The volatile organic compounds generated from the Maillard reaction between l-ascorbic acid and l-cysteine in hot compressed water.

BACKGROUND: Hot compressed water (HCW), also known as subcritical water (SCW), refers to high-temperature compressed water in a special physical and chemical state. It is an emerging technology for natural product extraction. The volatile organic compounds (VOCs) generated from the Maillard reaction between l-ascorbic acid (ASA) and l-cysteine (Cys) have attracted significant interest in the flavor and fragrance industry. This study aimed to explore the formation mechanism of VOCs from ASA and Cys and examine the effects of reaction parameters such as temperature, time, and pH in HCW. RESULTS: The identified VOCs were predominantly thiophene derivatives, polysulfides, and pyrazine derivatives in HCW. The findings indicated that thiophene derivatives were formed under various pH conditions, with polysulfide formation favored under acidic conditions and pyrazine derivative formation preferred under weak alkaline conditions, specifically at pH 8.0. CONCLUSION: The Maillard reaction between ASA and Cys mainly produced thiophene derivatives, polysulfides, and pyrazine derivatives in HCW. The generation mechanism was significantly dependent on the surrounding pH conditions. © 2024 Society of Chemical Industry.

Emerging role of exosome-derived non-coding RNAs in tumor-associated angiogenesis of tumor microenvironment.

The tumor microenvironment (TME) is an intricate ecosystem that is actively involved in various stages of cancer occurrence and development. Some characteristics of tumor biological behavior, such as proliferation, migration, invasion, inhibition of apoptosis, immune escape, angiogenesis, and metabolic reprogramming, are affected by TME. Studies have shown that non-coding RNAs, especially long-chain non-coding RNAs and microRNAs in cancer-derived exosomes, facilitate intercellular communication as a mechanism for regulating angiogenesis. They stimulate tumor growth, as well as angiogenesis, metastasis, and reprogramming of the TME. Exploring the relationship between exogenous non-coding RNAs and tumor-associated endothelial cells, as well as their role in angiogenesis, clinicians will gain new insights into treatment as a result.

PPARα is involved in high-fat diet-induced risk avoidance impairment via the regulation of hippocampal BDNF.

Risk avoidance behaviors are essential for survival. "Uncontrollable" risk-taking behaviors in animals or humans may have severe adverse consequences. In humans, a large proportion of psychiatric disorders are accompanied by impairments in risk avoidance. Obesity is associated with psychiatric disorders. Peroxisome proliferator-activated receptor α (PPARα) takes part in regulating lipid metabolism and neuronal function. Here, we investigated the effect of high-fat diet (HFD)-induced obesity on risk avoidance and the role of PPARα in this behavior. Male PPARα-null (KO) mice and wild-type (WT) mice were assigned to four different groups: WT-CON and KO-CON (normal diet); WT-HFD and KO-HFD (high fat diet). The HFD began at week 6 and was continued until sampling. A series of behavioral tests were performed at week 11. We found that WT but not KO mice fed with a HFD exhibited weight gain and risk avoidance impairment, compared with the mice fed with a normal diet. The staining of c-Fos revealed that the hippocampus was the main brain region involved in risk avoidance behavior. Moreover, biochemical analysis suggested that the decreased levels of the brain-derived neurotrophic factor (BDNF) in the hippocampus might contribute to risk avoidance impairment induced by a HFD. These results indicated that PPARα is involved in HFD-induced risk avoidance impairment via the regulation of hippocampal BDNF.

Sp1-mediated miR-193b suppresses atopic dermatitis by regulating HMGB1.

