Embryonic alcohol exposure in zebrafish predisposes adults to cardiomyopathy and diastolic dysfunction.

AIMS: Fetal alcohol spectrum disorders (FASDs) impact up to 0.8% of the global population. However, cardiovascular health outcomes in adult patients, along with predictive biomarkers for cardiac risk stratification, remain unknown. Our aim was to utilize a longitudinal cohort study in an animal model to evaluate the impact of embryonic alcohol exposure (EAE) on cardiac structure, function, and transcriptional profile across the lifespan. METHODS AND RESULTS: Using zebrafish, we characterized the aftereffects of embryonic alcohol exposure (EAE) in adults binned by congenital heart defect (CHD) severity. Chamber sizes were quantified on dissected adult hearts to identify structural changes indicative of cardiomyopathy. Using echocardiography, we quantified systolic function based on ejection fraction and longitudinal strain, and diastolic function based on ventricular filling dynamics, ventricular wall movement, and estimated atrial pressures. Finally, we performed RNA sequencing on EAE ventricles and assessed how differentially expressed genes (DEGs) correlated with cardiac function. Here, we demonstrate that embryonic alcohol exposure (EAE) causes cardiomyopathy and diastolic dysfunction through persistent alterations to ventricular wall structure and gene expression. Following abnormal ventricular morphogenesis, >30% of all EAE adults developed increased atrial-to-ventricular size ratios, abnormal ventricular filling dynamics, and reduced myocardial wall relaxation during early diastole despite preserved systolic function. RNA sequencing of the EAE ventricle revealed novel and heart failure-associated genes (slc25a33, ankrd9, dusp2, dusp4, spry4, eya4, and edn1) whose expression levels were altered across the animal's lifespan or correlated with the degree of diastolic dysfunction detected in adulthood. CONCLUSIONS: Our study identifies EAE as a risk factor for adult-onset cardiomyopathy and diastolic dysfunction, regardless of CHD status, and suggests novel molecular indicators of adult EAE-induced heart disease.

2'-O-methylation at internal sites on mRNA promotes mRNA stability.

2'-O-methylation (Nm) is a prominent RNA modification well known in noncoding RNAs and more recently also found at many mRNA internal sites. However, their function and base-resolution stoichiometry remain underexplored. Here, we investigate the transcriptome-wide effect of internal site Nm on mRNA stability. Combining nanopore sequencing with our developed machine learning method, NanoNm, we identify thousands of Nm sites on mRNAs with a single-base resolution. We observe a positive effect of FBL-mediated Nm modification on mRNA stability and expression level. Elevated FBL expression in cancer cells is associated with increased expression levels for 2'-O-methylated mRNAs of cancer pathways, implying the role of FBL in post-transcriptional regulation. Lastly, we find that FBL-mediated 2'-O-methylation connects to widespread 3' UTR shortening, a mechanism that globally increases RNA stability. Collectively, we demonstrate that FBL-mediated Nm modifications at mRNA internal sites regulate gene expression by enhancing mRNA stability.

Transcriptional inhibition after irradiation occurs preferentially at highly expressed genes in a manner dependent on cell cycle progression.

In response to DNA double strand damage, ongoing transcription is inhibited to facilitate accurate DNA repair while transcriptional recovery occurs after DNA repair is complete. However, the mechanisms at play and identity of the transcripts being regulated in this manner are unclear. In contrast to the situation following UV damage, we found that transcriptional recovery after ionizing radiation (IR) occurs in a manner independent of the HIRA histone chaperone. Sequencing of the nascent transcripts identified a programmed transcriptional response, where certain transcripts and pathways are rapidly downregulated after IR, while other transcripts and pathways are upregulated. Specifically, most of the loss of nascent transcripts occurring after IR is due to inhibition of transcriptional initiation of the highly transcribed histone genes and the rDNA. To identify factors responsible for transcriptional inhibition after IR in an unbiased manner, we performed a whole genome gRNA library CRISPR / Cas9 screen. Many of the top hits in our screen were factors required for protein neddylation. However, at short times after inhibition of neddylation, transcriptional inhibition still occurred after IR, even though neddylation was effectively inhibited. Persistent inhibition of neddylation blocked transcriptional inhibition after IR, and it also leads to cell cycle arrest. Indeed, we uncovered that many inhibitors and conditions that lead to cell cycle arrest in G1 or G2 phase also prevent transcriptional inhibition after IR. As such, it appears that transcriptional inhibition after IR occurs preferentially at highly expressed genes in cycling cells.

