A critical analysis of sources, pollution, and remediation of selenium, an emerging contaminant.

Selenium (Se) is an essential metalloid and is categorized as emerging anthropogenic contaminant released to the environment. The rise of Se release into the environment has raised concern about its bioaccumulation, toxicity, and potential to cause serious damages to aquatic and terrestrial ecosystem. Therefore, it is extremely important to monitor Se level in environment on a regular basis. Understanding Se release, anthropogenic sources, and environmental behavior is critical for developing an effective Se containment strategy. The ongoing efforts of Se remediation have mostly emphasized monitoring and remediation as an independent topics of research. However, our paper has integrated both by explaining the attributes of monitoring on effective scale followed by a candid review of widespread technological options available with specific focus on Se removal from environmental media. Another novel approach demonstrated in the article is the presentation of an overwhelming evidence of limitations that various researchers are confronted with to overcome achieving effective remediation. Furthermore, we followed a holistic approach to discuss ways to remediate Se for cleaner environment especially related to introducing weak magnetic field for ZVI reactivity enhancement. We linked this phenomenal process to electrokinetics and presented convincing facts in support of Se remediation, which has led to emerge 'membrane technology', as another viable option for remediation. Hence, an interesting, innovative and future oriented review is presented, which will undoubtedly seek attention from global researchers.

Metabolomics Reveal Nanoplastic-Induced Mitochondrial Damage in Human Liver and Lung Cells.

Plastic debris in the global biosphere is an increasing concern, and nanoplastic (NPs) toxicity in humans is far from being understood. Studies have indicated that NPs can affect mitochondria, but the underlying mechanisms remain unclear. The liver and lungs have important metabolic functions and are vulnerable to NP exposure. In this study, we investigated the effects of 80 nm NPs on mitochondrial functions and metabolic pathways in normal human hepatic (L02) cells and lung (BEAS-2B) cells. NP exposure did not induce mass cell death; however, transmission electron microscopy analysis showed that the NPs could enter the cells and cause mitochondrial damage, as evidenced by overproduction of mitochondrial reactive oxygen species, alterations in the mitochondrial membrane potential, and suppression of mitochondrial respiration. These alterations were observed at NP concentrations as low as 0.0125 mg/mL, which might be comparable to the environmental levels. Nontarget metabolomics confirmed that the most significantly impacted processes were mitochondrial-related. The metabolic function of L02 cells was more vulnerable to NP exposure than that of BEAS-2B cells, especially at low NP concentrations. This study identifies NP-induced mitochondrial dysfunction and metabolic toxicity pathways in target human cells, providing insight into the possibility of adverse outcomes in human health.

Emerging role of lncRNAs as mechanical signaling molecules in mechanotransduction and their association with Hippo-YAP signaling: a review. / LncRNAsåœ¨æœºæ¢°è½¬å¯¼ä¸­çš„ä½œç”¨åŠå ¶ä¸ŽHippo-YAPä¿¡å·è½¬å¯¼çš„å ³è”.

Cells within tissues are subject to various mechanical forces, including hydrostatic pressure, shear stress, compression, and tension. These mechanical stimuli can be converted into biochemical signals through mechanoreceptors or cytoskeleton-dependent response processes, shaping the microenvironment and maintaining cellular physiological balance. Several studies have demonstrated the roles of Yes-associated protein (YAP) and its homolog transcriptional coactivator with PDZ-binding motif (TAZ) as mechanotransducers, exerting dynamic influence on cellular phenotypes including differentiation and disease pathogenesis. This regulatory function entails the involvement of the cytoskeleton, nucleoskeleton, integrin, focal adhesions (FAs), and the integration of multiple signaling pathways, including extracellular signal-regulated kinase (ERK), wingless/integrated (WNT), and Hippo signaling. Furthermore, emerging evidence substantiates the implication of long non-coding RNAs (lncRNAs) as mechanosensitive molecules in cellular mechanotransduction. In this review, we discuss the mechanisms through which YAP/TAZ and lncRNAs serve as effectors in responding to mechanical stimuli. Additionally, we summarize and elaborate on the crucial signal molecules involved in mechanotransduction.

[The role of iron-uptake factor PiuB in pathogenicity of soybean pathogen Xanthomonas axonopodis pv. glycines].

