Reconstructing the electron and spin structures of nanoscale iron sulfide through a biosurfactant layer towards radical-nonradical co-dominant regime.

Radical-nonradical co-dominant pathways have become a hot topic in advanced oxidation, but achieving this on transition metal sulfides (TMS) remains challenging because their inherently higher electron and spin densities always induce radicals rather than nonradicals. Herein, a biosurfactant layer (BLR) was introduced to redistribute the electron and spin structure of nanoscale iron sulfide (FeS), which allowed both radical and nonradical to co-dominate the catalytic reaction. The resulting BLR-encased FeS hybrid (BLR@FeS) exhibited satisfactory removal efficiency (98.5 %) for hydrogen peroxide (H2O2) activation, outperforming both the constituent components [FeS (70.9 %) and BLR (86.2 %)]. Advanced characterizations showed that C, O, N-related sites (-CO and -NC) in BLR attracted electrons in FeS due to their strong electronegativity and electron-withdrawing capacity, which not only decreased electron density in FeS, but also resulted in a shift of the Fe/S sites from the high-spin to the medium-spin state. The reaction routes established by the BLR@FeS/H2O2 system maintained desirable stability against environmental interferences such as common inorganic anions, humic acid and changes in pH. Our study provides a state-of-the-art, molecule-level understanding of tunable co-dominant pathways and expands the targeted applications in the field of advanced oxidation.

Novel Mouse Model of Myocardial Infarction, Plaque Rupture, and Stroke Shows Improved Survival With Myeloperoxidase Inhibition.

BACKGROUND: Thromboembolic events, including myocardial infarction (MI) or stroke, caused by the rupture or erosion of unstable atherosclerotic plaques are the leading cause of death worldwide. Although most mouse models of atherosclerosis develop lesions in the aorta and carotid arteries, they do not develop advanced coronary artery lesions. Moreover, they do not undergo spontaneous plaque rupture with MI and stroke or do so at such a low frequency that they are not viable experimental models to study late-stage thrombotic events or to identify novel therapeutic approaches for treating atherosclerotic disease. This has stymied the development of more effective therapeutic approaches for reducing these events beyond what has been achieved with aggressive lipid lowering. Here, we describe a diet-inducible mouse model that develops widespread advanced atherosclerosis in coronary, brachiocephalic, and carotid arteries with plaque rupture, MI, and stroke. METHODS: We characterized a novel mouse model with a C-terminal mutation in the scavenger receptor class B, type 1 (SR-BI), combined with Ldlr knockout (designated SR-BI∆CT/∆CT/Ldlr-/-). Mice were fed Western diet (WD) for 26 weeks and analyzed for MI and stroke. Coronary, brachiocephalic, and carotid arteries were analyzed for atherosclerotic lesions and indices of plaque stability. To validate the utility of this model, SR-BI∆CT/∆CT/Ldlr-/- mice were treated with the drug candidate AZM198, which inhibits myeloperoxidase, an enzyme produced by activated neutrophils that predicts rupture of human atherosclerotic lesions. RESULTS: SR-BI∆CT/∆CT/Ldlr-/- mice show high (>80%) mortality rates after 26 weeks of WD feeding because of major adverse cardiovascular events, including spontaneous plaque rupture with MI and stroke. Moreover, WD-fed SR-BI∆CT/∆CT/Ldlr-/- mice displayed elevated circulating high-sensitivity cardiac troponin I and increased neutrophil extracellular trap formation within lesions compared with control mice. Treatment of WD-fed SR-BI∆CT/∆CT/Ldlr-/- mice with AZM198 showed remarkable benefits, including >90% improvement in survival and >60% decrease in the incidence of plaque rupture, MI, and stroke, in conjunction with decreased circulating high-sensitivity cardiac troponin I and reduced neutrophil extracellular trap formation within lesions. CONCLUSIONS: WD-fed SR-BI∆CT/∆CT/Ldlr-/- mice more closely replicate late-stage clinical events of advanced human atherosclerotic disease than previous models and can be used to identify and test potential new therapeutic agents to prevent major adverse cardiac events.

A qualitative exploration of facilitators and barriers to adopting a healthy lifestyle among Black, Hispanic, and American Indian males with diabetes or at risk for type 2 diabetes.