Autoimmune receptor encephalitis in ApoE­/­ mice induced by active immunization with NMDA1.

Subacute progressive neuropsychiatric symptoms with cognitive and motor impairment and autoimmune seizures are some of the typical symptoms of anti­N­methyl­D­aspartate receptor (anti­NMDAR) encephalitis. The mechanisms underlying this disease are yet to be elucidated, which could be partly attributed to the lack of appropriate animal models. The present study aimed to establish an active immune mouse model of anti­NMDAR encephalitis. Mice were immunized with the extracellular segment of the NMDA1 protein, then subjected to open­field and novel object recognition experiments. Plasma was collected after euthanasia on day 30 after immunization and anti­NMDA1 antibodies were detected using ELISA. Furthermore, brain slices were analyzed to measure postsynaptic density protein 95 (PSD­95) and NMDA1 expression. Western blot analysis of NMDA1 and PSD­95 protein expression levels in the hippocampus was also performed. In addition, protein expression levels of PSD­95 and NMDA1 in mouse neuronal HT­22 cells were evaluated. Compared with controls, mice immunized with NMDA1 exhibited anxiety, depression and memory impairment. Moreover, high anti­NMDA1 antibody titers were detected with ELISA and the levels of anti­NMDA1 antibody reduced postsynaptic NMDA1 protein density in the mouse hippocampus. These findings demonstrated the successful construction of a novel mouse model of anti­NMDAR encephalitis by actively immunizing the mice with the extracellular segment of the NMDA1 protein. This model may be useful for studying the pathogenesis and drug treatment of anti­NMDAR encephalitis in the future.

A newly predicted stable calcium argon compound byab initiocalculations under high pressure.

High pressure can change the valence electron arrangement of the elements, and it can be as a new method for the emergence of unexpected new compounds. In this paper, the Ca-Ar compounds at 0-200 GPa are systematically investigated by using CALYPSO structure prediction methods combined with first principles calculations. The study of the Ca-Ar system can provide theoretical guidance for the exploration of new structures of inert elemental Ar compounds under high pressure. A stable structure:P63/mmc-CaAr and six metastable structures:Rm-CaAr2,P4/mmm-CaAr2,Pm1-CaAr3,P4/mmm-CaAr3,P21/m-CaAr4andPm1-CaAr5were obtained. Our calculations show that the only stable phaseP63/mmc-CaAr can be synthesized at high pressure of 90 GPa. All the structures are ionic compounds of metallic nature, and surprisingly all Ar atoms attract electrons and act as an oxidant under high pressure conditions. The calculation results ofab initiomolecular dynamics show thatP63/mmc-CaAr compound maintains significant thermodynamic stability at high temperatures up to 1000 K. The high-pressure structures and electronic behaviors of the Ca-Ar system are expected to expand the understanding of the high-pressure chemical reactivity of compounds containing inert elements, and provide important theoretical support for the search of novel anomalous alkaline-earth metal inert element compounds.

Low RNA stability signifies strong expression regulatability of tumor suppressors.

RNA expression of a gene is determined by not only transcriptional regulation, but also post-transcriptional regulation of RNA decay. The precise regulation of RNA stability in the cell plays an important role in normal development. Dysregulation of RNA stability can lead to diseases such as cancer. Here we found tumor suppressor RNAs tended to decay fast in normal cell types when compared with other RNAs. Consistent with a negative effect of m6A modification on RNA stability, we observed preferential deposition of m6A on tumor suppressor RNAs. Moreover, abundant m6A and fast decay of tumor suppressor RNAs both tended to be further enhanced in prostate cancer cells relative to normal prostate epithelial cells. Further, knockdown of m6A methyltransferase METTL3 and reader YTHDF2 in prostate cancer cells both posed stronger effect on tumor suppressor RNAs than on other RNAs. These results indicated a strong post transcriptional expression regulatability mediated by abundant m6A modification on tumor suppressor RNAs.

Design of Superlubricity System Using Si3N4/Polyimide as the Friction Pair and Nematic Liquid Crystals as the Lubricant.

Polyimide (PI) is a high-performance engineering plastic used as a bearing material. A superlubricity system using Si3N4/PI as the friction pair and nematic liquid crystals (LCs) as the lubricant was designed. The superlubricity performance was studied by simulating the start-stop condition of the machine, and it was found that the superlubricity system had good reproducibility and stability. In the superlubricity system, friction aligned with the PI molecules, and this alignment was less relevant compared to which substance was rubbing on the PI. Oriented PI molecules induced LC molecule alignment when the pretilt angle was very small, and the LC molecules were almost parallel to the PI molecules due to the one-dimensional ordered arrangement of LC molecules and low viscosity, which is conducive to the occurrence of the superlubricity phenomenon.

