Breaking the Activity-Selectivity Trade-off for CH4-to-C2H6 Photoconversion.

Photocatalytic conversion of methane (CH4) to ethane (C2H6) has attracted extensive attention from academia and industry. Typically, the traditional oxidative coupling of CH4 (OCM) reaches a high C2H6 productivity, yet the inevitable overoxidation limits the target product selectivity. Although the traditional nonoxidative coupling of CH4 (NOCM) can improve the product selectivity, it still encounters unsatisfied activity, arising from being thermodynamically unfavorable. To break the activity-selectivity trade-off, we propose a conceptually new mechanism of H2O2-triggered CH4 coupling, where the H2O2-derived ·OH radicals are rapidly consumed for activating CH4 into ·CH3 radicals exothermically, which bypasses the endothermic steps of the direct CH4 activation by photoholes and the interaction between ·CH3 and ·OH radicals, affirmed by in situ characterization techniques, femtosecond transient absorption spectroscopy, and density-functional theory calculation. By this pathway, the designed Au-WO3 nanosheets achieve unprecedented C2H6 productivity of 76.3 mol molAu-1 h-1 with 95.2% selectivity, and TON of 1542.7 (TOF = 77.1 h-1) in a self-designed flow reactor, outperforming previously reported photocatalysts regardless of OCM and NOCM pathways. Also, under outdoor natural sunlight irradiation, the Au-WO3 nanosheets exhibit similar activity and selectivity toward C2H6 production, showing the possibility for practical applications. Interestingly, this strategy can be applied to other various photocatalysts (Au-WO3, Au-TiO2, Au-CeO2, Pd-WO3, and Ag-WO3), showing a certain universality. It is expected that the proposed mechanism adds another layer to our understanding of CH4-to-C2H6 conversion.

Light-Driven C-C Coupling for Targeted Synthesis of CH3 COOH with Nearly 100 % Selectivity from CO2.

Targeted synthesis of acetic acid (CH3 COOH) from CO2 photoreduction under mild conditions mainly limits by the kinetic challenge of the C-C coupling. Herein, we utilized doping engineering to build charge-asymmetrical metal pair sites for boosted C-C coupling, enhancing the activity and selectivity of CO2 photoreduction towards CH3 COOH. As a prototype, the Pd doped Co3 O4 atomic layers are synthesized, where the established charge-asymmetrical cobalt pair sites are verified by X-ray photoelectron spectroscopy and X-ray absorption near edge spectroscopy spectra. Theoretical calculations not only reveal the charge-asymmetrical cobalt pair sites caused by Pd atom doping, but also manifest the promoted C-C coupling of double *COOH intermediates through shortening of the coupled C-C bond distance from 1.54 to 1.52 Å and lowering their formation energy barrier from 0.77 to 0.33 eV. Importantly, the decreased reaction energy barrier from the protonation of two*COOH into *CO intermediates for the Pd-Co3 O4 atomic layer slab is 0.49 eV, higher than that of the Co3 O4 atomic layer slab (0.41 eV). Therefore, the Pd-Co3 O4 atomic layers exhibit the CH3 COOH evolution rate of ca. 13.8 µmol g-1 h-1 with near 100% selectivity, both of which outperform all previously reported single photocatalysts for CO2 photoreduction towards CH3 COOH under similar conditions.

CTRP3 inhibits myocardial fibrosis through the P2X7R-NLRP3 inflammasome pathway in SHR rats.