OBJECTIVES: Higher prevalence of several chronic diseases occurs in men in the United States, including diabetes and prediabetes. Of the 34 million adults with diabetes and 88 million with prediabetes there is a higher prevalence of both conditions in men compared to women. Black, Hispanic, and American Indian men have some of the highest rates of diabetes and diabetes complications. Adopting a healthy lifestyle including healthy eating and physical activity, is important in preventing type 2 diabetes and diabetes complications. DESIGN: This study included six focus groups that explored facilitators and barriers to adopting a healthy lifestyle in Black, Hispanic, and American Indian men with diabetes or at risk for type 2 diabetes. Thematic analysis was used to identify facilitators and barriers to adopting a healthy lifestyle. RESULTS: Participants included males 18 years of age and older identifying as Black, Hispanic, or American Indian and diagnosed with prediabetes, diabetes, hypertension, or otherwise at risk for type 2 diabetes. Thirty-seven men participated, 19 diagnosed with diabetes and 18 at risk for type 2 diabetes. Fourteen Black, 14 Hispanic, and 9 American Indian men participated. The themes of facilitators to a healthy lifestyle included: family and the social network; psychosocial factors; health status, health priorities and beliefs about aging; knowledge about health and healthy behavior; and healthy community resources. Themes of barriers to a healthy lifestyle also included: mistrust of the health care system, cost, and low socioeconomic status. CONCLUSIONS: This study underscores the complexity of factors involved in adopting a healthy lifestyle for some racial and ethnic minority men with diabetes or at risk for type 2 diabetes.

Recovery of Y(III) from wastewater by Pseudomonas psychrotolerans isolated from a mine soil.

While microbial technologies, which are considered to be environmentally friendly, have great potential for the recovery of rare earth elements (REEs) from mining wastewater, their applications have been restricted due to a lack of efficient biosorbents. In this study, a strain of Pseudomonas psychrotolerans isolated from yttrium-enriched mine soil was used to recover yttrium (Y(III)) from rare-earth mining wastewater. At an initial Y(III) dose of 50 mg L-1, the amount of Y(III) adsorbed by P. psychrotolerans reached 99.9 % after 24 h. Various characterization techniques revealed that P. psychrotolerans adsorbed Y(III) mainly through complexation of oxygen-containing functional groups and electrostatic interactions. A high level of adsorption efficiency (>99.9 %) was maintained after five consecutive adsorption/desorption cycles, indicating that P. psychrotolerans was highly reusable. While the efficiency of adsorbing Y(III) by P. psychrotolerans decreased (34.4 %) in actual rare earth mining wastewater, selectivity toward other REEs (≤ 18.4 %) was still observed. Consequently, this study provides a promising green, environmentally friendly and sustainable microbial approach for the selective recovery of REEs from rare earth wastewater.

Enhanced removal of 2,4-dichlorophenol by a novel biotic-abiotic hybrid system based on zeolitic imidazolate framework-8.

Biotic-abiotic hybrid systems have recently emerged as a potential technique for stable and efficient removal of persistent contaminants due to coupling of microbial catabolic with abiotic adsorption/redox processes. In this study, Burkholderia vietnamensis C09V (B.V.C09V) was successfully integrated with a Zeolitic Imidazolate Framework-8 (ZIF-8) to construct a state-of-art biotic-abiotic system using polyvinyl alcohol/ sodium alginate (PVA/SA) as media. The biotic-abiotic system (PVA/SA-ZIF-8 @B.V.C09V) was able to remove 99.0 % of 2,4-DCP within 168 h, which was much higher than either PVA/SA, PVA/SA-ZIF-8 or PVA/SA@B.V.C09V (53.8 %, 72.6 % and 67.2 %, respectively). Electrochemical techniques demonstrated that the carrier effect of PVA/SA and the driving effect of ZIF-8 collectively accelerated electron transfer processes associated with enzymatic reactions. In addition, quantitative-PCR (Q-PCR) revealed that ZIF-8 stimulated B.V.C09V to up-regulate expression of tfdB, tfdC, catA, and catC genes (2.40-, 1.68-, 1.58-, and 1.23-fold, respectively), which encoded the metabolism of related enzymes. Furthermore, the effect of key physical, chemical, and biological properties of PVA/SA-ZIF-8 @B.V.C09V on 2,4-DCP removal were statistically investigated by Spearman correlation analysis to identify the key factors that promoted synergistic removal of 2,4-DCP. Overall, this study has created an innovative new strategy for the sustainable remediation of 2,4-DCP in aquatic environments.

