PM2.5-induced iron homeostasis imbalance triggers cardiac hypertrophy through ferroptosis in a selective autophagy crosstalk manner.

Exposure to PM2.5 is correlated with cardiac remodeling, of which cardiac hypertrophy is one of the main clinical manifestations. Ferroptosis plays an important role in cardiac hypertrophy. However, the potential mechanism of PM2.5-induced cardiac hypertrophy through ferroptosis remains unclear. This study aimed to explore the molecular mechanism of cardiac hypertrophy caused by PM2.5 and the intervention role of MitoQ involved in this process. The results showed that PM2.5 could induce cardiac hypertrophy and dysfunction in mice. Meanwhile, the characteristics of ferroptosis were observed, such as iron homeostasis imbalance, lipid peroxidation, mitochondrial damage and abnormal expression of key molecules. MitoQ treatment could effectively mitigate these alternations. After treating human cardiomyocyte AC16 with PM2.5, ferroptosis activator (Erastin) and inhibitor (Fer-1), it was found that PM2.5 could promote ferritinophagy and lead to lipid peroxidation, mitochondrial dysfunction as well as the accumulation of intracellular and mitochondrial labile iron. Subsequently, mitophagy was activated and provided an additional source of labile iron, enhancing the sensitivity of AC16 cells to ferroptosis. Furthermore, Fer-1 alleviated PM2.5-induced cytotoxicity and iron overload in the cytoplasm and mitochondria of AC16 cells. It was worth noting that during the process of PM2.5 caused ferroptosis, abnormal iron metabolism mediated the activation of ferritinophagy and mitophagy in a temporal order. In addition, NCOA4 knockdown reversed the iron homeostasis imbalance and lipid peroxidation caused by PM2.5, thereby alleviating ferroptosis. In summary, our study found that iron homeostasis imbalance-mediated the crosstalk of ferritinophagy and mitophagy played an important role in PM2.5-induced ferroptosis and cardiac hypertrophy.

Associations of long-term particulate matter exposure with cardiometabolic diseases: A systematic review and meta-analysis.

BACKGROUND: This review aimed to establish a holistic perspective of long-term PM exposure and cardiometabolic diseases, identify long-term PM-related cardiovascular and metabolic risk factors, and provide practical significance to preventative measures. METHOD: A combination of computer and manual retrieval was used to search for keywords in PubMed (2903 records), Embase (2791 records), Web of Science (5488 records) and Cochrane Library (163 records). Finally, a total of 82 articles were considered in this meta-analysis. Stata 13.0 was accustomed to inspecting the studies' heterogeneity and calculating the combined effect value (RR) by selecting the matching models. The subgroup analysis, sensitivity analysis and publication bias tests were also performed. RESULTS: Meta-analysis figured an association between PM and cardiometabolic diseases. PM2.5 (per 10 µg/m3 increase) boosted the risk of hypertension (RR = 1.14, 95 % CI: 1.09-1.19), coronary heart disease (CHD) (RR = 1.21, 95 % CI: 1.08-1.35), diabetes (RR = 1.16, 95 % CI: 1.11-1.21) and stroke (including ischemic stroke and hemorrhagic stroke). PM10 (per 10 µg/m3 increase) elevated the incidence of hypertension (RR = 1.11, 95 % CI: 1.07-1.16) and diabetes (RR = 1.26, 95 % CI: 1.08-1.47). PM1 (per 10 µg/m3 increase) exposure increased the risk of total dyslipidemia, yielding the RR of 1.10 (95 % CI: 1.01-1.18). Furthermore, the elderly, overweight and higher background pollutant level were potentially susceptible to related diseases. CONCLUSION: There was a virtual connection between long-term exposure to PM and cardiometabolic diseases. PM2.5 or PM10 (per 10 µg/m3) increased the risk of hypertension, CHD, diabetes, stroke and dyslipidemia, causing cardiovascular "multimorbidity" in high-risk populations.