Effect of classical music on growth performance, stress level, antioxidant index, immune function and meat quality in broilers at different stocking densities.

High-stocking density is one of the factors that can easily cause oxidative stress and inflammatory reaction of broilers. Currently, music therapy has been proposed to help animals relieve stress to some extent. However, it is still unclear whether classical music can alleviate stress in broilers at high stocking densities. Hence, this study aimed to investigate the effects of classical music on growth performance, stress level, antioxidant index, immune function and meat quality of broilers under different stocking densities. A total of 540 one-day-old broilers with similar body weight were randomly divided into 6 treatment groups, with 6 replicates per group, which included two feeding environments (with/without classical music) and three stocking densities (15.5, 17.9, and 20.3 birds/m2), thereby making a 2 × 3 factorial arrangement. The results showed as follows: increasing stocking density decreased the average daily feed intake and average daily gain (ADG), increased feed-to-gain ratio (F/G) and mortality of broilers. Moreover, increased density resulted in an increase in serum corticosterone (CORT) and adrenocorticotropic hormone (ACTH) levels. Increasing stocking density decreased spleen and bursal indices, serum immunoglobulin A (IgA), immunoglobulin G (IgG), and immunoglobulin M (IgM) levels. Increasing stocking density elevated serum malondialdehyde (MDA) and decreased catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activities. Increasing stocking density decreased serum total protein (TP) levels and increased total cholesterol (TC) and glucose (GLU) levels. Additionally, increasing stocking density decreased the cooking liss of pectoralis and increased the L*24h value of pectoralis. Meanwhile, playing classical music for broilers increased their ADG and decreased F/G, and decreased serum CORT, ACTH, GLU content. In addition, the bursa of Fabricius index, serum IgA and IgG contents as well as the a*24h value of pectoralis was increased under the music therapy. In conclusion, high-stocking density (20.3 birds/m2) harmed the growth performance and health of broilers, and the classical music stimulus ameliorated the negative effects to some extent.

Low RNA stability signifies increased post-transcriptional regulation of cell identity genes.

Cell identity genes are distinct from other genes with respect to the epigenetic mechanisms to activate their transcription, e.g. by super-enhancers and broad H3K4me3 domains. However, it remains unclear whether their post-transcriptional regulation is also unique. We performed a systematic analysis of transcriptome-wide RNA stability in nine cell types and found that unstable transcripts were enriched in cell identity-related pathways while stable transcripts were enriched in housekeeping pathways. Joint analyses of RNA stability and chromatin state revealed significant enrichment of super-enhancers and broad H3K4me3 domains at the gene loci of unstable transcripts. Intriguingly, the RNA m6A methyltransferase, METTL3, preferentially binds to chromatin at super-enhancers, broad H3K4me3 domains and their associated genes. METTL3 binding intensity is positively correlated with RNA m6A methylation and negatively correlated with RNA stability of cell identity genes, probably due to co-transcriptional m6A modifications promoting RNA decay. Nanopore direct RNA-sequencing showed that METTL3 knockdown has a stronger effect on RNA m6A and mRNA stability for cell identity genes. Our data suggest a run-and-brake model, where cell identity genes undergo both frequent transcription and fast RNA decay to achieve precise regulation of RNA expression.

Epigenetic landscape reveals MECOM as an endothelial lineage regulator.

A comprehensive understanding of endothelial cell lineage specification will advance cardiovascular regenerative medicine. Recent studies found that unique epigenetic signatures preferentially regulate cell identity genes. We thus systematically investigate the epigenetic landscape of endothelial cell lineage and identify MECOM to be the leading candidate as an endothelial cell lineage regulator. Single-cell RNA-Seq analysis verifies that MECOM-positive cells are exclusively enriched in the cell cluster of bona fide endothelial cells derived from induced pluripotent stem cells. Our experiments demonstrate that MECOM depletion impairs human endothelial cell differentiation, functions, and Zebrafish angiogenesis. Through integrative analysis of Hi-C, DNase-Seq, ChIP-Seq, and RNA-Seq data, we find MECOM binds enhancers that form chromatin loops to regulate endothelial cell identity genes. Further, we identify and verify the VEGF signaling pathway to be a key target of MECOM. Our work provides important insights into epigenetic regulation of cell identity and uncovered MECOM as an endothelial cell lineage regulator.