IL-1ß Inhibition Partially Negates the Beneficial Effects of Diet-Induced Atherosclerosis Regression in Mice.

BACKGROUND: Thromboembolic events secondary to rupture or erosion of advanced atherosclerotic lesions is the global leading cause of death. The most common and effective means to reduce these major adverse cardiovascular events, including myocardial infarction and stroke, is aggressive lipid lowering via a combination of drugs and dietary modifications. However, we know little regarding the effects of reducing dietary lipids on the composition and stability of advanced atherosclerotic lesions, the mechanisms that regulate these processes, and what therapeutic approaches might augment the benefits of lipid lowering. METHODS: Smooth muscle cell lineage-tracing Apoe-/- mice were fed a high-cholesterol Western diet for 18 weeks and then a zero-cholesterol standard laboratory diet for 12 weeks before treating them with an IL (interleukin)-1ß or control antibody for 8 weeks. We assessed lesion size and remodeling indices, as well as the cellular composition of aortic and brachiocephalic artery lesions, indices of plaque stability, overall plaque burden, and phenotypic transitions of smooth muscle cell and other lesion cells by smooth muscle cell lineage tracing combined with single-cell RNA sequencing, cytometry by time-of-flight, and immunostaining plus high-resolution confocal microscopic z-stack analysis. RESULTS: Lipid lowering by switching Apoe-/- mice from a Western diet to a standard laboratory diet reduced LDL cholesterol levels by 70% and resulted in multiple beneficial effects including reduced overall aortic plaque burden, as well as reduced intraplaque hemorrhage and necrotic core area. However, contrary to expectations, IL-1ß antibody treatment after diet-induced reductions in lipids resulted in multiple detrimental changes including increased plaque burden and brachiocephalic artery lesion size, as well as increasedintraplaque hemorrhage, necrotic core area, and senescence as compared with IgG control antibody-treated mice. Furthermore, IL-1ß antibody treatment upregulated neutrophil degranulation pathways but downregulated smooth muscle cell extracellular matrix pathways likely important for the protective fibrous cap. CONCLUSIONS: Taken together, IL-1ß appears to be required for the maintenance of standard laboratory diet-induced reductions in plaque burden and increases in multiple indices of plaque stability.

Recovery of rare earth elements from mine wastewater using alginate microspheres encapsulated with zeolitic imidazolate framework-8.

There is increasing demand and interest in efficient methods for the recovery of rare earth elements (REEs) from wastewater because of the growing concerns associated with the negative impacts of REEs-rich waste discharged on pristine ecosystems. Here, we designed a ZIF-8@ALG composite hydrogel by encapsulating zeolitic imidazolate frameworks-8 (ZIF-8) into sodium alginate and poly (vinyl alcohol) double cross-linked networks (ALG) for the recovery of REEs from mine wastewater. ZIF-8@ALG showed exceptional REEs adsorption performance with the most superior separation factor (Ho/Mn) of 597.5. For the REEs considered, the ZIF-8@ALG composite exhibited a preference for heavy REEs with high adsorption efficiencies (65.3 ∼ 97.2%) and distribution coefficients (2045.5 ∼ 28500.0 mL·g-1). Adsorption involved a combination of electrostatic attraction, complexation and ion exchange mechanisms. REEs adsorbed on ZIF-8@ALG could also be desorbed using sodium citrate via ion-exchange and complexation, thus achieving efficient REEs recovery. In addition, ZIF-8@ALG was stable and reusable, maintaining effective adsorption in wastewater over four consecutive cycles, where the optimal adsorption efficiency reached 80.0%. Overall, this study provided an effective and feasible method for the recovery of REEs in mine wastewater, and confirmed that ZIF-8-based materials have significant potential for REEs recovery applications in wastewater engineering treatment.

Enhanced removal of Pb(II) from acid mine drainage using green reduced graphene oxide/silver nanoparticles.