A New Grey Wolf Optimizer Tuned Extended Generalized Predictive Control for Distillation Process.

The distillation process plays an essential role in the petrochemical industry. However, the high-purity distillation column has complicated dynamic characteristics such as strong coupling and large time delay. To control the distillation column accurately, we proposed an extended generalized predictive control (EGPC) method inspired by the principles of extended state observer and proportional-integral-type generalized predictive control method; the proposed EGPC can adaptively compensate the system for the effects of coupling and model mismatch online and performs well in controlling time-delay systems. The strong coupling of the distillation column needs fast control, and the large time delay requires soft control. To balance the requirement for fast and soft control at the same time, a grey wolf optimizer with reverse learning and adaptive leaders number strategies (RAGWO) was proposed to tune the parameters of EGPC, and these strategies enable RAGWO to have a better initial population and improve its exploitation and exploration ability. The benchmark test results indicate that the RAGWO outperforms the existing optimizers for most of the selected benchmark functions. Extensive simulations show that the proposed method in terms of fluctuation and response time is superior to other methods for controlling the distillation process.

Melatonin-mediated development and abiotic stress tolerance in plants.

Melatonin is a multifunctional molecule that has been widely discovered in most plants. An increasing number of studies have shown that melatonin plays essential roles in plant growth and stress tolerance. It has been extensively applied to alleviate the harmful effects of abiotic stresses. In view of its role in regulating aspects of plant growth and development, we ponder and summarize the scientific discoveries about seed germination, root development, flowering, fruit maturation, and senescence. Under abiotic and biotic stresses, melatonin brings together many pathways to increase access to treatments for the symptoms of plants and to counteract the negative effects. It has the capacity to tackle regulation of the redox, plant hormone networks, and endogenous melatonin. Furthermore, the expression levels of several genes and the contents of diverse secondary metabolites, such as polyphenols, terpenoids, and alkaloids, were significantly altered. In this review, we intend to examine the actions of melatonin in plants from a broader perspective, explore the range of its physiological functions, and analyze the relationship between melatonin and other metabolites and metabolic pathways.

An integral perspective of canonical cigarette and e-cigarette-related cardiovascular toxicity based on the adverse outcome pathway framework.

BACKGROUND: Nowadays, cigarette smoking remains the leading cause of chronic disease and premature death, especially cardiovascular disease. As an emerging tobacco product, e-cigarettes have been advocated as alternatives to canonical cigarettes, and thus may be an aid to promote smoking cessation. However, recent studies indicated that e-cigarettes should not be completely harmless to the cardiovascular system. AIM OF REVIEW: This review aimed to build up an integral perspective of cigarettes and e-cigarettes-related cardiovascular toxicity. KEY SCIENTIFIC CONCEPTS OF REVIEW: This review adopted the adverse outcome pathway (AOP) framework as a pivotal tool and aimed to elucidate the association between the molecular initiating events (MIEs) induced by cigarette and e-cigarette exposure to the cardiovascular adverse outcome. Since the excessive generation of reactive oxygen species (ROS) has been widely approved to play a critical role in cigarette smoke-related CVD and may also be involved in e-cigarette-induced toxic effects, the ROS overproduction and subsequent oxidative stress are regarded as essential parts of this framework. As far as we know, this should be the first AOP framework focusing on cigarette and e-cigarette-related cardiovascular toxicity, and we hope our work to be a guide in exploring the biomarkers and novel therapies for cardiovascular injury.

Co-exposure of PM2.5 and high-fat diet induce lipid metabolism reprogramming and vascular remodeling.

