Geochemical characteristics of biogenic barium in sediments of the Antarctica Ross Sea and their indication for paleoproductivity

241-248In this paper, the biogenic Ba of Column R11 in the Antarctic Ross Sea and its implications to the paleo oceanographic productivity since the late of Late Quaternary were discussed, combined with the organic carbon, opal and biogenic calcium carbonate. The biogenic Ba contents ranged from 51.8 to 508.4 μg/g overall, exhibiting a gradually rising trend from the bottom to the top. It highly correlated both with TOC and opal, revealing that on one hand biogenic Ba can be used to study the change of productivity in the Ross Sea; and on the other hand, the marine productivity gradually increased since the late Pleistocene. The new productivity based on Francois model varied from 0.40 to 233.90 gC/(m2•a). The high values were mainly concentrated at the depth from 32 to 48 cm, but the new productivity values of the bottom were lower. It was inferred that the change in marine productivity in the Ross Sea was possibly affected by the ice cover since the late Pleistocene

Spatiotemporal evolution and drivers of carbon inequalities in urban agglomeration:An MLD-IDA inequality indicator decomposition

Increasing countries are articulating ambitious goals of carbon neutrality. However, large inequalities in regional emissions within a country may hinder progress toward a carbon–neutral future, as the unequal distribution of reduction responsibilities among regions could impair just transition and exacerbate uneven development, which necessitates an in-depth understanding of the mechanism of multi-scale carbon inequalities within country, region, and city. Yet, the evolution of carbon inequalities within urban agglomerations and the differences between adjacent or distant urban agglomerations have not been well understood, especially in countries undergoing rapid urbanization. Using the data of 89 cities in China’s Yangtze River Economic Belt (YREB) during 2006–2021, this paper quantifies carbon emissions inequality (CEI) at different scales in a systematic regional-urban agglomeration-city hierarchical structure. Then, under the integrated mean logarithmic deviation-logarithmic mean Divisia index (MLD-LMDI) decomposition framework, multi-scale CEIs are perfectly decomposed into six interrelated drivers, i.e., industrial emission structure, energy emission intensity, industrial energy mix, energy intensity, industrial structure, and economic development. The results show that economic development, energy intensity, and industrial energy mix disparities are the main determinants accounting for CEIs at different scales. The decreasing CEI in YREB is mainly due to the changes in industrial structure and economic development, while the energy intensity effect partially hinders the mitigation of CEI. In the upper reaches of the YREB, the energy intensity effect accounts for over 94% growth of CEI during 2006–2021, while the decline in CEIs in middle and lower reaches is primarily caused by the effects of industrial energy mix and industrial structure, respectively. Further spatial decomposition analysis reveals more refined city-level heterogeneous effects and emphasizes the prioritized emission reduction direction for each city. This paper offers implications for reducing carbon inequality and insights into coordinated carbon emissions mitigation at the regional level for a carbon–neutral future

MOF-derived ultrathin cobalt molybdenum phosphide nanosheets for efficient electrochemical overall water splitting

Altres ajuts: IREC is funded by the CERCA Programme/Generalitat de Catalunya. ICN2 is funded by the CERCA Programme/Generalitat de Catalunya.The development of high-performance and cost-effective earth-abundant transition metal-based electrocatalysts is of major interest for several key energy technologies, including water splitting. Herein, we report the synthesis of ultrathin CoMoP nanosheets through a simple ion etching and phosphorization method. The obtained catalyst exhibits outstanding electrocatalytic activity and stability towards oxygen and hydrogen evolution reactions (OER and HER), with overpotentials down to 273 and 89 mV at 10 mA cm −2, respectively. The produced CoMoP nanosheets are also characterized by very small Tafel slopes, 54.9 and 69.7 mV dec −1 for OER and HER, respectively. When used as both cathode and anode electrocatalyst in the overall water splitting reaction, CoMoP-based cells require just 1.56 V to reach 10 mA cm −2 in alkaline media. This outstanding performance is attributed to the proper composition, weak crystallinity and two-dimensional nanosheet structure of the electrocatalyst

Protectin conjugates in tissue regeneration 1 alleviates sepsis-induced acute lung injury by inhibiting ferroptosis

Background: Acute lung injury (ALI) is a common and serious complication of sepsis with high mortality. Ferroptosis, categorized as programmed cell death, contributes to the development of lung injury. Protectin conjugates in tissue regeneration 1 (PCTR1) is an endogenous lipid mediator that exerts protective effects against multiorgan injury. However, the role of PCTR1 in the ferroptosis of sepsis-related ALI remains unknown. Methods: A pulmonary epithelial cell line and a mouse model of ALI stimulated with lipopolysaccharide (LPS) were established in vitro and in vivo. Ferroptosis biomarkers, including ferrous (Fe2+), glutathione (GSH), malondialdehyde (MDA) and 4-Hydroxynonenal (4-HNE), were assessed by relevant assay kits. Glutathione peroxidase 4 (GPX4) and prostaglandin-endoperoxide synthase 2 (PTGS2) protein levels were determined by western blotting. Lipid peroxides were examined by fluorescence microscopy and flow cytometry. Cell viability was determined by a CCK-8 assay kit. The ultrastructure of mitochondria was observed with transmission electron microscopy. Morphology and inflammatory cytokine levels predicted the severity of lung injury. Afterward, related inhibitors were used to explore the potential mechanism by which PCTR1 regulates ferroptosis. Results: PCTR1 treatment protected mice from LPS-induced lung injury, which was consistent with the effect of the ferroptosis inhibitor ferrostatin-1. PCTR1 treatment decreased Fe2+, PTGS2 and lipid reactive oxygen species (ROS) contents, increased GSH and GPX4 levels and ameliorated mitochondrial ultrastructural injury. Administration of LPS or the ferroptosis agonist RSL3 resulted in reduced cell viability, which was rescued by PCTR1. Mechanistically, inhibition of the PCTR1 receptor lipoxin A4 (ALX), protein kinase A (PKA) and transcription factor cAMP-response element binding protein (CREB) partly decreased PCTR1 upregulated GPX4 expression and a CREB inhibitor blocked the effects ofPCTR1 on ferroptosis inhibition and lung protection. Conclusion: This study suggests that PCTR1 suppresses LPS-induced ferroptosis via the ALX/PKA/CREB signaling pathway, which may offer promising therapeutic prospects in sepsis-related ALI