Mining activities can potentially release high levels of Pb(II) in acid mine drainage (AMD), which thereafter poses a significant threat to ecological security. In this study, green reduced graphene oxide/silver nanoparticles (rGO/Ag NPs) were successfully synthesized via a one-step approach using a green tea extract and subsequently used as a cost-effective absorbent to remove Pb(II) from AMD. Fourier transform infrared spectroscopy and X-ray photoelectron spectroscopy indicated that organic functional groups in the green tea extracts, such as C=O-C, CO, and CC, acted both as reductants and stabilizers in the synthesis of rGO/Ag NPs. In addition, the removal efficiency of Pb(II) by rGO/Ag NPs (84.2 %) was much better than either rGO (75.4 %) or Ag NPs (12.3 %) alone. Also, in real AMD, the distribution coefficient (Kd) of Pb(II) (4528 mL/g), was much higher than other heavy metal indicating the adsorbent had a high selective affinity for Pb(II). Interestingly, after five cycles of use, the removal efficiency of Pb(II) by rGO/Ag NPs from AMD actually increased from 46.4 to 65.2 % due to iron oxides (i.e., Fe2O3 and Fe3O4) being generated when rGO/Ag NPs was exposed to AMD. The removal of Pb(II) via adsorption on the rGO/Ag NPs surface involved formation of hexagonal rod-like precipitates. This work demonstrated the potential of rGO/Ag NPs to be continuously used for the removal of Pb(II) from AMD.

Integrative analysis of the lncRNA-miRNA-mRNA interactions in smooth muscle cell phenotypic transitions.

Objectives: We previously found that the pluripotency factor OCT4 is reactivated in smooth muscle cells (SMC) in human and mouse atherosclerotic plaques and plays an atheroprotective role. Loss of OCT4 in SMC in vitro was associated with decreases in SMC migration. However, molecular mechanisms responsible for atheroprotective SMC-OCT4-dependent effects remain unknown. Methods: Since studies in embryonic stem cells demonstrated that OCT4 regulates long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), making them candidates for OCT4 effect mediators, we applied an in vitro approach to investigate the interactions between OCT4-regulated lncRNAs, mRNAs, and miRNAs in SMC. We used OCT4 deficient mouse aortic SMC (MASMC) treated with the pro-atherogenic oxidized phospholipid POVPC, which, as we previously demonstrated, suppresses SMC contractile markers and induces SMC migration. Differential expression of lncRNAs, mRNAs, and miRNAs was obtained by lncRNA/mRNA expression array and small-RNA microarray. Long non-coding RNA to mRNA associations were predicted based on their genomic proximity and association with vascular diseases. Given a recently discovered crosstalk between miRNA and lncRNA, we also investigated the association of miRNAs with upregulated/downregulated lncRNA-mRNA pairs. Results: POVPC treatment in SMC resulted in upregulating genes related to the axon guidance and focal adhesion pathways. Knockdown of Oct4 resulted in differential regulation of pathways associated with phagocytosis. Importantly, these results were consistent with our data showing that OCT4 deficiency attenuated POVPC-induced SMC migration and led to increased phagocytosis. Next, we identified several up- or downregulated lncRNA associated with upregulation of the specific mRNA unique for the OCT4 deficient SMC, including upregulation of ENSMUST00000140952-Hoxb5/6 and ENSMUST00000155531-Zfp652 along with downregulation of ENSMUST00000173605-Parp9 and, ENSMUST00000137236-Zmym1. Finally, we found that many of the downregulated miRNAs were associated with cell migration, including miR-196a-1 and miR-10a, targets of upregulated ENSMUST00000140952, and miR-155 and miR-122, targets of upregulated ENSMUST00000155531. Oppositely, the upregulated miRNAs were anti-migratory and pro-phagocytic, such as miR-10a/b and miR-15a/b, targets of downregulated ENSMUST00000173605, and miR-146a/b and miR-15b targets of ENSMUST00000137236. Conclusion: Our integrative analyses of the lncRNA-miRNA-mRNA interactions in SMC indicated novel potential OCT4-dependent mechanisms that may play a role in SMC phenotypic transitions.

Single-Cell Gene-Regulatory Networks of Advanced Symptomatic Atherosclerosis.