Fine particulate matter (PM2.5) exposure has been proved to increase the cardiovascular disease risk. However, there is a lack of comprehensive knowledge on whether a high-fat diet (HFD) affects PM2.5-induced cardiovascular disease. The purpose of this study was to investigate the impairment of lipid metabolism and vascular function by PM2.5 and HFD exposure in ApoE-/- mice. Oil red O staining indicated that co-treatment of PM2.5 and HFD resulted in markedly lipid deposition in the mice aorta. Blood biochemical analysis demonstrated that co-exposure of PM2.5 and HFD could cause dyslipidemia in vivo. Vascular Doppler ultrasound and histopathological analysis found that the functional and structural alterations with fibrosis and calcified remodeling of the vessels were detected after PM2.5 and HFD exposure. For in-depth study, the genome-wide transcriptional analysis performed in macrophages was further revealed that the endoplasmic reticulum stress, immune system process, regulation of cell proliferation etc. were response to PM2.5 exposure; while Lipid and atherosclerosis signaling pathways had a critical role in PM2.5-induced vascular injury. Results from validation experiments manifested that the release of supernatant in PM2.5- or ox-LDL-treated macrophages could decrease the cell viability and increase the lipid ROS in vascular smooth muscle cells (VSMCs). Moreover, the up-regulations of CCL2, IL-6 and IL-1ß in aortic arch of mice were observed after co-exposure with PM2.5 and HFD. Our data hinted that PM2.5 could affect the lipid metabolism reprogramming and induce vascular remodeling, accompanied with synergistic effects of HFD.

PM2.5 induce the defective efferocytosis and promote atherosclerosis via HIF-1α activation in macrophage.

Epidemiological studies demonstrate that fine particulate matter (PM2.5) promotes the development of atherosclerosis. However, the mechanism insight of PM2.5-induced atherosclerosis is still lacking. The aim of this study was to explore the biological effects of hypoxia-inducible factor 1α (HIF-1α) on PM2.5-triggered atherosclerosis. The vascular stiffness, carotid intima-media thickness (CIMT), lipid and atherosclerotic lesion were increased when von Hippel-Lindau (VHL)-null mice were exposed to PM2.5. Yet, knockout of HIF-1α markedly decreased the PM2.5-triggered atherosclerotic lesion. We firstly performed microarray analysis in PM2.5-treated bone morrow-derived macrophages (BMDMs), which showed that PM2.5 significantly changed the genes expression patterns and affected biological processes such as phagocytosis, apoptotic cell clearance, cellular response to hypoxia, apoptotic process and inflammatory response. Moreover, the data showed knockout of HIF-1α remarkably relieved PM2.5-induced defective efferocytosis. Mechanistically, PM2.5 inhibited the level of genes and proteins of efferocytosis receptor c-Mer tyrosine kinase (MerTK), especially in VHL-null BMDMs. In addition, PM2.5 increased the genes and proteins of a disintegrin and metallopeptidase domain 17 (ADAM17), which caused the MerTK cleavage to form soluble MerTK (sMer) in plasma and cellular supernatant. The sMer was significantly up-regulated in plasma of VHL-null PM2.5-exposed mice. Moreover, PM2.5 could induce defective efferocytosis and activate inflammatory response through MerTK/IFNAR1/STAT1 signaling pathway in macrophages. Our results demonstrate that PM2.5 could induce defective efferocytosis and inflammation by activating HIF-1α in macrophages, ultimately resulting in accelerating atherosclerotic lesion formation and development. Our data suggest HIF-1α in macrophages might be a potential target for PM2.5-related atherosclerosis.

Metabolomics-based safety evaluation of acute exposure to electronic cigarettes in mice.

