A multi-stakeholder analysis of the economic efficiency of industrial energy efficiency policies: Empirical evidence from ten years of the Italian White Certificate Scheme

© 2019 There is growing interest worldwide in more effective policies to promote industrial energy efficiency and mitigate climate change. The White Certificates Scheme is a market-based mechanism aimed at stimulating the adoption of Energy Efficiency Measures. The Italian White Certificates scheme - one of the most long-standing and articulated - is a successful example of industrial energy efficiency policies, considered an interesting and remarkable case by other countries, especially due to its robustness in terms of the volume of certificates traded. Despite the considerable interest in White Certificates, an in-depth analysis of the economic efficiency of the mechanism from the perspective of different stakeholders is still lacking. To address this gap, this study develops a cost-benefit evaluation framework and a multi-stakeholder economic efficiency analysis of the Italian White Certificates scheme focusing on the Italian State, utilities, players in the energy efficiency value chain, and energy users. Our findings (also corroborated with sensitivity analyses) show that the White Certificates Scheme has led to several positive impacts for almost all stakeholders involved, with the exception of energy utilities that have suffered a major economic loss mainly due to a reduction of energy sold to end users. Such loss is likely to promote a deep change in the role of utilities in the energy market in terms of the services they offer and their business models. Our findings, in addition to providing useful directions for future research, offer interesting insights and implications for policymakers who may take inspiration from the pros and cons of the Italian White Certificates scheme when promoting energy efficiency through incentive mechanisms

Modelling and simulation of biased agonism dynamics at a G protein-coupled receptor.

Theoretical models of G protein-coupled receptor (GPCR) concentration-response relationships often assume an agonist producing a single functional response via a single active state of the receptor. These models have largely been analysed assuming steady-state conditions. There is now much experimental evidence to suggest that many GPCRs can exist in multiple receptor conformations and elicit numerous functional responses, with ligands having the potential to activate different signalling pathways to varying extents-a concept referred to as biased agonism, functional selectivity or pluri-dimensional efficacy. Moreover, recent experimental results indicate a clear possibility for time-dependent bias, whereby an agonist's bias with respect to different pathways may vary dynamically. Efforts towards understanding the implications of temporal bias by characterising and quantifying ligand effects on multiple pathways will clearly be aided by extending current equilibrium binding and biased activation models to include G protein activation dynamics. Here, we present a new model of time-dependent biased agonism, based on ordinary differential equations for multiple cubic ternary complex activation models with G protein cycle dynamics. This model allows simulation and analysis of multi-pathway activation bias dynamics at a single receptor for the first time, at the level of active G protein (αGTP), towards the analysis of dynamic functional responses. The model is generally applicable to systems with NG G proteins and N* active receptor states. Numerical simulations for NG=N*=2 reveal new insights into the effects of system parameters (including cooperativities, and ligand and receptor concentrations) on bias dynamics, highlighting new phenomena including the dynamic inter-conversion of bias direction. Further, we fit this model to 'wet' experimental data for two competing G proteins (Gi and Gs) that become activated upon stimulation of the adenosine A1 receptor with adenosine derivative compounds. Finally, we show that our model can qualitatively describe the temporal dynamics of this competing G protein activation

Protecting backaction-evading measurements from parametric instability

Noiseless measurement of a single quadrature in systems of parametrically coupled oscillators is theoretically possible by pumping at the sum and difference frequencies of the two oscillators, realizing a backaction-evading (BAE) scheme. Although this would hold true in the simplest scenario for a system with pure three-wave mixing, implementations of this scheme are hindered by unwanted higher-order parametric processes that destabilize the system and add noise. We show analytically that detuning the two pumps from the sum and difference frequencies can stabilize the system and fully recover the BAE performance, enabling operation at otherwise inaccessible cooperativities. We also show that the acceleration demonstrated in a weak signal detection experiment [PRX QUANTUM 4, 020302 (2023)] was only achievable because of this detuning technique.Comment: 7 pages, 3 figure

Autophagy in motor neuron disease: Key pathogenetic mechanisms and therapeutic targets

Autophagy is a lysosome-dependant intracellular degradation process that eliminates long-lived proteins as well as damaged organelles from the cytoplasm. An increasing body of evidence suggests that dysregulation of this system plays a pivotal role in the etiology and/or progression of neurodegenerative diseases including motor neuron disorders. Herein, we review the latest findings that highlight the involvement of autophagy in the pathogenesis of amyotrophic lateral sclerosis (ALS) and the potential role of this pathway as a target of therapeutic purposes. Autophagy promotes the removal of toxic, cytoplasmic aggregate-prone pathogenetic proteins, enhances cell survival, and modulates inflammation. The existence of several drugs targeting this pathway can facilitate the translation of basic research to clinical trials for ALS and other motor neuron diseases

Hereditary neuropathy with liability to pressure palsy (HNPP): Report of a family with a new point mutation in PMP22 gene

Background: Hereditary neuropathy with liability to pressure palsy (HNPP) is an autosomal dominant disorder most commonly presenting with acute-onset, non-painful focal sensory and motor mononeuropathy. Approximately 80% of patients carry a 1.5 Mb deletion of chromosome 17p11.2 involving the peripheral myelin protein 22 gene (PMP22), the same duplicated in Charcot-Marie-Tooth 1A patients. In a small proportion of patients the disease is caused by PMP22 point mutations. Case presentation: We report on a familial case harbouring a new point mutation in the PMP22 gene. The proband is a 4-years-old girl with acute onset of focal numbness and weakness in her right hand. Electroneurography demonstrated transient sensory and motor radial nerves involvement. In her father, reporting chronic symptoms (cramps and exercise-induced myalgia), we uncovered mild atrophy and areflexia on clinical examination and a mixed (predominantly demyelinating) polyneuropathy with sensory-motor involvement on electrophysiological study. Both carried a nucleotidic substitution c.178 + 2 T > C on intron 3 of the PMP22 gene, involving the splicing donor site, not reported on databases but predicted to be likely pathogenic. Conclusions: We described a previously unreported point mutation in PMP22 gene, which led to the development of a HNPP phenotype in a child and her father. In children evaluated for a sensory and motor transient episode, HNPP disorder due to PMP22 mutations should be suspected. Clinical and electrophysiological studies should be extended to all family members even in the absence of previous episodes suggestive for HNPP

Quantum interference of tunneling paths under a double-well barrier

The tunnel effect, a hallmark of the quantum realm, involves motion across a classically forbidden region. In a driven nonlinear system, two or more tunneling paths may coherently interfere, enhancing or cancelling the tunnel effect. Since individual quantum systems are difficult to control, this interference effect has only been studied for the lowest energy states of many-body ensembles. In our experiment, we show a coherent cancellation of the tunneling amplitude in the ground and excited state manifold of an individual squeeze-driven Kerr oscillator, a consequence of the destructive interference of tunneling paths in the classically forbidden region. The tunnel splitting vanishes periodically in the spectrum as a function of the frequency of the squeeze-drive, with the periodicity given by twice the Kerr coefficient. This resonant cancellation, combined with an overall exponential reduction of tunneling as a function of both amplitude and frequency of the squeeze-drive, reduces drastically the well-switching rate under incoherent environment-induced evolution. The control of tunneling via interference effects can be applied to quantum computation, molecular, and nuclear physics