Fe(II)-Modulated Microporous Electrocatalytic Membranes for Organic Microcontaminant Oxidation and Fouling Control: Mechanisms of Regulating Electron Transport toward Enhanced Reactive Oxygen Species Activation.

Regulation of the fast electron transport process for the generation and utilization of reactive oxygen species (ROS) by achieving fortified electron "nanofluidics" is effective for electrocatalytic oxidation of organic microcontaminants. However, limited available active sites and sluggish mass transfer impede oxidation efficiency. Herein, we fabricated a conductive electrocatalytic membrane decorated with hierarchical porous vertically aligned Fe(II)-modulated FeCo layered double hydroxide nanosheets (Fe(II)-FeCo LDHs) in an electro-Fenton system to maximize exposure of active sites and expedite mass transfer. The nanospaced interlayers of Fe(II)-FeCo LDHs within the microconfined porous structure formed by its vertical nanosheets highly boost the micro/nanofluidic distribution of target pollutants to active centers/species, achieving accelerated mass transferability. Aliovalent substitution by Fe(II) activates in-plane metallics to maximize the available active sites and makes each Fe(II)-FeCo LDH nanosheet a geometrical nanocarrier for constructing a fast electron "nanofluidic" to accelerate Fe(II) regeneration in Fe(III)/Fe(II) cycles. As a result, the Fe(II)-FeCo LDHs exhibited improved reactivity in catalyzing H2O2 to •OH and 1O2. Accordingly, the membrane exhibited a higher atrazine degradation kinetic (0.0441 min-1) and degradation rate (93.2%), which were 4.7 and 2.1 times more than those of the bare carbon nanotube membrane, respectively. Additionally, the enhanced hydrophilic and strongly oxidized reactivity synergistically mitigated the organic fouling occurring in the pores and surface of the membrane. These findings clarify the activation mechanism of ROS over an innovative electrocatalytic membrane reactor design for organic microcontaminant treatment.

Enhanced anaerobic degradation of azo dyes by biofilms supported by novel functionalized carriers.

Azo dyes are significant organic pollutants known for their adverse effects on humans and aquatic life. In this study, anthraquinone-2-sulfonate (AQS) immobilized on biochar (BC) was employed as a novel carrier in up-flow anaerobic fixed-bed reactors to induce specific biofilm formation and promote the biotransformation efficiency of azo dyes. Novel carrier-packed reactor 1 (R1) and BC-packed reactor 2 (R2) were used to treat red reactive 2 (RR2) under continuous operation for 175 days. The decolorization rates of R1 and R2 were 96-83% and 91-73%, respectively. The physicochemical characteristics and extracellular polymeric substances (EPS) of the biofilm revealed a more stable structure in R1. Furthermore, the microbial community in R1 interacted more closely with each other and contained more keystone genera. Overall, this study provides a feasible method for improving the biotransformation of azo dyes, thus providing support for practical applications in wastewater treatment projects.

CD45 Is Sufficient to Initiate Endothelial-to-Mesenchymal Transition in Human Endothelial Cells-Brief Report.

BACKGROUND: Endothelial-to-mesenchymal transition (EndMT) is a dynamic process in which endothelial cells acquire mesenchymal properties and in turn contribute to tissue remodeling and growth. Previously, we found EndMT associated with mitral valve adaptation after myocardial infarction. Furthermore, mitral valve endothelial cells collected at 6 months post-myocardial infarction expressed the pan-leukocyte marker CD45 and EndMT markers. Additionally, mitral valve endothelial cells induced to undergo EndMT with TGF (transforming growth factor)-ß1 strongly coexpressed CD45 but not CD11b or CD14. Pharmacologic inhibition of the CD45 PTPase (protein tyrosine phosphatase) domain in mitral valve endothelial cells blocked TGFß-induced EndMT. This prompted us to speculate that, downstream of TGFß, CD45 induces EndMT. METHODS: We activated the endogenous CD45 promoter in human endothelial colony forming cells (ECFCs) using CRISPR (cluster regularly interspaced short palindromic repeats)/inactive Cas9 (CRISPR-associated protein 9) transcriptional activation. Bulk RNA sequencing was performed on control ECFCs and CD45-positive ECFCs to identify transcriptomic changes. Three functional assays-cellular migration, collagen gel contraction, and transendothelial electrical resistance-were conducted to assess mesenchymal properties in CD45-positive ECFCs. RESULTS: Activation of the endogenous CD45 promoter in ECFC and 3 additional sources of endothelial cells induced expression of several genes implicated in EndMT. In addition, CD45-positive ECFCs showed increased migration, a hallmark of EndMT, increased collagen gel contraction, a hallmark of mesenchymal cells, and decreased cell-cell barrier integrity, indicating reduced endothelial function. CONCLUSIONS: CD45 is sufficient to incite an EndMT phenotype and acquisition of mesenchymal cell properties in normal human ECFCs. We speculate that CD45, through its C-terminal PTPase domain, initiates signaling events that drive EndMT.

