GSDME-mediated Pyroptosis Contributes to Chemotherapy-induced Platelet Hyperactivity and Thrombotic Potential.

Thrombotic complications due to platelet hyperreactivity are a major cause of death in patients undergoing chemotherapy. However, the underlying mechanisms are not fully understood. Herein, using human and GSDME-/- mouse platelets, we showed that GSDME is functionally expressed in anucleate platelets and GSDME-mediated pyroptosis, a newly identified form of cell death in mammalian nucleated cells, contributes to platelet hyperactivity in cisplatin-based chemotherapy. Cisplatin or etoposide activates caspase-3 to cleave GSDME, thereby releasing the N-terminal fragment of GSDME (GSDME-N) toward the platelet plasma membrane, subsequently forming membrane pores and facilitating platelet granule release. This eventually promotes platelet hyperactivity and thrombotic potential. We identified flotillin-2, a scaffold protein, as a GSDME-N interactor that recruits GSDME-N to the platelet membrane. loss of GSDME protects mice from cisplatin-induced platelet hyperactivity. Our results provide evidence that targeting GSDME-mediated pyroptosis could reduce thrombotic potential in chemotherapy.

Double-stranded DNA enhances platelet activation, thrombosis, and myocardial injury via cyclic GMP-AMP synthase.

AIMS: Elevated dsDNA levels in STEMI patients are associated with increased infarct size and worse clinical outcomes. However, the direct effect of dsDNA on platelet activation remains unclear. This study aims to investigate the direct influence of dsDNA on platelet activation, thrombosis, and the underlying mechanisms. METHODS AND RESULTS: Analysis of clinical samples revealed elevated plasma dsDNA levels in STEMI patients, which positively correlated with platelet aggregation and markers of neutrophil extracellular traps (NETs) such as MPO-DNA and CitH3. Platelet assays demonstrated the activation of the cGAS-STING pathway in platelets from STEMI patients. DsDNA directly potentiated platelet activation and thrombus formation. Mechanistic studies using G150 (cGAS inhibitor), H151 (STING inhibitor), and MCC950 (NLRP3 inhibitor), as well as cGAS-/-, STING-/- and NLRP3-/- mice showed that dsDNA activated cGAS, a previously unreported DNA sensor in platelets, and induced activation of the STING/NLRP3/caspase-1/IL-1ß axis. This cascade enhanced platelet activation and thrombus formation. Platelet cGAS depletion or Palbociclib, a cGAS-STING inhibitor, approved by the FDA for advanced breast cancer, ameliorated myocardial ischemia-reperfusion injury in ApoE-/- mice fed with a high-fat diet for 12 weeks. CONCLUSIONS: These results suggested that dsDNA is a novel driver of platelet activation and thrombus formation in STEMI patients. TRANSLATIONAL PERSPECTIVE: ST-elevated myocardial infarction (STEMI) patients exhibit high levels of plasma double-stranded DNA (dsDNA), which directly potentiates platelet activation through the platelet cGAS/STING/NLRP3/caspase-1/IL-1ß signaling pathway. STEMI patients may benefit from cGAS inhibition in the prevention of platelet hyperactivity and thrombus formation.

Spatial variation, emissions, transport, and risk assessment of organophosphate esters in two large petrochemical complexes in southern China.

Organophosphate esters (OPEs) serve as significant flame retardants and plasticizers in various petrochemical downstream products. The petrochemical industry could be a potential source of atmospheric OPEs, but their emissions from this industry are poorly understood. The present study revealed the spatial variation, emission, and atmospheric transport of traditional and novel OPEs (TOPEs and NOPEs, respectively) in atmospheric particulate matter (PM) across Hainan and Guangdong petrochemical complexes (HNPC and GDPC, respectively) in southern China. The total concentrations of TOPEs ranged from 232 to 46,002 pg/m3 and from 200 to 20,347 pg/m3 in the HNPC and GDPC, respectively, which were substantially higher than those of NOPEs (HNPC: 23.5-147 pg/m3, GDPC: 13.9-465 pg/m3). Enterprises involved in the production of downstream petrochemical products presented relatively high concentrations of OPEs, indicating evident emissions of these pollutants in the petrochemical industry. The correlations of PM-bound OPEs in the atmosphere are determined mainly by their coaddition to industrial products or their coexistence in technical mixtures. The annual emissions of TOPEs and NOPEs in the HNPC were 42.6 kg and 0.34 kg, respectively, and those in the GDPC were 116 kg and 1.85 kg, respectively. OPEs from the HNPC can reach Vietnam, Cambodia, and Guangxi Province, China, and those from the GDPC can reach Guangxi Province and Hunan Province via atmospheric transmission after 24 h of emission. The OPE concentrations reaching the receptor regions were generally less than 3.20 pg/m3. Risk assessment revealed that OPE inhalation exposure on two petrochemical complexes likely poses minor risks for people living in the study areas, but the risk resulting from two chlorinated OPEs should be noted since they are close to the threshold values. This study has implications for enhancing control measures for OPE emissions to reduce health risks related to the petrochemical industry.