BACKGROUND: While our understanding of the single-cell gene expression patterns underlying the transformation of vascular cell types during the progression of atherosclerosis is rapidly improving, the clinical and pathophysiological relevance of these changes remains poorly understood. METHODS: Single-cell RNA sequencing data generated with SmartSeq2 (≈8000 genes/cell) in 16 588 single cells isolated during atherosclerosis progression in Ldlr-/-Apob100/100 mice with human-like plasma lipoproteins and from humans with asymptomatic and symptomatic carotid plaques was clustered into multiple subtypes. For clinical and pathophysiological context, the advanced-stage and symptomatic subtype clusters were integrated with 135 tissue-specific (atherosclerotic aortic wall, mammary artery, liver, skeletal muscle, and visceral and subcutaneous, fat) gene-regulatory networks (GRNs) inferred from 600 coronary artery disease patients in the STARNET (Stockholm-Tartu Atherosclerosis Reverse Network Engineering Task) study. RESULTS: Advanced stages of atherosclerosis progression and symptomatic carotid plaques were largely characterized by 3 smooth muscle cells (SMCs), and 3 macrophage subtype clusters with extracellular matrix organization/osteogenic (SMC), and M1-type proinflammatory/Trem2-high lipid-associated (macrophage) phenotypes. Integrative analysis of these 6 clusters with STARNET revealed significant enrichments of 3 arterial wall GRNs: GRN33 (macrophage), GRN39 (SMC), and GRN122 (macrophage) with major contributions to coronary artery disease heritability and strong associations with clinical scores of coronary atherosclerosis severity. The presence and pathophysiological relevance of GRN39 were verified in 5 independent RNAseq data sets obtained from the human coronary and aortic artery, and primary SMCs and by targeting its top-key drivers, FRZB and ALCAM in cultured human coronary artery SMCs. CONCLUSIONS: By identifying and integrating the most gene-rich single-cell subclusters of atherosclerosis to date with a coronary artery disease framework of GRNs, GRN39 was identified and independently validated as being critical for the transformation of contractile SMCs into an osteogenic phenotype promoting advanced, symptomatic atherosclerosis.

Intensive ammonium fertilizer addition activates iron and carbon conversion coupled cadmium redistribution in a paddy soil under gradient redox conditions.

While over-fertilization and nitrogen deposition can lead to the enrichment of nitrogen in soil, its effects on heavy metal fractions under gradient moisture conditions remains unclear. Here, the effect of intensive ammonium (NH4+) addition on the conversion and interaction of cadmium (Cd), iron (Fe) and carbon (C) was studied. At relatively low (30-80 %) water hold capacity (WHC) NH4+ application increased the carbonate bound Cd fraction (F2Cd), while at relatively high (80-100 %) WHC NH4+ application increased the organic matter bound Cd fraction (F4Cd). Iron­manganese oxide bound Cd fractions (F3Cd) and oxalate-Fe decreased, but DCB-Fe increased in NH4+ treatments, indicating that amorphous Fe was the main carrier of F3Cd. The variations in F1Cd and F4Cd observed under the 100-30-100 % WHC treatment were similar to those observed under low moisture conditions (30-60 % WHC). The C=O/C-H ratio of organic matter in soil decreased under the 30-60 % WHC treatment, but increased under the 80-100 % WHC treatment, which was the dominant factor influencing F4Cd changes. The conversion of NH4+ declined with increasing soil moisture content, and the impact on oxalate-Fe was greater at 30-60 % WHC than at 80-100 % WHC. Correspondingly, genetic analysis showed the effect of NH4+ on Fe and C metabolism at 30-60 % WHC was greater than at 80-100 % WHC. Specifically, NH4+ treatment enhanced the expression of genes encoding extracellular Fe complexation (siderophore) at 30-80 % WHC, while inhibiting genes encoding Fe transmembrane transport at 30-60 % WHC, indicating that siderophores simultaneously facilitated Cd detoxification and Fe complexation. Furthermore, biosynthesis of sesquiterpenoid, steroid, butirosin and neomycin was significantly correlated with F4Cd, while glycosaminoglycan degradation metabolism and assimilatory nitrate reduction was significantly correlated with F2Cd. Overall, this study gives a more comprehensive insight into the effect of NH4+ on activated Fe and C conversion on soil Cd redistribution under gradient moisture conditions.

Deciphering silver nanoparticles perturbation effects and risks for soil enzymes worldwide: Insights from machine learning and soil property integration.