Atopic dermatitis (AD) is a chronic and recurrent inflammatory skin disease. Keratinocyte dysfunction plays a central role in AD development. MicroRNA is a novel player in many inflammatory and immune skin diseases. In this study, we investigated the potential function and regulatory mechanism of miR-193b in AD. Inflamed human keratinocytes (HaCaT) were established by tumor necrosis factor (TNF)-α/interferon (IFN)-γ stimulation. Cell viability was measured using MTT assay, while the cell cycle was analyzed using flow cytometry. The cytokine levels were examined by enzyme-linked immunosorbent assay. The interaction between Sp1, miR-193b, and HMGB1 was analyzed using dual luciferase reporter and/or chromatin immunoprecipitation (ChIP) assays. Our results revealed that miR-193b upregulation enhanced the proliferation of TNF-α/IFN-γ-treated keratinocytes and repressed inflammatory injury. miR-193b negatively regulated high mobility group box 1 (HMGB1) expression by directly targeting HMGB1. Furthermore, HMGB1 knockdown promoted keratinocyte proliferation and inhibited inflammatory injury by repressing nuclear factor kappa-B (NF-κB) activation. During AD progression, HMGB1 overexpression abrogated increase of keratinocyte proliferation and repression of inflammatory injury caused by miR-193b overexpression. Moreover, transcription factor Sp1 was identified as the biological partner of the miR-193b promoter in promoting miR-193b expression. Therefore, Sp1 upregulation promotes keratinocyte proliferation and represses inflammatory injury during AD development via promoting miR-193b expression and repressing HMGB1/NF-κB activation.

Synergistic between autotrophic and heterotrophic microorganisms for denitrification using bio-S as electron donor.

In recent years, biological sulfur (bio-S) was employed in sulfur autotrophic denitrification (SAD) in which autotrophic Thiobacillus denitrificans and heterotrophic Stenotrophomonas maltophilia played a key role. The growth pattern of T.denitrificans and S.maltophilia exhibited a linear relationship between OD600 and CFU when OD600 < 0.06 and <0.1, respectively. When S.maltophilia has applied alone, the NorBC and NosZ were undetected, and denitrification was incomplete. The DsrA of S.maltophilia could produce sulfide as an alternative electron donor for T.denitrificans. Even though T.denitrificans had complete denitrification genes, its efficiency was low when used alone. The interaction of T.denitrificans and S.maltophilia reduced nitrite accumulation, leading to complete denitrification. A sufficient quantity of S.maltophilia may trigger the autotrophic denitrification activity of T.denitrificans. When the colony-forming units (CFU) ratio of S.maltophilia to T.denitrificans was reached at 2:1, the highest denitrification performance was achieved at 2.56 and 12.59 times higher than applied alone. This research provides a good understanding of the optimal microbial matching for the future application of bio-S.

Lateral septal nucleus, dorsal part, and dentate gyrus are necessary for spatial and object recognition memory, respectively, in mice.

Introduction: Cognitive impairment includes the abnormality of learning, memory and judgment, resulting in severe learning and memory impairment and social activity impairment, which greatly affects the life quality of individuals. However, the specific mechanisms underlying cognitive impairment in different behavioral paradigms remain to be elucidated. Methods: The study utilized two behavioral paradigms, novel location recognition (NLR) and novel object recognition (NOR), to investigate the brain regions involved in cognitive function. These tests comprised two phases: mice were presented with two identical objects for familiarization during the training phase, and a novel (experiment) or familiar (control) object/location was presented during testing. Immunostaining quantification of c-Fos, an immediate early gene used as a neuronal activity marker, was performed in eight different brain regions after the NLR or NOR test. Results: The number of c-Fos-positive cells was significantly higher in the dorsal part of the lateral septal nucleus (LSD) in the NLR and dentate gyrus (DG) in the NOR experiment group than in the control group. We further bilaterally lesioned these regions using excitotoxic ibotenic acid and replenished the damaged areas using an antisense oligonucleotide (ASO) strategy. Discussion: These data reinforced the importance of LSD and DG in regulating spatial and object recognition memory, respectively. Thus, the study provides insight into the roles of these brain regions and suggests potential intervention targets for impaired spatial and object recognition memory.

Impact of Reperfusion on Temporal Immune Cell Dynamics After Myocardial Infarction.

