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In recent decades, global warming has significantly altered both the spatial and temporal distribution of rainfall patterns. This change has heightened the risk of rainfall-induced landslides, which are the most prevalent natural disasters in the mountainous regions of southwestern China. These events pose unpredictable and severe threats to the region, making it essential to forecast future rainfall trends and assess how landslide susceptibility will respond to these changes. Understanding these dynamics is crucial for developing effective strategies to mitigate and adapt to the changing rainfall patterns that influence landslides. This study focuses on Sichuan Province, China, and uses annual cumulative rainfall (ACR) as a key dynamic variable to create landslide susceptibility maps (LSMs). The goal is to explore the evolving relationship between rainfall and landslide susceptibility and use future rainfall projections to predict these risks. To achieve this, a historical landslide geospatial database was compiled across five temporal categories: 2000, 2001–2005, 2006–2010, 2011–2015, and 2016–2020. The extreme learning machine (ELM) was applied to generate LSMs for the years 2000 to2020, while an elasticity framework was used to assess how sensitive landslide susceptibility is to rainfall variations. To project future scenarios, a long short-term memory (LSTM) model was employed to project the ACR for 2030, using monthly rainfall data from 2000 to 2020. This projected ACR was then used to estimate future landslide susceptibility. Results showed a marked increase in high landslide susceptibility areas: 5.6 % by 2005, 0.3 % by 2010, 0.2 % by 2015, and 12.9 % by 2020, all relative to the year 2000. The elasticity analysis revealed that from 2000 to 2020, a 1 % change in rainfall would cause an average 1.35 % change in landslide susceptibility. Looking forward to 2030, the projected rise in ACR is expected to lead to a 2.44 % increase in areas of high landslide susceptibility. Multiple validation techniques were applied to ensure reliability and robustness of these findings.

Microplastics (MPs) have attracted increasing attention worldwide owing to their widespread presence and potential risks to terrestrial and marine ecosystems. Estimating the pollution status and risk levels of MPs in coastal ecosystems is necessary; however, these are poorly understood in coastal megacities. Here, the abundance and characteristics of MPs in seawater, marine sediment, marine organisms, and beaches in the Shenzhen coastal ecosystems and land sources (river and sewage outfall) were simultaneously investigated, and the annual MPs load of rivers and MP-induced ecological risks were evaluated. The results showed that MPs pollution was prevalent in Shenzhen coastal ecosystems, with the average abundances of 2.40 ± 2.48 items/m3, 404.21 ± 431.48 items/kg, 1.66 ± 1.96 items/individual, and 1648.99 ± 1908.19 items/kg in seawater, marine sediment, marine organisms, and beach sands, respectively. The detected MPs were predominantly fibrous/granular, transparent/white, < 1 mm in size, and polyethylene terephthalate/polyethylene/polystyrene. The spatial distribution patterns of marine MPs are influenced mainly by anthropogenic activities and freshwater inflows (rivers and sewage outfalls). Pollution hotspots of MPs were identified in the Pearl River Estuary, which has a high population, gross domestic product, and river and wastewater discharge. Furthermore, the negative correlation between the abundance of MPs in seawater and salinity indicates that freshwater inflow carrying MPs to the sea is an important source of marine MPs pollution. It has been estimated that approximately 8320 billion MPs particles, weighing 274.55 tons, flow into the Shenzhen coast annually through river input. Based on the MPs polymer types and quantities, the ecological risk of MPs pollution in the Shenzhen coastal ecosystem is moderate and deserves further attention. These findings deepen the understanding of MPs pollution, sources, and ecological risks in the southern coastal region of China, and are helpful for employing effective management strategies to control marine MPs pollution.

ABSTRACT: Avian reovirus (ARV) is the causative agent of avian viral arthritis and causes significant economic losses to the global poultry industry. For clinical diagnosis, detecting ARV-specific antibodies is crucial. We successfully expressed the ARV-σC protein in insect cells using the baculovirus expression vector system, achieving an expression level of approximately 200 mg/L. We developed an indirect enzyme-linked immunosorbent assay (iELISA) using the ARV-σC protein as a coating antigen to detect antibodies against it. The inter-batch and intrabatch coefficients of iELISA variation were less than 10%. Its sensitivity (1:12,800 diluted in serum) was 4 times higher than that of the indirect immunofluorescence assay (IFA; 1:3200 diluted in serum), and it showed no cross-reactivity with antibodies against other common avian viruses (such as Infectious bursal disease virus, Newcastle disease virus). The practicality of the iELISA was further evaluated using clinical samples. 300 clinical sera from chickens vaccinated with the ARV attenuated vaccine and 20 SPF sera were tested using both the iELISA and the IFA, demonstrating a 100% conformity rate. In conclusion, these results suggest that the iELISA developed in this study is a rapid, sensitive, and specific method that could serve as an effective diagnostic tool for monitoring and controlling avian viral arthritis.

Superparamagnetic iron oxide nanoparticles (SPION) are widely used in cardiovascular applications. However, their potential to induce ferroptosis in myocardial cells post-ischemia-reperfusion hinders clinical adoption. We investigated the mechanisms behind SPION-induced cytotoxicity in myocardial cells and explored whether co-loading SPION with SS-31 (a kind of mitochondrial-targeted antioxidant peptide) could counteract this toxicity.To create SPION@SS-31, SS-31 was physically adsorbed onto SPION. To study the dose- and time-dependent cytotoxic effects and assess the influence of SS-31 on reducing SPION-induced damage, hypoxia/reoxygenation(H/R) H9C2 cells were treated with either SPION or SPION@SS-31. We examined the relationship between SPION and ferroptosis by measuring mitochondrial ROS, mitochondrial membrane potential (MMP), lipid peroxidation products, ATP, GSH, GPX4, mitochondrial structure, nonheme iron content, cellular iron regulation, and typical ferroptosis markers.The findings showed that SPION induced concentration- and time-dependent toxicity, marked by a significant cell viability loss and an increase in LDH levels. In contrast, SPION@SS-31 produced results comparable to the H/R group, implying that SS-31 can notably reduce cell damage induced by SPION. SPION disrupted cellular iron homeostasis, with FtH and FtMt expression increased and reduced levels of FPN1 and ABCB8, which led to the overload of mitochondrial iron. This iron dysregulation damaged mitochondrial function and integrity, causing ATP depletion, MMP loss, and decreased GPX4 and GSH levels, accompanied by a burst of mitochondrial lipid peroxidation, ultimately resulting in ferroptosis in H/R cardiomyocytes. Notably, SS-31 significantly alleviated SPION-induced ferroptosis by decreasing mitochondrial MDA production and maintaining GSH and GPX4 levels, indicating its possibility to reverse SPION-induced cytotoxicity. The viability of H/R cells and cells treated with SPION and Fer-1 did not differ statistically, whereas cells exposed to SPION along with inhibitors like 3-MA, zVAD, or Nec-1 showed a substantial loss in viability, implying that ferroptosis is the primary mechanism behind SPION-induced myocardial toxicity.SPION triggers mitochondrial lipid peroxidation by causing overload of iron, leading to ferroptosis in H/R H9C2 cells. Mitochondria appear to be the primary target of SPION-induced toxic effects. SS-31 demonstrates potential in inhibiting this ferroptosis by acting as a mitochondria-targeted antioxidant, suggesting that the modification of mitochondria-targeted antioxidant peptides represents an innovative and practical approach to attenuate the myocardial toxicity associated with SPION.

Background: Studies have shown that abnormal temperature at night is a risk factor for respiratory health. However, there is limited evidence on the impact of hot and cold nights on cause-specific diseases such as pneumonia, which is a leading cause of morbidity and mortality in children. Methods: We collected daily data on pneumonia hospitalisations in children under five years from 2011 to 2017 in three low-, middle- and high-income countries (Bangladesh, China, and Australia). The intensity of hot and cold nights was measured by excess temperature. A space–time-stratified case-crossover analysis was used to estimate the association between hot and cold nights and childhood pneumonia hospitalisations. We further estimated the fraction of childhood pneumonia hospitalisations attributable to hot and cold nights. Results: Both hot and cold nights were associated with an increased risk of hospitalisations for childhood pneumonia in low-, middle-, and high-income countries, with a greater disease burden from hot nights. Specifically, the fraction of childhood pneumonia attributable to hot nights was the largest in Australia [21.2%, 95% confidence interval (CI): 11.8%-28.1%], followed by Bangladesh (15.2%, 95% CI: 4.1%–23.8%) and China (2.7%, 95% CI: 0.4%-4.7%). Additionally, the fraction of childhood pneumonia attributable to cold nights was 1.3% (95% CI: 0.4%-2.0%) in Bangladesh and 0.4% (95% CI: 0.1%-0.7%) in China. Conclusion: This multi-country study suggests that hot and cold nights are not only associated with a higher risk of pneumonia hospitalisations in children but also responsible for substantial fraction of hospitalisations, with a greater impact from hot nights.