INTRODUCTION: A growing number of epidemiological evidence reveals that electronic cigarettes (E-cigs) were associated with pneumonia, hypertension and atherosclerosis, but the toxicological evaluation and mechanism of E-cigs were largely unknown. OBJECTIVE: Our study was aimed to explore the adverse effects on organs and metabolomics changes in C57BL/6J mice after acute exposure to E-cigs. METHODS AND RESULTS: Hematoxylin and eosin (H&E) staining found pathological changes in tissues after acute exposure to E-cigs, such as inflammatory cell infiltration, nuclear pyknosis, and intercellular interstitial enlargement. E-cigs could increase apoptosis-positive cells in a time-dependent way using Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay. Oxidative damage indicators of reactive oxygen species (ROS), malondialdehyde (MDA) and 4-hydroxynonena (4-HNE) were also elevated after E-cigs exposure. There was an increasing trend of total glycerol and cholesterol in serum, while the glucose and liver enzymes including alanine aminotransferase (ALT), aspartate transaminase (AST), gamma-glutamyltranspeptidase (γ-GT) had no significant change compared to that of control. Further, Q Exactive high field (HF) mass spectrometer was used to conduct metabolomics, which revealed that differential metabolites including l-carnitine, Capryloyl glycine, etc. Trend analysis showed the type of compounds that change over time. Pathway enrichment analysis indicated that E-cigs affected 24 metabolic pathways, which were mainly regulated amino acid metabolism, further affected the tricarboxylic acid (TCA) cycle. Additionally, metabolites-diseases network analysis found that the type 2 diabetes mellitus, propionic acidemia, defect in long-chain fatty acids transport and lung cancer may be related to E-cigs exposure. CONCLUSIONS: Our findings provided important clues for metabolites biomarkers of E-cigs acute exposure and are beneficial for disease prevention.

Ecophysiological Leaf Traits of Forty-Seven Woody Species under Long-Term Acclimation in a Botanical Garden.

Ex situ conservation plays an important role in the conservation and utilization of plant resources. In recent years, botanical gardens have greatly improved the ex situ conservation of plants, and research has mainly focused on morphological characteristics, reproduction technology, and conservation value. There are few studies on the ecophysiological traits of plants after conservation. Forty-seven plants that are frequently used in North China and were grown in the Beijing Botanic Garden were selected to measure their photosynthetic traits, light-use efficiency (LUE), water-use efficiency (WUE), specific leaf area (SLA), relative chlorophyll content (SPAD), and leaf water potential (φ). An analysis of variance showed that there were significant differences in the ecophysiological traits of the leaves of 47 woody species. The light saturation point (LSP), net photosynthetic rate at light saturation (Pnmax), φ, and SLA had significant differences among different plant life forms. The SLA and SPAD of leaves were significantly different among the families. The LUE of all species reached its maximum under a low light intensity, and species with a large difference between the light saturation point and light compensation point had larger Pnmax values. This research further adds to the understanding of the adaptation mechanisms of plants to the environment under the conditions of a botanical garden as well as the environmental fitness in a long-term ex situ domestication and then helps with scientifically setting up artificial management conditions.

The critical role of epigenetic mechanisms involved in nanotoxicology.

Over the past decades, nanomaterials (NMs) have been widely applied in the cosmetic, food, engineering, and medical fields. Along with the prevalence of NMs, the toxicological characteristics exhibited by these materials on health and the environment have gradually attracted attentions. A growing number of evidences have indicated that epigenetics holds an essential role in the onset and development of various diseases. NMs could cause epigenetic alterations such as DNA methylation, noncoding RNA (ncRNA) expression, and histone modifications. NMs might alternate either global DNA methylation or the methylation of specific genes to affect the biological function. Abnormal upregulation or downregulation of ncRNAs might also be a potential mechanism for the toxic effects caused by NMs. In parallel, the phosphorylation, acetylation, and methylation of histones also take an important part in the process of NMs-induced toxicity. As the adverse effects of NMs continue to be explored, mechanisms such as chromosomal remodeling, genomic imprinting, and m6 A modification are also gradually coming into the limelight. Since the epigenetic alterations often occur in the early development of diseases, thus the relevant studies not only provide insight into the pathogenesis of diseases, but also screen for the prospective biomarkers for early diagnosis and prevention. This review summarizes the epigenetic alterations elicited by NMs, hoping to provide a clue for nanotoxicity studies and security evaluation of NMs. This article is categorized under: Toxicology and Regulatory Issues in Nanomedicine > Toxicology of Nanomaterials.

