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As climate change intensifies, food security has received widespread attention. This study examines the development of Japan’s food security index and its relationship with climate change. From these findings, a food security indicator system for Japan was established. The food security system has six dimensions: availability, nutrition, climate change, society, economics, and fertilizer. The factors affecting food security are complex and variable, and this paper adds the Fertilizer Security Index (FSI) to the previous studies. The overuse of fertilizers directly contributes to soil and atmospheric pollution, which can indirectly lead to issues of food quality insecurity. Including this factor within the food security system is fully justified. This enhances the precision of the food security index system to some degree. The results showed that Japan’s overall food security index exhibited a slight downward trend from 0.113 in 1980 to 0.099 in 2022. Food security reached its lowest point of about 0.067 in 1993. In addition, all five indicators, except the fertilizer index, put pressure on the food security index. Due to the uncertainty inherent in climate change, specifically its ambiguous positive and negative impacts on food security, the Climate Change Security Index provides detailed evidence in this paper supporting whether climate change contributes to or undermines food security. Finally, the study put forward recommendations to ensure food security.

Background Berberine (BBR), a compound extracted from a variety of medicinal herbs, has been shown multiple pharmacological effects against cancer cells of different origins. Cisplatin (DDP) is known as an effective chemotherapeutic agent against cancer by inducing DNA damage and cell apoptosis. However, the effect of the combined used of BBR and DDP on cell necroptosis in ovarian cancer has not been reported. Methods OVCAR3 and three patient-derived primary ovarian cancer cell lines (POCCLs) were chosen as the experimental objects. To determine the potential anti-cancer activity of BBR and DDP in combination, we firstly treated OVCAR3 and POCCLs cells with BBR and/or DDP. The cell viability of OVCAR3 and POCCLs with treatment of BBR or DDP for different hours was measured by CCK-8 assay. Flow cytometry was used to analyze cell cycle distribution and changes in apoptotic cells after treatment with BBR and/or DDP. The morphological changes of OVCAR3 cells were observed by using Transmission electron microscopy (TEM) analysis. Proliferation, apoptosis and necroptosis related markers of OVCAR3 and POCCLs with treatment of BBR or DDP were measured by RT-qPCR, western blotting and immunofluorescence assay. Results Our results demonstrated that BBR significantly inhibited the proliferation of OVCAR3 and primary ovarian cancer cells in a dose- and time-dependent manner. The combination treatment of BBR and DDP had a prominent inhibitory effect on cancer cell growth and induced G0/G1 cell cycle arrest. TEM revealed that the majority of cells after BBR or DDP treatment had an increasing tendency of typical apoptotic and necrotic cell death morphology. Besides, BBR and DDP inhibited the expression of PCNA and Ki67 and enhanced the expression and activation of Caspase-3, Caspase-8, RIPK3 and MLKL. Conclusion This study proposed that the combination therapy of BBR and DDP markedly enhanced more ovarian cancer cell death by inducing apoptosis and necroptosis, which may improve the anticancer effect of chemotherapy drugs. The apoptosis involved the caspase-dependent pathway, while the necroptosis involved the activation of the RIPK3–MLKL pathway. We hope our findings might provide a new insight for the potential of BBR as a therapeutic agent in the treatment of ovarian cancer.

Developing single-site catalysts featuring maximum atom utilization efficiency is urgently desired to improve oxidation-reduction efficiency and cycling capability of lithium-oxygen batteries. Here, we report a green method to synthesize isolated cobalt atoms embedded ultrathin nitrogen-rich carbon as a dual-catalyst for lithium-oxygen batteries. The achieved electrode with maximized exposed atomic active sites is beneficial for tailoring formation/decomposition mechanisms of uniformly distributed nano-sized lithium peroxide during oxygen reduction/evolution reactions due to abundant cobalt-nitrogen coordinate catalytic sites, thus demonstrating greatly enhanced redox kinetics and efficiently ameliorated over-potentials. Critically, theoretical simulations disclose that rich cobalt-nitrogen moieties as the driving force centers can drastically enhance the intrinsic affinity of intermediate species and thus fundamentally tune the evolution mechanism of the size and distribution of final lithium peroxide. In the lithium-oxygen battery, the electrode affords remarkably decreased charge/discharge polarization (0.40 V) and long-term cyclability (260 cycles at 400 mA g −1 ). The performance of Li-O 2 batteries is largely determined by the oxygen electrocatalytic reactions at the cathode. Here, the authors report cobalt single-atom catalysts anchored on carbon nanosheets. The design improves oxygen redox kinetics and enables good electrochemical performance.