The widespread use of plasticizers like phthalate esters (PAEs) has led to environmental and health concerns. The neurobehavioral toxicity of these compounds in marine environments, particularly regulated by the “brain-gut” axis, remains unclear, especially concerning wild demersal fish of high ecological value. Our investigation into the behavioral effects of three common PAEs, i.e., dimethyl phthalate (DMP), di-n-butyl phthalate (DBP), and di(2-ethylhexyl) phthalate (DEHP), and their molecular mechanisms on juvenile Sebastes schlegelii, revealed alarming results from molecular to population levels. After a 20-day foodborne exposure at a low marine environmental concentration (1.0 μg g−1), we observed that all three PAEs significantly increased the thigmotaxis (behavioral tendency to stay close to physical boundaries) and mobility of juvenile fish by 28.2–59.4 % and 23.3–74.5 %, respectively, indicating anxiety-like behavior of fish. DEHP exhibited the most pronounced effects, followed by DBP and DMP. PAEs accumulated in the juvenile fish in the order of brain > liver > gut > muscle, with DEHP showing the highest brain concentrations (23.2 ± 2.98 μg g−1). This accumulation led to oxidative damage, inflammatory responses, and neurodegenerative changes in the optic tectum, resulting in cholinergic system dysfunction. In the gut, PAEs caused inflammatory lesions, disrupted the gut barrier, and altered the gut microbiome, exacerbating the neurotoxicity via “brain-gut” communication. These findings underscore the significant neurobehavioral toxicity of PAEs, emphasizing their critical impact on fish behavior. We also stress the crucial need for further research on fish and other marine species beyond the laboratory scale to fully understand the broader implications of PAE exposure in marine ecosystems and to guide future conservation efforts.

The autogenous self-sealing model has been researched in previous work, which could help to characterize the self-sealing process with crystalline products. The model outcome was presented in the form of leakage water flow, which demonstrates the self-sealing capacity or the recovery of watertightness. While in the research area of cement-based material self-sealing, the expansive agent cannot be neglectable, for example the superabsorbent polymer (SAP). Especially for the building components exposed to free water, an efficient water flow blockage after cracking is crucial to ensure stable service. Hence in this study, the self-sealing process of a granular expansive agent inside the crack of cement-based material was simulated. The model outputs were compared with experimental results to verify the reliability. Additionally, the autogenous self-sealing model was incorporated into this model to simulate the “crystallization-expansion” synergetic self-sealing. The contribution of crystalline product and expanded EA to water flow blockage were compared during the crystallizing process. Overall, this model is of great use to evaluate the role of expansive agent on water flow blockage after the cement-based material cracking in hydraulic engineering or engineering components exposed to water.

Real-time monitoring of milling parameters is essential to improve machining efficiency and quality, especially for the workpieces with complex geometry. Its main task is to build the relationship between the parameters and the monitoring data. As the relationship is challenging to be established solely through mechanism-driven or data-driven methods, the physics informed method, based on prior physical laws between physical signals and milling parameters, becomes the optimal method. However, this method is limited due to the lack of a high-quality dataset. Therefore, a multi-sensor monitoring dataset for the milling process with various milling parameters and milling materials is built. The variables include cutting depth, cutting width, feed rate, spindle speed and workpiece materials (aluminium alloy 7030 and CK45 steel). The multi-sensor includes force, vibration, noise, and current. A dataset comprising 115 samples is built, including 100 samples collected using the 'all factors' method, and 15 slot milling samples using two different workpiece materials. The 15 slot milling samples are used to calibrate mechanical milling force coefficients, which is beneficial for developing a physics-informed machine learning algorithm.

Model mismatches can cause multi-dimensional uncertainties for the receding horizon control strategies of automated vehicles (AVs). The uncertainties may lead to potentially hazardous behaviors when the AV tracks ideal trajectories that are individually optimized by the AV's planning layer. To address this issue, this study proposes a safe motion planning and control (SMPAC) framework for AVs. For the control layer, a dynamic model including multi-dimensional uncertainties is established. A zonotopic tube-based robust model predictive control scheme is proposed to constrain the uncertain system in a bounded minimum robust positive invariant set. A flexible tube with varying cross-sections is constructed to reduce the controller conservatism. For the planning layer, a concept of safety sets, representing the geometric boundaries of the ego vehicle and obstacles under uncertainties, is proposed. The safety sets provide the basis for the subsequent evaluation and ranking of the generated trajectories. An efficient collision avoidance algorithm decides the desired trajectory through the intersection detection of the safety sets between the ego vehicle and obstacles. A numerical simulation and hardware-in-the-loop experiment validate the effectiveness and real-time performance of the SMPAC. The result of two driving scenarios indicates that the SMPAC can guarantee the safety of automated driving under multi-dimensional uncertainties.

Curcumin (CUR) is a compound extracted from turmeric that has a variety of functions including antioxidant and anti-inflammatory. As an estrogen-like mycotoxin, zearalenone (ZEN) not only attacks the reproductive system, but also has toxic effects on the liver. However, whether CUR can alleviate ZEN-induced liver injury remains unclear. This paper aims to investigate the protective effect of CUR against ZEN-induced liver injury in mice and explore the molecular mechanism involved. BALB/c mice were randomly divided into control (CON) group, CUR group (200 mg/kg b. w. CUR), ZEN group (40 mg/kg b. w. ZEN) and CUR+ZEN group (200 mg/kg b. w. CUR+40 mg/kg b. w. ZEN). 28 d after ZEN exposure and CUR treatment, blood and liver samples were collected for subsequent testing. The results showed that CUR reversed ZEN-induced hepatocyte swelling and necrosis in mice. It significantly reduced the serum alkaline phosphatase (ALP), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in mice (p < 0.05). In addition, CUR significantly reduced hepatic ROS, malondialdehyde, hydrogen peroxide and apoptosis levels in mice (p < 0.05). Quantitative RT-PCR and Western blot results showed that CUR significantly reduced the expression of Bax and Caspase3, and reversed the increase of Nrf2, HO-1 and NQO1 expression in the liver of mice induced by ZEN (p < 0.05). In conclusion, CUR alleviated ZEN-induced liver injury in mice by scavenging ROS and inhibiting the mitochondrial apoptotic pathway.

Introduction: Extracellular vesicles (EVs)-mediated cell-to-cell communication is crucial for hypoxia-induced cell proliferation and tissue repair, but its function in endogenous cardiac regeneration is still unknown. Objectives: Herein, we aimed to determine whether hypoxia-inducible circWhsc1 in endothelial EVs promoted cardiomyocyte (CM) proliferation and cardiac regeneration. Methods: RNA-sequence data was used to identify EV circRNAs that were involved into endogenous cardiac regeneration. Quantitative polymerase chain reactions were conducted to determine circRNA expression in tissue, cells and EVs. Gain- and loss-of-function assays were performed to explore the function of EV-derived circWhsc1 during cardiac regeneration. Western blotting and RNA pulldown assays were used to investigate its underlying mechanism. Results: We found that circWhsc1 was enriched in neonatal mouse hearts, particularly in cardiac ECs, and was further upregulated both in ECs and EC-derived EVs under hypoxic conditions. When cocultured with hypoxia-preconditioned neonatal ECs or their secreted EVs, both neonatal and adult CMs exhibited an increased proliferation rate and G2/M ratio, which could be attenuated by knockdown of circWhsc1 in ECs. In vivo, EC-restricted overexpression of circWhsc1 and EV-mediated delivery of circWhsc1 induced CM proliferation, alleviated cardiac fibrosis and restored cardiac function following myocardial infarction in adult mice. Mechanistic studies revealed that EV-derived circWhsc1 activated TRIM59 by enhancing its phosphorylation, thereby reinforcing the binding of TRIM59 to STAT3, phosphorylating STAT3 and inducing CM proliferation. Conclusion: The current study demonstrated that hypoxia-inducible circWhsc1 in EC-derived EVs induces CM proliferation and heart regeneration. EC-CM communication mediated by EV-derived circWhsc1 might represent a prospective therapeutic target for inducing cardiac repair post-myocardial infarction.

