster (within approximately 1 h), suggesting that extracellular effects can substitute for intracellular delivery of granzymes by perforin. Thus, electrical silencing is an immediate consequence of MHC I-restricted interaction of CD8(+) T cells with neurons. This mechanism is clearly perforin-dependent and precedes, but is not causally linked, to neuronal cell death
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