Optimal Climate Policy and the Future of World Economic Development

How much should the present generations sacrifice to reduce emissions today, in order to reduce the future harms of climate change? Within climate economics, debate on this question has been focused on so-called “ethical parameters” of social time preference and inequality aversion. We show that optimal climate policy similarly importantly depends on the future of the developing world. In particular, although global poverty is falling and the economic lives of the poor are improving worldwide, leading models of climate economics may be too optimistic about two central predictions: future population growth in poor countries, and future convergence in total factor productivity (TFP). We report results of small modifications to a standard model: under plausible scenarios for high future population growth (especially in sub-Saharan Africa) and for low future TFP convergence, we find that optimal near-term carbon taxes could be substantially larger

The importance of health co-benefits under different climate policy cooperation frameworks

Reducing greenhouse gas emissions has the 'co-benefit' of also reducing air pollution and associated impacts on human health. Here, we incorporate health co-benefits into estimates of the optimal climate policy for three different climate policy regimes. The first fully internalizes the climate externality at the global level via a uniform carbon price (the 'cooperative equilibrium'), thus minimizing total mitigation costs. The second connects to the concept of 'common but differentiated responsibilities' where nations coordinate their actions while accounting for different national capabilities considering socioeconomic conditions. The third assumes nations act only in their own self-interest. We find that air quality co-benefits motivate substantially reduced emissions under all three policy regimes, but that some form of global cooperation is required to prevent runaway temperature rise. However, co-benefits do warrant high levels of mitigation in certain regions even in the self-interested case, suggesting that air quality impacts may expand the range of possible policy outcomes whereby global temperatures do not increase unabated

The impact of human health co-benefits on evaluations of global climate policy

The health co-benefits of CO2 mitigation can provide a strong incentive for climate policy through reductions in air pollutant emissions that occur when targeting shared sources. However, reducing air pollutant emissions may also have an important co-harm, as the aerosols they form produce net cooling overall. Nevertheless, aerosol impacts have not been fully incorporated into cost-benefit modeling that estimates how much the world should optimally mitigate. Here we find that when both co-benefits and co-harms are taken fully into account, optimal climate policy results in immediate net benefits globally, overturning previous findings from cost-benefit models that omit these effects. The global health benefits from climate policy could reach trillions of dollars annually, but will importantly depend on the air quality policies that nations adopt independently of climate change. Depending on how society values better health, economically optimal levels of mitigation may be consistent with a target of 2 °C or lower

Priority for the Worse Off and the Social Cost of Carbon

The social cost of carbon (SCC) is a monetary measure of the harms from carbon emission. Specifically, it is the reduction in current consumption that produces a loss in social welfare equivalent to that caused by the emission of a ton of CO2. The standard approach is to calculate the SCC using a discounted-utilitarian social welfare function (SWF)—one that simply adds up the well-being numbers (utilities) of individuals, as discounted by a weighting factor that decreases with time. The discounted-utilitarian SWF has been criticized both for ignoring the distribution of well-being, and for including an arbitrary preference for earlier generations. Here, we use a prioritarian SWF, with no time-discount factor, to calculate the SCC in the integrated assessment model RICE. Prioritarianism is a well-developed concept in ethics and theoretical welfare economics, but has been, thus far, little used in climate scholarship. The core idea is to give greater weight to well-being changes affecting worse off individuals. We find substantial differences between the discounted-utilitarian and non-discounted prioritarian SCC

Observation of Josephson harmonics in tunnel junctions

Approaches to developing large-scale superconducting quantum processors must cope with the numerous microscopic degrees of freedom that are ubiquitous in solid-state devices. State-of-the-art superconducting qubits employ aluminium oxide (AlO$_x$) tunnel Josephson junctions as the sources of nonlinearity necessary to perform quantum operations. Analyses of these junctions typically assume an idealized, purely sinusoidal current–phase relation. However, this relation is expected to hold only in the limit of vanishingly low-transparency channels in the AlO$_x$ barrier. Here we show that the standard current–phase relation fails to accurately describe the energy spectra of transmon artificial atoms across various samples and laboratories. Instead, a mesoscopic model of tunnelling through an inhomogeneous AlO$_x$ barrier predicts percent-level contributions from higher Josephson harmonics. By including these in the transmon Hamiltonian, we obtain orders of magnitude better agreement between the computed and measured energy spectra. The presence and impact of Josephson harmonics has important implications for developing AlOx-based quantum technologies including quantum computers and parametric amplifiers. As an example, we show that engineered Josephson harmonics can reduce the charge dispersion and associated errors in transmon qubits by an order of magnitude while preserving their anharmonicity