The role of acoustic cavitation in various surface cleaning disciplines is important. However, the physical mechanisms underlying acoustic cavitation-induced surface cleansing are poorly understood. This is due to the combination of microscopic and ultrashort timescales associated with the dynamics of acoustic cavitation bubbles. Here, we have precisely controlled single-bubble cavitation in both space and time. Ultrasonic excitation leads to the cavitation of generated single bubbles. A synchronous ultrafast photomicrographic system simultaneously records the dynamics of single acoustic cavitation bubbles (SACBs) and the cleaning process of the nearby surface in liquids with varying viscosities. Finally, we analysed the correlation between bubble dynamics and surface cleaning situations. The differences in the typical dynamic characteristics of the bubbles during collapse in liquids with varying viscosities reveal two main mechanisms underlying surface cleaning by acoustic cavitation, which are respective the Laplace pressure during the bubble’s movement and liquid jets during bubble collapse. Our study provides a better physical understanding of the ultrasonic cleaning process based on acoustic cavitation, and will help to optimize and facilitate the applications of surface cleaning, especially for the cleaning of substrates with tightly attached dirt.

Based on the self-developed high permeability water pressure loading system, the physical and mechanical properties and pore structure evolution under various high permeability water pressures were studied. This study aims to reveal the microscopic damage mechanism of concrete when subjected to high permeability water pressures. The results indicate that the internal water content increases with the rising of water pressure under various high permeability conditions. Furthermore, the higher the water pressure, the greater the reduction in strength, particularly evident in low-strength-grade concrete. High permeability water pressure causes to the expansion of gelatinized pores with small sizes into transition pores. Moreover, there is a concurrent alteration in both pore size and pore number under high permeability water pressure.

Microplastics (MPs) weather after entering the environment gradually, and the interaction with metal ions in the aqueous environment has received extensive attention. However, there are few studies on Hg(Ⅱ), especially the effect of MPs on the release of Hg0(DEM) in water after entering the aqueous environment. In this study, four types of MPs (PP, PE, PET, PVC) were selected to study the adsorption and desorption behavior of Hg(Ⅱ) after photoaging and to explore the influence of MPs on the release of DEM in seawater under different lighting conditions. The results showed that the specific surface area, negative charges, and oxygen-containing functional group of MPs increased after aging. The adsorption capacity of aged MPs for Hg(Ⅱ) was significantly improved, which was consistent with the pseudo-first-order and pseudo-second-order model, indicating that the adsorption process was a chemical and physical adsorption. The fitting results of the in-particle diffusion model indicated that the adsorption was controlled by multiple steps. Hg(Ⅱ) was easier to desorb in the simulated gastric fluid environment. Because the aged MPs had the stronger binding force to Hg(Ⅱ), their desorption rate is lower than new MPs. Under visible light and UVA irradiation, MPs inhibited the release of Hg0. Under UVA, the mass of DEM produced in seawater with aged PE and PVC was higher than that of new PE and PVC. The aged PE and PVC could produce more ·O2-, which was conducive to the reduction of mercury. However, in UVB irradiation, the addition of MPs promoted the release of DEM, and ·O2- also played an important contribution in affecting the photochemical reaction of mercury. Therefore, the presence of aged MPs will significantly affect the water-air exchange of Hg in water. Compared with new MPs, aged MPs improved the contribution of free radicals in Hg transformation by releasing reactive oxygen species. This study extends the understanding of the effects of MPs on the geochemical cycle of Hg(Ⅱ) in seawater, better assesses the potential combined ecological risks of MPs and Hg(Ⅱ), and provides certain guidance for the pollution prevention and control of MPs.

Background: Pulmonary hypertension (PH) is characterized with vascular remodeling, which is intiated by vascular endothelial dysfunction. N6-methyladenosine (m6A) modification mediates gene expression in many ways including mediating RNA degradation, splicing, nuclear export et al. m6A modification have been found to be associated with the development of PH. However, the role of m6A regulators in pulmonary artery endothelial cells (PAECs) dysfunction of PH is still under research. Methods: The expression levels of m6A regulators in PAECs were analyzed with the single-cell sequencing Data(scRNA). Next, the target differentially expressed genes (DEGs) of m6A regulators in PAECs were functionally annotated. The analysis of cellular interactions included the examination of receptor—ligand pairs regulated by m6A regulators. Pseudo-time trajectory analyses and a ceRNA network involving lncRNAs, miRNAs, and mRNAs were conducted in PAECs. Furthermore, microarray data (GSE180169) for Sugen Hypoxia PH (SuHx PH) mouse models was screened for DEGs and m6A regulators in PAECs. Moreover, the expression of YTHDC1 in the lung samples of SuHx PH models was determined using immunofluorescence. In vitro, the mRNA expression of YTHDC1 in HPAECs under hypoxia conditions was detected. The effect of YTHDC1 recombinant protein on HPAEC proliferation was detected by Cell Counting Kit-8 (CCK8). Results: Dysregulation of m6A regulators was observed in mouse PAECs. The m6A reader of YTHDC1 was decreased in PAECs in scRNA data and RNAseq data of isolated PAECs of SuHx PH models. Downregulation of YTHDC1 was caused by hypoxia in PAECs in vitro and similar results was observed in PAECs of SuHx PH mouse models. Next, YTHDC1 recombinant protein was found to inhibit HPAECs proliferation. The DEGs targeted by YTHDC1 were enriched in angiogenesis, endothelial cell migration, fluid shear stress, and stem cell maintenance. Analysis indicates that interactions among endothelial cells, smooth muscle cells, fibroblasts, and immune cells, mediated by specific YTHDC1 target genes (e.g., PTPRC-MRC1, ITBG2-ICAM1, COL4A1-CD44), contribute to PH development. Also, the YTHDC1 expression were consistent with Thioredoxin interacting protein (TXNIP). What's more, the predicted transcription factors showed that NFKB1, Foxd3 may be involved in the regulation of YTHDC1. Lastly, our data suggest that YTHDC1 may be involved in regulating PAECs dysfunction through lncRNA/miRNA/mRNA network. Conclusion: For the first time, we analyzed changes in the expression and biological functions of m6A regulators in SuHx PH mouse models. We causatively linked YTHDC1 to PAECs dysfunction, providing novel insight into and opportunities to diagnose and treat PH.

Background: The incidence of renal clear cell carcinoma (ccRCC) is steadily growing, and cellular metastasis and extensive infiltration of CD8+ T cells are the primary factors contributing to its undesirable prognosis. GLIPR2 (GLI pathogenesis related 2) belongs to the PR-1 family, and it was upregulated in hepatocellular carcinoma, playing a role in the regulation of epithelial cell to mesenchymal transition (EMT). However, its involvement in ccRCC remains unknown. Methods: Genes associated with tumor metastasis and CD8+ T cell levels were identified through weighted gene coexpression network analysis (WGCNA) leveraging the TCGA and GEO databases. Afterwards we follow survival, univariate Cox regression, receiver operating characteristic (ROC) and drug susceptibility analyses confirmed the most influential gene. Further exploration of its molecular, metastatic, and immune properties was carried out through bioinformatics analysis and experimental validation. Results: Initially, GLIPR2 was identified as the most influential gene via WGCNA. Our findings indicated that GLIPR2 exhibited high expression levels in ccRCC and metastatic ccRCC, and its over-expression is significantly correlated with an unfavorable prognosis. Competing endogenous RNAs (CeRNA) network analysis offered insights into the potential regulatory mechanisms governing its expression. Pathway enrichment analysis revealed the involvement of GLIPR2 in multiple pathways intertwined with immune and cellular metastasis. Meanwhile, experiments provided confirmation that GLIPR2 may facilitate the metastasis of ccRCC through EMT. However, the specific mechanisms by which GLIPR2 regulated EMT to promote invasion and migration in ccRCC required in-depth exploration. Single-cell sequencing, immune infiltration, immune survival, and immunotherapy analysis demonstrated the close association between GLIPR2 and CD8+ T cells in ccRCC, as well as its potential for immunotherapeutic intervention. Conclusions: The upregulation of GLIPR2 in ccRCC is associated with cellular metastasis and enrichment of CD8+ T cells. Herein, it may hold promising potential as a predictive independent biomarker for ccRCC metastasis, immune infiltration, and prognosis.

