Human-induced intensified seasonal cycle of sea surface temperature.

Changes in the seasonal cycle of sea surface temperature (SST) have far-reaching ecological and societal implications. Previous studies have found an intensified SST seasonal cycle under global warming, but whether such changes have emerged in historical records remains largely unknown. Here, we reveal that the SST seasonal cycle globally has intensified by 3.9 ± 1.6% in recent four decades (1983-2022), with hotspot regions such as the northern subpolar gyres experiencing an intensification of up to 10%. Increased greenhouse gases are the primary driver of this intensification, and decreased anthropogenic aerosols also contribute. These changes in anthropogenic emissions lead to shallower mixed layer depths, reducing the thermal inertia of upper ocean and enhancing the seasonality of SST. In addition, the direct impacts of increased ocean heat uptake and suppressed seasonal amplitude of surface heat flux also contribute in the North Pacific and North Atlantic. The temperature seasonal cycle is intensified not only at the ocean surface, but throughout the mixed layer. The ramifications of this intensified SST seasonal cycle extend to the seasonal variation in upper-ocean oxygenation, a critical factor for most ocean ecosystems.

Atmosphere teleconnections from abatement of China aerosol emissions exacerbate Northeast Pacific warm blob events.

During 2010 to 2020, Northeast Pacific (NEP) sea surface temperature (SST) experienced the warmest decade ever recorded, manifested in several extreme marine heatwaves, referred to as "warm blob" events, which severely affect marine ecosystems and extreme weather along the west coast of North America. While year-to-year internal climate variability has been suggested as a cause of individual events, the causes of the continuous dramatic NEP SST warming remain elusive. Here, we show that other than the greenhouse gas (GHG) forcing, rapid aerosol abatement in China over the period likely plays an important role. Anomalous tropospheric warming induced by declining aerosols in China generated atmospheric teleconnections from East Asia to the NEP, featuring an intensified and southward-shifted Aleutian Low. The associated atmospheric circulation anomaly weakens the climatological westerlies in the NEP and warms the SST there by suppressing the evaporative cooling. The aerosol-induced mean warming of the NEP SST, along with internal climate variability and the GHG-induced warming, made the warm blob events more frequent and intense during 2010 to 2020. As anthropogenic aerosol emissions continue to decrease, there is likely to be an increase in NEP warm blob events, disproportionately large beyond the direct radiative effects.

Increased Asian aerosols drive a slowdown of Atlantic Meridional Overturning Circulation.

Observational evidence and climate model experiments suggest a slowdown of the Atlantic Meridional Overturning Circulation (AMOC) since the mid-1990s. Increased greenhouse gases and the declined anthropogenic aerosols (AAs) over North America and Europe are believed to contribute to the AMOC slowdown. Asian AAs continue to increase but the associated impact has been unclear. Using ensembles of climate simulations, here we show that the radiative cooling resulting from increased Asian AAs drives an AMOC reduction. The increased AAs over Asia generate circumglobal stationary Rossby waves in the northern midlatitudes, which shift the westerly jet stream southward and weaken the subpolar North Atlantic westerlies. Consequently, reduced transport of cold air from North America hinders water mass transformation in the Labrador Sea and thus contributes to the AMOC slowdown. The link between increased Asian AAs and an AMOC slowdown is supported by different models with different configurations. Thus, reducing emissions of Asian AAs will not only lower local air pollution, but also help stabilize the AMOC.

Freshwater Flux Variability Lengthens the Period of the Low-Frequency AMOC Variability.

Atlantic Meridional Overturning Circulation (AMOC) exhibits interdecadal to multidecadal variability, yet the role of surface freshwater flux (FWF) variability in this AMOC variability remains unclear. This study isolates the contribution of FWF variability in modulating AMOC through a partially coupled experiment, in which the effect of the interactive FWF is disabled. It is demonstrated that the impact of the coupled FWF variability enhances the persistence of density and deep convection anomalies in the Labrador Sea (LS), thus lengthening the period of the AMOC oscillation on multidecadal timescale and suppressing its ∼30-year periodicity. Further lead-lag regressions illuminate that the more persistent LS density anomalies are maintained by two mechanisms: (a) The local temperature-salinity coupling through the evaporation and (b) a downstream propagation along the East Greenland Current of the extra salinity anomaly due to the sea ice melting changes associated with an atmosphere forcing over the southern Greenland tip.