Globally extensive research into how silver nanoparticles (AgNPs) affect enzyme activity in soils with differing properties has been limited by cost-prohibitive sampling. In this study, customized machine learning (ML) was used to extract data patterns from complex research, with a hit rate of Random Forest > Multiple Imputation by Chained Equations > Decision Tree > K-Nearest Neighbors. Results showed that soil properties played a pivotal role in determining AgNPs' effect on soil enzymes, with the order being pH > organic matter (OM) > soil texture ≈ cation exchange capacity (CEC). Notably, soil enzyme activity was more sensitive to AgNPs in acidic soil (pH < 5.5), while elevated OM content (>1.9 %) attenuated AgNPs toxicity. Compared to soil acidification, reducing soil OM content is more detrimental in exacerbating AgNPs' toxicity and it emerged that clay particles were deemed effective in curbing their toxicity. Meanwhile sand particles played a very different role, and a sandy soil sample at > 40 % of the water holding capacity (WHC), amplified the toxicity of AgNPs. Perturbation mapping of how soil texture alters enzyme activity under AgNPs exposure was generated, where soils with sand (45-65 %), silt (< 22 %), and clay (35-55 %) exhibited even higher probability of positive effects of AgNPs. The average calculation results indicate the sandy clay loam (75.6 %), clay (74.8 %), silt clay (65.8 %), and sandy clay (55.9 %) texture soil demonstrate less AgNPs inhibition effect. The results herein advance the prediction of the effect of AgNPs on soil enzymes globally and determine the soil types that are more sensitive to AgNPs worldwide.

Secreted Protein Profiling of Human Aortic Smooth Muscle Cells Identifies Vascular Disease Associations.

BACKGROUND: Smooth muscle cells (SMCs), which make up the medial layer of arteries, are key cell types involved in cardiovascular disease, the leading cause of mortality and morbidity worldwide. In response to microenvironment alterations, SMCs dedifferentiate from a contractile to a synthetic phenotype characterized by an increased proliferation, migration, production of ECM (extracellular matrix) components, and decreased expression of SMC-specific contractile markers. These phenotypic changes result in vascular remodeling and contribute to the pathogenesis of cardiovascular disease, including coronary artery disease, stroke, hypertension, and aortic aneurysms. Here, we aim to identify the genetic variants that regulate ECM secretion in SMCs and predict the causal proteins associated with vascular disease-related loci identified in genome-wide association studies. METHODS: Using human aortic SMCs from 123 multiancestry healthy heart transplant donors, we collected the serum-free media in which the cells were cultured for 24 hours and conducted liquid chromatography-tandem mass spectrometry-based proteomic analysis of the conditioned media. RESULTS: We measured the abundance of 270 ECM and related proteins. Next, we performed protein quantitative trait locus mapping and identified 20 loci associated with secreted protein abundance in SMCs. We functionally annotated these loci using a colocalization approach. This approach prioritized the genetic variant rs6739323-A at the 2p22.3 locus, which is associated with lower expression of LTBP1 (latent-transforming growth factor beta-binding protein 1) in SMCs and atherosclerosis-prone areas of the aorta, and increased risk for SMC calcification. We found that LTBP1 expression is abundant in SMCs, and its expression at mRNA and protein levels was reduced in unstable and advanced atherosclerotic plaque lesions. CONCLUSIONS: Our results unravel the SMC proteome signature associated with vascular disorders, which may help identify potential therapeutic targets to accelerate the pathway to translation.

Uptake and transport mechanisms of rare earth hyperaccumulators: A review.

Due to their use in a number of advanced electronic technologies, Rare earth elements (REEs) have recently emerged as a key strategic resource for many nations worldwide. The significant increase in demand for REEs has thus greatly increased the mining of these substances, but this industrial-scale expansion of mining activities also poses potential risks to the surrounding environment, flora, fauna, and humans. Hence efficient REE remediation is one potential remediation process involving in situ clean-up of contaminated soil which has gained much attention in recent years, due to its low cost and lack of secondary pollution. However, some crucial aspects of phytoremediation, such as the precise-mechanisms of absorption, transport, and tolerance of REEs by hyperaccumulators -are poorly understood. This review briefly discusses the environmental risks associated with excess REEs, the efficacy of phytoremediation technologies coupled with, appropriate hyperaccumulator species to migrate REEs exposure. While REEs hyperaccumulator species should ideally be large-biomass trees and shrubs suitable for cropping in subtropical regions areas, such species have not yet been found. Specifically, this review focuses on the factors affecting the bioavailability of REEs in plants, where organic acids are critical ligands promoting efficient transport and uptake. Thus the uptake, transport, and binding forms of REEs in the above-ground parts of hyperaccumulators, especially the transporters isolated from the heavy metal transporter families, are discussed in detail. Finally, having summarized the current state of research in this area, this review proceeds to discuss current knowledge gaps and research directions. With a focus on hyperaccumulators, this review serves as a basis for future phytoremediation strategies of rare earth mining-impacted environments and addresses ecosystem/environmental degradation issues resulting from such mining activity.

Treatment of advanced atherosclerotic mice with ABT-263 reduced indices of plaque stability and increased mortality.