Energy flux in food webs is a fundamental feature of ecosystems and an important link between biodiversity and ecosystem function. Studies of energy flow through the soil nematode food web have emerged in recent year; however, it is not clear whether and how the nematode food web structure affects the energy flow. In this study, the structures and carbon flux of soil nematode food webs in four different ecosystems, namely, forageland, cropland, secondary forest, and grass-shrubland, were assessed. The food web structure was represented by nematode community indices such as maturity index, structure index, genus and trophic group diversity, and slope of size spectra. The results showed that carbon flux through the nematode food webs was the highest and lowest in the secondary forest and forageland, respectively. The total carbon flux of nematode food web was higher in the cropland than that in the grass-shrubland. The magnitudes of bacterial and fungal energy channels were basically equal in the forageland and secondary forest. The energy flow through the bacterial channel was greater than that through the fungal channel in the grass-shrubland, whereas the pattern was reversed in the cropland. The total carbon flux through the nematode food web, the carbon fluxes through the bacterial or fungal channel, and the energy flow uniformity were positively correlated with the nematode structure index, maturity index, and genus diversity index. The trophic group diversity and size spectra slope of nematode communities were not significantly correlated with the carbon flux. The results indicate that mature and complex soil communities support high energy flux across soil food webs.

Toxoplasmosis is a major infectious disease, affecting approximately one-third of the world's population; its main clinical manifestation, ocular toxoplasmosis (OT), is a severe sight-threatening disease. Nevertheless, the diagnosis of OT is based on clinical findings, which needs improvement, even with biochemical tests, such as polymerase chain reaction and antibody detections. Furthermore, the efficacy of OT-targeted treatment is limited; thus, additional measures for diagnosis and treatments are needed. Here, we for the first time report a significantly reduced iron concentration in the vitreous humor (VH) of human patients infected with OT. To obtain further insights into molecular mechanisms, we established a mouse model of T. gondii infection, in which intravitreally injected tracer 57Fe, was accumulated in the neurosensory retina. T. gondii-infected eyes showed increased lipid peroxidation, reduction of glutathione peroxidase-4 expression and mitochondrial deformity in the photoreceptor as cristae loss. These findings strongly suggest the involvement of ferroptotic process in the photoreceptor of OT. In addition, deferiprone, an FDA-approved iron chelator, reduced the iron uptake but also ameliorated toxoplasma-induced retinochoroiditis by reducing retinal inflammation. In conclusion, the iron levels in the VH could serve as diagnostic markers and iron chelators as potential treatments for OT.

Cipher-block chaining (CBC) is a widely used encryption mode for smart grid data, however, the chain structure leads to low encryption and decryption efficiency. To overcome this issue, this paper proposes a novel tree-CBC (TCBC) block encryption method. First, the smart grid plaintext is preprocessed according to the security level of the data. Second, the chain structure of the CBC mode is converted into a tree structure, and for the data block with a higher security level, its location is deeper in the encryption tree. Third, since the overall security and encryption time of data encrypted by TCBC depend on the number of forks of the encryption tree, this paper proposes a method to determine the optimal number of forks of TCBC based on the weights of the encryption time and security of the data blocks. The experiment shows that the encryption efficiency of the TCBC mode is improved by nearly 50% compared to the original CBC mode. And as the data size increases, the efficiency improvement becomes more obvious. Furthermore, compared with widely used encryption modes such as CFB, OFB, CTR, and PCBC, the proposed TCBC mode has higher encryption and decryption efficiency.

Tumors are among the leading causes of death worldwide. Cell-derived biomimetic functional materials have shown great promise in the treatment of tumors. These materials are derived from cell membranes, extracellular vesicles and bacterial outer membrane vesicles and may evade immune recognition, improve drug targeting and activate antitumor immunity. However, their use is limited owing to their low drug-loading capacity and complex preparation methods. Liposomes are artificial bionic membranes that have high drug-loading capacity and can be prepared and modified easily. Although they can overcome the disadvantages of cell-derived biomimetic functional materials, they lack natural active targeting ability. Lipids can be hybridized with cell membranes, extracellular vesicles or bacterial outer membrane vesicles to form lipid-hybrid cell-derived biomimetic functional materials. These materials negate the disadvantages of both liposomes and cell-derived components and represent a promising delivery platform in the treatment of tumors. This review focuses on the design strategies, applications and mechanisms of action of lipid-hybrid cell-derived biomimetic functional materials and summarizes the prospects of their further development and the challenges associated with it.

Collision-free navigation of mobile robots is a challenging task, especially in unknown environments, and various studies have been carried out in this regard. However, the previous studies have shortcomings, such as low performance in cluttered and unknown environments, high computational costs, and multiple controller models for navigation. This paper proposes an adaptive neuro-fuzzy inference system (ANFIS) and global positioning system (GPS) for control and navigation to overcome these problems. The proposed method automates the navigation of a mobile robot while averting obstacles in unknown and densely cluttered environments. Furthermore, the mobile robots’ global path planning and steering are controlled using GPS and heading sensor data fusion to achieve the target coordinates. A fuzzy inference system (FIS) is adopted to model obstacle avoidance where distance sensors data is converted into fuzzy linguistics. Moreover, a type-1 Takagi–Sugeno FIS is used to train a five-layered neural network for the local planning of the robot, and ANFIS parameters are tuned using a hybrid learning method. In addition, an algorithm is designed to generate a dataset for testing and training the ANFIS controller. All the testing and training are conducted in MATLAB, while simulations are carried out using CoppeliaSim. Comprehensive experiments are performed to validate the robustness of the proposed method. The results of the experiments show that the proposed approach outperforms various state-of-the-art neuro-fuzzy, CS-ANFIS, multi-ANFIS, and hybrid ANFIS navigation and obstacle avoidance methods in finding a near-optimal path in unknown environments.

Blockchain technology provides the possibility for the realization of decentralized energy trading. However, the blockchain confronts privacy risks and efficiency issues, which hinder its application in energy trading. In this paper, to solve this problem, we propose an efficient and privacy-preserving decentralized energy trading scheme in a blockchain environment. We propose an account mapping algorithm to solve the privacy attack problem. We propose a new transaction processing method, which can protect private data and improve execution efficiency by two-layer transaction processing. Finally, we verify the effectiveness of the proposed scheme for privacy protection and trading efficiency of decentralized energy transactions through experiments.

This paper explores three new competitive heuristic procedures, which are compared with the mixed integer linear programming (MILP), all used to commit units within a hydroplant to give the maximal electrical production during a study horizon, given the cascade operation has already determined the quarter-hourly releases from individual reservoirs. The problem incorporates constraints on the unit up/down hours and its shutdown times. The procedures are applied to seven hydroplants, with 2, 3, 4, 5, 6, 9 and 18 units installed respectively. The application suggests that the MILP performs the best in minimizing spillages and improving generating efficiency but volatile in computation time when the number of units is more than 4 in a hydroplant, while the heuristic procedures can obtain fairly good results and have a significant advantage in computation time when committing more than 6 units in a hydroplant. The heuristic procedures are valuable when incorporating unit commitment into a large-scale operational problem of cascaded hydropower reservoirs.

Salt-affected soil has become one of the major threats to soil health. However, the evaluation of biochar amendment effects and the underlying mechanisms on the physical, chemical, and biological indicators used for assessing the health of salt-affected soils is lacking. This review summarized biochar performance and mechanisms in improving the health of salt-affected soils. Biochar addition significantly improved soil physico-chemical properties by enhancing aggregate stability (15.0–34.9%), porosity (8.9%), and water retention capacity (7.8–18.2%), increasing cation exchange capacity (21.1%), soil organic carbon (63.1%), and nutrient availability (31.3–39.9%), as well as decreasing bulk density (6.0%) and alleviating salt stress (4.1–40.0%). Following biochar incorporation, soil biological health can also be improved, particularly enhancing microbial biomass (7.1–25.8%), facilitating enzyme activity (20.2–68.9%), and ultimately increasing plant growth. To properly assess the health of salt-affected soils, it is important to select indicators related to ecological service functions including plant production, water quality, climate change, and human health. This will improve the evaluation of soil multifunctionality and enhance current soil health assessment methods. Finally, limitations and future needs of biochar research and biochar-based technologies for soil health assessment in salt-affected soils are discussed. Based on a global meta-analysis to illustrate biochar effects on salt-affected soil health indicators, this review offers valuable insights for developing sustainable biochar-based tools for remediating salt-affected soil.

