[Research advances of prostaglandin E2 receptor 1 (EP1)].

Prostaglandin E2 (PGE2) is an important lipid molecule derived from arachidonic acid, which regulates a variety of physiological and pathological activities. Based on the inhibition of inflammatory PGE2 production, non-steroidal anti-inflammatory drugs (NSAIDs) are considered as the most commonly used drugs to treat inflammatory diseases and to relieve fever and pain symptoms. PGE2 mediates its functions via four different G protein-coupled receptors, named EP1-EP4. Though the limited distribution and low PGE2 affinity of EP1, it plays important roles in the maintenance of many physiological functions and homeostasis. Moreover, EP1 is widely involved in the inflammatory response, pain perception and multisystem pathological function regulation. In this review, we will briefly summarize the recent advances on the physiological and pathophysiological function of EP1 and its targeted drugs development.

Enhancing singlet oxygen production of dioxygen activation on the carbon-supported rare-earth oxide nanocluster and rare-earth single atom catalyst to remove antibiotics.

Singlet oxygen (1O2) is extensively employed in the fields of chemical, biomedical and environmental. However, it is still a challenge to produce high- concentration 1O2 by dioxygen activation. Herein, a system of carbon-supported rare-earth oxide nanocluster and single atom catalysts (named as RE2O3/RE-C, RE=La, Ce, Pr, Nd, Sm, Eu, Gd, Tb, Dy, Ho, Er, Tm, Yb, Lu, Sc and Y) with similar morphology, structure, and physicochemical characteristic are constructed to activate dissolved oxygen (DO) to enhance 1O2 production. The catalytic activity trends and mechanisms are revealed experimentally and are also proven by theoretical analyses and calculations. The 1O2 generation activity trend is Gd2O3/Gd-C>Er2O3/Er-C>Sm2O3/Sm-C>pristine carbon (C). More than 95.0% of common antibiotics (ciprofloxacin, ofloxacin, norfloxacin and carbamazepine) can be removed in 60 min by Gd2O3/Gd-C. Density functional theory calculations indicate that Gd2O3 nanoclusters and Gd single atoms exhibit the moderate adsorption energy of ·O2- to enhance 1O2 production. This study offers a universal strategy to enhance 1O2 production in dioxygen activation for future application and reveals the natural essence of basic mechanisms of 1O2 production via rare-earth oxide nanoclusters and rare-earth single atoms.

Visualizing plant intracellular inorganic orthophosphate distribution.

Intracellular inorganic orthophosphate (Pi) distribution and homeostasis profoundly affect plant growth and development. However, its distribution patterns remain elusive owing to the lack of efficient cellular Pi imaging methods. Here we develop a rapid colorimetric Pi imaging method, inorganic orthophosphate staining assay (IOSA), that can semi-quantitatively image intracellular Pi with high resolution. We used IOSA to reveal the alteration of cellular Pi distribution caused by Pi starvation or mutations that alter Pi homeostasis in two model plants, rice and Arabidopsis, and found that xylem parenchyma cells and basal node sieve tube element cells play a critical role in Pi homeostasis in rice. We also used IOSA to screen for mutants altered in cellular Pi homeostasis. From this, we have identified a novel cellular Pi distribution regulator, HPA1/PHO1;1, specifically expressed in the companion and xylem parenchyma cells regulating phloem Pi translocation from the leaf tip to the leaf base in rice. Taken together, IOSA provides a powerful method for visualizing cellular Pi distribution and facilitates the analysis of Pi signalling and homeostasis from the level of the cell to the whole plant.

Circadian control of ConA-induced acute liver injury and inflammatory response via Bmal1 regulation of Junb.