Deciphering the fate of osmotic stress priming on enhanced microorganism acclimation for purified terephthalic acid wastewater treatment with high salinity and organic load.

Osmotic stress priming (OSP) was an effective management strategy for improving microbial acclimation to salt stress. In this study, the interaction between pollutants and microbiota, and microbial osmoregulation were investigated triggered by OSP (alternately increasing salinity and organic loading). Results showed that OSP significantly improved COD removal from 31.53 % to 67.99 % and mitigated the terephthalate inhibition produced by toluate, decreasing from 1908.08 mg/L to 837.16 mg/L compared with direct priming. Due to an increase in salinity, Pelotomaculum and Mesotoga were enriched to facilitate terephthalate degradation and syntrophic acetate oxidation (SAO). And organic load promoted acetate formation through syntrophic metabolism of Syntrophorhabdus/Pelotomaculum and SAO-dependent hydrogenotrophic methanogenesis. K+ absorbing, proline and trehalose synthesis participated in osmoregulation at 0.5 % salinity, while only ectoine alleviated intracellular osmolarity under 1.0 % salinity with OLR of 0.44 kg COD /m3. This study provided in-depth insight for microbial acclimation process of anaerobic priming of saline wastewater.

Epsin Nanotherapy Regulates Cholesterol Transport to Fortify Atheroma Regression.

BACKGROUND: Excess cholesterol accumulation in lesional macrophages elicits complex responses in atherosclerosis. Epsins, a family of endocytic adaptors, fuel the progression of atherosclerosis; however, the underlying mechanism and therapeutic potential of targeting Epsins remains unknown. In this study, we determined the role of Epsins in macrophage-mediated metabolic regulation. We then developed an innovative method to therapeutically target macrophage Epsins with specially designed S2P-conjugated lipid nanoparticles, which encapsulate small-interfering RNAs to suppress Epsins. METHODS: We used single-cell RNA sequencing with our newly developed algorithm MEBOCOST (Metabolite-mediated Cell Communication Modeling by Single Cell Transcriptome) to study cell-cell communications mediated by metabolites from sender cells and sensor proteins on receiver cells. Biomedical, cellular, and molecular approaches were utilized to investigate the role of macrophage Epsins in regulating lipid metabolism and transport. We performed this study using myeloid-specific Epsin double knockout (LysM-DKO) mice and mice with a genetic reduction of ABCG1 (ATP-binding cassette subfamily G member 1; LysM-DKO-ABCG1fl/+). The nanoparticles targeting lesional macrophages were developed to encapsulate interfering RNAs to treat atherosclerosis. RESULTS: We revealed that Epsins regulate lipid metabolism and transport in atherosclerotic macrophages. Inhibiting Epsins by nanotherapy halts inflammation and accelerates atheroma resolution. Harnessing lesional macrophage-specific nanoparticle delivery of Epsin small-interfering RNAs, we showed that silencing of macrophage Epsins diminished atherosclerotic plaque size and promoted plaque regression. Mechanistically, we demonstrated that Epsins bound to CD36 to facilitate lipid uptake by enhancing CD36 endocytosis and recycling. Conversely, Epsins promoted ABCG1 degradation via lysosomes and hampered ABCG1-mediated cholesterol efflux and reverse cholesterol transport. In a LysM-DKO-ABCG1fl/+ mouse model, enhanced cholesterol efflux and reverse transport due to Epsin deficiency was suppressed by the reduction of ABCG1. CONCLUSIONS: Our findings suggest that targeting Epsins in lesional macrophages may offer therapeutic benefits for advanced atherosclerosis by reducing CD36-mediated lipid uptake and increasing ABCG1-mediated cholesterol efflux.

Temperature-regulated and starvation-induced refractory para-toluic acid anaerobic biotransformation.