Urban built environment quality along the travel route is positively correlated with active mobility. However, most previous personalized route recommendation research for cycling emphasizes non-visual attributes, ignoring the significance of visual attributes such as the built environment. Therefore, to take the built environment into consideration in the cycling route planning, we propose the personalized bikeability-based cycling route recommendation (PBCRR) method. The method consists of three steps: (1) deep neural networks are utilized to achieve statistics on built environment attributes and features of bikeability; (2) the weights road impedance calculation function is used to calculate route recommendation indicators according to minimum impedance sum of road segments; and (3) the recommended cycling route is found and shown to the user based on the calculated indicators. The results indicate that our PBCRR presents a high level of effectiveness and differences, and achieves better results than the current route recommendation algorithm in guiding cyclists towards routes with a better built environment.

Based on self-developed ultra high frequency pulse Metal-Inert Gas Welding (UFP-MIG) power source, the ultra-high frequency pulse (UFP) current was studied as an effective way for improving the microstructure and properties of 2219 aluminum alloy joints. The welding pores reduction performance, microstructures, microhardness, and tensile properties of conventional pulsed MIG(CP-MIG) welds and the UFP-MIG welds with different modes and frequencies were investigated. The results indicated that the UFP-MIG process could almost completely eliminate welding porosity in the joints of 2219 aluminum alloy. Compared with CP-MIG welding process, the grain size of the UFP-MIG welding zone was reduced and gradually decreased as the frequency of UFP increased. Similarly, the grain refinement effect also appeared in the heat affected zone (HAZ) near the welds, and the grain size could be reduced by up to 14.85%. Meanwhile, the morphology and uniformity of θ phases and α+θ eutectics along grain boundaries of UFP-MIG welds were also improved. The microhardness in the weld zone and partially melted zone (PMZ) of UFP-MIG weld joints with different modes and frequencies were significantly improved. The highest joint average microhardness occurred at peak pulse mode (PP) with 40 kHz(75.17HV), which was 27.9% higher than that of CP-MIG (58.74HV). The strength and ductility of welded joints were simultaneously improved by UFP-MIG weld process. Fracture analysis results showed that the large reduction of weld pores, the refinement of weld grains, and the lower segregation of Cu element in the eutectic were responsible for the joint tensile properties improvement.

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway plays a vital role in sensing viral DNA in the cytosol, stimulating type I interferon (IFN) production and triggering the innate immune response against DNA virus infection. However, viruses have evolved effective inhibitors to impede this sensing pathway. Chicken anemia virus (CAV), a nonenveloped ssDNA virus, is a ubiquitous pathogen causing great economic losses to the poultry industry globally. CAV infection is reported to downregulate type I IFN induction. However, whether the cGAS-STING signal axis is used by CAV to regulate type I IFN remains unclear. Our results demonstrate that CAV infection significantly elevates the expression of cGAS and STING at the mRNA level, whereas IFN-β levels are reduced. Furthermore, IFN-β activation was completely blocked by the structural protein VP1 of CAV in interferon stimulatory DNA (ISD) or STING-stimulated cells. VP1 was further confirmed as an inhibitor by interacting with interferon regulatory factor 7 (IRF7) by binding its C-terminal 143–492 aa region. IRF7 dimerization induced by TANK binding kinase 1 (TBK1) could be inhibited by VP1 in a dose-dependent manner. Together, our study demonstrates that CAV VP1 is an effective inhibitor that interacts with IRF7 and antagonizes cGAS-STING pathway-mediated IFN-β activation. These findings reveal a new mechanism of immune evasion by CAV.

Summary: Background: A growing number of studies have reported an increased risk of cardiovascular disease (CVD) and respiratory disease (RD) within hours after exposure to ambient air pollution or temperature. We assemble published evidence on the sub-daily associations of CVD and RD with ambient air pollution and temperature. Methods: Databases of PubMed and Web of Science were searched for original case-crossover and time-series designs of English articles examining the intra-day effects of ambient air pollution [particulate matter with aerodynamic diameter ≤2.5 μm (PM2.5), ≤10 μm (PM10), 2.5–10μm (PM10-2.5), and < 7 μm (SPM), O3, SO2, NO2, CO, and NO] and temperatures (heat and cold) on cardiorespiratory diseases within 24 h after exposure in the general population by comparing with exposure at different exposure levels or periods. Meta-analyses were conducted to pool excess risks (ERs, absolute percentage increase in risk) of CVD and RD morbidities associated with an increase of 10 μg/m3 in particulate matters, 0.1 ppm in CO, and 10 ppb in other gaseous pollutants. Findings: Final analysis included thirty-three papers from North America, Europe, Oceania, and Asia. Meta-analysis found an increased risk of total CVD morbidity within 3 h after exposure to PM2.5 [ER%: 2.65% (95% CI: 1.00% to 4.34%)], PM10-2.5 [0.31% (0.02% to 0.59%)], O3 [1.42% (0.14% to 2.73%)], and CO [0.41% (0.01% to 0.81%)]. The risk of total RD morbidity elevated at lag 7–12 h after exposure to PM2.5 [0.69% (0.14% to 1.24%)] and PM10 [0.38% (0.02% to 0.73%)] and at lag 12–24 h after exposure to SO2 [2.68% (0.94% to 4.44%)]. Cause-specific CVD analysis observed an increased risk of myocardial infarction morbidity within 6 h after exposure to PM2.5, PM10, and NO2, and an increased risk of out-of-hospital cardiac arrest morbidity within 12 h after exposure to CO. Risk of total CVD also increased within 24 h after exposure to heat. Interpretation: This study supports a sudden risk increase of cardiorespiratory diseases within a few hours after exposure to air pollution or heat, and some acute and highly lethal diseases such as myocardial infarction and cardiac arrest could be affected within a shorter time. Funding: The National Natural Science Foundation of China (Grant No. 42105165; 81773518), the High-level Scientific Research Foundation of Anhui Medical University (Grant No. 0305044201), and the Discipline Construction of Anhui Medical University (Grant No. 0301001836).

Aims: Metabolic switching during heart development contributes to postnatal cardiomyocyte (CM) cell cycle exit and loss of regenerative capacity in the mammalian heart. Metabolic control has potential for developing effective CM proliferation strategies. We sought to determine whether lactate dehydrogenase A (LDHA) regulated CM proliferation by inducing metabolic reprogramming. Methods and results: LDHA expression was high in P1 hearts and significantly decreased during postnatal heart development. CM-specific LDHA knockout mice were generated using CRISPR/Cas9 technology. CM-specific LDHA knockout inhibited CM proliferation, leading to worse cardiac function and a lower survival rate in the neonatal apical resection model. In contrast, CM-specific overexpression of LDHA promoted CM proliferation and cardiac repair post-MI. The α-MHC-H2B-mCh/CAG-eGFP-anillin system was used to confirm the proliferative effect triggered by LDHA on P7 CMs and adult hearts. Metabolomics, proteomics and Co-IP experiments indicated that LDHA-mediated succinyl coenzyme A reduction inhibited succinylation-dependent ubiquitination of thioredoxin reductase 1 (Txnrd1), which alleviated ROS and thereby promoted CM proliferation. In addition, flow cytometry and western blotting showed that LDHA-driven lactate production created a beneficial cardiac regenerative microenvironment by inducing M2 macrophage polarization. Conclusions: LDHA-mediated metabolic reprogramming promoted CM proliferation by alleviating ROS and inducing M2 macrophage polarization, indicating that LDHA might be an effective target for promoting cardiac repair post-MI.

Summary: Contagious itch behavior informs conspecifics of adverse environment and is crucial for the survival of social animals. Gastrin-releasing peptide (GRP) and its receptor (GRPR) in the suprachiasmatic nucleus (SCN) of the hypothalamus mediates contagious itch behavior in mice. Here, we show that intrinsically photosensitive retina ganglion cells (ipRGCs) convey visual itch information, independently of melanopsin, from the retina to GRP neurons via PACAP-PAC1R signaling. Moreover, GRPR neurons relay itch information to the paraventricular nucleus of the thalamus (PVT). Surprisingly, neither the visual cortex nor superior colliculus is involved in contagious itch. In vivo calcium imaging and extracellular recordings reveal contagious itch-specific neural dynamics of GRPR neurons. Thus, we propose that the retina-ipRGC-SCN-PVT pathway constitutes a previously unknown visual pathway that probably evolved for motion vision that encodes salient environmental cues and enables animals to imitate behaviors of conspecifics as an anticipatory mechanism to cope with adverse conditions.

