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• The transcriptome characteristics of CSDS were more focused on neuronal and synapse. • The transcriptome characteristics of FMT were more focused on inflammation. • The common transcriptome characteristics of two models was energy metabolism. • The CSDS had large more alternative splicing events than FMT. Depression is a complex disorder with multiple contributing factors, and chronic stress has previously been recognized as a major causative factor, while gut microbes have also been found to be involved in depression recently. However, gene expression in depression models with different etiologies is unclear. Here, we compared the transcriptomes of the striatum in chronic social defeat stress (CSDS) model of C57BL/6J male mice and fecal microbiota transplant (FMT) model of Kumming male mice. We found that the proportion of shared differentially expressed genes (DEGs) between the two models was only 24 %. The specific DEGs of FMT model were enriched in immune and inflammatory, and are associated with changes in vascular and ciliated ependymal cells. The specific DEGs of CSDS model were enriched in neuron and synapse. The results of network analysis suggested the expression patterns and biological function of depressive-like behaviors-related modules in the two models are different. Further, the alternative splicing events of CSDS are more than FMT. Our results suggested models of depression induced by different etiologies differ significantly in gene expression and biological function. Our study also suggested us to pay attention to the characteristics of models of depression of different etiologies and provided a more comprehensive understanding of the heterogeneity of depression. [ABSTRACT FROM AUTHOR]

This paper presents a multi-objective optimization model for a green supply chain management scheme that minimizes the inherent risk occurred by hazardous materials, associated carbon emission and economic cost. The model related parameters are capitalized on a big data analysis. Three scenarios are proposed to improve green supply chain management. The first scenario divides optimization into three options: the first involves minimizing risk and then dealing with carbon emissions (and thus economic cost); the second minimizes both risk and carbon emissions first, with the ultimate goal of minimizing overall cost; and the third option attempts to minimize risk, carbon emissions, and economic cost simultaneously. This paper provides a case study to verify the optimization model. Finally, the limitations of this research and approach are discussed to lay a foundation for further improvement. [ABSTRACT FROM AUTHOR]

Di-2-Ethylhexyl Phthalate (DEHP) is often used as an additive in polyvinyl chloride (PVC) to give plastics flexibility, which makes DEHP widely used in food packaging, daily necessities, medical equipment, and other products. However, due to the unstable combination of DEHP and polymer, it will migrate to the environment in the materials and eventually contact the human body. It has been recorded that low-dose DEHP will increase neurotoxicity in the nervous system, and the human health effects of DEHP have been paid attention to because of the extensive exposure to DEHP and its high absorption during brain development. In this study, we review the evidence that DEHP exposure is associated with neurodevelopmental abnormalities and neurological diseases based on human epidemiological and animal behavioral studies. Besides, we also summarized the oxidative damage, apoptosis, and signal transduction disorder related to neurobehavioral abnormalities and nerve injury, and described the potential mechanisms of neurotoxicity caused by DEHP. Overall, we found exposure to DEHP during the critical developmental period will increase the risk of neurobehavioral abnormalities, depression, and autism spectrum disorders. This effect is sex-specific and will continue to adulthood and even have an intergenerational effect. However, the research results on the sex-dependence of DEHP neurotoxicity are inconsistent, and there is a lack of systematic mechanisms research as theoretical support. Future investigations need to be carried out in a large-scale population and model organisms to produce more consistent and convincing results. And we emphasize the importance of mechanism research, which can enhance the understanding of the environmental and human health risks of DEHP exposure. [Display omitted] • DEHP is more likely to cause neurotoxicity to humans and animals in early life. • The neurotoxicity of DEHP has sex-specific, long-term, and transgenerational effects. • Oxidative stress and apoptosis are the main mechanisms to cause DEHP neurotoxicity. • DEHP can cause nerve cell abnormal enzyme activity and ion channel imbalance. • Nerve cell damage is one of the important reasons for DEHP neurotoxicity. [ABSTRACT FROM AUTHOR]