TBC1D4 antagonizes RAB2A-mediated autophagic and endocytic pathways.

Macroautophagic/autophagic and endocytic pathways play essential roles in maintaining homeostasis at different levels. It remains poorly understood how both pathways are coordinated and fine-tuned for proper lysosomal degradation of diverse cargoes. We and others recently identified a Golgi-resident RAB GTPase, RAB2A, as a positive regulator that controls both autophagic and endocytic pathways. In the current study, we report that TBC1D4 (TBC1 domain family member 4), a TBC domain-containing protein that plays essential roles in glucose homeostasis, suppresses RAB2A-mediated autophagic and endocytic pathways. TBC1D4 bound to RAB2A through its N-terminal PTB2 domain, which impaired RAB2A-mediated autophagy at the early stage by preventing ULK1 complex activation. During the late stage of autophagy, TBC1D4 impeded the association of RUBCNL/PACER and RAB2A with STX17 on autophagosomes by direct interaction with RUBCNL via its N-terminal PTB1 domain. Disruption of the autophagosomal trimeric complex containing RAB2A, RUBCNL and STX17 resulted in defective HOPS recruitment and eventually abortive autophagosome-lysosome fusion. Furthermore, TBC1D4 inhibited RAB2A-mediated endocytic degradation independent of RUBCNL. Therefore, TBC1D4 and RAB2A form a dual molecular switch to modulate autophagic and endocytic pathways. Importantly, hepatocyte- or adipocyte-specific tbc1d4 knockout in mice led to elevated autophagic flux and endocytic degradation and tissue damage. Together, this work establishes TBC1D4 as a critical molecular brake in autophagic and endocytic pathways, providing further mechanistic insights into how these pathways are intertwined both in vitro and in vivo.Abbreviations: ACTB: actin beta; ATG9: autophagy related 9; ATG14: autophagy related 14; ATG16L1: autophagy related 16 like 1; CLEM: correlative light electron microscopy; Ctrl: control; DMSO: dimethyl sulfoxide; EGF: epidermal growth factor; EGFR: epidermal growth factor receptor; FL: full length; GAP: GTPase-activating protein; GFP: green fluorescent protein; HOPS: homotypic fusion and protein sorting; IP: immunoprecipitation; KD: knockdown; KO: knockout; LAMP1: lysosomal associated membrane protein 1; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; OE: overexpression; PG: phagophore; PtdIns3K: class III phosphatidylinositol 3-kinase; SLC2A4/GLUT4: solute carrier family 2 member 4; SQSTM1/p62: sequestosome 1; RUBCNL/PACER: rubicon like autophagy enhancer; STX17: syntaxin 17; TAP: tandem affinity purification; TBA: total bile acid; TBC1D4: TBC1 domain family member 4; TUBA1B: tubulin alpha 1b; ULK1: unc-51 like autophagy activating kinase 1; VPS39: VPS39 subunit of HOPS complex; WB: western blot; WT: wild type.

Mechanistic insights into tris(2-chloroisopropyl) phosphate biomineralization coupled with lead (II) biostabilization driven by denitrifying bacteria.