Little research was focused on the anerobic degradation of refractory para-toluic acid at present. Thus, temperature-regulated anaerobic system of para-toluic acid fed as sole substrate was built and investigated via microbiota, metabolism intermediates, and function prediction in this study. Results showed that low methane yield was produced in para-toluic acid anaerobic system at alkaline condition. And the causes were owing to anaerobic methane oxidation and potentially H2S production at 37 °C, N2 production by denitrification before starvation and propionic acid occurrence after starvation at 27 °C, and production of N2 and free ammonia, and accumulation of acetic acid at 52 °C. Simultaneously, hydrogenotrophic methanogenesis dependent on syntrophic acetate oxidation (SAO) was predominant, facilitating the removal of para-toluic acid at 52 °C. Moreover, the key intermediate changed from phthalic acid of 37 °C and 27 °C before starvation to terephthalic acid of 52 °C. Starvation promoted removal of para-toluic acid through benzoyl-CoA pathway by Syntrophorhabdus, enrichment of syntrophic propionate degraders of Bacteroidetes and Ignavibacteriaceae, and increase of methylotrophic methanogens.

StripeDiff: Model-based algorithm for differential analysis of chromatin stripe.

Multiple recent studies revealed stripes as an architectural feature of three-dimensional chromatin and found stripes connected to epigenetic regulation of transcription. Whereas a couple of tools are available to define stripes in a single sample, there is yet no reported method to quantitatively measure the dynamic change of each stripe between samples. Here, we developed StripeDiff, a bioinformatics tool that delivers a set of statistical methods to detect differential stripes between samples. StripeDiff showed optimal performance in both simulation data analysis and real Hi-C data analysis. Applying StripeDiff to 12 sets of Hi-C data revealed new insights into the connection between change of chromatin stripe and change of chromatin modification, transcriptional regulation, and cell differentiation. StripeDiff will be a robust tool for the community to facilitate understanding of stripes and their function in numerous biological models.

A passive-active combined strategy for ultrafiltration membrane fouling control in continuous oily wastewater purification.

Membrane-based technology has been confirmed as an effective way to treat emulsified oily wastewater, however, membrane fouling is still one of practical challenges in long-term operation. Herein, a novel passive-active combined strategy was proposed to control membrane fouling in continuous oily wastewater purification, where the δ-MnO2 decoration layer helped to reduce the total fouling ratio (passive strategy for fouling mitigation) and the catalytic cleaning effectively removed the irreversible oil fouling (active strategy for fouling removal). The functional membrane was prepared via in-situ modification, referred to as δ-MnO2@TA-PES. The morphology, crystalline phase, chemical structure and surface properties of the membranes were systematically characterized. Compared with PES, the δ-MnO2@TA-PES possessed superhydrophilicity, enhanced electronegativity and narrowed pore size. The δ-MnO2@TA-PES achieved high water permeation flux of 723.9 L·m - 2·h - 1·bar-1, excellent oil rejection with separation efficiency above 98.5% for various emulsions, and durable anti-oil-fouling performance with FRRb of 98.0%. Notably, the oil cake layer fouling on δ-MnO2@TA-PES was greatly alleviated owing to its enhanced surface properties. In addition, δ-MnO2@TA-PES showed high cleaning efficiency in the peroxymonosulfate (PMS) cleaning process, where the radical and nonradical pathways occurred simultaneously. And the active substances generated in the nonradical process (especially 1O2) were considered as the main contributor to the reduction of irreversible fouling. Overall, the novel strategy of fouling control ensured the efficient operation of ultrafiltration membranes for the continuous oily wastewater purification.

Crystal structure and Hirshfeld surface analysis of 7,7-dimethyl-2-phenyl-3,3a,4,6,7,8,9,9a-octa-hydro-1H-benzo[f]iso-indole-1,5(2H)-dione.

The title compound, C20H23NO2, was obtained via the reaction of N-allyl-N-phenyl-acryl-amide with 3-iodo-cyclo-hex-2-en-1-one using PdCl2(PPh3)2 as a catalyst. The compound crystallizes in the monoclinic space group P21/c. The fused-ring system is not planar and the five- and six-membered rings are trans-fused. The mol-ecular geometry is partially stabilized by an intra-molecular C-H⋯O hydrogen bond, forming an S(6) ring motif. In the crystal, mol-ecules are linked by C-H⋯O and C-H⋯π inter-actions into a three-dimensional network. To further analyse the inter-molecular inter-actions, a Hirshfeld surface analysis was performed. The results indicate that the most important contributions to the overall surface are from H⋯H (65.5%), O⋯H/H⋯O (17.5%) and C⋯H/H⋯C (14.3%) inter-actions.