[Display omitted] • AhR gene plays an important role in maintaining the migration ability of glioblastoma. • TCDD and FICZ inhibit the migration of glioblastoma through AhR pathway. • IL24 is a downstream gene of AhR pathway in glioblastoma cells. • AhR agonists inhibit the migration of glioblastoma by up-regulated IL24 expression. Cancer occurrence and development are closely related to the environment. Aryl hydrocarbon receptor (AhR) is an important receptor mediating the toxic effects of many environmental compounds, and is also involved in regulating tumor cell migration. Glioblastoma is the most malignant glioma and exhibits high motility, but the effects of AhR on the migration of glioblastoma are still unclear. We aimed to understand the role of AhR in the migration of this type of tumor cell and to explore the underlying molecular mechanism. In cultured human neuroblastoma cells (U87), we found that AhR overexpression or knockdown increased or suppressed the migration ability of U87 cells, respectively. Furthermore, inhibition of basal activation of the AhR pathway suppressed migration ability, suggesting a positive correlation between endogenous activity of the AhR pathway and cell migration. When the AhR pathway was activated by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 6-formyl [3,2-b] carbazole (FICZ), the migration of U87 cells was inhibited by inducing the expression of a tumor suppressor, IL24, which is a downstream responsive gene of AhR activation. Moreover, a similar AhR-IL24-dependent mechanism for migration inhibition of TCDD was documented in a breast cancer cell line and a lung cancer cell line. This study demonstrated that AhR plays important roles in regulating the migration of glioblastoma, and the induction of the AhR-IL24 axis mediates the inhibition of migration in response to TCDD or FICZ treatment. [ABSTRACT FROM AUTHOR]

• Intranasal exposure to ZnO NPs affect cholinergic neurotransmission in rat brain. • The release of key neurotransmitter acetylcholine (ACh) is increased. • ACh synthesis is enhanced and the vesicular ACh transporter is upregulated. • AChE activity is suppressed by Zn-AChE interaction or a down-regulation mechanism. • The observed biological effects are mainly derived from released Zn2+. The neurotoxicity of inhaled ZnO nanoparticles (NPs) and the underlying mechanisms remain largely unknown. In this study, ZnO NPs (30 ± 6 nm) were intranasally instilled to rats via a single dose (13 mg Zn/kg BW), with ZnSO 4 as the ionic control, and analysis 7-days post exposure. The hippocampus was found to be the main target for Zn accumulation for both ZnO NPs and ZnSO 4. Synchrotron radiation based X-ray absorption fine structure (XAFS) analysis showed that no particulate ZnO was found, suggesting the occurrence of dissolution and transformation of ZnO NPs. Multi-omics analysis, including transcriptomics, proteomics and metabolomics, demonstrated that cholinergic neurotransmission was the main biological process affected following both treatments. The release of the key neurotransmitter acetylcholine (ACh) was increased by enhanced ACh synthesis, upregulation of vesicular ACh transporter, and suppression of the activity of ACh hydrolysis enzyme (AChE), either by direct Zn-AChE interaction or a transcriptional down-regulation mechanism. In addition, ZnO NPs and ZnSO 4 induced similar molecular consequences and exhibited the same Zn chemical speciation (100 % of Zn complexes) in the hippocampal region evidenced by XAFS analysis, suggesting that the observed biological effects were mainly derived from Zn2+ released from the ZnO NPs. This study not only evidences a new pathway for the impact of ZnO NPs on the brain, but also identifies the origin of the impact as ionic Zn, which provides the basis for safe-by-design of ZnO NPs. [ABSTRACT FROM AUTHOR]

Biological rhythms denote the cyclical patterns of life activities anchored to a 24-hour cycle. Research shows that depression exhibits disturbances in biological rhythms. Yet, the relationship between these biological rhythms and concomitant anxiety symptoms is insufficiently investigated in structured clinical assessments. This multicenter study, carried out in four Chinese hospitals, comprehensively examined the relationship between anxiety and disruptions in biological rhythms among patients with depression. The study encompassed 218 patients diagnosed with depression and 205 matched healthy controls. The Chinese version of the Biological Rhythms Interview of Assessment in Neuropsychiatry was utilized to evaluate the participants' biological rhythms, focusing on four dimensions: sleep, activity, social, and diet. In patients with depression, there is a significant positive correlation between the severity of anxiety symptoms and the disturbances in biological rhythms. The severity of anxiety and depression, along with the quality of life, are independently associated with disruptions in biological rhythms. The mediation model reveals that anxiety symptoms mediate the relationship between depressive symptoms and biological rhythms. This research highlights the role of anxiety within the spectrum of depressive disorders and the associated disturbances in biological rhythms. Our findings shed light on potential pathways towards more targeted preventive strategies and therapeutic interventions for individuals battling depression and anxiety. [ABSTRACT FROM AUTHOR]