The ubiquity and persistence of organophosphate esters (OPEs) and heavy metal (HMs) pose global environmental risks. This study explored tris(2-chloroisopropyl)phosphate (TCPP) biomineralization coupled to lead (Pb2+) biostabilization driven by denitrifying bacteria (DNB). The domesticated DNB achieved synergistic bioremoval of TCPP and Pb2+ in the batch bioreactor (efficiency: 98 %).TCPP mineralized into PO43- and Cl-, and Pb2+ precipitated with PO43-. The TCPP-degrading/Pb2+-resistant DNB: Achromobacter, Pseudomonas, Citrobacter, and Stenotrophomonas, dominated the bacterial community, and synergized TCPP biomineralization and Pb2+ biostabilization. Metagenomics and metaproteomics revealed TCPP underwent dechlorination, hydrolysis, the TCA cycle-based dissimilation, and assimilation; Pb2+ was detoxified via bioprecipitation, bacterial membrane biosorption, EPS biocomplexation, and efflux out of cells. TCPP, as an initial donor, along with NO3-, as the terminal acceptor, formed a respiratory redox as the primary energy metabolism. Both TCPP and Pb2+ can stimulate phosphatase expression, which established the mutual enhancements between their bioconversions by catalyzing TCPP dephosphorylation and facilitating Pb2+ bioprecipitation. TCPP may alleviate the Pb2+-induced oxidative stress by aiding protein phosphorylation. 80 % of Pb2+ converted into crystalized pyromorphite. These results provide the mechanistic foundations and help develop greener strategies for synergistic bioremediation of OPEs and HMs.

The Role of Place Attachment in the Relationship between Attitudes toward Aging and Subjective Well-Being among Community-Dwelling Older Adults in Taiwan.

Subjective well-being presents a societal challenge for vulnerable older adults. This study aims to investigate the mediating role of place attachment in the relationship between attitudes toward aging and subjective well-being among community-dwelling older adults in Taiwan. Two waves of investigations were conducted to examine the interplay between attitudes toward aging, subjective well-being, and place attachment among older adults. In Wave I, 1190 participants were enrolled, revealing predominantly younger cohorts with substantial educational levels. The subsequent Wave II involved 483 participants, maintaining continuity in characteristics. Subjective well-being remained moderate across waves, with prevalent positive attitudes toward aging. Place attachment scores indicated moderate to high associations. After controlling for demographics, structural equation modeling (SEM) in both waves revealed significant positive associations: attitudes toward aging influenced well-being, attitudes toward aging were positively associated with place attachment, and place attachment was positively related to well-being. Mediation testing confirmed the mediating role of place attachment in the relationship between attitudes toward aging and well-being. These findings underscore the important role of place attachment. It is evident that improving attitudes toward aging is an effective intervention which can lead to a better sense of well-being by enhancing place attachment to empower civil society.

Tuning nitrogen adsorption and activation performances of Three-Atom transition metal clusters by modulating external electric fields.

Three-atom transition metal clusters (TATMCs) with remarkable catalytic activities, especially Nb3, Zr3, and Y3, are proven to be suitable candidates for efficient ammonia production. The pursuit of effective strategies to further promote the ammonia synthesis performance of TATMCs is necessary. In this study, we systematically investigate the effect of external electric fields on tuning the N2 adsorption and NN* activation performances of Nb3, Zr3, and Y3. Our findings demonstrate that the medium and low positive fields promote the N2 adsorption performance of Nb3, while both positive and negative fields enhance nitrogen adsorption on Zr3. Additionally, electric fields may impede N2 fixation on Y3, yet the N2 adsorption performance of Y3 remains considerable. Negative electric fields enhance the NN* activation performance of Nb3 and Y3. But only high negative fields weaken the NN bond on Zr3, which is attributed to the promotion of the charge accumulation around two N atoms. Notably, Nb3 and Zr3 are identified as two TATMCs with the potential for simultaneous optimization of their EN and ICOHP values. This work sheds light on the field effects on the N2 adsorption and NN* activation performances of TATMCs and guides the design of catalysts for achieving more sustainable ammonia synthesis.

ANKFY1 bridges ATG2A-mediated lipid transfer from endosomes to phagophores.