Background & Aims: Circadian rhythms play significant roles in immune responses, and many inflammatory processes in liver diseases are associated with malfunctioning molecular clocks. However, the significance of the circadian clock in autoimmune hepatitis (AIH), which is characterised by immune-mediated hepatocyte destruction and extensive inflammatory cytokine production, remains unclear. Methods: We tested the difference in susceptibility to the immune-mediated liver injury induced by concanavalin A (ConA) at various time points throughout a day in mice and analysed the effects of global, hepatocyte, or myeloid cell deletion of the core clock gene, Bmal1 (basic helix-loop-helix ARNT-like 1), on liver injury and inflammatory responses. Multiple molecular biology techniques and mice with macrophage-specific knockdown of Junb, a Bmal1 target gene, were used to investigate the involvement of Junb in the circadian control of ConA-induced hepatitis. Results: The susceptibility to ConA-induced liver injury is highly dependent on the timing of ConA injection. The treatment at Zeitgeber time 0 (lights on) triggers the highest mortality as well as the severest liver injury and inflammatory responses. Further study revealed that this timing effect was driven by macrophage, but not hepatocyte, Bmal1. Mechanistically, Bmal1 controls the diurnal variation of ConA-induced hepatitis by directly regulating the circadian transcription of Junb and promoting M1 macrophage activation. Inhibition of Junb in macrophages blunts the administration time-dependent effect of ConA and attenuates liver injury. Moreover, we demonstrated that Junb promotes macrophage inflammation by regulating AKT and extracellular signal-regulated kinase (ERK) signalling pathways. Conclusions: Our findings uncover a critical role of the Bmal1-Junb-AKT/ERK axis in the circadian control of ConA-induced hepatitis and provide new insights into the prevention and treatment of AIH. Impact and Implications: This study unveils a critical role of the Bmal1-Junb-AKT/ERK axis in the circadian control of ConA-induced liver injury, providing new insights into the prevention and treatment of immune-mediated hepatitis, including autoimmune hepatitis (AIH). The findings have scientific implications as they enhance our understanding of the circadian regulation of immune responses in liver diseases. Furthermore, clinically, this research offers opportunities for optimising treatment strategies in immune-mediated hepatitis by considering the timing of therapeutic interventions.

PGC-1α regulates critical period onset/closure, mediating cortical plasticity.

Peroxisome proliferator-activated receptor PPARγ coactivator-α (PGC-1α) is concentrated in inhibitory interneurons and plays a vital role in neuropsychiatric diseases. We previously reported some characteristic features of schizophrenia (SZ) in GABAergic neuron-specific Pgc-1alpha knockout (KO) mice (Dlx5/6-Cre: Pgc-1alphaf/f). However, there is a fundamental gap in the molecular mechanism by which the Pgc-1alpha gene is involved in the neurobehavioral abnormalities of SZ. The loss of critical period (CP) triggers-maturations of parvalbumin interneurons (PVIs) and brakes-and the formation of perineuronal nets (PNNs) implicates mistimed trajectories during adult brain development. In this study, using the Pgc-1alpha KO mouse line, we investigated the association of Pgc-1alpha gene deletion with SZ-like behavioral deficits, PVI maturation, PNN integrity and synaptic ultrastructure. These findings suggest that Pgc-1alpha gene deletion resulted in a failure of CP onset and closure, thereby prolonging cortical plasticity timing. To determine whether the manipulation of the PNN structure is a potential method of altering neuronal plasticity, GM6001, a broad-spectrum matrix metalloproteinase (MMP)-inhibitor was applied. Here we confirmed that the treatment could effectively correct the CP plasticity window and ameliorate the synaptic ultrastructure in the Pgc-1alpha KO brain. Moreover, the intervention effect on neuronal plasticity was followed by the rescue of short-term habituation deficits and the mitigation of aberrant salience, which are some characteristic features of SZ. Taken collectively, these findings suggest that the role of PGC-1α in regulating cortical plasticity is mediated, at least partially, through the regulation of CP onset/closure. Strategically introduced reinforcement of molecular brakes may be a novel preventive therapy for psychiatric disorders associated with PGC-1α dysregulation.

An ethylene-induced NAC transcription factor acts as a multiple abiotic stress responsor in conifer.