BACKGROUND AND PURPOSE: Reducing hypertensive myocardial fibrosis is the fundamental approach to preventing hypertensive ventricular remodelling. C1q/TNF-related protein-3 (CTRP3) is closely associated with hypertension. However, the role and mechanism of CTRP3 in hypertensive myocardial fibrosis are unclear. In this study, we aimed to explore the effect of CTRP3 on hypertensive myocardial fibrosis and the potential mechanism. METHODS AND RESULTS: WKY and SHR rats were employed, blood pressure, body weight, heart weight, H/BW were measured, and fibrotic-related proteins, CTRP3 and Collagen I were tested in myocardium at 12 and 20 weeks by immunohistochemical staining and Western blotting, respectively. The results showed that compared with the WKY, SBP, DBP, mean arterial pressure and heart rate (HR) were all significantly increased in SHR at 12 and 20 weeks, while heart weight and H/BW were only increased at 20 weeks. Meanwhile, CTRP3 decreased, while Collagen I increased significantly in the SHR rat myocardium at 20 weeks, which compared to the WKY. Moreover, the expression of α-SMA increased from 12 weeks, Collagen I/III and MMP2/9 increased and TIMP-2 decreased until 20 weeks. In order to explore the function and mechanism of CTRP3 in hypertensive fibrosis, Angiotensin II (Ang II) was used to induce hypertension in primary neonatal rat cardiac fibroblasts in vitro . CTRP3 significantly inhibited the Ang II induced activation of fibrotic proteins, purinergic 2X7 receptor (P2X7R)-NLRP3 inflammasome pathway. The P2X7R agonist BzATP significantly exacerbated Ang II-induced NLRP3 inflammasome activation, which was decreased by the P2X7R antagonists A43079, CTRP3 and MCC950. CONCLUSION: CTRP3 expression was decreased in the myocardium of SHR rats, and exogenous CTRP3 inhibited Ang II-induced fibrosis in cardiac fibroblasts by regulating the P2X7R-NLRP3 inflammasome pathway, suggesting that CTRP3 is a potential drug for alleviating myocardial fibrosis in hypertensive conditions.

Potential Application of Intestinal Organoids in Intestinal Diseases.

To accurately reveal the scenario and mecahnism of gastrointestinal diseases, the establishment of in vitro models of intestinal diseases and drug screening platforms have become the focus of attention. Over the past few decades, animal models and immortalized cell lines have provided valuable but limited insights into gastrointestinal research. In recent years, the development of intestinal organoid culture system has revolutionized in vitro studies of intestinal diseases. Intestinal organoids are derived from self-renewal and self-organization intestinal stem cells (ISCs), which can replicate the genetic characteristics, functions, and structures of the original tissues. Consequently, they provide new stragety for studying various intestinal diseases in vitro. In the review, we will discuss the culture techniques of intestinal organoids and describe the use of intestinal organoids as research tools for intestinal diseases. The role of intestinal epithelial cells (IECs) played in the pathogenesis of inflammatory bowel diseases (IBD) and the treatment of intestinal epithelial dysfunction will be highlighted. Besides, we review the current knowledge on using intestinal organoids as models to study the pathogenesis of IBD caused by epithelial dysfunction and to develop new therapeutic approaches. Finally, we shed light on the current challenges of using intestinal organoids as in vitro models.

A chitosan-based conductive double network hydrogel doped by tannic acid-reduced graphene oxide with excellent stretchability and high sensitivity for wearable strain sensors.

Conductive hydrogels usually suffer from weak mechanical properties and are easily destroyed, resulting in limited applications in flexible electronics. Concurrently, adding conductive additives to the hydrogel solution increases the probability of agglomeration and uneven dispersion issues. In this study, the biocompatible natural polymer chitosan was used as the network substrate. The rigid network employed was the Cit3-ion crosslinked chitosan (CS) network, and the MBA chemically crosslinked polyacrylamide (PAM) network was used as the flexible network. Tannic acid-reduced graphene oxide (TA-rGO), which has excellent conductivity and dispersibility, is used as a conductive filler. Thus, a CS/TA-rGO/PAM double network conductive hydrogel with excellent performance, high toughness, high conductivity, and superior sensing sensitivity was prepared. The prepared CS/TA-rGO/PAM double network conductive hydrogels have strong tensile properties (strain and toughness as high as 2009 % and 1045 kJ/cm3), excellent sensing sensitivity (GF value was 4.01), a wider strain detection range, high cycling stability and durability, good biocompatibility, and antimicrobial properties. The hydrogel can be assembled into flexible wearable devices that can not only dynamically detect human movements, such as joint bending, facial expression changes, swallowing, and saying, but also recognize handwriting and enable human-computer interaction.

Total flavonoids extracted from Penthorum chinense Pursh mitigates CCl4-induced hepatic fibrosis in rats via inactivation of TLR4-MyD88-mediated NF-κB pathways and regulation of liver metabolism.