Melatonin alleviates PM2.5-triggered macrophage M1 polarization and atherosclerosis via regulating NOX2-mediated oxidative stress homeostasis.

It is reported that oxidative stress homeostasis was involved in PM2.5-induced foam cell formation and progression of atherosclerosis, but the exact molecular mechanism is still unclear. Melatonin is an effective antioxidant that could reverse the cardiopulmonary injury. The main purpose of this study is to investigate the latent mechanism of PM2.5-triggered atherosclerosis development and the protective role of melatonin administration. Vascular Doppler ultrasound showed that PM2.5 exposure reduced aortic elasticity in ApoE-/- mice. Meanwhile, blood biochemical and pathological analysis demonstrated that PM2.5 exposure caused dyslipidemia, elicited oxidative damage of aorta and was accompanied by an increase in atherosclerotic plaque area; while the melatonin administration could effectively alleviate PM2.5-induced macrophage M1 polarization and atherosclerosis in mice. Further investigation verified that NADPH oxidase 2 (NOX2) and mitochondria are two prominent sources of PM2.5-induced ROS production in vascular macrophages. Whereas, the combined use of two ROS-specific inhibitors and adopted with melatonin markedly rescued PM2.5-triggered macrophage M1 polarization and foam cell formation by inhibiting NOX2-mediated crosstalk of Keap1/Nrf2/NF-κB and TLR4/TRAF6/NF-κB signaling pathways. Our results demonstrated that NOX2-mediated oxidative stress homeostasis is critical for PM2.5-induced atherosclerosis and melatonin might be a potential treatment for air pollution-related cardiovascular diseases.

Adverse outcome pathway of fine particulate matter leading to increased cardiovascular morbidity and mortality: An integrated perspective from toxicology and epidemiology.

Fine particulate matter (PM2.5) exposure is a major threat to public health, and is listed as one of the leading factors associated with global premature mortality. Among the adverse health effects on multiple organs or tissues, the influence of PM2.5 exposure on cardiovascular system has drawn more and more attention. Although numerous studies have investigated the mechanisms responsible for the cardiovascular toxicity of PM2.5, the various mechanisms have not been integrated due to the variety of the study models, different levels of toxicity assessment endpoints, etc. Adverse Outcome Pathway (AOP) framework is a useful tool to achieve this goal so as to facilitate comprehensive understanding of toxicity assessment of PM2.5 on cardiovascular system. This review aims to illustrate the causal mechanistic relationships of PM2.5-triggered cardiovascular toxicity from different levels (from molecular/cellular/organ to individual/population) by using AOP framework. Based on the AOP Wiki and published literature, we propose an AOP framework focusing on the cardiovascular toxicity induced by PM2.5 exposure. The molecular initiating event (MIE) is identified as reactive oxygen species generation, followed by the key events (KEs) of oxidative damage and mitochondria dysfunction, which induces vascular endothelial dysfunction via vascular endothelial cell autophagy dysfunction, vascular fibrosis via vascular smooth muscle cell activation, cardiac dysregulation via myocardial apoptosis, and cardiac fibrosis via fibroblast proliferation and myofibroblast differentiation, respectively; all of the above cardiovascular injuries ultimately elevate cardiovascular morbidity and mortality in the general population. As far as we know, this is the first work on PM2.5-related cardiovascular AOP construction. In the future, more work needs to be done to explore new markers in the safety assessment of cardiovascular toxicity induced by PM2.5.

The critical role of epigenetic mechanism in PM2.5-induced cardiovascular diseases.

