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  1. Abstract

    The ocean’s major circulation system, the Atlantic Meridional Overturning Circulation (AMOC), is slowing down. Such weakening is consistent with warming associated with increasing greenhouse gases, as well as with recent decreases in industrial aerosol pollution. The impact of biomass burning aerosols on the AMOC, however, remains unexplored. Here, we use the Community Earth System Model version 1 Large Ensemble to quantify the impact of both aerosol types on the AMOC. Despite relatively small changes in North Atlantic biomass burning aerosols, significant AMOC evolution occurs, including weakening from 1920 to ~1970 followed by AMOC strengthening. These changes are largely out of phase relative to the corresponding AMOC evolution under industrial aerosols. AMOC responses are initiated by thermal changes in sea surface density flux due to altered shortwave radiation. An additional dynamical mechanism involving the North Atlantic sea-level pressure gradient is important under biomass-burning aerosols. AMOC-induced ocean salinity flux convergence acts as a positive feedback. Our results show that biomass-burning aerosols reinforce early 20th-century AMOC weakening associated with greenhouse gases and also partially mute industrial aerosol impacts on the AMOC. Recent increases in wildfires suggest biomass-burning aerosols may be an important driver of future AMOC variability.

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  2. Abstract

    In the era of escalating climate change, understanding human impacts on marine heatwaves (MHWs) becomes essential. This study harnesses climate model historical and single forcing simulations to delve into the individual roles of anthropogenic greenhouse gases (GHGs) and aerosols in shaping the characteristics of global MHWs over the past several decades. The results suggest that GHG variations lead to longer-lasting, more frequent, and intense MHWs. In contrast, anthropogenic aerosols markedly curb the intensity and growth of MHWs. Further analysis of the sea surface temperature (SST) probability distribution reveals that anthropogenic GHGs and aerosols have opposing effects on the tails of the SST probability distribution, causing the tails to expand and contract, respectively. Climate extremes such as MHWs are accordingly promoted and reduced. Our study underscores the significant impacts of anthropogenic GHGs and aerosols on MHWs, which go far beyond the customary concept that these anthropogenic forcings modulate climate extremes by shifting global SST probabilities via modifying the mean-state SST.

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    Free, publicly-accessible full text available January 16, 2025
  3. Free, publicly-accessible full text available November 15, 2024
  4. Free, publicly-accessible full text available December 1, 2024
  5. Abstract

    The Pacific Decadal Oscillation has been suggested to play an important role in driving marine heatwaves in the Northeast Pacific during recent decades. Here we combine observations and climate model simulations to show that marine heatwaves became longer, stronger and more frequent off the Northeast Pacific coast under a positive Pacific Decadal Oscillation scenario, unlike what is found during a negative Pacific Decadal Oscillation scenario. This primarily results from the different mean-state sea surface temperatures between the two Pacific Decadal Oscillation phases. Compared to the cool (negative) phase of the Pacific Decadal Oscillation, warmer coastal sea surface temperatures occur during the positive Pacific Decadal Oscillation phase due to reduced coastal cold upwelling and increased net downward surface heat flux. Model results show that, relative to the background anthropogenic global warming, the positive Pacific Decadal Oscillation in the period 2013–2022 prolongs marine heatwaves duration by up to 43% and acts to increase marine heatwaves annual frequency by up to 32% off the Northeast Pacific coast.

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    Free, publicly-accessible full text available December 1, 2024
  6. Abstract

    Uncovering gene-phenotype relationships can be enabled by precise gene modulation in human induced pluripotent stem-cell-derived cardiomyocytes (iPSC-CMs) and follow up phenotyping using scalable all-optical electrophysiology platforms. Such efforts towards human functional genomics can be aided by recent CRISPR-derived technologies for reversible gene inhibition or activation (CRISPRi/a). We set out to characterize the performance of CRISPRi in post-differentiated iPSC-CMs, targeting key cardiac ion channel genes,KCNH2,KCNJ2, andGJA1, and providing a multiparametric quantification of the effects on cardiac repolarization, stability of the resting membrane potential and conduction properties using all-optical tools. More potent CRISPRi effectors, e.g., Zim3, and optimized viral delivery led to improved performance on par with the use of CRISPRi iPSC lines. Confirmed mild yet specific phenotype changes when CRISPRi is deployed in non-dividing differentiated heart cells is an important step towards more holistic pre-clinical cardiotoxicity testing and for future therapeutic use in vivo.

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  7. Free, publicly-accessible full text available December 6, 2024
  8. Abstract

    Genetic association signals have been mostly found in noncoding regions through genome-wide association studies (GWAS), suggesting the roles of gene expression regulation in human diseases and traits. However, there has been limited success in colocalizing expression quantitative trait locus (eQTL) with disease-associated variants. Mediated expression score regression (MESC) is a recently proposed method to quantify the proportion of trait heritability mediated by genetically regulated gene expressions (GReX). Applications of MESC to GWAS results have yielded low estimation of mediated heritability for many traits. As MESC relies on stringent independence assumptions between cis-eQTL effects, gene effects, and nonmediated SNP effects, it may fail to characterize the true relationships between those effect sizes, which leads to biased results. Here, we consider the robustness of MESC to investigate whether the low fraction of mediated heritability inferred by MESC reflects biological reality for complex traits or is an underestimation caused by model misspecifications. Our results suggest that MESC may lead to biased estimates of mediated heritability with misspecification of gene annotations leading to underestimation, whereas misspecification of SNP annotations may lead to overestimation. Furthermore, errors in eQTL effect estimates may lead to underestimation of mediated heritability.

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  9. Free, publicly-accessible full text available November 2, 2024
  10. Free, publicly-accessible full text available July 14, 2024