The proper response to various abiotic stresses is essential for plants' survival to overcome their sessile nature, especially for perennial trees with very long-life cycles. However, in conifers, the molecular mechanisms that coordinate multiple abiotic stress responses remain elusive. Here, the transcriptome response to various abiotic stresses like salt, cold, drought, heat shock and osmotic were systematically detected in Pinus tabuliformis (P. tabuliformis) seedlings. We found that four transcription factors were commonly induced by all tested stress treatments, while PtNAC3 and PtZFP30 were highly up-regulated and co-expressed. Unexpectedly, the exogenous hormone treatment assays and the content of the endogenous hormone indicates that the upregulation of PtNAC3 and PtZFP30 are mediated by ethylene. Time-course assay showed that the treatment by ethylene immediate precursor, 1-aminocyclopropane-1-carboxylic acid (ACC), activated the expression of PtNAC3 and PtZFP30 within 8 hours. We further confirm that the PtNAC3 can directly bind to the PtZFP30 promoter region and form a cascade. Overexpression of PtNAC3 enhanced unified abiotic stress tolerance without growth penalty in transgenic Arabidopsis and promoted reproductive success under abiotic stress by shortening the lifespan, suggesting it has great potential as a biological tool applied to plant breeding for abiotic stress tolerance. This study provides novel insights into the hub nodes of the abiotic stresses response network as well as the environmental adaptation mechanism in conifers, and provides a potential biofortification tool to enhance plant unified abiotic stress tolerance.

Enhanced selective separation of vanadium(V) and chromium(VI) using the CeO2 nanorod containing oxygen vacancies.

Adsorption of vanadium from wastewater defends the environment from toxic ions and contributes to recover the valuable metal. However, it is still challenging for the separation of vanadium (V5+) and chromium (Cr6+) because of their similar properties. Herein, a kind of CeO2 nanorod containing oxygen vacancies is facilely synthesized which displays ultra-high selectivity of V5+ against various competitive ions (i.e., Fe, Mn, Cr, Ni, Cu, Zn, Ga, Cd, Ba, Pb, Mg, Be, and Co). Moreover, a large separation factor (SFV/Cr) of 114,169.14 for the selectivity of V5+ is achieved at the Cr6+/V5+ ratio of 80 with the trace amount of V5+ (~ 1 mg/L). The results show that the process of V5+ uptake is the monolayer homogeneous adsorption and is controlled by external and intraparticle diffusions. In addition, it also shows that V5+ is reduced to V3+ and V4+ and then formation of V-O complexation. This work offers a novel CeO2 nanorod material for efficient separation of V5+ and Cr6+ and also clarifies the mechanism of the V5+ adsorption on the CeO2 surface.

NIGT1 represses plant growth and mitigates phosphate starvation signaling to balance the growth response tradeoff in rice.

Inorganic phosphate (Pi) availability is an important factor which affects the growth and yield of crops, thus an appropriate and effective response to Pi fluctuation is critical. However, how crops orchestrate Pi signaling and growth under Pi starvation conditions to optimize the growth defense tradeoff remains unclear. Here we show that a Pi starvation-induced transcription factor NIGT1 (NITRATE-INDUCIBLE GARP-TYPE TRANSCRIPTIONAL REPRESSOR 1) controls plant growth and prevents a hyper-response to Pi starvation by directly repressing the expression of growth-related and Pi-signaling genes to achieve a balance between growth and response under a varying Pi environment. NIGT1 directly binds to the promoters of Pi starvation signaling marker genes, like IPS1, miR827, and SPX2, under Pi-deficient conditions to mitigate the Pi-starvation responsive (PSR). It also directly represses the expression of vacuolar Pi efflux transporter genes VPE1/2 to regulate plant Pi homeostasis. We further demonstrate that NIGT1 constrains shoot growth by repressing the expression of growth-related regulatory genes, including brassinolide signal transduction master regulator BZR1, cell division regulator CYCB1;1, and DNA replication regulator PSF3. Our findings reveal the function of NIGT1 in orchestrating plant growth and Pi starvation signaling, and also provide evidence that NIGT1 acts as a safeguard to avoid hyper-response during Pi starvation stress in rice.

Deletion of Cyclic GMP-AMP Synthase Aggravates Concanavalin A-Induced Acute Hepatic Injury by Facilitating Leukocyte Chemotaxis.