This study aims to explore consumers' perception, their purchase intention and willingness to pay for carbon-labeled products through a questionnaire survey. By taking Chengdu as a case study city, the results show that urban consumers had an overall low perception on carbon-labeled products. While most consumers indicated their intentions to buy carbon labeled products, the level of product premium they were willing to accept was relatively low. The acceptance level on such low carbon products had a significant impact on consumers' perception on carbon-labeled products. Perceived benefits significantly influenced purchase intention in relation to carbon-labeled products. Perceived consumers’ effectiveness, occupation, and income level had a significant effect on the willingness to pay for carbon-labeled products. From policy point of view, this study may provide valuable policy insights to develop a carbon labeling system and promote carbon-labeled products in China so that low-carbon consumption can be fostered in the future. [ABSTRACT FROM AUTHOR]

This study explores the transformation of peanut shells, an abundant agricultural waste, into high-efficiency activated carbon for CO 2 capture using a two-step pyrolysis and K 2 CO 3 activation method. Observations indicated that with an increasing impregnation ratio, the activated carbon demonstrates remarkable improvements in structural properties, achieving specific surface areas and pore volumes of 1150.02 m2/g and 0.46 cm3/g, respectively. Among the prepared samples, the activated carbon obtained with a peanut shell to K 2 CO 3 impregnation mass ratio of 1:2 exhibits superior CO 2 adsorption capacity at 1 bar, with values of 3.76 mmol/g at 25 °C and 5.70 mmol/g at 0 °C. The CO 2 adsorption isotherms of the activated carbon conform to the Langmuir and Freundlich models. These results demonstrate the potential of this method in addressing environmental concerns, particularly in mitigating CO 2 emissions, and highlight the broader application prospects of biomass-derived activated carbon in environmental management. • Activated carbon from peanut shells was prepared using a simple two-step method with K 2 CO 3 activation and high cyclic adsorption stability. • The maximum specific surface area of the sample reached 1150.02 m2/g and exhibited a high CO 2 adsorption capacity of 5.7 mmol/g. • Thermodynamic results indicate that the adsorption of CO 2 is physical adsorption and is an exothermic process. [ABSTRACT FROM AUTHOR]

Waste activated sludge (WAS) is generated continuously in sewage treatment plants (STPs) which requires ongoing treatment mode. Persulfate(PS)-based approaches have been demonstrated to stimulate VFAs production successfully via batch tests but whether they can be suitable to continuous flow is still unknown. Herein, the long-term performance of utilizing Persulfate(PS)-based approaches to promote volatile fatty acids (VFAs) production as well as the potential microbiological mechanisms are investigated and revealed. Results indicated that PS-based treatments stimulated stable acetic acid-enriched VFAs promotion by 3.1- and 14.1-fold that of the blank. The key genes for substrate metabolism (i.e., carbohydrates and amino acid metabolism), pyruvate metabolism (i.e., pdhA and aceE) and fatty acid biosynthesis (i.e., fabB and ACSL) were up-regulated by PS-based treatments via metagenomic analysis. The differential gene expression was primarily attributed to the variation of fermentative bacteria (i.e., Clostridium and Fonticella). Further explorations demonstrated that accompanied with more abundant bioavailable organics, the critical genes encoding oxidative defensive enzymes (i.e., SOD2 and katE) were activated to counteract the oxidative toxicity to anaerobes and maintain high metabolic functions in the PS-based treatment systems. This study provides the foundation for applying PS-based treatment to WAS treatment continuously. [Display omitted] • PS-based treatments induced VFAs promotion by 3.1-(PS) and 14.1-fold (PS/Fe) that of the control. • PS-based treatments could provide sufficient bioavailable organic matter continuously for microbial exploitation. • PS-based treatments promote the metabolic capacities of the primary substrates. • PS-based treatments up-regulated the key genes related to VFAs biosynthesis. • The antioxidant system was activated by PS-based treatments to maintain bacterial activity. [ABSTRACT FROM AUTHOR]