Background: Penthorum chinense Pursh (PCP) is widely utilized in China to treat a variety of liver diseases. It has been shown that flavonoids inhibit inflammation and have the potential to attenuate tissue damage and fibrosis. However, the mechanisms underlying how total flavonoids isolated from PCP (TFPCP) exert their anti-fibrotic effects remain unclear. Methods: The chemical composition of TFPCP was determined using UHPLC-Q-Orbitrap HRMS. Subsequently, rats were randomly assigned to a control group (Control), a carbon tetrachloride (CCl4)-induced hepatic fibrosis model group (Model), a positive control group [0.2 mg/(kg∙day)] of Colchicine), and three TFPCP treatment groups [50, 100, and 150 mg/(kg∙day)]. All substances were administered by gavage and treatments lasted for 9 weeks. Simultaneously, rats were intraperitoneally injected with 10%-20% CCl4 for 9 weeks to induce liver fibrosis. At the end of the experiment, the liver ultrasound, liver histomorphological, biochemical indicators, and inflammatory cytokine levels were tested respectively. The underlying mechanisms were assessed using Western blot, immunohistochemistry, immunofluorescence, RT-qPCR, and metabolomics. Results: Fourteen flavonoids were identified in TFPCP. Compared with control animals, CCl4-treated rats demonstrated obvious liver injury and fibrosis, manifested as increases in gray values, distal diameter of portal vein (DDPV) and a decrease in blood flow velocity (VPV) in the ultrasound analysis; increased biochemical index values (serum levels of ALT, AST, TBIL, and ALP); marked increases in the contents of fibrotic markers (PC III, COL4, LN, HA) and inflammatory factors (serum TNF-α, IL-6, and IL-1ß); and significant pathological changes. However, compared with the Model group, the ultrasound parameters were significantly improved and the serum levels of inflammatory cytokines were reduced in the TFPCP group. In contrast, the expression of TGF-ß1, TLR4, and MyD88, as well as the p-P65/P65 and p-IκBα/IκBα ratios, were considerably reduced following TFPCP treatment. In addition, we identified 32 metabolites exhibiting differential abundance in the Model group. Interestingly, TFPCP treatment resulted in the restoration of the levels of 20 of these metabolites. Conclusion: Our findings indicated that TFPCP can ameliorate hepatic fibrosis by improving liver function and morphology via the inactivation of the TLR4/MyD88-mediated NF-κB pathway and the regulation of liver metabolism.

Insight into extracellular vesicles in vascular diseases: intercellular communication role and clinical application potential.

BACKGROUND: Cells have been increasingly known to release extracellular vesicles (EVs) to the extracellular environment under physiological and pathological conditions. A plethora of studies have revealed that EVs contain cell-derived biomolecules and are found in circulation, thereby implicating them in molecular trafficking between cells. Furthermore, EVs have an effect on physiological function and disease development and serve as disease biomarkers. MAIN BODY: Given the close association  between EV circulation and vascular disease, this review aims to provide a brief introduction to EVs, with a specific focus on the EV cargoes participating in pathological mechanisms, diagnosis, engineering, and clinical potential, to highlight the emerging evidence suggesting promising targets in vascular diseases. Despite the expansion of research in this field, some noticeable limitations remain for clinical translational research. CONCLUSION: This review makes a novel contribution to a summary of recent advances and a perspective on the future of EVs in vascular diseases. Video Abstract.

TRIP6 disrupts tight junctions to promote metastasis and drug resistance and is a therapeutic target in colorectal cancer.