Observation of Josephson Harmonics in Tunnel Junctions

Superconducting quantum processors have a long road ahead to reach fault-tolerant quantum computing. One of the most daunting challenges is taming the numerous microscopic degrees of freedom ubiquitous in solid-state devices. State-of-the-art technologies, including the world's largest quantum processors, employ aluminum oxide (AlO$_x$) tunnel Josephson junctions (JJs) as sources of nonlinearity, assuming an idealized pure $\sin\varphi$ current-phase relation (C$\varphi$R). However, this celebrated $\sin\varphi$ C$\varphi$R is only expected to occur in the limit of vanishingly low-transparency channels in the AlO$_x$ barrier. Here we show that the standard C$\varphi$R fails to accurately describe the energy spectra of transmon artificial atoms across various samples and laboratories. Instead, a mesoscopic model of tunneling through an inhomogeneous AlO$_x$ barrier predicts %-level contributions from higher Josephson harmonics. By including these in the transmon Hamiltonian, we obtain orders of magnitude better agreement between the computed and measured energy spectra. The reality of Josephson harmonics transforms qubit design and prompts a reevaluation of models for quantum gates and readout, parametric amplification and mixing, Floquet qubits, protected Josephson qubits, etc. As an example, we show that engineered Josephson harmonics can reduce the charge dispersion and the associated errors in transmon qubits by an order of magnitude, while preserving anharmonicity

Epigenetic Silencing of Spermatocyte-Specific and Neuronal Genes by SUMO Modification of the Transcription Factor Sp3

SUMO modification of transcription factors is linked to repression of transcription. The physiological significance of SUMO attachment to a particular transcriptional regulator, however, is largely unknown. We have employed the ubiquitously expressed murine transcription factor Sp3 to analyze the role of SUMOylation in vivo. We generated mice and mouse embryonic fibroblasts (MEFs) carrying a subtle point mutation in the SUMO attachment sequence of Sp3 (IKEE553D mutation). The E553D mutation impedes SUMOylation of Sp3 at K551 in vivo, without affecting Sp3 protein levels. Expression profiling revealed that spermatocyte-specific genes, such as Dmc1 and Dnahc8, and neuronal genes, including Paqr6, Rims3, and Robo3, are de-repressed in non-testicular and extra-neuronal mouse tissues and in mouse embryonic fibroblasts expressing the SUMOylation-deficient Sp3E553D mutant protein. Chromatin immunoprecipitation experiments show that transcriptional de-repression of these genes is accompanied by the loss of repressive heterochromatic marks such as H3K9 and H4K20 tri-methylation and impaired recruitment of repressive chromatin-modifying enzymes. Finally, analysis of the DNA methylation state of the Dmc1, Paqr6, and Rims3 promoters by bisulfite sequencing revealed that these genes are highly methylated in Sp3wt MEFs but are unmethylated in Sp3E553D MEFs linking SUMOylation of Sp3 to tissue-specific CpG methylation. Our results establish SUMO conjugation to Sp3 as a molecular beacon for the assembly of repression machineries to maintain tissue-specific transcriptional gene silencing

Polygenic burden in focal and generalized epilepsies

Rare genetic variants can cause epilepsy, and genetic testing has been widely adopted for severe, paediatric-onset epilepsies. The phenotypic consequences of common genetic risk burden for epilepsies and their potential future clinical applications have not yet been determined. Using polygenic risk scores (PRS) from a European-ancestry genome-wide association study in generalized and focal epilepsy, we quantified common genetic burden in patients with generalized epilepsy (GE-PRS) or focal epilepsy (FE-PRS) from two independent non-Finnish European cohorts (Epi25 Consortium, n = 5705; Cleveland Clinic Epilepsy Center, n = 620; both compared to 20 435 controls). One Finnish-ancestry population isolate (Finnish-ancestry Epi25, n = 449; compared to 1559 controls), two European-ancestry biobanks (UK Biobank, n = 383 656; Vanderbilt biorepository, n = 49 494), and one Japaneseancestry biobank (BioBank Japan, n = 168 680) were used for additional replications. Across 8386 patients with epilepsy and 622 212 population controls, we found and replicated significantly higher GE-PRS in patients with generalized epilepsy of European-ancestry compared to patients with focal epilepsy (Epi25: P = 1.64 710-15; Cleveland: P = 2.85 710-4; Finnish-ancestry Epi25: P = 1.80 710-4) or population controls (Epi25: P = 2.35 710-70; Cleveland: P = 1.43 710-7; Finnish-ancestry Epi25: P = 3.11 710-4; UK Biobank and Vanderbilt biorepository meta-analysis: P = 7.99 710-4). FE-PRS were significantly higher in patients with focal epilepsy compared to controls in the non-Finnish, non-biobank cohorts (Epi25: P = 5.74 710-19; Cleveland: P = 1.69 710-6). European ancestry-derived PRS did not predict generalized epilepsy or focal epilepsy in Japanese-ancestry individuals. Finally, we observed a significant 4.6-fold and a 4.5-fold enrichment of patients with generalized epilepsy compared to controls in the top 0.5% highest GE-PRS of the two non-Finnish European cohorts (Epi25: P = 2.60 710-15; Cleveland: P = 1.39 710-2). We conclude that common variant risk associated with epilepsy is significantly enriched in multiple cohorts of patients with epilepsy compared to controls-in particular for generalized epilepsy. As sample sizes and PRS accuracy continue to increase with further common variant discovery, PRS could complement established clinical biomarkers and augment genetic testing for patient classification, comorbidity research, and potentially targeted treatment