Macroautophagy is a process that cells engulf cytosolic materials by autophagosomes and deliver them to lysosomes for degradation. The biogenesis of autophagosomes requires ATG2 as a lipid transfer protein to transport lipids from existing membranes to phagophores. It is generally believed that endoplasmic reticulum is the main source for lipid supply of the forming autophagosomes; whether ATG2 can transfer lipids from other organelles to phagophores remains elusive. In this study, we identified a new ATG2A-binding protein, ANKFY1. Depletion of this endosome-localized protein led to the impaired autophagosome growth and the reduced autophagy flux, which largely phenocopied ATG2A/B depletion. A pool of ANKFY1 co-localized with ATG2A between endosomes and phagophores and depletion of UVRAG, ANKFY1 or ATG2A/B led to reduction of PI3P distribution on phagophores. Purified recombinant ANKFY1 bound to PI3P on membrane through its FYVE domain and enhanced ATG2A-mediated lipid transfer between PI3P-containing liposomes. Therefore, we propose that ANKFY1 recruits ATG2A to PI3P-enriched endosomes and promotes ATG2A-mediated lipid transfer from endosomes to phagophores. This finding implicates a new lipid source for ATG2A-mediated phagophore expansion, where endosomes donate PI3P and other lipids to phagophores via lipid transfer.

Spatiotemporal variations, sources, and atmospheric transformation potential of volatile organic compounds in an industrial zone based on high-resolution measurements in three plants.

Industrial emissions are significant sources of volatile organic compounds (VOCs). This study conducted a field campaign at high temporal and spatial resolution to monitor VOCs within three plants in an industrial park in southern China. VOC concentrations showed significant spatial variability in this industrial zone, with median concentrations of 75.22, 40.53, and 29.41 µg/m3 for the total VOCs in the three plants, respectively, with oxygenated VOCs (OVOCs) or aromatics being the major VOCs. Spatial variability within each plant was also significant but VOC-dependent. Seasonal variations in the VOC levels were governed by their industrial emissions, meteorological conditions, and photochemical losses, and they were different for the four groups of VOCs. The temporal and spatial variations in the VOC compositions suggest similar sources of each class of VOCs during different periods of the year in each plant. The diurnal patterns of VOCs (unimodal or bimodal) clearly differed from those at most industrial/urban locations previously, reflecting a dependence on industrial activities. The secondary transformation potential of VOCs also varied temporally and spatially, and aromatics generally made the predominant contributions in this industrial park. The loss rate of OH radicals and ozone formation potential were highly correlated, but the linear relationship substantially changed in summer and autumn due to the intensive emissions of an OVOC species. The lifetime cancer and non-cancer risks via occupational inhalation of the VOCs in the plants were acceptable but merit attention. Taking the secondary transformation potential and health risks into consideration, styrene, xylene, toluene, trichloroethylene, and benzene were proposed to be the priority VOCs regulated in the plants.

Impact of fine particulate matter on liver injury: evidence from human, mice and cells.

BACKGROUND: A recently discovered risk factor for chronic liver disease is ambient fine particulate matter (PM2.5). Our research aims to elucidate the effects of PM2.5 on liver injury and the potential molecular mechanisms. METHODS AND RESULTS: A population-based longitudinal study involving 102,918 participants from 15 Chinese cities, using linear mixed-effect models, found that abnormal alterations in liver function were significantly associated with long-term exposure to PM2.5. The serum levels of alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, direct bilirubin, and triglyceride increased by 2.05%, 2.04%, 0.58%, 2.99%, and 1.46% with each 10 µg/m3 increase in PM2.5. In contrast, the serum levels of total protein, albumin, and prealbumin decreased by 0.27%, 0.48%, and 2.42%, respectively. Mice underwent chronic inhalation exposure to PM2.5 experienced hepatic inflammation, steatosis and fibrosis. In vitro experiments found that hepatocytes experienced an inflammatory response and lipid metabolic dysregulation due to PM2.5, which also activated hepatic stellate cells. The down-regulation and mis-localization of polarity protein Par3 mediated PM2.5-induced liver injury. CONCLUSIONS: PM2.5 exposure induced liver injury, mainly characterized by steatosis and fibrosis. The down-regulation and mis-localization of Par3 were important mechanisms of liver injury induced by PM2.5.