Metastasis is the primary cause of death in colorectal cancer (CRC). Thyroid hormone receptor interacting protein 6 (TRIP6) is an adaptor protein that regulates cell motility. Here, we aim to elucidate the role of TRIP6 in driving CRC tumorigenesis and metastasis and evaluate its potential as a therapeutic target. TRIP6 mRNA is up-regulated in CRC compared to adjacent normal tissues in three independent cohorts (all P < 0.0001), especially in liver metastases (P < 0.001). High TRIP6 expression predicts poor prognosis of CRC patients in our cohort (P = 0.01) and TCGA cohort (P = 0.02). Colon-specific TRIP6 overexpression (Trip6KIVillin-Cre) in mice accelerated azoxymethane (AOM)-induced CRC (P < 0.05) and submucosal invasion (P < 0.0001). In contrast, TRIP6 knockout (Trip6+/- mice) slowed tumorigenesis (P < 0.05). Consistently, TRIP6 overexpression in CRC cells promoted epithelial-mesenchymal transition (EMT), cell migration/invasion in vitro, and metastases in vivo (all P < 0.05), whereas knockdown of TRIP6 exerted opposite phenotypes. Mechanistically, TRIP6 interacted PDZ domain-containing proteins such as PARD3 to impair tight junctions, evidenced by decreased tight junction markers and gut permeability dysfunction, inhibit PTEN, and activate oncogenic Akt signaling. TRIP6-induced pro-metastatic phenotypes and Akt activation depends on PARD3. Targeting TRIP6 by VNP-encapsulated TRIP6-siRNA synergized with Oxaliplatin and 5-Fluorouracil to suppress CRC liver metastases. In conclusion, TRIP6 promotes CRC metastasis by directly interacting with PARD3 to disrupt tight junctions and activating Akt signaling. Targeting of TRIP6 in combination with chemotherapy is a promising strategy for the treatment of metastatic CRC.

Preparation and Electromagnetic Wave Absorption Properties of N-Doped SiC Nanowires.

Enhancing the conductivity loss of SiC nanowires through doping is beneficial for improving their electromagnetic wave absorption performance. In this work, N-doped SiC nanowires were synthesized using three different methods. The results indicate that a large amount of Si2ON will be generated during the microwave synthesis of SiC nanowires in a nitrogen atmosphere. In addition, the secondary heat-treatment of the as-synthesized SiC nanowires under nitrogen atmosphere will significantly reduce their stacking fault density. When ammonium chloride is introduced as a doped nitrogen source in the reaction raw material, the N-doped SiC nanowires with high-density stacking faults can be synthesized by microwave heating. Therefore, the polarization loss induced by faults and the conductivity loss caused by doping will synergistically enhance the dielectric and EMW absorption properties of SiC nanowires in the range of 2-18 GHz. When the filling ratio of N-doped SiC nanowires is 20 wt.%, the composite shows a minimum reflection loss of -22.2 dB@17.92 GHz, and an effective absorption (RL ≤ -10 dB) bandwidth of 4.24 GHz at the absorber layer thickness of 2.2 mm. Further, the N-doped SiC nanowires also exhibit enhanced high-temperature EMW absorption properties with increasing temperature.

PDZK1 improves ventricular remodeling in hypertensive rats by regulating the stability of the Mas receptor.

Ventricular remodeling is one of the main causes of mortality from heart failure due to hypertension. Exploring its mechanism and finding therapeutic targets have become urgent scientific problems to be solved. A number of studies have shown that Mas, as an Ang-(1-7) specific receptor, was significantly reduced in myocardial tissue of rats undergoing hypertensive ventricular remodeling. It has been reported that Mas receptor levels are significantly downregulated in myocardium undergoing ventricular remodeling, but studies focused on intracellular and post-translational modifications of Mas are lacking. The results of this research are as follows: (1) PDZK1 interacts with the carboxyl terminus of Mas through its PDZ1 domain; (2) the expression of PDZK1 and Mas is decreased in rats undergoing hypertensive ventricular remodeling, and PDZK1 upregulation can ameliorate hypertensive myocardial fibrosis and myocardial hypertrophy; (3) PDZK1 enhances the stability of Mas protein through the proteasome pathway, and the proteasome inhibitor MG132 promotes hypertensive ventricular remodeling. PDZK1 improves ventricular remodeling in hypertensive rats by regulating Mas receptor stability. This study provides a scientific basis for the prevention and treatment of ventricular remodeling.

Alcohol Intake Provoked Cardiomyocyte Apoptosis Via Activating Calcium-Sensing Receptor and Increasing Endoplasmic Reticulum Stress and Cytosolic [Ca2+]i.