Excessive inflammation and impaired healing of cardiac tissue following a myocardial infarction (MI) can drive the development of heart failure. Cardiac repair begins immediately after the onset of MI and continues for months. The repair process can be divided into the following 3 overlapping phases, each having distinct functions and sequelae: the inflammatory phase, the proliferative phase, and the maturation phase. Macrophages, neutrophils, and lymphocytes are present in the myocardium throughout the repair process and govern the duration and function of each of these phases. However, changes in the functions of these cell types across each phase are poorly characterized. Numerous immunomodulatory therapies that specifically target inflammation have been developed for promoting cardiac repair and preventing heart failure after MI. However, these treatments have been largely unsuccessful in large-scale clinical randomized controlled trials. A potential explanation for this failure is the lack of a thorough understanding of the time-dependent evolution of the functions of immune cells after a major cardiovascular event. Failure to account for this temporal plasticity in cell function may reduce the efficacy of immunomodulatory approaches that target cardiac repair. This review is concerned with how the functions of different immune cells change with time following an MI. Improved understanding of the temporal changes in immune cell function is important for the future development of effective and targeted treatments for preventing heart failure after MI.

Multifunctional terahertz absorber based on the Dirac semimetal and vanadium dioxide.

In this paper, a multifunctional terahertz (THz) absorber based on Dirac semimetal and vanadium dioxide (V O 2) is proposed. By modulating the temperature of V O 2, the absorber can be switched between the narrow band and wide band. When V O 2 is in the metallic state, the absorber has a broadband absorption effect with a bandwidth of approximately 4 THz. It has the advantages of insensitivity to polarization and wide-angle absorption. When V O 2 is in the insulating state, the absorber has two absorption peaks with absorptivity exceeding 90% and sensitivities of 297.7 and 402 GHz/RIU, and thus can be used as a highly sensitive sensor for cell detection. When the Fermi level of the Dirac semimetal is changed, the absorption characteristics can be modulated. The absorber has broad application prospects in multifunctional modulated devices.

A pH-responsive metal-organic framework for the co-delivery of HIF-2α siRNA and curcumin for enhanced therapy of osteoarthritis.

The occurrence of osteoarthritis (OA) is highly correlated with the reduction of joint lubrication performance, in which persistent excessive inflammation and irreversible destruction of cartilage dominate the mechanism. The inadequate response to monotherapy methods, suboptimal efficacy caused by undesirable bioavailability, short retention, and lack of stimulus-responsiveness, are few unresolved issues. Herein, we report a pH-responsive metal-organic framework (MOF), namely, MIL-101-NH2, for the co-delivery of anti-inflammatory drug curcumin (CCM) and small interfering RNA (siRNA) for hypoxia inducible factor (HIF-2α). CCM and siRNA were loaded via encapsulation and surface coordination ability of MIL-101-NH2. Our vitro tests showed that MIL-101-NH2 protected siRNA from nuclease degradation by lysosomal escape. The pH-responsive MIL-101-NH2 gradually collapsed in an acidic OA microenvironment to release the CCM payloads to down-regulate the level of pro-inflammatory cytokines, and to release the siRNA payloads to cleave the target HIF-2α mRNA for gene-silencing therapy, ultimately exhibiting the synergetic therapeutic efficacy by silencing HIF-2α genes accompanied by inhibiting the inflammation response and cartilage degeneration of OA. The hybrid material reported herein exhibited promising potential performance for OA therapy as supported by both in vitro and in vivo studies and may offer an efficacious therapeutic strategy for OA utilizing MOFs as host materials.

Remodeling the Tumor Microenvironment with Core-Shell Nanosensitizer Featuring Dual-Modal Imaging and Multimodal Therapy for Breast Cancer.