Cell differentiation is an important characteristic of multicellular organisms which produce new-typed cells to engage in diverse life functions. Irreversible differentiation, as an important differentiation pattern, describes cells differentiated by determined trajectories to form specialized cell types. It has been found that differentiated cell types often show different death rates. Yet, it is still unclear what role cell death plays in shaping the formation of irreversible cell differentiation. Here, we establish a theoretical model to investigate the impact of cell death on the evolution of irreversible cell differentiation in multicellular organisms. Irreversible differentiation refers to the loss of a cell type’s differentiation potential, and it is constructed by the sequences of differentiation probabilities of a cell type across cell divisions. We show that irreversible differentiation is more likely to occur when cell death rates between cell types are linear. Meanwhile, differences in death rates between cell types affect the emergence conditions of irreversible differentiation, whereas no significant impacts on that from equal cell death rates. Additionally, we found that cell death impacts the cell number and cell composition of a mature organism. These findings provide insights into understanding the role of cell death in the formation of cells’ irreversible differentiation.

We investigate the steady-state solar wind in spherical coordinates using a low-dissipation Harten–Lax–van Leer-Discontinuities Riemann solver, in which the magnetic field is decomposed into an initial potential field B0 and a time-dependent part B1. A constrained transport method is employed to effectively preserve the divergence-free condition, with the relative divergence errors maintained at truncation level throughout the simulation. The solar wind plasma and magnetic field equations are solved using a one-step MUSCL-type time integration scheme, combined with spacetime reconstruction at cell interfaces and edges. Prior to the solar wind simulation, the accuracy and robustness of the numerical method are verified through benchmark tests, including the smooth Alfvén wave problem, the Mach 800 dense MHD jet, and the MHD blast wave in spherical polar coordinates. The results confirm that the scheme achieves second-order accuracy and remains stable under challenging physical conditions. The validated scheme is then applied to simulate the structured solar wind during Carrington Rotation 2236, using Helioseismic and Magnetic Imager 720 s cadence line-of-sight magnetograms as input. The simulation successfully reproduces key large-scale solar wind features, such as polar and extended coronal holes, open and closed magnetic field regions, helmet streamers, pseudo-streamers, the heliospheric current sheet, and the spatial distribution of fast and slow solar wind streams. Comparisons with remote sensing observations and in situ measurements demonstrate reasonable agreement. However, discrepancies remain in the temporal variations of plasma parameters and the detailed structure of coronal holes, suggesting areas for further model refinement.

As an environmentally friendly energy recovery technology, microwave pyrolysis has huge development potential in sludge resource treatment. This paper comprehensively reviews the progress of microwave pyrolysis of sludge, focusing on the mechanisms and development status of microwave pyrolysis equipment. The effects of pyrolysis temperature, heating rate, microwave absorbers, sludge properties and catalysts on microwave pyrolysis efficiency and its products are also discussed. Finally, the differentiation compared with conventional pyrolysis is summarized. It is suggested that target products can be controlled directionally by changing the pyrolysis conditions and exploring the harmful products produced in the microwave pyrolysis process. Future research directions are proposed to help the subsequent extensive application of microwave pyrolysis technology in sludge treatment.

Sepsis-associated delirium (SAD) is a common and severe complication in critically ill patients and is associated with increased mortality. Thiamine is an essential coenzyme in mitochondrial energy metabolism, and deficiency is frequent in critical illness. However, the association between thiamine supplementation and survival in ICU patients with SAD remains unclear. We conducted a retrospective cohort study using the MIMIC-IV (v3.1) database. Adult ICU patients meeting Sepsis-3 criteria and diagnosed with delirium during ICU stay were included. Patients were categorized according to thiamine supplementation during ICU admission. Propensity score–based methods, including matching, adjustment, and multiple weighting approaches, were applied to balance baseline covariates. The primary outcome was 30-day all-cause mortality. We performed survival, subgroup, and sensitivity analyses. We also conducted duration–response and dose–response analyses to evaluate whether thiamine treatment duration and average daily dose were associated with prognosis. In the MIMIC-IV cohort, 332 ICU patients with sepsis-associated delirium received thiamine supplementation, while 956 did not. Thirty-day mortality was significantly lower in the thiamine group compared with the non-thiamine group ( P  < 0.001). Thiamine use was associated with improved survival in crude analysis and remained significantly associated with lower 30-day mortality after multivariable adjustment (HR, 0.51; 95% CI, 0.33–0.79; P  = 0.002). Consistent associations were observed across propensity score analyses, including propensity score–adjusted analysis (HR, 0.59; 95% CI, 0.40–0.85; P  = 0.005), propensity score matching (HR, 0.59; 95% CI, 0.39–0.90; P  = 0.015), inverse probability of treatment weighting (HR, 0.54; 95% CI, 0.38–0.77; P  = 0.002), standardized mortality ratio weighting (HR, 0.68; 95% CI, 0.47–0.98; P  = 0.052), pairwise algorithmic weighting (HR, 0.63; 95% CI, 0.40–0.97; P  = 0.016), and overlap weight (HR, 0.60; 95% CI, 0.36–1.02; P  = 0.008). Weighted subgroup analyses demonstrated consistent associations across clinical strata, with a significant interaction by illness severity indicating a survival benefit of thiamine among patients with SOFA scores < 4. Duration-response and dose-response analyses suggested greater benefit with longer treatment courses and lower daily dosing. Thiamine supplementation was associated with reduced 30-day mortality in ICU patients with sepsis-associated delirium, with an observed interaction in the SOFA score subgroup, where a SOFA score below 4 was associated with survival benefit. Duration–response and dose–response analyses suggested greater benefit with longer treatment courses and lower daily dosing.