Growing evidence demonstrates that cyclic GMP-AMP synthase (cGAS), as a cytosolic DNA sensor, is essential for activating innate immunity and regulating inflammatory response against cellular damage. However, its role in immune-mediated hepatitis remains unclear. Here by challenging the cGAS knockout (KO) and their littermate wide-type (WT) mice with intravenous ConA injection to induce acute immune-mediated liver injury, we found that lack of cGAS drastically aggravated liver damage post ConA treatment for 24 h, reflected by increased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and amplified hepatic necrosis. The number of apoptotic hepatocytes was also significantly increased in the KO mice. RNA-sequencing analysis revealed that leukocyte chemotaxis and migration-related genes were remarkably upregulated in the KO livers. Consistently, immunofluorescence assays illustrated that the infiltrating F4/80-positive macrophages, Ly6G-positive neutrophils, and CD3-positive T cells were all significantly increased in the KO liver sections. The hepatic expression of the pro-inflammatory genes was elevated as well. Supporting the in vivo findings, the knockdown of cGAS in cultured macrophages showed promoted migration potential and enhanced pro-inflammatory gene expression. These results collectively demonstrated that deletion of cGAS could aggravate ConA-induced acute liver injury, at least at the 24-h time point, and its mechanism might be related to facilitating leukocyte chemotaxis and promoting liver inflammatory response.

Insights into the Selective Transformation of Ceria Sulfation and Iron/Manganese Mineralization for Enhancing the Selective Recovery of Rare Earth Elements.

To cope with the urgent and unprecedented demands for rare earth elements (REEs) in sophisticated industries, increased attention has been paid to REE recovery from recycled streams. However, the similar geochemical behaviors of REEs and transition metals often result in poor separation performance due to nonselectivity. Here, a unique approach based on the selective transformation between ceria sulfation and iron/manganese mineralization was proposed, leading to the enhancement of the selective separation of REEs. The mechanism of the selective transformation of minerals could be ascribed to the distinct geochemical and metallurgical properties of ions, resulting in different combinations of cations and anions. According to hard-soft acid-base (HSAB) theory, the strong Lewis acid of Ce(III) was inclined to combine with the hard base of sulfates (SO42-), while the borderline acid of Fe(II)/Mn(II) prefers to interact with oxygen ions (O2-). Both in situ characterization and density functional theory (DFT) calculation further revealed that such selective transformation might trigger by the generation of an oxygen vacancy on the surface of CeO2, leading to the formation of Ce2(SO4)3 and Fe/Mn spinel. Although the electron density difference of the configurations (CeO2-x-SO4, Fe2O3-x-SO4, and MnO2-x-SO4) shared a similar direction of the electron transfer from the metals to the sulfate-based oxygen, the higher electron depletion of Ce (QCe = -1.91 e) than Fe (QFe = -1.66 e) and Mn (QMn = -1.64 e) indicated the higher stability in the Ce-O-S complex, resulting in the larger adsorption energy of CeO2-x-SO4 (-6.88 eV) compared with Fe2O3-x-SO4 (-3.10 eV) and MnO2-x-SO4 (-2.49 eV). This research provided new insights into the selective transformation of REEs and transition metals in pyrometallurgy and thus offered a new approach for the selective recovery of REEs from secondary resources.

Alternative splicing of REGULATOR OF LEAF INCLINATION 1 modulates phosphate starvation signaling and growth in plants.

Phosphate (Pi) limitation represents a primary constraint on crop production. To better cope with Pi deficiency stress, plants have evolved multiple adaptive mechanisms for phosphorus acquisition and utilization, including the alteration of growth and the activation of Pi starvation signaling. However, how these strategies are coordinated remains largely unknown. Here, we found that the alternative splicing (AS) of REGULATOR OF LEAF INCLINATION 1 (RLI1) in rice (Oryza sativa) produces two protein isoforms: RLI1a, containing MYB DNA binding domain and RLI1b, containing both MYB and coiled-coil (CC) domains. The absence of a CC domain in RLI1a enables it to activate broader target genes than RLI1b. RLI1a, but not RLI1b, regulates both brassinolide (BL) biosynthesis and signaling by directly activating BL-biosynthesis and signaling genes. Both RLI1a and RLI1b modulate Pi starvation signaling. RLI1 and PHOSPHATE STARVATION RESPONSE 2 function redundantly to regulate Pi starvation signaling and growth in response to Pi deficiency. Furthermore, the AS of RLI1-related genes to produce two isoforms for growth and Pi signaling is widely present in both dicots and monocots. Together, these findings indicate that the AS of RLI1 is an important and functionally conserved strategy to orchestrate Pi starvation signaling and growth to help plants adapt to Pi-limitation stress.