To improve the efficiency of radiation therapy (RT) for breast cancer, a designable multifunctional core-shell nanocomposite of FeP@Pt is constructed using Fe(III)-polydopamine (denoted as FeP) as the core and platinum particles (Pt) as the shell. The hybrid structure is further covered with hyaluronic acid (HA) to give the final nanoplatform of FeP@Pt@HA (denoted as FPH). FPH exhibits good biological stability, prolongs blood circulation time, and is simultaneously endowed with tumor-targeting ability. With CD44-mediated endocytosis of HA, FPH can be internalized by cancer cells and activated by the tumor microenvironment (TME). The redox reaction between Fe3+ in FPH and endogenous glutathione (GSH) or/and hydrogen peroxide (H2O2) initiates ferroptosis therapy by promoting GSH exhaustion and •OH generation. Moreover, FPH has excellent photothermal conversion efficiency and can absorb near-infrared laser energy to promote the above catalytic reaction as well as to achieve photothermal therapy (PTT). Ferroptosis therapy and PTT are further accompanied by the catalase activity of Pt nanoshells to accelerate O2 production and the high X-ray attenuation coefficient of Pt for enhanced radiotherapy (RT). Apart from the therapeutic modalities, FPH exhibits dual-modal contrast enhancement in infrared (IR) thermal imaging and computed tomography (CT) imaging, offering potential in imaging-guided cancer therapy. In this article, the nanoplatform can remodel the TME through the production of O2, GSH- and H2O2-depletion, coenhanced PTT, ferroptosis, and RT. This multimodal nanoplatform is anticipated to shed light on the design of TME-activatable materials to enhance the synergism of treatment results and enable the establishment of efficient nanomedicine.

Bufalin Inhibits Tumorigenesis and SREBP-1-Mediated Lipogenesis in Hepatocellular Carcinoma via Modulating the ATP1A1/CA2 Axis.

Altered lipid metabolism is a hallmark of hepatocellular carcinoma (HCC), a common malignancy with a dismal prognosis against which there is a lack of effective therapeutic strategies. Bufalin, a classical Na[Formula: see text]-K[Formula: see text]-ATPase (NKA) inhibitor, shows a potent antitumor effect against HCC. However, the role of bufalin in regulating lipid metabolism-related pathways of HCC remains unclear. In this study, we examined the interaction between bufalin and its target molecule, ATP1A1/CA2, in vitro and in vivo and explored the intersected downstream pathways in silico. A multi-omics analysis of transcriptomics and metabolomics was employed to screen for potential action targets. The results were verified and correlated with the downstream lipid de novo synthesis pathway and the bufalin/ATP1A1/CA2 axis. We found that bufalin suppressed the ATP1A1/CA2 ratio in the treated HCC cells and showed a negative correlation with bufalin drug sensitivity. Functionally, ATP1A1 overexpression and CA2 down-regulation inhibited the bufalin-suppressed HCC proliferation and metastasis. Furthermore, down-regulation of CA2 induced epithelial-mesenchymal transition and bufalin resistance in HCC cells by up-regulating ATP1A1. Mechanistically, lipid metabolism-related signaling pathways were enriched in low ATP1A1 and high CA2 expression subgroups in GSEA. The multi-omics analysis also showed that bufalin was closely related to lipid metabolism. We demonstrated that bufalin inhibits lipogenesis and tumorigenesis by down-regulating SREBP-1/FASN/ACLY via modulating the ATP1A1/CA2 axis in HCC.

FAS-mediated circRNA-miRNA-mRNA Crosstalk Network Regulates Immune Cell Infiltration in Cerebral Infarction.