Cardiovascular disease (CVD) has become the leading cause of death worldwide, which seriously threatens human life and health. Epidemiological studies have confirmed the occurrence and development of CVD are closely related to air pollution. In particular, fine particulate matter (PM2.5) is recognized as an important environmental factor contributing to increased morbidity, mortality and hospitalization rates among adults and children. However, the underlying mechanism by which PM2.5 promotes CVD development remains unclear. With the development of epigenetics, recent studies have shown that PM2.5 exposure may induce or aggravate CVD through epigenetic changes. In order to better understand the potential mechanisms, this paper reviews the epigenetic changes of CVD caused by PM2.5. We summarized the epigenetic mechanisms of PM2.5 causing cardiovascular pathological damage and functional changes, mainly involving DNA methylation, non-coding RNA, histone modification and chromosome remodeling. It will provide important clues for exploring the biological mechanisms affecting cardiovascular health.

The mitochondria-targeted antioxidant MitoQ attenuated PM2.5-induced vascular fibrosis via regulating mitophagy.

Short-term PM2.5 exposure is related to vascular remodeling and stiffness. Mitochondria-targeted antioxidant MitoQ is reported to improve the occurrence and development of mitochondrial redox-related diseases. At present, there is limited data on whether MitoQ can alleviate the vascular damage caused by PM2.5. Therefore, the current study was aimed to evaluate the protective role of MitoQ on aortic fibrosis induced by PM2.5 exposure. Vascular Doppler ultrasound manifested PM2.5 damaged both vascular function and structure in C57BL/6J mice. Histopathological analysis found that PM2.5 induced aortic fibrosis and disordered elastic fibers, accompanied by collagen I/III deposition and synthetic phenotype remodeling of vascular smooth muscle cells; while these alterations were partially alleviated following MitoQ treatment. We further demonstrated that mitochondrial dysfunction, including mitochondrial reactive oxygen species (ROS) overproduction and activated superoxide dismutase 2 (SOD2) expression, decreased mitochondrial membrane potential (MMP), oxygen consumption rate (OCR), ATP and increased intracellular Ca2+, as well as mitochondrial fragmentation caused by increased Drp1 expression and decreased Mfn2 expression, occurred in PM2.5-exposed aorta or human aortic vascular smooth muscle cells (HAVSMCs), which were reversed by MitoQ. Moreover, the enhanced expressions of LC3II/I, p62, PINK1 and Parkin regulated mitophagy in PM2.5-exposed aorta and HAVSMCs were weakened by MitoQ. Transfection with PINK1 siRNA in PM2.5-exposed HAVSMCs further improved the effects of MitoQ on HAVSMCs synthetic phenotype remodeling, mitochondrial fragmentation and mitophagy. In summary, our data demonstrated that MitoQ treatment had a protective role in aortic fibrosis after PM2.5 exposure through mitochondrial quality control, which regulated by mitochondrial ROS/PINK1/Parkin-mediated mitophagy. Our study provides a possible targeted therapy for PM2.5-induced arterial stiffness.

Cardiovascular toxicity assessment of polyethylene nanoplastics on developing zebrafish embryos.

Environmental exposure to nanoplastics is inevitable as the application of nanoplastics in our daily life is more and more extensively. So, the adverse effects of nanoplastics on human health are also gaining greater concerns. However, the subsequent toxicological response to nanoplastics, especially on cardiovascular damage was still largely unknown. In this regard, the evaluation of cardiovascular effects of nanoplastics was performed in zebrafish embryos. The results indicated that the no observed adverse effect level (NOAEL) of nanoplastics is 50 µg/mL. The pericardial toxicity and hemodynamic changes were assessed by Albino (melanin allele) mutant zebrafish line. Severe pericardial edema was observed in zebrafish embryos after exposure to nanoplastics. At the concentration higher than NOAEL, nanoplastics significantly decreased the cardiac output (CO) and blood flow velocity. The fluorescence images manifested that the nanoplastics could inhibit the subintestinal angiogenesis of transgenic zebrafish embryos line Tg (fli-1: EGFP), which might disturb the cardiovascular formation and development. The resulting vascular endothelial dysfunction and hypercoagulable state of circulating blood further accelerated thrombosis. Reactive oxidative stress (ROS) and systemic inflammation were also found in Wild AB and Tg (mpo: GFP) zebrafish embryos, respectively. We also found many neutrophils recruiting in the tail vein where the zebrafish embryo thrombosis occurred. Our data suggested that nanoplastics could trigger the cardiovascular toxicity in zebrafish embryos, which could provide an essential clue for the safety assessment of nanoplastics.