Disposable Plastic Waste and Associated Antioxidants and Plasticizers Generated by Online Food Delivery Services in China: National Mass Inventories and Environmental Release.

China's online food delivery (OFD) services consume enormous amounts of disposable plastics. Here, we investigated and modeled the national mass inventories and environmental release of plastics and chemical additives in the plastic. The extra-tree regression identified six key descriptors in determining OFD sales in Chinese cities. Approximately 847 kt of OFD plastic waste was generated in 2021 (per capita 1.10 kg/yr in the megacities and 0.39 kg/yr in other cities). Various additives were extensively detected, with geomean concentrations of 140.96, 4.76, and 0.25 µg/g for ∑8antioxidants, ∑21phthalates, and bisphenol A (BPA), respectively. The estimated mass inventory of these additives in the OFD plastics was 164.7 t, of which 51.1 t was released into the atmosphere via incineration plants and 51.0 t was landfilled. The incineration also released 8.07 t of polycyclic aromatic hydrocarbons and 39.1 kt of particulate matter into the atmosphere. Takeout food may increase the dietary intake of phthalates and BPA by 30% to 50% and raise concerns about considerable exposure to antioxidant transformation products. This study provides profound environmental implications for plastic waste in the Chinese OFD industry. We call for a sustainable circular economy action plan for waste disposal, but mitigating the hazardous substance content and their emissions is urgent.

A mitophagy sensor PPTC7 controls BNIP3 and NIX degradation to regulate mitochondrial mass.

Mitophagy mediated by BNIP3 and NIX critically regulates mitochondrial mass. Cellular BNIP3 and NIX levels are tightly controlled by SCFFBXL4-mediated ubiquitination to prevent excessive mitochondrial loss and lethal disease. Here, we report that knockout of PPTC7, a mitochondrial matrix protein, hyperactivates BNIP3-/NIX-mediated mitophagy and causes perinatal lethality that is rescued by NIX knockout in mice. Biochemically, the PPTC7 precursor is trapped by BNIP3 and NIX to the mitochondrial outer membrane, where PPTC7 scaffolds assembly of a substrate-PPTC7-SCFFBXL4 holocomplex to degrade BNIP3 and NIX, forming a homeostatic regulatory loop. PPTC7 possesses an unusually weak mitochondrial targeting sequence to facilitate its outer membrane retention and mitophagy control. Starvation upregulates PPPTC7 expression in mouse liver to repress mitophagy, which critically maintains hepatic mitochondrial mass, bioenergetics, and gluconeogenesis. Collectively, PPTC7 functions as a mitophagy sensor that integrates homeostatic and physiological signals to dynamically control BNIP3 and NIX degradation, thereby maintaining mitochondrial mass and cellular homeostasis.

Qa-SNARE syntaxin 18 mediates lipid droplet fusion with SNAP23 and SEC22B.

Lipid droplets (LDs) are dynamic lipid storage organelles that can sense and respond to changes in systemic energy balance. The size and number of LDs are controlled by complex and delicate mechanisms, among which, whether and which SNARE proteins mediate LD fusion, and the mechanisms governing this process remain poorly understood. Here we identified a SNARE complex, syntaxin 18 (STX18)-SNAP23-SEC22B, that is recruited to LDs to mediate LD fusion. STX18 targets LDs with its transmembrane domain spanning the phospholipid monolayer twice. STX18-SNAP23-SEC22B complex drives LD fusion in adiposome lipid mixing and content mixing in vitro assays. CIDEC/FSP27 directly binds STX18, SEC22B, and SNAP23, and promotes the lipid mixing of SNAREs-reconstituted adiposomes by promoting LD clustering. Knockdown of STX18 in mouse liver via AAV resulted in smaller liver and reduced LD size under high-fat diet conditions. All these results demonstrate a critical role of the SNARE complex STX18-SNAP23-SEC22B in LD fusion.

The Pyroptosis-Related Signature Composed of GSDMC Predicts Prognosis and Contributes to Growth and Metastasis of Hepatocellular Carcinoma.