Neutrophils have a pathogenic function in inflammation via releasing pro-inflammatory mediators or neutrophil extracellular traps (NETs). However, their heterogeneity and pro-inflammatory mechanisms remain unclear. Here, we demonstrate that CXCR4 hi neutrophils accumulate in the blood and inflamed skin in human psoriasis, and correlate with disease severity. Compared to CXCR4 lo neutrophils, CXCR4 hi neutrophils have enhanced NETs formation, phagocytic function, neutrophil degranulation, and overexpression of pro-inflammatory cytokines and chemokines in vitro. This is accompanied by a metabolic shift in CXCR4 hi neutrophils toward glycolysis and lactate release, thereby promoting vascular permeability and remodeling. CXCR4 expression in neutrophils is dependent on CREB1, a transcription factor activated by TNF and CXCL12, and regulated by de novo synthesis. In vivo, CXCR4 hi neutrophil infiltration amplifies skin inflammation, whereas blockade of CXCR4 hi neutrophils through CXCR4 or CXCL12 inhibition leads to suppression of immune responses. In this work, our study identifies CREB1 as a critical regulator of CXCR4 hi neutrophil development and characterizes the contribution of CXCR4 hi neutrophils to vascular remodeling and inflammatory responses in skin. The mechanistic functions of neutrophils in skin inflammation are not fully understood. Here the authors use human psoriasis samples and a mouse model of skin inflammation to study neutrophils and find a CXCR4 hi population of NET-forming, phagocytic neutrophils whose induction depends on the transcription factor CREB1.

Triggering receptor expressed on myeloid cells 2 (TREM2) is a membrane receptor on myeloid cells and plays an important role in the body's immune defense. Recently, TREM2 has received extensive attention from researchers, and its activity has been found in Alzheimer's disease, neuroinflammation, and traumatic brain injury. The appearance of TREM2 is usually accompanied by changes in apolipoprotein E (ApoE), and there has been a lot of research into their structure, as well as the interaction mode and signal pathways involved in them. As two molecules with broad and important roles in the human body, understanding their correlation may provide therapeutic targets for certain diseases. In this article, we reviewed several diseases in which TREM2 and ApoE are synergistically involved in the development. We further discussed the positive or negative effects of the TREM2-ApoE pathway on nervous system immunity and inflammation.

Epidermal infiltration of neutrophils is a hallmark of psoriasis, where their activation leads to release of neutrophil extracellular traps (NETs). The contribution of NETs to psoriasis pathogenesis has been unclear, but here we demonstrate that NETs drive inflammatory responses in skin through activation of epidermal TLR4/IL-36R crosstalk. This activation is dependent upon NETs formation and integrity, as targeting NETs with DNase I or CI-amidine improves disease in the imiquimod (IMQ)-induced psoriasis-like mouse model, decreasing IL-17A, lipocalin2 (LCN2), and IL-36G expression. Proinflammatory activity of NETs, and LCN2 induction, is dependent upon activation of TLR4/IL-36R crosstalk and MyD88/nuclear factor-kappa B (NF-κB) down-stream signaling, but independent of TLR7 or TLR9. Notably, both TLR4 inhibition and LCN2 neutralization alleviate psoriasis-like inflammation and NETs formation in both the IMQ model and K14-VEGF transgenic mice. In summary, these results outline the mechanisms for the proinflammatory activity of NETs in skin and identify NETs/TLR4 as novel therapeutic targets in psoriasis.