The use of senolytic agents to remove senescent cells from atherosclerotic lesions is controversial. A common limitation of previous studies is the failure to rigorously define the effects of senolytic agent ABT-263 (Navitoclax) on smooth muscle cells (SMC) despite studies claiming that these cells are the major source of senescent cells. Moreover, there are no studies on the effect of ABT-263 on endothelial cells (EC), which - along with SMC - comprise 90% of α-smooth muscle actin+ (α-SMA+) myofibroblast-like cells in the protective fibrous cap. Here we tested the hypothesis that treatment of advanced atherosclerotic mice with ABT-263 will reduce lesion size and increase plaque stability. SMC (Myh11-CreERT2-eYFP) and EC (Cdh5-CreERT2-eYFP) lineage tracing Apoe-/- mice were fed a western diet (WD) for 18 weeks, followed by ABT-263 at 100 mg/kg/bw for 6 weeks or 50 mg/kg/bw for 9 weeks. ABT-263 treatment did not change lesion size or lumen area of the brachiocephalic artery (BCA). However, ABT-263 treatment reduced SMC by 90% and increased EC contributions to lesions via EC-to-mesenchymal transition (EndoMT) by 60%. ABT-263 treatment also reduced α-SMA+ fibrous cap thickness by 60% and was associated with a > 50% mortality rate. Taken together, ABT-263 treatment of WD-fed Apoe-/- mice with advanced lesions resulted in multiple detrimental changes, including reduced indices of stability and increased mortality.

Ferrous sulfide nanoparticles can be biosynthesized by sulfate-reducing bacteria: Synthesis, characterization and removal of heavy metals from acid mine drainage.

Ferrous sulfide nanoparticles (nFeS) have proven to be effective in removing heavy metals (HMs) from wastewater. One such approach, which has garnered much attention as a sustainable technology, is via the in situ microbial synthesis of nFeS. Here, a sulfate-reducing bacteria (SRB) strain, Geobacter sulfurreducens, was used to initially biosynthesize ferrous sulfide nanoparticles (SRB-nFeS) and thereafter remove HMs from acid mine drainage (AMD). SRB-nFeS was characterized by X-ray powder diffraction (XRD), scanning electron microscopy (SEM) coupled to an energy dispersive spectrometer (EDS), three-dimensional excitation-emission matrix (3D-EEM) spectroscopy, Fourier transform infrared (FTIR) spectroscopy and X-ray photoelectron spectroscopy (XPS). Such characterization showed that SRB mediated the reduction of SO42- to S2- to form nFeS, where the metabolized substances functioned as complexing agents which coordinated with nFeS to form biofunctional SRB-nFeS with improved stability. One advantage of this synthetic route was that the attachment of nFeS to the bacterial surface protected SRB cells from HM toxicity. Furthermore, due to a synergistic effect between nFeS and SRB, HM removal from both solution and AMD by SRB-nFeS was enhanced relative to the constituent components. Thus, after 5 consecutive cycles of HM removal, SRB-nFeS removed, Pb(Ⅱ) (92.6%), Cd(Ⅱ) (78.7%), Cu(Ⅱ) (76.0%), Ni(Ⅱ) (62.5%), Mn(Ⅱ) (62.2%), and Zn(Ⅱ) (88.5%) from AMD This study thus provides new insights into the biosynthesis of SRB-nFeS and its subsequent practical application in the removal of HMs from AMD.

Green rGO/FeNPs nanocomposites activated peroxydisulfate for the removal of mixed 17ß-estradiol and estriol.

Reduced graphene oxide/iron nanoparticles (rGO/FeNPs) synthesized by the chemical method have been used in Fenton oxidation of organic contaminants, yet little is known about biosynthesized rGO/FeNPs using green tea extract (GT) as how to activate persulfate in sulfate radical-based advanced oxidation processes. In this study, rGO/FeNPs were used to activate peroxydisulfate (PDS) for 17ß-estradiol (ßE2) and estriol (E3) removal. The rGO/FeNPs-PDS system removed 83.6% of ßE2 and 62.5% of E3 within 240 min, which was confirmed by a combination of adsorption and degradation via both radical and non-radical pathways. Four main reactive species in ßE2 and E3 degradation were observed, i.e., hydroxyl radical (·OH), sulfate radical (SO4·-), singlet oxygen (1O2) and electron transfer, with the respective contributions of ·OH (32.9 and 34.7%), SO4·- (16.1 and 19.7%), 1O2 (12.2 and 14.1%) and electron transfer (8.0 and 7.2%). Analysis of X-ray photoelectron spectroscopy (XPS), Fourier transform infrared (FTIR), Electron Paramagnetic Resonance (EPR) and electrochemical measurements all indicated that beside the well-known role of Fe, CO from rGO through the generation of ·OH, SO4·-, 1O2 and electron transfer, as well as GT through electron transfer also participated in the activation of PDS. Finally, the degradation pathways of ßE2/E3 were proposed. Overall, this study provides a new insight into the biosynthesis of rGO/FeNPs to activate PDS for the oxidation of mixed emerging contaminants.