Iron is an essential element for living organisms that plays critical roles in the process of bacterial growth and metabolism. However, it remains to be elucidated whether piuB encoding iron-uptake factor is involved in iron uptake and pathogenicity of Xanthomonas axonopodis pv. glycines (Xag). To investigate the function of piuB, we firstly generated a piuB deletion mutant (ΔpiuB) by homologous recombination. Compared with the wild-type, the piuB mutant exhibited significantly reduced growth and virulence in host soybean. The mutant displayed markedly increased siderophore secretory volume, and its sensitivity to Fe3+, Cu2+, Zn2+ and Mn2+ was significantly enhanced. Additionally, the H2O2 resistance, exopolysaccharide yield, biofilm formation, and cell mobility of ΔpiuB were significantly diminished compared to that of the wild-type. The addition of exogenous Fe3+ cannot effectively restore the above characteristics of ΔpiuB. However, expressing piuB in trans rescued the properties lost by ΔpiuB to the levels in the wild-type. Taken together, our results demonstrated that PiuB is a potential factor for Xag to assimilate Fe3+, and is necessary for Xag to be pathogenic in host soybean.

Proteome analysis develops novel plasma proteins classifier in predicting the mortality of COVID-19.

COVID-19 has been a global concern for 3 years, however, consecutive plasma protein changes in the disease course are currently unclear. Setting the mortality within 28 days of admission as the main clinical outcome, plasma samples were collected from patients in discovery and independent validation groups at different time points during the disease course. The whole patients were divided into death and survival groups according to their clinical outcomes. Proteomics and pathway/network analyses were used to find the differentially expressed proteins and pathways. Then, we used machine learning to develop a protein classifier which can predict the clinical outcomes of the patients with COVID-19 and help identify the high-risk patients. Finally, a classifier including C-reactive protein, extracellular matrix protein 1, insulin-like growth factor-binding protein complex acid labile subunit, E3 ubiquitin-protein ligase HECW1 and phosphatidylcholine-sterol acyltransferase was determined. The prediction value of the model was verified with an independent patient cohort. This novel model can realize early prediction of 28-day mortality of patients with COVID-19, with the area under curve 0.88 in discovery group and 0.80 in validation group, superior to 4C mortality and E-CURB65 scores. In total, this work revealed a potential protein classifier which can assist in predicting the outcomes of COVID-19 patients and providing new diagnostic directions.

Sensing of mitochondrial DNA by ZBP1 promotes RIPK3-mediated necroptosis and ferroptosis in response to diquat poisoning.

Diquat (DQ) poisoning is a severe medical condition associated with life-threatening implications and multiorgan dysfunction. Despite its clinical significance, the precise underlying mechanism remains inadequately understood. This study elucidates that DQ induces instability in the mitochondrial genome of endothelial cells, resulting in the accumulation of Z-form DNA. This process activates Z-DNA binding protein 1 (ZBP1), which then interacts with receptor-interacting protein kinase 3 (RIPK3), ultimately leading to RIPK3-dependent necroptotic and ferroptotic signaling cascades. Specific deletion of either Zbp1 or Ripk3 in endothelial cells simultaneously inhibits both necroptosis and ferroptosis. This dual inhibition significantly reduces organ damage and lowers mortality rate. Notably, our investigation reveals that RIPK3 has a dual role. It not only phosphorylates MLKL to induce necroptosis but also phosphorylates FSP1 to inhibit its enzymatic activity, promoting ferroptosis. The study further shows that deletion of mixed lineage kinase domain-like (Mlkl) and the augmentation of ferroptosis suppressor protein 1 (FSP1)-dependent non-canonical vitamin K cycling can provide partial protection against DQ-induced organ damage. Combining Mlkl deletion with vitamin K treatment demonstrates a heightened efficacy in ameliorating multiorgan damage and lethality induced by DQ. Taken together, this study identifies ZBP1 as a crucial sensor for DQ-induced mitochondrial Z-form DNA, initiating RIPK3-dependent necroptosis and ferroptosis. These findings suggest that targeting the ZBP1/RIPK3-dependent necroptotic and ferroptotic pathways could be a promising approach for drug interventions aimed at mitigating the adverse consequences of DQ poisoning.

Anti-aging effects of medicinal plants and their rapid screening using the nematode Caenorhabditis elegans.