[Display omitted] • Urea exhibits dose-dependent effects on VFAs biosynthesis. • The urea and generated FA promote SS solubilization and hydrolysis. • Urea contributed to the enrichment of hydrolytic and acidogenic microbes. • Urea promoted microbial functional traits related to VFAs production. Herein, a cost-effective method for improving the anaerobic fermentation performance of sewage sludge (SS) is proposed. The highest volatile fatty acids (VFAs) reached up to 5550 mg COD/L with the supplementation of 0.2 g urea/g total suspended solids (TSS). Intensive exploration showed that SS decomposition was profoundly triggered by urea and the free ammonia generated due to the hydrolysis of urea, providing adequately bioaccessible substrates for acidogenic reactions and thus contributing to VFAs formation. Microbial composition analysis indicated that functional bacteria (i.e., Tissierella and Clostridium) associated with VFAs generation were enriched. Moreover, the metabolic activities of functional flora (i.e., membrane transport and fatty acid synthesis) were up-regulated due to the stimulation of urea. In general, the increase in bioavailable organic matter and functional microbes, and thus the increased microbial metabolic activities, improved the efficient production of VFAs. This study could provide a cost-effective approach for resource recovery from SS. [ABSTRACT FROM AUTHOR]

Abstract Autism spectrum disorder (ASD) has emerged as a major public health concern due to its fast-growing prevalence in recent decades. Environmental factors are thought to contribute substantially to the variance in ASD. Interest in environmental toxins as causes of ASD has arisen due to the high sensitivity of the developing human brain to toxic chemicals, particularly to dioxin and certain dioxin-like compounds (dioxins). As a group of typical persistent organic pollutants, dioxins have been found to exert adverse effects on human brain development. In this paper, we review the evidence for association of exposure to dioxins with neurodevelopmental abnormalities related to ASD based on both human epidemiological and animal studies. It has been documented that exposure to dioxins during critical developmental periods increased risk for ASD. This notion has been demonstrated in different populations exposed to high or background level of dioxins. Furthermore, the effects and mechanisms of action of dioxins relevant to the pathophysiology and pathogenesis of ASD are summarized, describing potential underlying mechanisms linking dioxin exposure with ASD onset. Further studies focusing on effects of prenatal/perinatal exposure to individual dioxin congeners or to mixtures of dioxins on ASD-associated behavioral and neurobiological consequences in animal models, and on the mechanisms of actions of dioxins, are needed in order to better understand how dioxin exposure might contribute to increased risk for ASD. Highlights • Human and animal studies indicate association of dioxin exposure with ASD. • Dioxin exposure is related to ASD pathophysiology. • Dioxin exposure is related to ASD pathogenesis. [ABSTRACT FROM AUTHOR]

Major depressive disorder, with serious impairment in cognitive and social functioning, is a complex psychiatric disorder characterized by pervasive and persistent low mood and a loss of interest or pleasure. However, the underlying molecular mechanisms of depression remain largely unknown. In this study, we used a non-targeted metabolomics approach based on gas chromatography–mass spectrometry of the prefrontal cortex in chronic restraint stress (CRS)-treated rats. CRS was induced in the stress group by restraining rats in a plastic restrainer for 6 h every day. This stress paradigm continued for 21 days. Body weight measurement and behavior tests were applied, including the sucrose preference test for anhedonia, the forced swimming test for despair-like behavior, and open field test and the elevated plus-maze to test for anxiety-like behaviors in rats after CRS. Differentially expressed metabolites associated with CRS-treated rats were identified by combining multivariate and univariate statistical analysis and corrected for multiple testing using the Benjamini-Hochberg procedure. A heat map of differential metabolites was constructed using Matlab. Ingenuity Pathways Analysis was applied to identify the predicted pathways and biological functions relevant to the bio-molecules of interest. Our findings showed that CRS induces depression-like behaviors and not anxiety-like behaviors. Thirty-six metabolites were identified as potential depression biomarkers involved in amino acid metabolism, energy metabolism and lipid metabolism, as well as a disturbance in neurotransmitters. Consequently, this study provides useful insights into the molecular mechanisms of depression. [ABSTRACT FROM AUTHOR]