BACKGROUND: Cardiomyocyte apoptosis plays an important role in alcoholic cardiac injury. However, the association between calcium-sensing receptor (CaSR) and alcohol-induced cardiomyocyte apoptosis remain unclear. Therefore, we investigated the role and its moleculer mechanism of CaSR in rat cardiomyocyte apoptosis induced by alcohol. METHODS: Alcohol-induced cardiomyocyte apoptosis in vivo and in vitro model of rats were applied in this study. The expression of CaSR, endoplasmic reticulum stress markers and apoptosis were tested by immunohistological staining, western blot, TUNEL and flow cytometry, respectively. [Ca2+]i were detected by confocal laser scanning microscopy. RESULTS: Compared with the control group, alcohol intake (AI) led to abnormal arrangements of cardiomyocytes and obvious increase of myocardial apoptosis. Moreover, AI also significantly upregulated protein expression of CaSR, GRP94, caspase-12 and CHOP. Alcohol induced apoptosis of cultured cardiomyocytes of rats in a dose-dependent way. Activation of CaSR markedly enhanced cardiomyocyte apoptosis and ERS induced by alcohol, ERS inducer also significantly increased cardiomyocyte apoptosis without activating CaSR. Furthermore, GdCl3 augmented alcohol-induced increase of [Ca2+]i in cardiomyocytes, which was attenuated by NPS2390 but not 4-PBA pre-treatment. CONCLUSIONS: Alcohol could induce cardiomyocyte apoptosis in rats in vivo and in vitro, which was mediated probably via activating CaSR, and then ERS and the increase of the cytosolic [Ca2+]i. This provides a potential target for preventing cardiomyocyte apoptosis and cardiomyopathy induced by alochol.

Patchouli alcohol against renal fibrosis of spontaneously hypertensive rats via Ras/Raf-1/ERK1/2 signalling pathway.

OBJECTIVES: The present study was designed to obverse the protection of patchouli alcohol (PA) ameliorates hypertensive nephropathy in spontaneously hypertensive rats (SHR) and reveals potential mechanism. METHODS: Briefly, the adult spontaneously hypertensive rats (SHR) or Wistar-Kyoto (WKY) rats (half male and half female) were intragastric gavaged or not with PA (80, 40 and 20 mg/kg) for 8 weeks. Body weight, blood pressure (BP), renal weight, renal function and renal morphology were measured. Further, western blotting and immunohistochemical analysis were used to study the underlying mechanism. KEY FINDINGS: Compared with the WKY group, plasmatic levels of renin, angiotensin II (Ang-II), transforming growth factor beta 1(TGF-ß1), plasminogen activator inhibitor-1(PAI-1), creatinine (Cr), blood urea nitrogen (BUN), renal index, mRNA levels of ERK1/2 and α-SMA were significantly increased in SHR. Histology results showed that renal tubular injury and tubulointerstitial fibrosis occurred in SHR. After administration, SBP of captopril group decreased at each week after administration, especially at 3, 5, 6 7 and 8 weeks (P < 0.05 or P < 0.01). There is no significant effect was assessed in the olive oil group. Decreased plasma Cr, Renin, Ang-II, TGF-ß1, PAI-1, SCFAs and Renin, TGF-ß1, PAI-1 in renal tissues were observed significantly in captopril (P <0.05 or P < 0.01). Plasma BUN, Ang-II, TGF-ß1 and PAI-1 in renal tissues decreased in the olive oil group significantly (P <0.05 or P < 0.01). PA (80, 40 and 20 mg/kg) lowered BP and plasmatic levels of Renin, Ang-II, TGF-ß1 and PAI-1. Treatment with PA (40, 20 mg/kg) decreased levels of Cr, BUN and suppressed of activation of pro-fibrosis cytokines including TGF-ß1 in kidney. There is no ameliorative change in the olive oil group and the captopril group (P > 0.05) while PA treatment alleviated renal tubular injury and produced dramatic collagen fibre area reductions in mesangial membrane, basement membrane, and renal interstitium obviously (P < 0.05 or P < 0.01). Treatment of SHR with PA-inhibited MFB activation and downregulated mRNA of α-SMA. Treatment with PA suppressed excessive production of the extracellular matrix (ECM) via decreasing Col I, III and FN, downregulating mRNA of tissue inhibitor of TIMP-1 along with upregulating mRNA of MMP-9. The expression of Col III and MMP-9 mRNA-reduced in the captopril group (P < 0.05). In addition, the expression of ERK1/2 and pERK1/2 also reduced in the captopril group significantly (P < 0.05 or P < 0.01). Treatment with PA (20 mg/kg) downregulated proteins expression of Raf-1, ERK1/2 and pERK1/2 and mRNA expression of Ras, Raf-1 and ERK1/2. CONCLUSIONS: Overall, PA restored normal BP, alleviated renal dysfunction and renal fibrosis, possibly by suppressing Ang II and TGF-ß1-mediated Ras/Raf-1/ERK1/2 signalling pathway.