BACKGROUND: Aging is the primary risk factor of most chronic diseases in humans, including cardiovascular diseases, osteoporosis and neurodegenerative diseases, which extensively damage the quality of life for elderly individuals. Aging is a multifaceted process with numerous factors affecting it. Efficient model organisms are essential for the research and development of anti-aging agents, particularly when investigating pharmacological mechanisms are needed. PURPOSE: This review discusses the application of Caenorhabditis elegans for studying aging and its related signaling pathways, and presents an overview of studies exploring the mechanism and screening of anti-aging agents in C. elegans. Additionally, the review summarizes related clinical trials of anti-aging agents to inspire the development of new medications. METHOD: Literature was searched, analyzed, and collected using PubMed, Web of Science, and Science Direct. The search terms used were "anti-aging", "medicinal plants", "synthetic compounds", "C. elegans", "signal pathway", etc. Several combinations of these keywords were used. Studies conducted in C. elegans or humans were included. Articles were excluded, if they were on studies conducted in silico or in vitro or could not offer effective data. RESULTS: Four compounds mainly derived through synthesis (metformin, rapamycin, nicotinamide mononucleotide, alpha-ketoglutarate) and four active ingredients chiefly obtained from plants (resveratrol, quercetin, Astragalus polysaccharide, ginsenosides) are introduced emphatically. These compounds and active ingredients exhibit potential anti-aging effects in preclinical and clinical studies. The screening of these anti-aging agents and the investigation of their pharmacological mechanisms can benefit from the use of C. elegans. CONCLUSION: Medicinal plants provide valuable resource for the treatment of diseases. A wide source of raw materials for the particular plant medicinal compounds having anti-aging effects meet diverse pharmaceutical requirements, such as immunomodulatory, anti-inflammation and alleviating oxidative stress. C. elegans possesses advantages in scientific research including short life cycle, small size, easy maintenance, genetic tractability and conserved biological processes related to aging. C. elegans can be used for the efficient and rapid evaluation of compounds with the potential to slow down aging.

High-throughput profiling of RNA modifications by ultra-performance liquid chromatography coupled to complementary mass spectrometry: Methods, quality control, and applications.

Although next-generation sequencing technology has been used to delineate RNA modifications in recent years, the paucity of appropriate converting reactions or specific antibodies impedes the accurate characterization and quantification of numerous RNA modifications, especially when these modifications demonstrate wide variations across developmental stages and cell types. In this study, we developed a high-throughput analytical platform coupling ultra-performance liquid chromatograph (UPLC) with complementary mass spectrometry (MS) to identify and quantify RNA modifications in both synthetic and biological samples. Sixty-four types of RNA modifications, including positional isomers and hypermodified ribonucleosides, were successfully monitored within a 16-min single run of UPLC-MS. Two independent methods to cross-validate the purity of RNA extracted from Caenorhabditis elegans (C. elegans) were developed using the coexisting C. elegans and Escherichia coli (E. coli) as a surveillance system. To test the validity of the method, we investigated the RNA modification landscape of three model organisms, C. elegans, E. coli, and Arabidopsis thaliana (A. thaliana). Both the identity and molarity of modified ribonucleosides markedly varied among the species. Moreover, our platform is not only useful for exploring the dynamics of RNA modifications in response to environmental cues (e.g., cold shock) but can also help with the identification of RNA-modifying enzymes in genetic studies. Cumulatively, our method presents a novel platform for the comprehensive analysis of RNA modifications, which will be of benefit to both analytical chemists involved in biomarker discovery and biologists conducting functional studies of RNA modifications.

LncRNA modulates Hippo-YAP signaling to reprogram iron metabolism.

Iron metabolism dysregulation is tightly associated with cancer development. But the underlying mechanisms remain poorly understood. Increasing evidence has shown that long noncoding RNAs (lncRNAs) participate in various metabolic processes via integrating signaling pathway. In this study, we revealed one iron-triggered lncRNA, one target of YAP, LncRIM (LncRNA Related to Iron Metabolism, also named ZBED5-AS1 and Loc729013), which effectively links the Hippo pathway to iron metabolism and is largely independent on IRP2. Mechanically, LncRIM directly binds NF2 to inhibit NF2-LATS1 interaction, which causes YAP activation and increases intracellular iron level via DMT1 and TFR1. Additionally, LncRIM-NF2 axis mediates cellular iron metabolism dependent on the Hippo pathway. Clinically, high expression of LncRIM correlates with poor patient survival, suggesting its potential use as a biomarker and therapeutic target. Taken together, our study demonstrated a novel mechanism in which LncRIM-NF2 axis facilitates iron-mediated feedback loop to hyperactivate YAP and promote breast cancer development.

Perceived accessibility and mental health consequences of COVID-19 containment policies.

