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Methylmercury (MeHg) and, to a lesser extent, inorganic mercury (IHg) contamination of rice is a global public health concern, but little is known about how soil and grain Hg concentrations respond to elevated CO2 (ECO2), or how ECO2 alters movement of Hg through the soil-plant-grain system. To advance knowledge of how Hg contamination of rice will change in the future, this study explored the effect of elevated CO2 (ECO2, c. 800 ppm) on soil, iron plaque, root, stem/leaf, and grain concentrations of MeHg and IHg. We observed evidence that ECO2 increased accumulation of MeHg, but not IHg, in rice grain. For IHg, ECO2 did not alter its uptake from the soil, translocation through the plant, or concentration in rice grain. However, ECO2 did reduce uptake of IHg from the air into leaf tissues, likely as a result of the reduced stomatal conductivity and thus more limited direct uptake from the air. Methylmercury concentrations in the grain of plants grown at ECO2 were significantly higher than those of plants grown at ambient CO2. Moreover, MeHg concentrations were also elevated in stem/leaf (82 %) and root tissue (37 %) for ECO2 plants, although the root-tissue results were not statistically significant. In contrast, soil MeHg concentrations were virtually indistinguishable between treatments, indicating that higher rice grain MeHg concentrations were not likely due to higher microbial IHg methylation in soil. Plant uptake of MeHg into stem/leaves and grain from the soil was significantly greater in the ECO2 treatment; however, translocation patterns of MeHg within the plant itself did not differ between treatments. Notably, these patterns existed despite consistently lower transpiration in the ECO2 treatment, and thus less mass flow of solute towards and through the plant. Our results indicate that as CO2 concentrations rise, the human health risks related to MeHg in grain will likely increase. 

Abstract The tropical Pacific warming pattern since the 1950s exhibits two warming centers in the western Pacific (WP) and eastern Pacific (EP), encompassing an equatorial central Pacific (CP) cooling and a hemispheric asymmetry in the subtropical EP. The underlying mechanisms of this warming pattern remain debated. Here, we conduct ocean heat decompositions of two coupled model large ensembles to unfold the role of wind-driven ocean circulation. When wind changes are suppressed, historical radiative forcing induces a subtropical northeastern Pacific warming, thus causing a hemispheric asymmetry that extends toward the tropical WP. The tropical EP warming is instead induced by the cross-equatorial winds associated with the hemispheric asymmetry, and its driving mechanism is southward warm Ekman advection due to the off-equatorial westerly wind anomalies around 5°N, not vertical thermocline adjustment. Climate models fail to capture the observed CP cooling, suggesting an urgent need to better simulate equatorial oceanic processes and thermal structures. 

Abstract Cancer immunotherapy with autologous chimeric antigen receptor (CAR) T cells faces challenges in manufacturing and patient selection that could be avoided by using ‘off-the-shelf’ products, such as allogeneic CAR natural killer T (^AlloCAR-NKT) cells. Previously, we reported a system for differentiating human hematopoietic stem and progenitor cells into^AlloCAR-NKT cells, but the use of three-dimensional culture and xenogeneic feeders precluded its clinical application. Here we describe a clinically guided method to differentiate and expand IL-15-enhanced^AlloCAR-NKT cells with high yield and purity. We generated^AlloCAR-NKT cells targeting seven cancers and, in a multiple myeloma model, demonstrated their antitumor efficacy, expansion and persistence. The cells also selectively depleted immunosuppressive cells in the tumor microenviroment and antagonized tumor immune evasion via triple targeting of CAR, TCR and NK receptors. They exhibited a stable hypoimmunogenic phenotype associated with epigenetic and signaling regulation and did not induce detectable graft versus host disease or cytokine release syndrome. These properties of^AlloCAR-NKT cells support their potential for clinical translation. 