Recently, foam glass thermal insulating decorative integrated board has been proposed as advanced external wall insulation. In the present study, the temperature and strain monitoring program is designed to investigate the synergistic of the integrated board and the base wall after installation on the building exterior wall. Moreover, variations of the temperature and strain fields of the system in different aging stages are studied. The obtained results show that the foam glass integrated board has an excellent performance in heat and cold preservation. It is found that the temperature difference between the concrete base layer and the finishing layer reaches 40°C. The temperature fluctuation range of the base layer is only 4°C and 9°C in hot-rain cycles and the heat-cold cycles, respectively. Moreover, it is found that the strain fluctuations of the finishing layer are relatively severe, and the deformation range of −1000με～+2500με and the plastic deformation of +1500με may occur in the hot-rain cycle, and the range of −2000με～+1500με and the plastic deformation of −600με may occur in the heat-cold cycle. Finally, the concept of thermal insulation degradation degree (DT) is proposed. The obtained results reveal that DT rises from 0 to 0.23 in the hot-rain cycle and from 0 to 0.36 in the heat-cold cycle. Through the analysis of the strain changes, the synergistic mechanism of the integrated board and the base wall in the aging process is studied. The present article is expected to provide a theoretical guideline to design foam glass integrated boards.

Using panel data from 242 cities in China, we examine the impact of government research and development (R&D) spending on corporate technological innovation. We find that listed firms located in cities with higher government R&D expenditures are more innovative than firms in other cities. Further, the positive effect of government R&D spending depends on fiscal instruments and factor allocation. Through subsidies and tax incentives, government R&D spending enhances firm innovation by alleviating financing constraints, improving employee creativity and ensuring efficient operations. We demonstrate that subsidies are more effective than taxes in spurring corporate technological innovation. We also show that the impact of government R&D spending is stronger for state-owned and high-tech enterprises than for other enterprises. Overall, our findings suggest that government R&D spending can substantially improve corporate technological innovation through fiscal instruments.

From an epidemiological perspective, previous research on COVID-19 has generally been based on classical statistical analyses. As a result, spatial information is often not used effectively. This paper uses image-based neural networks to explore the relationship between urban spatial risk and the distribution of infected populations, and the design of urban facilities. To achieve this objective, we use spatio-temporal data of people infected with new coronary pneumonia prior to 28 February 2020 in Wuhan. We then use kriging, which is a method of spatial interpolation, as well as core density estimation technology to establish the epidemic heat distribution on fine grid units. We further evaluate the influence of nine major spatial risk factors, including the distribution of agencies, hospitals, park squares, sports fields, banks and hotels, by testing them for significant positive correlation with the distribution of the epidemic. The weights of these spatial risk factors are used for training Generative Adversarial Network (GAN) models, which predict the distribution of cases in a given area. The input image for the machine learning model is a city plan converted by public infrastructures, and the output image is a map of urban spatial risk factors in the given area. The results of the trained model demonstrate that optimising the relevant point of interests (POI) in urban areas to effectively control potential risk factors can aid in managing the epidemic and preventing it from dispersing further.

Germline-mutation in BRCA1 tumor suppressor gene is an established risk for carcinogenesis not only in females but also in males. Deficiency in the repair of DNA double-strand breaks is hypothesized as a responsible mechanism for carcinogenesis. However, supporting data is insufficient both in the mutation spectra of cancers in the patients with BRCA1 germline-mutation and in murine knockout/knock-in models of Brca1 haploinsufficiency. Furthermore, information on the driving force toward carcinogenesis in BRCA1 mutation carriers is lacking. Here we applied Fenton reaction-based renal carcinogenesis to a rat heterozygously knockout model of BRCA1 haploinsufficiency (mutant [MUT] model; L63X/+). Rat MUT model revealed significant promotion of renal cell carcinoma (RCC) induced by ferric nitrilotriacetate (Fe-NTA). Array-based comparative genome hybridization of the RCCs identified significant increase in chromosomal amplification, syntenic to those in breast cancers of BRCA1 mutation carriers, including c-Myc, in comparison to those in the wild-type. Subacute-phase analysis of the kidney after repeated Fe-NTA treatment in the MUT model revealed dysregulated iron metabolism with mitochondrial malfunction assessed by expression microarray and electron microscopy, leading to renal tubular proliferation with iron overload. In conclusion, we for the first time demonstrate that biallelic wild-type BRCA1 provides more robust protection for mitochondrial metabolism under iron-catalyzed oxidative stress, preventing the emergence of neoplastic cells with chromosomal amplification. Our results suggest that oxidative stress via excess iron is a major driving force for carcinogenesis in BRCA1 haploinsufficiency, which can be a target for cancer prevention and therapeutics.

Background: Evidence suggests that particulate matter (PM) with smaller particle sizes (such as PM1, PM with an aerodynamic diameter≤1 µm) may have more toxic health effects. However, the short-term association between PM1 and asthma mortality remains largely unknown. Objective: This study aimed to examine the short-term effects of PM1 and PM2.5 on asthma mortality, as well as to investigate how neighborhood characteristics modified this association. Methods: Daily data on asthma mortality were collected from 13 cities in Jiangsu Province, China, between 2016 and 2017. A time-stratified case-crossover design was attempted to examine the short-term effects of PM1 and PM2.5 on asthma mortality. Individual exposure levels of PM1 and PM2.5 on case and control days were determined based on individual’s residential addresses. Stratified analyses by neighborhood characteristics (including green space, tree canopy, blue space, population density, nighttime light and street connectivity) were conducted to identify vulnerable living environments. Results: Mean daily concentrations of PM1 and PM2.5 on case days were 33.8 μg/m3 and 54.3 μg/m3. Each 10 μg/m3 increase in three-day-averaged (lag02) PM1 and PM2.5 concentrations were associated with an increase of 6.66% (95%CI:1.18%,12.44%) and 2.39% (95%CI: 0.05%−4.78%) asthma mortality, respectively. Concentration-response curves showed a consistent increase in daily asthma mortality with increasing PM1 and PM2.5 concentrations. Subgroup analyses indicated that the effect of PM1 appeared to be evident in neighborhood characteristics with high green space, low urbanization level and poor street connectivity. Conclusion: This study suggested an association between short-term PM1 and PM2.5 exposures and asthma mortality. Several neighborhood characteristics (such as green space and physical supportive environment) that could modify the effect of PM1 on asthma mortality should be further explored.

The synergism between cardiomyogenesis and angiogenesis is essential for cardiac regeneration. Circular RNAs (circRNAs) play pivotal roles in cell growth and angiogenesis, but their functions in cardiac regeneration are not yet known. In this study, we investigated the role and underlying mechanisms of circRNA Hipk3 (circHipk3) in both cardiomyogenesis and angiogenesis during cardiac regeneration. We found that circHipk3 was overexpressed in the fetal or neonatal heart of mice. The transcription factor Gata4 bound to the circHipk3 promoter and increased circHipk3 expression. Cardiomyocyte (CM) proliferation in vitro and in vivo was inhibited by circHipk3 knockdown and increased by circHipk3 overexpression. Moreover, circHipk3 overexpression promoted coronary vessel endothelial cell proliferation, migration, and tube-forming capacity and subsequent angiogenesis. More importantly, circHipk3 overexpression attenuated cardiac dysfunction and decreased fibrotic area after myocardial infarction (MI). Mechanistically, circHipk3 promoted CM proliferation by increasing Notch1 intracellular domain (N1ICD) acetylation, thereby increasing N1ICD stability and preventing its degradation. In addition, circHipk3 acted as a sponge for microRNA (miR)-133a to promote connective tissue growth factor (CTGF) expression, which activated endothelial cells. Our findings suggested that circHipk3 might be a novel therapeutic target for preventing heart failure post-MI.