Estimating the prevalence of depression using wastewater-based epidemiology: A case study in Qinghai Province, West China.

Wastewater-based epidemiology (WBE) is considered a cost-effective alternative approach capable of determining the consumption and prevalence of drug use in communities, however, the application of WBE for estimating the prevalence of depression has seldom been reported. In this study, the prevalence of antidepressants was estimated in five cities in Qinghai Province, west China to examine the feasibility of using WBE to estimate the depression prevalence. Residual concentrations of the drugs varied from different wastewater treatment plants (WWTPs) in five cities. Venlafaxine (0.06-720 ng/L), O-desmethylvenlafaxine (1.31-1659 ng/L), paroxetine (

The multifaceted biology of lncR-Meg3 in cardio-cerebrovascular diseases.

Cardio-cerebrovascular disease, related to high mortality and morbidity worldwide, is a type of cardiovascular or cerebrovascular dysfunction involved in various processes. Therefore, it is imperative to conduct additional research into the pathogenesis and new therapeutic targets of cardiovascular and cerebrovascular disorders. Long non-coding RNAs (lncRNAs) have multiple functions and are involved in nearly all cellular biological processes, including translation, transcription, signal transduction, and cell cycle control. LncR-Meg3 is one of them and is becoming increasingly popular. By binding proteins or directly or competitively binding miRNAs, LncR-Meg3 is involved in apoptosis, inflammation, oxidative stress, endoplasmic reticulum stress, epithelial-mesenchymal transition, and other processes. Recent research has shown that LncR-Meg3 is associated with acute myocardial infarction and can be used to diagnose this condition. This article examines the current state of knowledge regarding the expression and regulatory function of LncR-Meg3 in relation to cardiovascular and cerebrovascular diseases. The abnormal expression of LncR-Meg3 can influence neuronal cell death, inflammation, apoptosis, smooth muscle cell proliferation, etc., thereby aggravating or promoting the disease. In addition, we review the bioactive components that target lncR-Meg3 and propose some potential delivery vectors. A comprehensive and in-depth analysis of LncR-Meg3's role in cardiovascular disease suggests that targeting LncR-Meg3 may be an alternative therapy in the near future, providing new options for slowing the progression of cardiovascular disease.

NNMT Is an Immune-Related Prognostic Biomarker That Modulates the Tumor Microenvironment in Pan-Cancer.

Emerging evidence has revealed the significant roles of nicotinamide n-methyltransferase (NNMT) in cancer initiation, development, and progression; however, a pan-cancer analysis of NNMT has not been conducted. In this study, we first thoroughly investigated the expression and prognostic significance of NNMT and the relationship between NNMT and the tumor microenvironment using bioinformatic analysis. NNMT was significantly increased and associated with poor prognosis in many common cancers. NNMT expression correlated with the infiltration levels of cancer-associated fibroblasts and macrophages in pan-cancer. Function enrichment analysis discovered that NNMT related to cancer-promoting and immune pathways in various common cancers, such as colon adenocarcinoma, head and neck squamous cell carcinoma, ovarian serous cystadenocarcinoma, and stomach adenocarcinoma. NNMT expression was positively correlated with tumor-associated macrophages (TAMs), especially M2-like TAMs. The results suggest that NNMT might be a new biomarker for immune infiltration and poor prognosis in cancers, providing new direction on therapeutics of cancers.