Exposure to polydopamine nanoparticles induces neurotoxicity in the developing zebrafish.

Currently, the potential applications of polydopamine (PDA) nanoparticles in the biomedical field are being extensively studied, such as cell internalization, biocompatible surface modification, biological imaging, nano-drug delivery, cancer diagnosis, and treatment. However, the subsequent toxicological response to PDA nanoparticles, especially on nervous system damage was still largely unknown. In this regard, the evaluation of the neurotoxicity of PDA nanoparticles was performed in the developing zebrafish larvae. Results of the transmission electron microscope (TEM), diameter analysis, 1H NMR, and thermogravimetric analysis (TGA) indicated that PDA nanoparticles had high stability without any depolymerization; the maximum non-lethal dose (MNLD) and LD10 of PDA nanoparticles for zebrafish were determined to be 0.5 mg/mL and 4 mg/mL. Pericardial edema and uninflated swim bladders were observed in zebrafish larvae after exposure to PDA nanoparticles. At a concentration higher than MNLD, the fluorescence images manifested that the PDA nanoparticles could inhibit the axonal growth of peripheral motor neurons in zebrafish, which might affect the movement distances and speed, disturb the movement trace, finally resulting in impaired motor function. However, in further investigating the mechanism of PDA nanoparticles-induced neurotoxicity in zebrafish larvae, we did not find apoptosis of central neurocytes. Our data suggested that PDA nanoparticles might trigger neurotoxicity in zebrafish, which could provide an essential clue for the safety assessment of PDA nanoparticles.

Simulating highly disturbed vegetation distribution: the case of China's Jing-Jin-Ji region.

BACKGROUND: Simulating vegetation distribution is an effective method for identifying vegetation distribution patterns and trends. The primary goal of this study was to determine the best simulation method for a vegetation in an area that is heavily affected by human disturbance. METHODS: We used climate, topographic, and spectral data as the input variables for four machine learning models (random forest (RF), decision tree (DT), support vector machine (SVM), and maximum likelihood classification (MLC)) on three vegetation classification units (vegetation group (I), vegetation type (II), and formation and subformation (III)) in Jing-Jin-Ji, one of China's most developed regions. We used a total of 2,789 vegetation points for model training and 974 vegetation points for model assessment. RESULTS: Our results showed that the RF method was the best of the four models, as it could effectively simulate vegetation distribution in all three classification units. The DT method could only simulate vegetation distribution in units I and II, while the other two models could not simulate vegetation distribution in any of the units. Kappa coefficients indicated that the DT and RF methods had more accurate predictions for units I and II than for unit III. The three vegetation classification units were most affected by six variables: three climate variables (annual mean temperature, mean diurnal range, and annual precipitation), one geospatial variable (slope), and two spectral variables (Mid-infrared ratio of winter vegetation index and brightness index of summer vegetation index). Variables Combination 7, including annual mean temperature, annual precipitation, mean diurnal range and precipitation of driest month, produced the highest simulation accuracy. CONCLUSIONS: We determined that the RF model was the most effective for simulating vegetation distribution in all classification units present in the Jing-Jin-Ji region. The RF model produced high accuracy vegetation distributions in classification units I and II, but relatively low accuracy in classification unit III. Four climate variables were sufficient for vegetation distribution simulation in such region.

Mudstone creep experiment and nonlinear damage model study under cyclic disturbance load.