We present AntVis, a web-based visual analytics tool for exploring ant movement data collected from the video recording of ants moving on tree branches. Our goal is to enable domain experts to visually explore massive ant movement data and gain valuable insights via effective visualization, filtering, and comparison. This is achieved through a deep learning framework for automatic detection, segmentation, and labeling of ants, ant movement clustering based on their trace similarity, and the design and development of five coordinated views (the movement, similarity, timeline, statistical, and attribute views) for user interaction and exploration. We demonstrate the effectiveness of AntVis with several case studies developed in close collaboration with domain experts. Finally, we report the expert evaluation conducted by an entomologist and point out future directions of this study. Keywords: Ant movement, Object detection, Image segmentation, Visual analytics, Knowledge discovery

Summary: Possessing a characteristic sandwich-type structure, metallocenes have been widely used by the chemistry community. However, the direct catalytic C−H heteroarylation of metallocenes still remains underexplored. Here, we report an efficient catalytic protocol for C−H heteroarylation of group 8 metallocenes (M = Fe, Ru) under light irradiation. This intermolecular cross coupling features directing group free, mild conditions and a wide substrate scope. Preliminary mechanistic studies suggest that the newly formed C−C bond is constructed through electrophilic radical substitution of the metallocene with a heteroaryl radical, which is generated via an oxidative quenching pathway.

Owing to their lightweight design, high energy absorption capacity, and excellent thermal and sound insulation properties, lattice structures have many potential applications in the fields of security, aerospace, biomedicine, and heat dissipation. In this study, a gyroid-type triply periodic minimal surface is used to design lattice structures. Gyroid uniform lattice structures and gyroid graded lattice structures are mathematically designed and fabricated using selective laser melting with a SS 316 L stainless steel powder. The mechanical properties of these structures are studied under a compression load, and the deformation differences between the graded and uniform structures are compared. The finite element method is used to simulate the compression process, and the experimental and simulation results are qualitatively compared. Results show that during plastic deformation, the stress change in the graded structure is larger than that in the uniform structure. By controlling the volume fraction, mechanical properties can be specifically tailored, which provides the design guidelines for the application of this structure.

Ferroptosis is a form of regulated cell necrosis, as a consequence of Fe(II)-dependent lipid peroxidation. Although ferroptosis has been linked to cancer cell death, neurodegeneration and reperfusion injury, physiological roles of ferroptosis have not been elucidated to date mostly due to the lack of appropriate methodologies. Here, we show that 4-hydroxy-2-nonenal (HNE)-modified proteins detected by a HNEJ-1 mouse monoclonal antibody is a robust immunohistochemical technology to locate ferroptosis in tissues in combination with morphological nuclear information, based on various models of ferroptosis, including erastin-induced cysteine-deprivation, conditional Gpx4 knockout and Fe(II)-dependent renal tubular injury, as well as other types of regulated cell death. Specificity of HNEJ-1 with ferroptosis was endorsed by non-selective identification of HNE-modified proteins in an Fe(II)-dependent renal tubular injury model. We further comprehensively searched for signs of ferroptosis in different developmental stages of Fischer-344 rats from E9.5–2.5 years of age. We observed that there was a significant age-dependent increase in ferroptosis in the kidney, spleen, liver, ovary, uterus, cerebellum and bone marrow, which was accompanied by iron accumulation. Not only phagocytic cells but also parenchymal cells were affected. Epidermal ferroptosis in ageing SAMP8 mice was significantly promoted by high-fat or carbohydrate-restricted diets. During embryogenesis of Fischer-344 rats, we found ferroptosis in nucleated erythrocytes at E13.5, which disappeared in enucleated erythrocytes at E18.5. Administration of a ferroptosis inhibitor, liproxstatin-1, significantly delayed erythrocyte enucleation. Therefore, our results demonstrate for the first time the involvement of ferroptosis in physiological processes, such as embryonic erythropoiesis and aging, suggesting the evolutionally acquired mechanism and the inevitable side effects, respectively.

Acoustic cavitation is a very important hydrodynamic phenomenon, and is often implicated in a myriad of industrial, medical, and daily living applications. In these applications, the effect mechanism of liquid surface tension on improving the efficiency of acoustic cavitation is a crucial concern for researchers. In this study, the effects of liquid surface tension on the dynamics of an ultrasonic driven bubble near a rigid wall, which could be the main mechanism of efficiency improvement in the applications of acoustic cavitation, were investigated at the microscale level. A synchronous high-speed microscopic imaging method was used to clearly record the temporary evolution of single acoustic cavitation bubble in the liquids with different surface tension. Meanwhile, the bubble dynamic characteristics, such as the position and time of bubble collapse, the size and stability of the bubbles, the speed of bubble boundaries and the micro-jets, were analyzed and compared. In the case of the single bubbles near a rigid wall, it was found that low surface tension reduces the stability of the bubbles in the liquid medium. Meanwhile, the bubbles collapse earlier and farther from the rigid wall in the liquids with lower surface tension. In addition, the surface tension has no significant influence on the speed of the first micro-jet, but it can substantially increase the speed of second and the third micro-jets after the first collapse of the bubble. These effects of liquid surface tension on the bubble dynamics can explain the mechanism of surfactants in numerous fields of acoustic cavitation for facilitating its optimization and application.

Summary: Superhydrophobic coatings have tremendous potential for protecting porous structures from corrosion. However, the weak adhesion and poor abrasion resistance have long been challenges for their real-life applications. Inspired by tree roots, we prepared a robust superhydrophobic coating by spraying fluorinated nanodiamonds (FNDs) on a permeable epoxy coating. The epoxy can not only coat the surface but also permeate deeply inside a porous substrate and consolidate in situ as tree roots in soil. Thus, the structure is thoroughly reinforced where the pull-off strength reaches 9.4 MPa for concrete. On the other hand, the surface is covered with immobilized FNDs, forming a superhydrophobic surface. Thanks to the ultra-hard FNDs, the coating surface has high abrasion resistance and its superhydrophobicity holds even after 100 abrasion cycles. Moreover, it exhibits self-cleaning, anti-icing, and anticorrosion performance. It is promising in protecting various porous structures such as concrete, wood, and untreated corroded steel.

Non-thermal plasma (NTP), an engineered technology to generate reactive species, induces ferroptosis and/or apoptosis specifically in various-type cancer cells. NTP-activated Ringer's lactate (PAL) is another modality for cancer therapy at preclinical stage. Here we found that PAL induces selective ferroptosis of malignant mesothelioma (MM) cells, where non-targeted metabolome screening identified upregulated citrulline-nitric oxide (.NO) cycle as a PAL target. .NO probe detected biphasic peaks transiently at PAL exposure with time-dependent increase, which was responsible for inducible . NO synthase (iNOS) overexpression through NF-κB activation. .NO and lipid peroxidation occupied lysosomes as a major compartment with increased TFEB expression. Not only ferrostatin-1 but inhibitors for . NO and/or iNOS could suppress this ferroptosis. PAL-induced ferroptosis accompanied autophagic process in the early phase, as demonstrated by an increase in essential amino acids, LC3B-II, p62 and LAMP1, transforming into the later phase with boosted lipid peroxidation. Therefore, .NO-mediated lysosomal impairment is central in PAL-induced ferroptosis.

Rice (Oryza sativa L.) is one of the most important food crops worldwide and a model monocot plant for gene function analysis, so it is an ideal system for studying flower development. This study reports a mutant, named multi-floret spikelet 3 (mfs3), which is related to the spikelet development in rice and derived from the ethylmethane sulfonate (EMS)-treated rice cultivar XIDA 1B. In mfs3, the main body of palea (bop) was degenerated severely and only glume-like marginal regions of palea (mrp) remained, while other floral organs developed normally, indicating that the palea identity was seriously influenced by the mutation. It was also observed that the number of floral organs was increased in some spikelets, including 2 lemmas, 4 mrp, 4 lodicules, 8–10 stamens, and 2 pistils, which meant that the spikelet determinacy was lost to some degree in mfs3. Furthermore, genetic analysis demonstrated that the mfs3 trait was controlled by a single recessive gene. Using 426 F2 mutants derived from the cross between sterile line 56S and mfs3, the MULTI-FLORET SPIKELET 3 (MFS3) gene was mapped between the molecular markers RM19347 and RM19352 on Chr.6, with a physical distance of 106.3 kb. Sequencing of candidate genes revealed that an 83-bp fragment loss and a base substitution occurred in the LOC_Os06g04540 gene in the mutant, confirming preliminarily that the LOC_Os06g04540 gene was the MFS3 candidate gene. Subsequent qPCR analysis showed that the mutation caused the down-regulation of OsMADS1 and FON1 genes, and the up-regulation of OsIDS1 and SNB genes, which are all involved in the regulation of spikelet development. The MFS3 mutation also significantly reduced the transcription of the REP gene, which is involved in palea development. These results indicated that the MFS3 gene might be involved in the spikelet meristem determinacy and palea identity by regulating the expression of these related genes.