Effects of in situ leaching on the origin and migration of rare earth elements in aqueous systems of South China: Insights based on REE patterns, and Ce and Eu anomalies.

In situ leaching of ion-adsorption rare earth element (REE) deposits has released large amounts of REE-containing wastewater. However, the origin, speciation, distribution and migration of REEs in aqueous systems of the mining catchment are poorly understood. Groundwater, surface water, in situ leachates and weathered granite soil samples were collected from a catchment affected by mining activities in South China. The REE concentrations in groundwater (6.18 × 10-3-0.49 µmol L-1) and surface water (2.54-44.05 µmol L-1) decreased from upstream to downstream. REEs in groundwater were detected in organic matter associated (FA-REE) colloids, while the REE3+ and REE(SO4)+ were converted to REE(CO3)+ and FA-REE colloids from leachates and upstream surface water to downstream. The REE patterns of leachates and upstream groundwater (light and middle REE enrichment) resembled those of soil, but showed heavy REE enrichment due to FA-REE colloids in the downstream. REE in surface water were derived from middle REE enriched leachate. The Ce and Eu anomalies in the water samples indicated the REE origin (i.e., mining activities) and the hydrological variations (e.g., oxidation environment and water-rock interaction). Our results reveal the origin and fate of REE in aqueous systems of ion-adsorption REE mining catchments.

Biogeochemical dynamics of nutrients and rare earth elements (REEs) during natural succession from biocrusts to pioneer plants in REE mine tailings in southern China.

The exploitation of ion-adsorption rare earth element (REE) deposits has resulted in large quantities of abandoned mine tailings, which pose significant risks to the surrounding environment. However, the natural evolutional patterns at early successional stages and related biogeochemical dynamics (e.g. nutrient and REE cycling) on such mine tailings remains poorly understood. To this end, a chronosequence of REE mine tailings abandoned for up to 15 years was investigated in a post-mining site in south China. Our results showed that biocrusts were the earliest colonizers on these tailings, reaching a peak of 10% of surface coverage after 10 years of abandonment. Later on, after 15 years, the biocrusts began to be replaced by pioneer plants (e.g. Miscanthus sinensis), suggesting a rather rapid succession. This ecological succession was accompanied by obvious changes in soil nutrients and microbial community structure. Compared to bulk soils, both the biocrusts and rhizospheric soils favored an accumulation of nutrients (e.g. P, S, N, C). Notably, the autotrophic bacteria (e.g. Chloroflexi and Cyanobacteria) with C and N fixation abilities were preferentially enriched in biocrusts, while heterotrophic plant growth promoting bacteria (e.g. Pseudoocardiaceae and Acidobacteriales) were mainly present in the rhizosphere. Moreover, the biocrusts showed a remarkably high concentration of REEs (up to 1820 mg kg-1), while the rhizospheric soils tended to decrease REE concentrations (~400 mg kg-1) in comparison with bulk soils, indicating that the REEs could be redistributed by biological processes. Principal component analysis and mantel tests showed that the concentrations of nutrients and REEs were the most important factors affecting the microbial communities in biocrusts, rhizospheric and bulk soils. In sum, based on the observation of nutrient accumulation and pollutant (i.e. REE) dynamics in the initial successional stages, this work provides a feasible theoretical basis for future restoration practices on REE mine tailings.

A reciprocal inhibitory module for Pi and iron signaling.