BACKGROUND: Pyroptosis-related genes (PRG) are closely associated with the progression and metastasis of hepatocellular carcinoma (HCC). The predictive power of PRGs could be used to assess the clinical outcomes of HCC. METHODS: The Cancer Genome Atlas (TCGA) RNA-seq data and clinical information from patients with liver hepatocellular carcinoma (LIHC) were used to identify PRG with differentially expressed between HCC and normal samples. Univariate Cox regression, least absolute shrinkage and selection operator (LASSO) Cox method, and multivariate Cox regression analysis were used to develop a prognostic model that included three PRGs. Gene set enrichment analysis (GSEA) was performed to identify differential immune cells and their associated pathways. The expression of Gasdermin C (GSDMC) in the HCC samples was detected by western blotting, and the function of GSDMC in HCC proliferation and metastasis was detected by the Cell Counting Kit-8 (CCK-8), colony formation, cell invasion, and wound healing assays. RESULTS: Of 52 PRGs, GSDMC, Bcl-2 homologusantagonist/ killer 1 (BAK1), and NOD-like receptor thermal protein domain associated protein 6 (NLRP6) were selected to establish a prognostic model. The model successfully differentiated HCC patients with varied survival in the TCGA training and test cohorts, as well as the International Cancer Genome Consortium (ICGC) validation cohorts. The risk score was proven to be an independent prognostic factor. In addition, we also reported a marked upregulation of GSDMC in HCC tissues, which could be induced by CD274 (PD-L1). Overexpression of GSDMC contributes to HCC cells invasion, proliferation, and migration. CONCLUSIONS: The three PRGs signatures containing GSDMC independently predicted HCC prognosis. As a new driver molecule, GSDMC could play a tumor-promoting role by facilitating HCC growth and metastasis.

C9orf72-catalyzed GTP loading of Rab39A enables HOPS-mediated membrane tethering and fusion in mammalian autophagy.

The multi-subunit homotypic fusion and vacuole protein sorting (HOPS) membrane-tethering complex is required for autophagosome-lysosome fusion in mammals, yet reconstituting the mammalian HOPS complex remains a challenge. Here we propose a "hook-up" model for mammalian HOPS complex assembly, which requires two HOPS sub-complexes docking on membranes via membrane-associated Rabs. We identify Rab39A as a key small GTPase that recruits HOPS onto autophagic vesicles. Proper pairing with Rab2 and Rab39A enables HOPS complex assembly between proteoliposomes for its tethering function, facilitating efficient membrane fusion. GTP loading of Rab39A is important for the recruitment of HOPS to autophagic membranes. Activation of Rab39A is catalyzed by C9orf72, a guanine exchange factor associated with amyotrophic lateral sclerosis and familial frontotemporal dementia. Constitutive activation of Rab39A can rescue autophagy defects caused by C9orf72 depletion. These results therefore reveal a crucial role for the C9orf72-Rab39A-HOPS axis in autophagosome-lysosome fusion.

Dual roles of the Arabidopsis PEAT complex in histone H2A deubiquitination and H4K5 acetylation.

Histone H2A monoubiquitination is associated with transcriptional repression and needs to be removed by deubiquitinases to facilitate gene transcription in eukaryotes. However, the deubiquitinase responsible for genome-wide H2A deubiquitination in plants has yet to be identified. In this study, we found that the previously identified PWWP-EPCR-ARID-TRB (PEAT) complex components interact with both the ubiquitin-specific protease UBP5 and the redundant histone acetyltransferases HAM1 and HAM2 (HAM1/2) to form a larger version of PEAT complex in Arabidopsis thaliana. UBP5 functions as an H2A deubiquitinase in a nucleosome substrate-dependent manner in vitro and mediates H2A deubiquitination at the whole-genome level in vivo. HAM1/2 are shared subunits of the PEAT complex and the conserved NuA4 histone acetyltransferase complex, and are responsible for histone H4K5 acetylation. Within the PEAT complex, the PWWP components (PWWP1, PWWP2, and PWWP3) directly interact with UBP5 and are necessary for UBP5-mediated H2A deubiquitination, while the EPCR components (EPCR1 and EPCR2) directly interact with HAM1/2 and are required for HAM1/2-mediated H4K5 acetylation. Collectively, our study not only identifies dual roles of the PEAT complex in H2A deubiquitination and H4K5 acetylation but also illustrates how these processes collaborate at the whole-genome level to regulate the transcription and development in plants.