Background: We previously found that loss of lncRNA-AZIN2 splice variant (AZIN2-sv) increases cardiomyocyte (CM) proliferation and attenuates adverse ventricular remodelling post-myocardial infarction (MI). However, whether inhibition of AZIN2-sv can simultaneously induce angiogenesis and thus improve prognosis after MI is unclear. Methods: We used in situ hybridization and quantitative PCR to determine AZIN2-sv expression in endothelial cells. Knockdown and overexpression were performed to detect the role of AZIN2-sv in endothelial cell function, angiogenesis and prognosis after MI. RNA pulldown, RNA immunoprecipitation and luciferase reporter assays were used to determine the interaction with talin1 (Tln1) protein and miRNA-214 (miR-214). DNA pulldown and chromatin immunoprecipitation (ChIP) assays were used to study AZIN2-sv binding to upstream transcription factors. Findings: AZIN2-sv was enriched in cardiac endothelial cells. The loss of AZIN2-sv reduced endothelial cell apoptosis and promoted endothelial sprouting and capillary network formation in vitro. Moreover, in vivo, the loss of AZIN2-sv induced angiogenesis and improved cardiac function after MI. Mechanistically, AZIN2-sv reduced Tln1 and integrin β1 (ITGB1) protein levels to inhibit neovascularization. AZIN2-sv activated the ubiquitination-dependent degradation of Tln1 mediated by proteasome 26S subunit ATPase 5 (PSMC5). In addition, AZIN2-sv could bind to miR-214 and suppress the phosphatase and tensin homologue (PTEN)/Akt pathway to inhibit angiogenesis. With regard to the upstream mechanism, Bach1, a negative regulator of angiogenesis, bound to the promoter of AZIN2-sv and increased its expression. Interpretation: Bach1-activated AZIN2-sv could participate in angiogenesis by promoting the PSMC5-mediated ubiquitination-dependent degradation of Tln1 and blocking the miR-214/PTEN/Akt pathway. Inhibition of AZIN2-sv induced angiogenesis and myocardial regeneration simultaneously, thus, AZIN2-sv could be an ideal therapeutic target for improving myocardial repair after MI. Fund: National Natural Science Foundations of China. Keywords: AZIN2-sv, Angiogenesis, Tln1, Ubiquitination

This paper presents a method to solidify/stabilize the municipal solid waste incineration (MSWI) fly ash by originally employing the microbial induced carbonate precipitation (MICP) technique. In this method, the rich endogenous calcium in the MSWI fly ash was utilized to induce calcite precipitation, which is different from the operation of adding extra calcium source in previous researches. The fly ash sample had a CaO content of 44.5%, and its leaching concentrations of Zn, Cr and Pb exceed the limits of the identification standard for hazardous wastes in China. The optical density at 600 nm (OD600) of the bacterial solution was about 1.0 after the processes of bacterial activation and reproduction. The prepared fly ash sample was well mixed with bacterial solution at an ash-liquid ratio of 1 kg: 0.3 L and cured at a temperature of 20 °C and a humidity of ≥95% for 7 days. After treatment, the heavy metal leachability significantly reduced to meet the standard for pollution control of landfill site, and the unconfined compressive strength increased approximately 40%. The precipitated carbonates were verified by SEM-EDS analysis and quantified by measurement of carbonate content via acid-dissolving method. The results shone a light on the possibility of using MICP technique as a useful and efficient tool to stabilize the MSWI fly ash before being reused or properly stored in landfills. • The MICP method is efficient to reduce the heavy metal leachability and increase the compressive strength of MSWI fly ash. • The endogenous calcium in MSWI fly ash was utilized to induce calcite precipitation. • The heavy metals in MSWI fly ash were well immobilized by the formation of carbonates. Method name: Microbial induced solidification/stabilization method, Keywords: Microbial induced carbonate precipitation (MICP), Solidification/stabilization method, Municipal solid waste incineration (MSWI) fly ash, Endogenous calcium, Heavy metal leachability, Compressive strength

This is the second part of a two-part work on the unified mathematical theory of gapped and gapless edges of 2+1D topological orders. In Part I, we have developed the mathematical theory of chiral gapless edges. In Part II, we study boundary-bulk relation and non-chiral gapless edges. In particular, we explain how the notion of the center of an enriched monoidal category naturally emerges from the boundary-bulk relation. After the study of 0+1D gapless walls, we give the complete boundary-bulk relation for 2+1D topological orders with chiral gapless edges (including gapped edges) and 0d walls between edges. This relation is stated precisely and proved rigorously as a monoidal equivalence, which generalizes the functoriality of the usual Drinfeld center to an enriched setting. We also develop the mathematical theory of non-chiral gapless edges and 0+1D walls, and explain how to gap out certain non-chiral 1+1D gapless edges and 0+1D gapless walls categorically. In the end, we show that all anomaly-free 1+1D boundary-bulk rational CFT's can be recovered from 2d topological orders with chiral gapless edges via a dimensional reduction process. This provides physical meanings to some mysterious connections between mathematical results in fusion categories and those in rational CFT's.

Strategies to mitigate the spread of antibiotic resistance genes (ARGs) in soils are urgently needed. Therefore, a pristine pyroligneous acid (PA) from pyrolyzing blended woody waste at 450 °C and its three fractions distilled at 98, 130, and 220 °C (F1, F2, and F3) were used to evaluate their feasibility of reducing ARGs in soil. Application of PA, F2, and F3 effectively decreased the relative ARG abundance by 22.4–75.4% and 39.7–66.7% in the rhizosphere and bulk soil relative to control, respectively, and the removal efficiency followed an order of F3 > PA > F2. Contrarily, F1 increased the abundance of ARGs. The decreased abundance of two mobile genetic elements and impaired conjugative transfer of RP4 plasmid in the presence of PA, F2 and F3 demonstrated that the weakened horizontal gene transfer (HGT) contributed to the reduced ARG level. Variation partitioning analysis and structural equation models confirmed that ARG reduction was primarily driven by the weakened HGT, followed by the decreased co-selection of heavy metals and shifted bacterial community (e.g., reduced potential host bacteria of ARGs). Our findings provide practical and technical support for developing PA-based technology in remediating ARG-contaminated soil to ensure food safety and protect human health.

Absract: Background: Identifying effective drugs to suppress vascular inflammation is a promising strategy to delay the progression of abdominal aortic aneurysm (AAA). Itaconate has a vital role in regulating inflammatory activation in various inflammatory diseases. However, the role of itaconate in the progression of AAA is unknown. In this study, we explored the inhibitory effect of itaconate on AAA formation and its underlying mechanisms. Methods: Quantitative PCR, western blotting and immunohistochemistry were used to determine Irg1 and downstream Nrf2 expression in human and mouse AAA samples. Liquid chromatograph-mass spectrometry (LC-MS) analysis was performed to measure the abundance of itaconate. OI treatment and Irg1 knockdown were performed to study the role of OI in AAA formation. Nrf2 intervention in vivo was performed to detect the critical role of Nrf2 in the beneficial effect of OI on AAA. Findings: We found that itaconate suppressed the formation of angiotensin II (Ang II)-induced AAA in apolipoprotein E-deficient (Apoe−/−) mice, while Irg1 deficiency exerted the opposite effect. Mechanistically, itaconate inhibited vascular inflammation by enabling Nrf2 to function as a transcriptional repressor of downstream inflammatory genes via alkylation of Keap1. Moreover, Nrf2 deficiency significantly aggravated inflammatory factor expression and promoted AAA formation. In addition, Keap1 overexpression significantly promoted Ang II-induced AAA formation, which was inhibited by itaconate. Interpretation: Itaconate inhibited AAA formation by suppressing vascular inflammation, and therapeutic approaches to increase itaconate are potentially beneficial for preventing AAA formation. Funding: National Natural Science Foundations of China and Guangzhou regenerative medicine and Health Laboratory of Guangdong.