Phosphorous (P) and iron (Fe), two essential nutrients for plant growth and development, are highly abundant elements in the earth's crust but often display low availability to plants. Due to the ability to form insoluble complexes, the antagonistic interaction between P and Fe nutrition in plants has been noticed for decades. However, the underlying molecular mechanism modulating the signaling and homeostasis between them remains obscure. Here, we show that the possible iron sensors HRZs, the iron deficiency-induced E3 ligases, could interact with the central regulator of phosphate (Pi) signaling, PHR2, and prompt its ubiquitination at lysine residues K319 and K328, leading to its degradation in rice. Consistent with this, the hrzs mutants displayed a high Pi accumulation phenotype. Furthermore, we found that iron deficiency could attenuate Pi starvation signaling by inducing the expression of HRZs, which in turn trigger PHR2 protein degradation. Interestingly, on the other hand, rice PHRs could negatively regulate the expression of HRZs to modulate iron deficiency responses. Therefore, PHR2 and HRZs form a reciprocal inhibitory module to coordinate Pi and iron signaling and homeostasis in rice. Taken together, our results uncover a molecular link between Pi and iron master regulators, which fine-tunes plant adaptation to Pi and iron availability in rice.

Biogeochemical cycles of nutrients, rare earth elements (REEs) and Al in soil-plant system in ion-adsorption REE mine tailings remediated with amendment and ramie (Boehmeria nivea L.).

The exploitation of ion-adsorption rare earth element (REE) deposits in South China has left large areas of mine tailings. However, limited remediation practices on these tailings have been reported, and how the remediation strategies and economic plants cultivation affect the biogeochemical cycles of nutrients, REEs and Al remains unclear. The aim of the present study was to investigate the effects of the combination of the addition of soil amendment and the root development and activity of a fiber plant ramie (Boehmeria nivea L.) on the availability and distribution of nutrients, as well as of REEs and other potentially toxic elements (e.g. Al) in the soil-plant system. The results showed that the application of organic amendment and ramie planting induced a significant increase in soil pH, total carbon (C), nitrogen (N), and other nutrient (e.g. P and Ca) concentrations, while led to a decrease of 80-90% and 60-90% in soil extractable REE and Al concentrations respectively. Matrices of correlation showed that soil pH, total C, N, and P concentrations were among the most important factors controlling the availability of soil REEs and Al, and root characteristics (e.g. fine root length). The total C, N, P and extractable nutrient concentrations, and electrical conductivity were higher in the rhizosphere soils of ramie than those in the bulk soils. Moreover, more than 60% of the quantity of REE and Al in the whole ramie plant was stored within the thick roots. These results showed that, in addition to amendment, the effects induced by the roots of ramie could further improve soil properties through C input, nutrient mobilization and toxic element stabilization. Our study concludes that ramie planting with organic amendment is a promising phytostabilization strategy for the remediation of REE mine tailings in South China.

[Research advances of prostaglandin E2 synthases and receptors in cardiovascular diseases].

Prostaglandin E2 (PGE2) is an important lipid mediator derived from arachidonic acid. It is widely distributed in various tissues and involved in numerous physiological and pathophysiological processes. Based on the inhibition of inflammatory PGE2 production, non-steroidal anti-inflammatory drugs (NSAIDs) are considered as the most commonly used drugs to treat pain and inflammation. However, clinical trials have revealed that NSAIDs, especially cyclooxygenase-2 (COX-2) selective inhibitors, may predispose patients to a remarkably increased cardiovascular risk, including hypertension, myocardial infarction, and heart failure. This promotes scientists to develop new drugs to not only afford pain relief but also have cardiovascular efficacy. Microsomal prostaglandin E synthase-1 (mPGES-1), the key terminal enzyme catalyzing the synthesis of inflammatory PGE2, and the four PGE2 receptors (EP1-4) have gained more attention as the promising alternative drug targets for the development of novel NSAIDs. The role of mPGES-1 and EP receptors in cardiovascular diseases also has been widely studied. In this review, we highlight the most recent advances from our and other studies on the role of PGE2, particularly mPGES-1 and the four PGE2 receptors, in cardiovascular diseases.

Ameliorative effect of SIRT1 in postpartum depression mediated by upregulation of the glucocorticoid receptor.