Vacancy-cluster-mediated surface activation for boosting CO2 chemical fixation.

The cycloaddition of CO2 with epoxides towards cyclic carbonates provides a promising pathway for CO2 utilization. Given the crucial role of epoxide ring opening in determining the reaction rate, designing catalysts with rich active sites for boosting epoxide adsorption and C-O bond cleavage is necessary for gaining efficient cyclic carbonate generation. Herein, by taking two-dimensional FeOCl as a model, we propose the construction of electron-donor and -acceptor units within a confined region via vacancy-cluster engineering to boost epoxide ring opening. By combing theoretical simulations and in situ diffuse reflectance infrared Fourier-transform spectroscopy, we show that the introduction of Fe-Cl vacancy clusters can activate the inert halogen-terminated surface and provide reactive sites containing electron-donor and -acceptor units, leading to strengthened epoxide adsorption and promoted C-O bond cleavage. Benefiting from these, FeOCl nanosheets with Fe-Cl vacancy clusters exhibit enhanced cyclic carbonate generation from CO2 cycloaddition with epoxides.

Metagenomic surveillance of antibiotic resistome in influent and effluent of wastewater treatment plants located on the Qinghai-Tibetan Plateau.

As hotspots for the dissemination of antibiotic resistance genes (ARGs), wastewater treatment plants (WWTPs) have attracted global attention. However, there lacks a sufficient metagenomic surveillance of antibiotic resistome in the WWTPs located on the Qinghai-Tibet Plateau. Here, metagenomic approaches were used to comprehensively investigate the occurrence, mobility potential, and bacterial hosts of ARGs in influent and effluent of 18 WWTPs located on the Qinghai-Tibet Plateau. The total ARG relative abundances and diversity were significantly decreased from influent to effluent across the WWTPs. Multidrug, bacitracin, sulfonamide, aminoglycoside, and beta-lactam ARGs generally consisted of the main ARG types in effluent samples, which were distinct from influent samples. A group of 72 core ARGs accounting for 61.8-95.8 % of the total ARG abundances were shared by all samples. Clinically relevant ARGs mainly conferring resistance to beta-lactams were detected in influent (277 ARGs) and effluent (178 ARGs). Metagenomic assembly revealed that the genetic location of an ARG on a plasmid or a chromosome was related to its corresponding ARG type, demonstrating the distinction in the mobility potential of different ARG types. The abundance of plasmid-mediated ARGs accounted for a much higher proportion than that of chromosome-mediated ARGs in both influent and effluent. Moreover, the ARGs co-occurring with diverse mobile genetic elements in the effluent exhibited a comparable mobility potential with the influent. Furthermore, 137 metagenome-assembled genomes (MAGs) assigned to 13 bacterial phyla were identified as the ARG hosts, which could be effectively treated in most WWTPs. Notably, 46 MAGs were found to carry multiple ARG types and the potential pathogens frequently exhibited multi-antibiotic resistance. Some ARG types tended to be carried by certain bacteria, showing a specific host-resistance association pattern. This study highlights the necessity for metagenomic surveillance and will facilitate risk assessment and control of antibiotic resistome in WWTPs located on the vulnerable area.

Identification of Nrf2/Keap1 pathway and its transcriptional regulation of antioxidant genes after exposure to microcystins in freshwater mussel Cristaria plicata.