Binary Heterogroup-Templated Scaffolds of Polyoxopalladates as Precatalysts for Plasma-Assisted Ammonia Synthesis.

In addition to improving the synthetic efficiency, the template method can do a lot more in the chemistry of polyoxopalladates (POPs), such as the establishment of novel metal-oxo scaffolds. In this endeavor, a binary system comprising heterogroups of nonmetallic {As/SiO4} and metallic {VO4/5} successfully fulfills the templated growth of two POPs with unprecedented seesaw- and spindle-like prototypes. Of these, self-aggregation of heterogroups beacons an effective route to break the highly symmetrical PdII-oxo matrix and to force the arrangement of addenda in a nonconventional manner. Aside from the interest in their structural features, the as-made POPs are available for immobilization on the mesoporous SBA-15 as precatalysts for ammonia synthesis. The outer cover of heterogroups in the POP precursors contributes to the ultrafine size and uniform distribution of derived Pd0 nanoparticles (PdNPs). With the help of plasma activation on H2 and N2, such PdNPs-SBA15 catalysts significantly improve the production performance of NH3, showcasing the maximum synthesis rate of 64.42 µmol/(min·gcat) with the corresponding energy yield as high as 4.38 g-NH3/kWh.

Complex polycyclic aromatic compound mixtures in PM2.5 in a Chinese megacity: Spatio-temporal variations, toxicity, and source apportionment.

Polycyclic aromatic compounds (PACs) are important toxic organic components in fine particulate matter (PM2.5), whereas the links between PM2.5 toxicity and associated PACs in ambient air are poorly understood. This study investigated the spatial-temporal variations of PACs in PM2.5 collected from 11 sampling sites across a Chinese megacity and characterized the reactive oxygen species (ROS) generation and cytotoxicity induced by organic extracts of PM2.5 based on cellular assays. The extra trees regression model based on machine learning and ridge regression were used to identify the key toxicants among complex PAC mixtures. The total concentrations of these PACs varied from 2.12 to 71.7 ng/m3 across the study city, and polycyclic aromatic hydrocarbons (PAHs) are the main PACs. The spatial variations of the toxicological indicators generally resembled those of the PAC concentrations, and the PM2.5 related to waste treatment facilities exhibited the strongest toxic potencies. The ROS generation was highly correlated with high molecular weight PAHs (MW302 PAHs), followed by PAHs with MW<302 amu and oxygenated PAHs, but not with nitrated PAHs and the plastics additives. The cell mortality showed weak correlations with these organic constituents. The associations between the biological endpoints and these PM2.5-bound contaminants were further confirmed by exposure to authentic chemicals. Four primary sources of PACs were identified, among which coal and biomass combustion sources (30.2% of the total PACs) and industrial sources (31.0%) were predominant. PACs emitted from industrial sources were highly associated with ROS generation in this city. Our findings highlight the potent ROS-generating potential of MW302 PAHs and the importance of industrial sources contributing to PM2.5 toxicity in this megacity, raising public concerns and further administration.

WRKY transcription factors and OBERON histone-binding proteins form complexes to balance plant growth and stress tolerance.

WRKY transcription factors in plants are known to be able to mediate either transcriptional activation or repression, but the mechanism regulating their transcriptional activity is largely unclear. We found that group IId WRKY transcription factors interact with OBERON (OBE) proteins, forming redundant WRKY-OBE complexes in Arabidopsis thaliana. The coiled-coil domain of WRKY transcription factors binds to OBE proteins and is responsible for target gene selection and transcriptional repression. The PHD finger of OBE proteins binds to both histones and WRKY transcription factors. WRKY-OBE complexes repress the transcription of numerous stress-responsive genes and are required for maintaining normal plant growth. Several WRKY and OBE mutants show reduced plant size and increased drought tolerance, accompanied by increased expression of stress-responsive genes. Moreover, expression levels of most of these WRKY and OBE genes are reduced in response to drought stress, revealing a previously uncharacterized regulatory mechanism of the drought stress response. These results suggest that WRKY-OBE complexes repress transcription of stress-responsive genes, and thereby balance plant growth and stress tolerance.