High-throughput production of functional prototissues capable of producing NO for vasodilation.

Bottom-up synthesis of prototissues helps us to understand the internal cellular communications in the natural tissues and their functions, as well as to improve or repair the damaged tissues. The existed prototissues are rarely used to improve the function of living tissues. We demonstrate a methodology to produce spatially programmable prototissues based on the magneto-Archimedes effect in a high-throughput manner. More than 2000 prototissues are produced once within 2 h. Two-component and three-component spatial coded prototissues are fabricated by varying the addition giant unilamellar vesicles order/number, and the magnetic field distributions. Two-step and three-step signal communications in the prototissues are realized using cascade enzyme reactions. More importantly, the two-component prototissues capable of producing nitric oxide cause vasodilation of rat blood vessels in the presence of glucose and hydroxyurea. The tension force decreases 2.59 g, meanwhile the blood vessel relaxation is of 31.2%. Our works pave the path to fabricate complicated programmable prototissues, and hold great potential in the biomedical field.

The protective function of taurine on pesticide-induced permanent neurodevelopmental toxicity in juvenile rats.

Numerous studies have confirmed that prenatal or early postnatal exposure to pesticides can lead to functional deficits in the developing brain. This study aimed to investigate whether combined exposure to paraquat (PQ) and maneb (MB) during puberty could cause permanent toxic effects in the neural system of rats. In addition, the neuroprotective function of taurine (T) and its possible mechanism were investigated. Rats were administered PQ + MB intragastrically for 12 continuous weeks, while taurine dissolved in water was fed to the rats for 24 continuous weeks. In the behavioral tests, the rats' trajectories became complex, and the reaction latencies and mistake frequencies increased. Significant changes were found in the hippocampal neurons of the PQ + MB groups but not in the taurine treatment groups. PQ + MB stimulated cAMP to reduce the production of protein kinase A (PKA) and inhibited the activation of other elements, such as brain-derived neurotrophic factor (BDNF), cAMP response element binding protein (CREB), phospho-CREB (p-CREB), immediate-early genes (IEGs)Arc, and c-Fos. Importantly, taurine regulated the level of cAMP and the expression of the abovementioned proteins. Together, our findings implied that adolescent exposure to PQ + MB may impact the behavior and cognitive function of rats via the cAMP-PKA-CREB signaling pathway, while taurine may in turn exert neuroprotection by diminishing these impacts.

Dihydromethysticin, a natural molecule from Kava, suppresses the growth of colorectal cancer via the NLRC3/PI3K pathway.

Dihydromethysticin (DHM), a natural compound derived from Kava, has been reported to be effective against mental disorders and some malignant tumors. However, little is known about the inhibitory effect of DHM on colorectal cancer (CRC). First, we examined the impact of DHM on human colon cancer cell lines, which demonstrated that DHM inhibits proliferation, migration, and invasion and promotes apoptosis and cell cycle arrest in colon cancer cells in vitro. Using small hairpin RNA, we inhibited nucleotide-oligomerization domain-like receptor subfamily C3 (NLRC3)/phosphoinositide 3-kinase (PI3K) pathway to elucidate the partial signaling of DHM-mediated tumor suppression. Additionally, using an ectopic human CRC model, we verified whether DHM inhibits tumor growth and angiogenesis via the NLRC3/PI3K pathway in vivo. Overall, DHM showed an inhibitory effect on CRC by altering cell proliferation, migration, invasion, apoptosis, cell cycle, and angiogenesis, possibly via the NLRC3/PI3K pathway. Thus, DHM may be a promising candidate for CRC therapy.