Microcystins (MC) are one of the most abundant and widely distributed cyanotoxins in aquatic systems. MC inhibits the functions of protein phosphatase 1 and 2A (PP1/2A), which can seriously affect ecosystem integrity. The NF-E2-related nuclear factor 2 (Nrf2)/Kelch-like epichlorohydrin-related protein-1 (Keap1) signaling pathway protects against oxidative damage by activating phase II detoxification/antioxidant enzymes. Our previous study revealed that MC upregulates the expression and enhances the activities of the antioxidant enzymes by stimulating the CpNrf2 signaling pathway. In the current study, to further clarify the regulatory role of Keap1 in response to MC-induced oxidative stress in shellfish, we cloned the full-length cDNA of Keap1a and Keap1b from Cristaria plicata (designated CpKeap1a and CpKeap1b), which are 2952 and 3710 bp peptides, respectively. The amino acid sequence of CpKeap1a and CpKeap1b contained Tram-track and Bric-a-brac (BTB), Intervening region (IVR), and Double glycine repeat (DGR) domain. Additionally, CpKeap1a contained two cysteine residues analogous to Cys-273 and -288 in zebrafish, but CpKeap1b did not. Moreover, CpKeap1a and -1b formed a homodimer and heterodimer, respectively, and also formed a heterodimer with CpNrf2. In the hepatopancreas, the expression levels of CpKeap1a and -1b were the highest, but MC treatment down-regulated the expression of these proteins. Moreover, the transcription of antioxidant enzymes with antioxidant response element (ARE-driven enzymes), including CpMnSOD, CpCu/ZnSOD, CpTRX, CpPrx, CpSe-GPx, and Cpsigma-GST was upregulated by CpNrf2 in the hepatopancreas. Compared with the MC-induced group, CpKeap1a-siRNA1117 injection significantly increased the transcription of mRNAs for ARE-driven enzymes and Nrf2. CpKeap1a-siRNA1117 also enhanced the activities of antioxidation enzymes. These findings demonstrated that Keap1a negatively regulated the expression of Nrf2 protein and MC-induced oxidative stress response in C. plicata. Therefore, we speculated that CpKeap1a promoted CpNrf2 by recognizing and binding MC. These events then protected molluscs from MC-induced oxidative damage.

Investigation on consumption of psychoactive substances and their ecological risks using wastewater-based epidemiology: a case study on Qinghai-Tibet Plateau.

The Qinghai-Tibet Plateau is the third pole of the world, and information on the consumption of psychoactive substances (PSs) in this area is scarce. In this study, we selected Qinghai Province as the research area, and the per capita consumption and prevalence of PSs were investigated using wastewater-based epidemiology. Samples from 17 wastewater treatment plants (WWTPs) in 5 major cities in Qinghai Province were monitored, and 11 PSs were detected by ultra-high performance liquid chromatography-tandem mass spectrometry. Results showed that the target compounds were detected in all samples, with relatively high concentrations of ephedrine (2.1-4825.3 ng/L) and methamphetamine (1.5-295.7 ng/L). The consumption of methamphetamine in Xining City, Haidong City, and Haixi City was up to 78.4, 16.8, and 21.2 mg/1000 inh/d (the PS consumption per 1000 inhabitants in 1 day), respectively, higher than that in the other two cities, which was the result of the different consumption patterns and its relationship with the economic levels of each city. High consumption of methadone (47.9 mg/1000 inh/day) was found in Xining City, which might be related to the methadone maintenance therapy sites in the city. Methamphetamine was the most prevalent drug, with the prevalence ranging from 0.003 (Guoluo) to 0.197% (Xining), and the prevalence of other PSs was low. The ecological risk assessment of PSs in the effluent of WWTPs showed that methadone exerted a low risk to aquatic organisms in three sites, while other substances posed potential risk or no risk. However, the long-term effect of PSs cannot be ignored.

Near Infrared Reflection and Hydrophobic Properties of Composite Coatings Prepared from Hollow Glass Microspheres Coated with Needle-Shaped Rutile Shell.

Infrared thermal reflective coating is an effective material to reduce building energy consumption and carbon emission. In this work, needle-shaped-rutile-shell-coated hollow glass microbeads (HGM) were prepared by surface modification of HGM and thermohydrolysis of TiCl4, and the possible shell formation mechanism was also proposed. The near infrared (NIR) reflectance of the coated HGM reached 93.3%, which could be further increased to 97.3% after the rutile shell crystallinity was improved by heat treatment. Furthermore, HGM/styrene-acrylic composite reflective coating was prepared on the surface of gypsum board by facile blending and coating methods, and the thermal insulation performance was measured by an indigenously designed experimental heat set-up. The results show that the composite coating prepared by HGM coated with rutile shell shows better NIR reflectance and thermal insulation performance than that prepared by pure organic coating and uncoated HGM. Meanwhile, it also shows better surface hydrophobicity, which is conducive to long-term and stable infrared reflection performance.