• Intranasal exposure to ZnO NPs induced accumulation of Zn in liver of rat. • No accumulation of Zn in liver was found in ZnSO 4 treatment. • Persistence of NPs in liver 7 days post exposure was revealed by XAFS. • More and distinct metabolites in liver were altered by ZnO NPs than by ZnSO 4. • ZnO NPs induced particle-specific effects revealed by metabolomics. Toxicity of ZnO nanoparticles (NPs) are often related to the release of Zn2+ ions due to their dissolution. Studies also suggest that the toxicity of ZnO NPs cannot be solely explained by the release of Zn2+ ions; however, there is a lack of direct evidence of ZnO particulate effects. This study compared the acute toxicity of ZnO NPs and ZnSO 4 following intranasal exposure using a combination of metallomics and metabolomics approaches. Significant accumulation of Zn in the liver was only found in the ZnO NP treatment, with 29% of the newly accumulated Zn in the form of ZnO as revealed by X-ray fine structure spectroscopy (XAFS). This is the first direct evidence suggesting the persistence of ZnO NPs in liver upon intranasal exposure. Although both ZnO NPs and ZnSO 4 altered the metabolite profiles, with some overlaps and considerable specificity, of both liver and plasma samples, more and distinct metabolites in the liver and opposite effects in the plasma were altered by ZnO NPs compared with ZnSO 4 , consistent with no accumulation of Zn detected in liver from ZnSO 4. Specifically, a large number of antioxidant-related compounds and energetic substrates were exclusively elevated in the liver of ZnO NP-treated animals. These findings provided direct evidence that persistence of ZnO NPs induced particle-specific effects on the antioxidant systems and energy metabolism pathways. [ABSTRACT FROM AUTHOR]

• Dioxin upregulates the expression of NFL gene and protein in neuronal cells. • Dioxin leads to NFL protein accumulation in the cytoplasm of neurons. • AhR pathway interacts with the MAPK pathway in the nervous system. • Dioxin upregulates NFL via AhR mediated enhancement of ERK1/2 MAPK pathway. Dioxin exposure is reported to affect nervous system development and increase the risk of neurodegenerative diseases. Generally, dioxin exerts its neurotoxicity via aryl hydrocarbon receptor (AhR). Neurofilament (NF) light (NFL) protein is a biomarker for both neuronal differentiation and neurodegeneration and its expression is controlled by the mitogen-activated protein kinase (MAPK) pathway. However, the effects of dioxin on NFL expression and involved mechanisms are incompletely understood. We aimed to investigate the effects of 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) on NFL expression and elucidate the underlining signaling pathways and their potential crosstalk, specifically between MAPK and AhR pathway. We employed primary cultured rat cortical neurons to evaluate the effect of TCDD exposure on NFL expression. We also used nerve growth factor (NGF)-treated PC12 cells with specific inhibitors to investigate the involvement of and potential crosstalk between the MAPK pathway and the AhR pathway in mediating the effects of TCDD on NFL expression. After TCDD exposure, NFL mRNA and protein levels were upregulated in cultured neurons. NFL protein was preferentially found in the cell body compared with neurites of the cultured neurons. In PC12 cells, TCDD enhanced both NGF-induced NFL expression and phosphorylation of ERK1/2 and p38. The addition of MAPK-pathway inhibitors (PD98059 and SB230580) partially blocked the TCDD-induced NFL upregulation. CH223191, an AhR antagonist, reversed the upregulation of NFL and phosphorylation of ERK1/2 and p38 induced by TCDD. This study demonstrated TCDD-induced upregulation of NFL in cultured neurons, with protein retained in the cell body. TCDD action was dependent on activation of AhR and MAPK, while crosstalk was found between these two signaling pathways. [ABSTRACT FROM AUTHOR]