Smooth muscle cells-specific loss of OCT4 accelerates neointima formation after acute vascular injury.

Introduction: There is growing evidence that smooth muscle cell (SMC) phenotypic transitions play critical roles during normal developmental and tissue recovery processes and in pathological conditions such as atherosclerosis. However, the molecular mechanisms responsible for these transitions are not well understood. Recently, we found that the embryonic stem cell/induced pluripotent stem cell (iPSC) factor OCT4, which was believed to be silenced in somatic cells, plays an atheroprotective role in SMC, and regulates angiogenesis after corneal alkali burn and hindlimb ischemia by mediating microvascular SMC and pericyte migration. However, the kinetics of OCT4 activation in arterial SMC and its role in acute pathological conditions are still unknown. Methods and Results: Here, using an Oct4-IRES-GFP reporter mouse model, we found that OCT4 is reactivated in the carotid artery 18 hours post-acute ligation-induced injury, a common in vivo model of the SMC phenotypic transitions. Next, using a tamoxifen-inducible Myh11-CreERT2 Oct4 knockout mouse model, we found that the loss of OCT4, specifically in SMC, led to accelerated neointima formation and increased tunica media following carotid artery ligation, at least in part by increasing SMC proliferation within the media. Bulk RNA sequencing analysis on the cultured SMC revealed significant down-regulation of the SMC contractile markers and dysregulation of the genes belonging to the regulation of cell proliferation and, positive and negative regulation for cell migration ontological groups following genetic inactivation of Oct4. We also found that loss of Oct4 resulted in suppression of contractile SMC markers after the injury and in cultured aortic SMC. Further mechanistic studies revealed that OCT4 regulates SMC contractile genes, ACTA2 and TAGLN, at least in part by direct binding to the promoters of these genes. Conclusion: These results demonstrate that the pluripotency factor OCT4 is quickly activated in SMC after the acute vascular injury and inhibits SMC hyperproliferation, which may be protective in preventing excessive neointima formation.

Secreted protein profiling of human aortic smooth muscle cells identifies vascular disease associations.

Background: Smooth muscle cells (SMCs), which make up the medial layer of arteries, are key cell types involved in cardiovascular diseases (CVD), the leading cause of mortality and morbidity worldwide. In response to microenvironment alterations, SMCs dedifferentiate from a "contractile" to a "synthetic" phenotype characterized by an increased proliferation, migration, production of extracellular matrix (ECM) components, and decreased expression of SMC-specific contractile markers. These phenotypic changes result in vascular remodeling and contribute to the pathogenesis of CVD, including coronary artery disease (CAD), stroke, hypertension, and aortic aneurysms. Here, we aim to identify the genetic variants that regulate ECM secretion in SMCs and predict the causal proteins associated with vascular disease-related loci identified in genome-wide association studies (GWAS). Methods: Using human aortic SMCs from 123 multi-ancestry healthy heart transplant donors, we collected the serum-free media in which the cells were cultured for 24 hours and conducted Liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based proteomic analysis of the conditioned media. Results: We measured the abundance of 270 ECM and related proteins. Next, we performed protein quantitative trait locus mapping (pQTL) and identified 20 loci associated with secreted protein abundance in SMCs. We functionally annotated these loci using a colocalization approach. This approach prioritized the genetic variant rs6739323-A at the 2p22.3 locus, which is associated with lower expression of LTBP1 in SMCs and atherosclerosis-prone areas of the aorta, and increased risk for SMC calcification. We found that LTBP1 expression is abundant in SMCs, and its expression at mRNA and protein levels was reduced in unstable and advanced atherosclerotic plaque lesions. Conclusions: Our results unravel the SMC proteome signature associated with vascular disorders, which may help identify potential therapeutic targets to accelerate the pathway to translation.