Abstract Indian Ocean meridional heat transport (MHT_IO) drives climate and ecosystem impacts, through changes to ocean temperature. Improved understanding of natural variability in tropical and subtropical MHT_IOis needed to contextualize observations and future projections. Previous studies suggest that El Niño‐Southern Oscillation (ENSO) and Indian Ocean Dipole (IOD) can drive variability in MHT_IO. However, it is unclear whether internally generated IOD can drive variability in MHT_IO, or if the apparent relationship between IOD and MHT_IOarises because both are modulated by ENSO. Here, we use a model experiment which dynamically removes ENSO to determine the role of internally forced IOD on MHT_IO. We find that IOD is not linked to anomalies in MHT_IO. Nevertheless, internal atmospheric variability drives significant MHT_IOvariability. There is little evidence for decadal or multidecadal variability in MHT_IO, suggesting this may be a region where an anthropogenic trend rises above the level of internal variability sooner. 

Abstract Investigating Pacific Meridional Modes (PMM) without the influence of tropical Pacific variability is technically difficult if based on observations or fully coupled model simulations due to their overlapping spatial structures. To confront this issue, the present study investigates both North (NPMM) and South PMM (SPMM) in terms of their associated atmospheric forcing and response processes based on a mechanically decoupled climate model simulation. In this experiment, the climatological wind stress is prescribed over the tropical Pacific, which effectively removes dynamically coupled tropical Pacific variability (e.g., the El Niño-Southern Oscillation). Interannual NPMM in this experiment is forced not only by the North Pacific Oscillation, but also by a North Pacific tripole (NPT) pattern of atmospheric internal variability, which primarily forces decadal NPMM variability. Interannual and decadal variability of the SPMM is partly forced by the South Pacific Oscillation. In turn, both interannual and decadal NPMM variability can excite atmospheric teleconnections over the Northern Hemisphere extratropics by influencing the meridional displacement of the climatological intertropical convergence zone throughout the whole year. Similarly, both interannual and decadal SPMM variability can also excite atmospheric teleconnections over the Southern Hemisphere extratropics by extending/shrinking the climatological South Pacific convergence zone in all seasons. Our results highlight a new poleward pathway by which both the NPMM and SPMM feed back to the extratropical climate, in addition to the equatorward influence on tropical Pacific variability. 

Abstract Mitigation and adaptation strategies for climate change depend on accurate climate projections for the coming decades. While changes in radiative heat fluxes are known to contribute to surface warming, changes to ocean circulation can also impact the rate of surface warming. Previous studies suggest that projected changes to ocean circulation reduce the rate of global warming. However, these studies consider large greenhouse gas forcing scenarios, which induce a significant buoyancy‐driven decline of the Atlantic Meridional Overturning Circulation. Here, we use a climate model to quantify the previously unknown impact of changes to wind‐driven ocean circulation on global surface warming. Wind‐driven ocean circulation changes amplify the externally forced warming rate by 17% from 1979 to 2014. Accurately simulating changes to the atmospheric circulation is key to improving near‐term climate projections. 

Abstract Identifying the origins of wintertime climate variations in the Northern Hemisphere requires careful attribution of the role of El Niño–Southern Oscillation (ENSO). For example, Aleutian low variability arises from internal atmospheric dynamics and is remotely forced mainly via ENSO. How ENSO modifies the local sea surface temperature (SST) and North American precipitation responses to Aleutian low variability remains unclear, as teasing out the ENSO signal is difficult. This study utilizes carefully designed coupled model experiments to address this issue. In the absence of ENSO, a deeper Aleutian low drives a positive Pacific decadal oscillation (PDO)-like SST response. However, unlike the observed PDO pattern, a coherent zonal band of turbulent heat flux–driven warm SST anomalies develops throughout the subtropical North Pacific. Furthermore, non-ENSO Aleutian low variability is associated with a large-scale atmospheric circulation pattern confined over the North Pacific and North America and dry precipitation anomalies across the southeastern United States. When ENSO is included in the forcing of Aleutian low variability in the experiments, the ENSO teleconnection modulates the turbulent heat fluxes and damps the subtropical SST anomalies induced by non-ENSO Aleutian low variability. Inclusion of ENSO forcing results in wet precipitation anomalies across the southeastern United States, unlike when the Aleutian low is driven by non-ENSO sources. Hence, we find that the ENSO teleconnection acts to destructively interfere with the subtropical North Pacific SST and southeastern United States precipitation signals associated with non-ENSO Aleutian low variability.