BACKGROUND: Individuals have experienced various degrees of accessibility loss during the COVID-19 pandemic, which may consequently have influenced their mental health. Although efforts have been made to understand the mental health consequences of the pandemic and corresponding containment measures, the impacts of accessibility loss remain underexplored. METHODS: Based on 186 family interviews, a 569-respondent panel survey was designed and distributed monthly from February to October 2020 in Kunming, China. A 3-wave cross-lagged panel model was developed to understand the causal relationship between mental health and perceived accessibility of daily necessities, key services, and social activities. RESULTS: Goodness-of-fit indicators imply that the hypothesised model fits the observed data well: χ2/df = 2.221, AGFI = 0.910, NFI = 0.907, CFI = 0.933, RMSEA = 0.052. The results indicate that perceived accessibility of daily necessities and social activities had lagged effects on mental health status. The within-wave effects show that perceived accessibility of daily necessities (0.619, p < 0.01) and social activities (0.545, p < 0.01) significantly influenced respondents' mental health during the peak of the pandemic whilst perceived accessibility of social activities dominantly influenced their mental health after restrictions were lifted (0.779, p < 0.01). Perceived accessibility of public services such as healthcare did not significantly influence respondents' mental health in any wave. COVID-19 containment policies had different mental outcomes across population groups. Disadvantaged people experienced mental health issues due to accessibility loss for daily necessities and social activities until the lifting of compulsory QR-code-for-buses, whilst better-off populations had better mental health during the early phase of the outbreak and rapidly recovered their mental health after mobility restrictions eased. CONCLUSION: Reduced perceived accessibility of daily necessities and social activities may be an underlying cause of mental health problems. Relative accessibility deprivation exacerbated mental health inequities during the COVID-19 pandemic.

Impact of change in traffic flow on vehicle non-exhaust PM2.5 and PM10 emissions: A case study of the M25 motorway, UK.

This study quantifies the change in traffic flow on the M25 motorway in the UK due to the COVID-19 outbreak. Moreover, the impact of the change in traffic flow on non-exhaust PM2.5 and PM10 emissions for different categories of vehicle was explored. During the year of the COVID-19 outbreak (March 2020 to February 2021), the total traffic flows of passenger cars (PCs), light goods vehicles (LGVs), heavy goods vehicles (HGVs), and long HGVs on the M25 motorway decreased by 38.6%, 27.6%, 15.9% and 7.2%, respectively, in comparison to the previous year. Correspondingly, the total mass of non-exhaust emissions (PM2.5 and PM10) of PCs, LGVs, HGVs, and long HGVs reduced by 38.7%, 27.3%, 16.2% and 7%, respectively. The traffic flows per year before and during the COVID-19 outbreak of long HGVs were 87.2% and 80.7% less than those of PCs. Correspondingly, the long HGVs emitted 10.2% less but 36.3% more PM2.5 emissions, as well as 10.9% and 66.7% more PM10 emissions than the latter, indicating that long HGVs contribute much more to non-exhaust particles than PCs. In addition, it was found that resuspension of road dust on the M25 motorway was the largest contributor to air pollution among non-exhaust emissions, followed by road wear, tyre wear, and brake wear particles.

Toxic chemicals from uncontrolled e-waste recycling: Exposure, body burden, health impact.

Uncontrolled electronic-waste (e-waste) recycling processes have induced serious environmental pollution and human health impacts. This paper reviewed studies on the wide range of toxic chemicals through the use of primitive recycling techniques, their transfer to various ecological compartments, and subsequent health impacts. Results indicated that local food items were heavily polluted by the pollutants emitted, notably heavy metals in vegetables, rice, fish and seafood, and persistent organic pollutants (POPs) in livestock. Dietary exposure is the most important exposure pathway. The associations between exposure to e-waste and high body burdens of these pollutants were evident. It seems apparent that toxic chemicals emitted from e-waste activities are causing a number of major illnesses related to cardiovascular, digestive and respiratory systems, according to the information provided by a local hospital (Taizhou, an e-waste recycling hot spot in China). More epidemiological data should be made available to the general public. It is envisaged that there are potential dangers of toxic chemicals passing on to the next generation via placental transfer and lactation. There is a need to monitor the development and health impacts of infants and children, born and brought up in the e-waste sites.

Metabolomics and proteomics study reveals the effects of benzo[a]pyrene on the viability and migration of KYSE-150 esophageal cells.

