Stomatal closure is one of the main physiological responses to increasing CO2 concentration, which leads to a reduction in plant water loss. This response has the potential to trigger changes in the climate system by regulating surface energy budgets—a phenomenon known as CO2 physiological forcing. However, its remote impacts on the Arctic climate system are unclear. Here we show that vegetation at high latitudes enhances the Arctic amplification via remote and time-delayed physiological forcing processes. Surface warming occurs at mid-to-high latitudes due to the physiological acclimation-induced reduction in evaporative cooling and resultant increase in sensible heat flux. This excessive surface heat energy is transported to the Arctic ocean and contributes to the sea ice loss, thereby enhancing Arctic warming. The surface warming in the Arctic is further amplified by local feedbacks, and consequently the contribution of physiological effects to Arctic warming represents about 10% of radiative forcing effects.
Multilayered hard coatings with a CrN matrix and an Al2O3, TiO2, or nanolaminate-Al2O3/TiO2 sealing layer were designed by a hybrid deposition process combined with physical vapor deposition (PVD) and atomic layer deposition (ALD). The strategy was to utilize ALD thin films as pinhole-free barriers to seal the intrinsic defects to protect the CrN matrix. The influences of the different sealing layers added in the coatings on the microstructure, surface roughness, and corrosion behaviors were investigated. The results indicated that the sealing layer added by ALD significantly decreased the average grain size and improved the corrosion resistance of the CrN coatings. The insertion of the nanolaminate-Al2O3/TiO2 sealing layers resulted in a further increase in corrosion resistance, which was attributed to the synergistic effect of Al2O3 and TiO2, both acting as excellent passivation barriers to the diffusion of corrosive substances.
Stomatal closure is a major physiological response to the increasing atmospheric carbon dioxide (CO2), which can lead to surface warming by regulating surface energy fluxes—a phenomenon known as CO2 physiological forcing. The magnitude of land surface warming caused by physiological forcing is substantial and varies across models. Here we assess the continental warming response to CO2 physiological forcing and quantify the resultant climate feedback using carbon–climate simulations from phases 5 and 6 of the Coupled Model Intercomparison Project, with a focus on identifying the cause of inter-model spread. It is demonstrated that the continental (40°–70°N) warming response to the physiological forcing in summer (~0.55 K) is amplified primarily due to cloud feedback (~1.05 K), whereas the other climate feedbacks, ranged from –0.57 K to 0.20 K, show relatively minor contributions. In addition, the strength of cloud feedback varies considerably across models, which plays a primary role in leading large diversity of the continental warming response to the physiological forcing.
The El Niño-Southern Oscillation (ENSO) drives variations in terrestrial carbon fluxes by affecting the terrestrial ecosystem via atmospheric teleconnections and thus plays an important role in interannual variability of the global carbon cycle. However, we lack such knowledge on decadal time scales, that is, how the carbon cycle can be affected by decadal variations of ENSO characteristics. Here we examine how, and by how much, decadal ENSO variability affects decadal variability of the global carbon cycle by analyzing a 1,801-year preindustrial control simulation. We identify two different aspects, together explaining~36% of the decadal variations in the global carbon cycle. First, climate variations induced by decadal ENSO-like variability regulate terrestrial carbon flux and hence atmospheric CO 2 on decadal time scales. Second, decadal changes in the asymmetrical response of the terrestrial ecosystem, resulting from decadal modulation of ENSO amplitude and asymmetry, rectify the background mean state, thereby generating decadal variability of land carbon fluxes.Plain Language Summary The El Niño-Southern Oscillation (ENSO) is an important driver of year-to-year variation of the global carbon cycle due to its impacts on the global climate variability. For example, most parts of the tropical land experience drought during El Niño events, and therefore rainforests and savanna regions do not capture well carbon dioxide compared to normal years because a high temperature and a lack of precipitation during El Niño events lead to less photosynthesis over the tropics. This is a well-known feature in year-to-year variation, but not in decadal time scales due to a lack of long-term observations. Here we examine how, and by how much, decadal ENSO variability affects decadal variation in the global carbon cycle by analyzing a 1,801-year Earth System simulation. We found that two different aspects of decadal ENSO variability, associated with decadal changes in the tropical Pacific Ocean and asymmetric characteristics between El Niño and La Niña, drive decadal change in the terrestrial carbon fluxes. As a result, these two aspects together can explain~36% of the decadal variability in the global carbon cycle.It has long been established that the El Niño-Southern Oscillation (ENSO), a predominant mode of climate variability, leads to interannual variability of the global carbon cycle (Key Points: • About 36% of decadal variations in global NBP can be explained by two aspects of decadal ENSO variability • First, decadal ENSO-like variability induces interdecadal changes in terrestrial carbon fluxes via atmospheric teleconnections • Second, decadal ENSO modulations in amplitude and asymmetry lead to decadal NBP variability by changing ENSO-induced residual NBP Supporting Information: • Supporting Information S1
Loranthus tanakae Franch. & Sav. found in China, Japan, and Korea is traditionally used for managing arthritis and respiratory diseases. In this study, we analyzed the components of L. tanakae 70% ethanol extract (LTE) and investigated the therapeutic effects of LTE on pulmonary inflammation using cells exposed to cigarette smoke condensate (CSC) and lipopolysaccharide (LPS) in vitro and in vivo in mice and performed a network analysis between components and genes based on a public database. We detected quercitrin, afzelin, rhamnetin 3-rhamnoside, and rhamnocitrin 3-rhamnoside in LTE, which induced a significant reduction in inflammatory mediators including interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α and inflammatory cells in CSC exposed H292 cells and in mice, accompanied by a reduction in inflammatory cell infiltration into lung tissue. In addition, LTE increased translocation into the nuclei of nuclear factor erythroid-2-related factor 2 (Nrf2). By contrast, the activation of nuclear factor (NF)-κB, induced by CSC exposure, decreased after LTE application. These results were consistent with the network pharmacological analysis. In conclusion, LTE effectively attenuated pulmonary inflammation caused by CSC+LPS exposure, which was closely involved in the enhancement of Nrf2 expression and suppression of NF-κB activation. Therefore, LTE may be a potential treatment option for pulmonary inflammatory diseases including chronic obstructive pulmonary disease (COPD).
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