Recent evidence has confirmed the association of glucocorticoid receptor (GR) gene variants with the "stress" endocrine axis in postpartum depression (PPD). Sirtuin 1(SIRT1) is an NAD+-dependent histone deacetylase and transcriptional enhancer of GR. However, to date, the function of the SIRT1 gene in the regulation of GR expression in PPD remains to be fully determined. A hormone-stimulated pregnancy (HSP) and subsequent "postpartum" withdrawal of estrogen was employed to mimic the fluctuations in estradiol associated with pregnancy and postpartum. We confirmed that estradiol benzoate withdrawal (EW)-rats displayed depression- and anxiety-like behaviors. These behavioral dysfunctions are associated with attenuated expression of SIRT1 and GR in the hippocampus. To assess the role of SIRT1, as well as its regulatory target directly, a selective SIRT1 activator (SRT2104) was infused into the hippocampus of EW-rats. We found that pharmacological activation of hippocampal SIRT1 blocks the development of depression-related, but not anxiety-related, phenotypes of PPD. In addition, the activation of SIRT1 leads to an increase in hippocampal GR expression in EW-rats. We further confirmed that SIRT1 physically interacts with GR in a glucocorticoid-dependent manner. Taken together, our results suggest that neuropathology in PPD is caused, at least in part, by the inhibition of the SIRT1-GR signaling pathway. Elevating SIRT1 levels, either pharmacologically or through other means, could represent a therapeutic strategy for PPD.

Selective Leaching of Rare Earth Elements from Ion-Adsorption Rare Earth Tailings: A Synergy between CeO2 Reduction and Fe/Mn Stabilization.

The increasing demand for rare earth elements (REEs) motivates the development of novel strategies for cost-effective REE recovery from secondary sources, especially rare earth tailings. The biggest challenges in recovering REEs from ion-adsorption rare earth tailings are incomplete extraction of cerium (Ce) and the coleaching of iron (Fe) and manganese (Mn). Here, a synergistic process between reduction and stabilization was proposed by innovatively using elemental sulfur (S) as reductant for converting insoluble CeO2 into soluble Ce2(SO4)3 and transforming Fe and Mn oxides into inert FeFe2O4 and MnFe2O4 spinel minerals. After the calcination at 400 °C, 97.0% of Ce can be dissolved using a diluted sulfuric acid, along with only 3.67% of Fe and 23.3% of Mn leached out. Thermodynamic analysis reveals that CeO2 was indirectly reduced by the intermediates MnSO4 and FeS in the system. Density functional theory calculations indicated that Fe(II) and Mn(II) shared similar outer electron arrangements and coordination environments, favoring Mn(II) over Ce(III) as a replacement for Fe(II) in the FeO6 octahedral structure of FeFe2O4. Further investigation on the leaching process suggested that 0.5 mol L-1 H2SO4 is sufficient for the recovery of REEs (97.0%). This research provides a promising strategy to selectively recover REEs from mining tailings or secondary sources via controlling the mineral phase transformation.

Plant-Soil Feedbacks for the Restoration of Degraded Mine Lands: A Review.

Much effort has been made to remediate the degraded mine lands that bring severe impacts to the natural environments. However, it remains unclear what drives the recovery of biodiversity and ecosystem functions, making the restoration of these fragile ecosystems a big challenge. The interactions among plant species, soil communities, and abiotic conditions, i.e., plant-soil feedbacks (PSFs), significantly influence vegetation development, plant community structure, and ultimately regulate the recovery of ecosystem multi-functionality. Here, we present a conceptual framework concerning PSFs patterns and potential mechanisms in degraded mine lands. Different from healthy ecosystems, mine lands are generally featured with harsh physical and chemical properties, which may have different PSFs and should be considered during the restoration. Usually, pioneer plants colonized in the mine lands can adapt to the stressful environment by forming tolerant functional traits and gathering specific soil microbial communities. Understanding the mechanisms of PSFs would enhance our ability to predict and alter both the composition of above- and below-ground communities, and improve the recovery of ecosystem functions in degraded mine lands. Finally, we put forward some challenges of the current PSFs study and discuss avenues for further research in the ecological restoration of degraded mine lands.