A representative polycyclic aromatic hydrocarbon, benzo[a]pyrene (B[a]P), has been widely detected in environmental compartments and is highly carcinogenic to humans. Oral ingestion of B[a]P is the dominant exposure pathway. The esophagus acts as the first contact point when B[a]P enters the human body. However, its role in the development of human esophageal cancer is rarely discussed. Herein, we employed untargeted metabolomics in combination with proteomics to explore B[a]P-related intracellular responses in human esophageal cell lines. Our results demonstrated that B[a]P exposure induced significant metabolic disorders, further leading to overproduction of reactive oxygen species (ROS) and disturbance of the cellular viability process and migration ability of esophageal cells. In response, glutathione (GSH) was consumed to meet the demand for cellular detoxification, and thioredoxin (TXN) was upregulated to balance the cellular redox. These alterations caused the reregulation of some specific protein families, including S100A proteins, ribosomal proteins, and histone H1 proteins. Such changes impeded the viability and migration of esophageal cells, which could adversely affect wound healing of the epithelium. These cellular responses indicate that B[a]P will cause serious cellular damage to esophageal cells and increase the carcinogenic risk even as a result of short-term exposure. SYNOPSIS: Our omics study demonstrated how benzo[a]pyrene hampered the migration of esophageal cells and proposed a plausible mechanism underlying its carcinogenicity, which may contribute to our understanding of environmental pollutants.

Absorption, distribution, metabolism, excretion and toxicity of microplastics in the human body and health implications.

Microplastics (MPs; <5 mm) in the biosphere draws public concern about their potential health impacts. Humans are potentially exposed to MPs via ingestion, inhalation, and dermal contact. Ingestion and inhalation are the two major exposure pathways. An adult may consume approximately 5.1 × 103 items from table salts and up to 4.1 × 104 items via drinking water annually. Meanwhile, MP inhalation intake ranges from 0.9 × 104 to 7.9 × 104 items per year. The intake of MPs would be further distributed in different tissues and organs of humans depending on their sizes. The excretion has been discussed with the possible clearance ways (e.g., urine and feces). The review summarized the absorption, distribution, metabolic toxicity and excretion of MPs together with the attached chemicals. Moreover, the potential implications on humans are also discussed from in vitro and in vivo studies, and connecting the relationship between the physicochemical properties and the potential risks. This review will contribute to a better understanding of MPs as culprits and/or vectors linking to potential human health hazards, which will help outline the promising areas for further revealing the possible toxicity pathways.

Environmental emission, fate and transformation of microplastics in biotic and abiotic compartments: Global status, recent advances and future perspectives.

The intensive use and wide-ranging application of plastic- and plastic-derived products have resulted in alarming levels of plastic pollution in different environmental compartments worldwide. As a result of various biogeochemical mechanisms, this plastic litter is converted into small, ubiquitous and persistent fragments called microplastics (<5 mm), which are of significant and increasing concern to the scientific community. Microplastics have spread across the globe and now exist in virtually all environmental compartments (the soil, atmosphere, and water). Although these compartments are often considered to be independent environments, in reality, they are very closely linked. Ample research has been done on microplastics, but there are still questions and knowledge gaps regarding the emission, occurrence, distribution, detection, environmental fate and transport of MPs in different environmental compartments. The current article is intended to provide a systematic overview of MP emissions, pollution conditions, sampling and analytical approaches, transport, fates and transformation mechanisms in different environmental compartments. It also identifies research gaps and future research directions and perspectives.

Improved Calculation Model for the Shortest Spontaneous Combustion Period.

Disasters caused by the spontaneous combustion of coal have occurred in major coal-producing countries, resulting in the loss of resources and human life and severe environmental pollution. The development of an efficient model to calculate the shortest spontaneous combustion period (SSCP) has been a long-standing challenge. In this study, we propose a continuous model that calculates the SSCP by changing the traditional time summation form into a time integration form. The proposed model can reduce the calculation errors and determine the heating time to any temperature, which overcomes the limitations of the traditional model. The accuracy and convenience of the improved model were validated through a comparison with the results of the traditional model and a numerical model. The parameter sensitivities were analyzed in the improved model. The results showed that the SSCPs calculated using the improved continuous model are in good agreement with those of the traditional and numerical models. The results also indicated that the continuous model is more accurate and convenient than the traditional model. Parameters such as the heat release intensity, water content, specific heat capacity, and gas content influence the SSCP results in the sensitivity analysis. This model can potentially help prevent and control the risk of coal spontaneous combustion and should be further tested in practical mine management.