To study the creep characteristics of mudstone under disturbed load, creep rock triaxial compression disturbance tests under different disturbance amplitudes and frequencies are conducted using a self-made triaxial disturbed creep test bench for rock. The influence of different factors on the creep deformation law of each stage is analyzed. The results show that the disturbance effect has a significant impact on the creep properties of mudstone, and various factors have different effects on the creep stages. The instantaneous deformation variable, creep decay time, and steady creep rate change exponentially with the increase in axial pressure, and increase linearly with the increase in disturbance amplitude and disturbance frequency. The disturbance amplitude has a more significant effect on the instantaneous deformation, steady-state creep rate, and accelerated creep. According to the analysis of the test results, a nonlinear disturbance creep damage model based on Burger's model is established. The model is identified and calculated by the improved least squares method based on pattern search. The influence of different disturbance factors on the creep parameters is analyzed. The model fitting results and experimental results are compared to demonstrate that the model is used to simulate different disturbances. It was observed that rock creep under certain conditions exhibits certain adaptability. It is of great significance to carry out rock disturbance creep experiments and study the theory of disturbance creep to ensure the long-term stability of deep rock mass in complex environment.

Evaluating physiological changes of grass and semishrub species with seasonality for understanding the process of shrub encroachment in semiarid grasslands.

Shrub encroachment occurs worldwide, especially in arid and semiarid grasslands. Changes in soil water in different layers affect the process of shrub encroachment. Understanding the biological and physiological responses of plant species to shrub encroachment is essential for explaining shrub encroachment. The dominant species in six typical plant communities changed from Stipa bungeana Trin. to Artemisia ordosica Krasch., representing different shrub-encroached grasslands. The gravimetric soil water content (SWC) and enzyme and osmotic adjustment compounds of the dominant species across shrub encroachment stages and growing seasons were measured to explain the shrub encroachment. Results showed that SWC decreased and then increased during the growing seasons. With the process of shrub encroachment, SWC first increased, then decreased. With increasing soil depth, SWC increased or decreased. Across seasons with decreasing SWC, enzyme activity decreased and then increased, and malondialdehyde content and osmotic adjustment compounds increased. With the process of shrub encroachment, enzyme activity, malondialdehyde content and osmotic adjustment compounds increased or decreased. The two dominant species (S. bungeana and A. ordosica) enhanced their drought resistance abilities by regulating their antioxidant systems and osmotic adjustment compounds when soil water in a specific layer was not over the threshold. We recommend increasing the clay content to increase the water holding capacity in the surface soil layer to restore the zonal vegetation of S. bungeana.

Changes in levels of enzymes and osmotic adjustment compounds in key species and their relevance to vegetation succession in abandoned croplands of a semiarid sandy region.

Reclamation of cropland from grassland is regarded as a main reason for grassland degradation; understanding succession from abandoned cropland to grassland is thus crucial for vegetation restoration in arid and semiarid areas. Soil becomes dry when cropland is reverted to grassland, and enzyme and osmotic adjustment compounds may help plants to adapt to a drying environment. Croplands that were abandoned in various years on the Ordos Plateau in China, were selected for the analysis of the dynamics of enzymes and osmotic adjustment compounds in plant species during vegetation succession. With increasing number of years since abandonment, levels of superoxide dismutase increased in Stipa bungeana, first decreased and then increased in Lespedeza davurica and Artemisia frigida, and fluctuated in Heteropappus altaicus. Levels of peroxidase and catalase in the four species fluctuated; levels of proline, soluble sugar, and soluble protein either decreased or first increased and then generally decreased. According to a drought resistance index, the drought resistance of the four species was ranked in descending order as follows: S. bungeana > A. frigida > H. altaicus > L. davurica. The drought resistance ability of the different species was closely linked with vegetation succession from communities dominated by annual and biennial species (with main accompanying species of L. davurica and H. altaicus) to communities dominated by perennial species (S. bungeana and A. frigida) when soil became dry owing to increasing evapotranspiration after cropland abandonment. The restoration of S. bungeana steppe after cropland abandonment on the Ordos Plateau is recommended both as high-quality forage and for environmental sustainability.