Catestatin Enhances Neuropathic Pain Mediated by P2X4 Receptor of Dorsal Root Ganglia in a Rat Model of Chronic Constriction Injury

Background/Aims: Neuropathic pain (NPP) is the consequence of a number of central nervous system injuries or diseases. Previous studies have shown that NPP is mediated by P2X4 receptors that are expressed on satellite glial cells (SGCs) of dorsal root ganglia (DRG). Catestatin (CST), a neuroendocrine multifunctional peptide, may be involved in the pathogenesis of NPP. Here, we studied the mechanism through which CST affects NPP. Methods: We made rat models of chronic constriction injury (CCI) that simulate neuropathic pain. Rat behavioral changes were estimated by measuring the degree of hyperalgesia as assessed by the mechanical withdrawal threshold (MWT) and the thermal withdrawal latency (TWL). P2X4 mRNA expression was detected by quantitative real-time reverse transcription-polymerase chain reaction. P2X4 protein level and related signal pathways were assessed by western blot. Additionally, double-labeled immunofluorescence was employed to visualize the correspondence between the P2X4 receptor and glial fibrillary acidic protein. An enzyme-linked immunosorbent assay was performed to determine the concentration of CST and inflammatory factors. Results: CST led to lower MWT and TWL and increased P2X4 mRNA and protein expression on the SGCs of model rats. Further, CST upregulated the expression of phosphor-p38 and phosphor-ERK 1/2 on the SGCs of CCI rats. However, the expression level of phosphor-JNK and phosphor-p65 did not obviously change. Conclusion: Taken together, CST might boost NPP by enhancing the sensitivity of P2X4 receptors in the DRG of rats, which would provide us a novel perspective and research direction to explore new therapeutic targets for NPP

Inhibition the ubiquitination of ENaC and Na,K-ATPase with erythropoietin promotes alveolar fluid clearance in sepsis-induced acute respiratory distress syndrome

Sepsis-induced acute respiratory distress syndrome (ARDS) causes significant fatalities worldwide and lacks pharmacological intervention. Alveolar fluid clearance (AFC) plays a pivotal role in the remission of ARDS and is markedly impaired in the pathogenesis of ARDS. Here, we demonstrated that erythropoietin could effectively ameliorate lung injury manifestations and lethality, restore lung function and promote AFC in a rat model of lipopolysaccharide (LPS)-induced ARDS. Moreover, it was proven that EPO-induced restoration of AFC occurs through triggering the total protein expression of ENaC and Na,K-ATPase channels, enhancing their protein abundance in the membrane, and suppressing their ubiquitination for degeneration. Mechanistically, the data indicated the possible involvement of EPOR/JAK2/STAT3/SGK1/Nedd4–2 signaling in this process, and the pharmacological inhibition of the pathway markedly eliminated the stimulating effects of EPO on ENaC and Na,K-ATPase, and subsequently reversed the augmentation of AFC by EPO. Consistently, in vitro studies of alveolar epithelial cells paralleled with that EPO upregulated the expression of ENaC and Na,K-ATPase, and patch-clamp studies further demonstrated that EPO substantially strengthened sodium ion currents. Collectively, EPO could effectively promote AFC by improving ENaC and Na,K-ATPase protein expression and abundance in the membrane, dependent on inhibition of ENaC and Na,K-ATPase ubiquitination, and resulting in diminishing LPS-associated lung injuries

In Situ Measurements of the Mechanical Properties of Electrochemically Deposited Li₂CO₃ and Li₂O Nanorods

Solid-electrolyte interface (SEI) is “the most important but least understood (component) in rechargeable Li-ion batteries”. The ideal SEI requires high elastic strength and can resist the penetration of a Li dendrite mechanically, which is vital for inhibiting the dendrite growth in lithium batteries. Even though Li$_{2}$CO$_{3}$ and Li$_{2}$O are identified as the major components of SEI, their mechanical properties are not well understood. Herein, SEI-related materials such as Li$_{2}$CO$_{3}$ and Li$_{2}$O were electrochemically deposited using an environmental transmission electron microscopy (ETEM), and their mechanical properties were assessed by in situ atomic force microscopy (AFM) and inverse finite element simulations. Both Li$_{2}$CO$_{3}$ and Li$_{2}$O exhibit nanocrystalline structures and good plasticity. The ultimate strength of Li$_{2}$CO$_{3}$ ranges from 192 to 330 MPa, while that of Li$_{2}$O is less than 100 MPa. These results provide a new understanding of the SEI and its related dendritic problems in lithium batteries