New data are accumulating on the involvement of interaction among circular RNAs (circRNAs), microRNAs (miRNAs/miRs), and messenger RNAs (mRNAs) in cerebral infarction (CI). This study aims to illustrate the GEO database-based identification of a circRNA-miRNA-mRNA crosstalk network underlying immune cell infiltration in CI. The differential analysis suggested that 1696 circRNAs, 1989 miRNAs, and 5550 mRNAs that were differentially expressed in CI samples were retrieved from GEO database. GO and KEGG functional enrichment analyses showed that the differentially expressed mRNAs were mainly associated with common risk factors of CI, such as immune and inflammatory response. Next, the circRNA-miRNA pairs and miRNA-mRNA pairs were predicted, and the circRNA-miRNA-mRNA network was constructed by Cytoscape software. Totally, 436 circRNA-miRNA pairs were obtained through the online database, and 2033 miRNA-mRNA pairs were used to construct the circRNA-miRNA-mRNA crosstalk network. A protein-protein interaction (PPI) network was constructed on the basis of the ceRNA network, followed by key gene identification in the GSE9877 dataset. FAS was identified as the key gene in CI. The constructed FAS-mediated circRNA-miRNA-mRNA crosstalk network included five upregulated circRNAs (hsa_circ_0075341, hsa_circ_0049637, hsa_circ_0001085, hsa_circ_0004808 and hsa_circ_0092337) and five downregulated miRNAs (hsa-miR-92a-2-5p, hsa-miR-1245b-3p, hsa-miR-592, hsa-miR-224-5p, and hsa-miR-30e-3p). Furthermore, the CIBERSORT algorithm indicated that FAS was associated with immune cell infiltration in CI. In conclusion, this study revealed a role for FAS-centered circRNA-miRNA-mRNA crosstalk network in regulating immune cell infiltration of CI, which may be a viable target for CI prevention.

Element sulfur-based autotrophic denitrification constructed wetland as an efficient approach for nitrogen removal from low C/N wastewater.

Constructed wetlands (CWs) integrated with sulfur autotrophic denitrification to stimulate high-rate nitrogen removal from carbon-limited wastewater holds particular application prospect due to no excessive carbon source addition, high efficiency, and good stability. In this study, we conducted elemental sulfur-based constructed wetland (SCW) and traditional constructed wetland (CW) under different C/N (2, 1, and 0.5) to explore the feasibility and mechanisms for nitrogen removal from low C/N wastewater. Compared with CW, SCW was demonstrated more robust in nitrogen removal in the case of low C/N influent. When the influent C/N control was at 0.5, SCW observed total nitrogen (TN) and nitrate removal efficiency of 69.36 ± 3.96% and 81.71 ± 3.96%, with the corresponding removal rate of 1.18 ± 0.66 and 1.70 ± 0.92 g-N·m-2·d-1, which were 2.11 and 10.03 times of CW, respectively. The nitrate removal rate constant k in the SCW was 1.05, 3.83, and 10.33 times higher than the CW with C/N of 2, 1 and 0.5. Furthermore, 14.40, 54.51, and 79.82% of nitrogen were removed by the sulfur autotrophic denitrification (SAD) in SCW, which also contributed 43.89, 73.68, and 71.70% of sulfate production. Moreover, the combined system of CW-SCW is proved be an efficient operation mode for simultaneously removing total ammonia nitrogen (TAN) and nitrate. In the SCW, the richness of the microbial community was improved and sulfur-oxidizing genera (e.g. Thiobacillus, Sulfurimonas) was selectively enriched, which affect the performance the elemental sulfur-based denitrification process. The nitrate reduction pathway was overwhelmed by denitrification and the dissimilatory nitrate reduction process. These findings offer elemental sulfur-based autotrophic denitrification constructed wetland has excellent potential to enhance nitrogen removal from carbon-limited wastewater.

NIR-PTT/ROS-Scavenging/Oxygen-Enriched Synergetic Therapy for Rheumatoid Arthritis by a pH-Responsive Hybrid CeO2-ZIF-8 Coated with Polydopamine.

Rheumatoid arthritis (RA) is an inflammatory type of arthritis that causes joint pain and damage. The inflammatory cell infiltration (e.g., M1 macrophages), the poor O2 supply at the joint, and the excess reactive oxygen species (ROS)-induced oxidative injury are the main causes of RA. We herein report a polydopamine (PDA)-coated CeO2-dopped zeolitic imidazolate framework-8 (ZIF-8) nanocomposite CeO2-ZIF-8@PDA (denoted as CZP) that can synergistically treat RA. Under near-infrared (NIR) light irradiation, PDA efficiently scavenges ROS and results in an increased temperature in the inflamed area because of its good light-to-heat conversion efficiency. The rise of temperature serves to obliterate hyper-proliferative inflammatory cells accumulated in the diseased area while vastly promoting the collapse of the acidic-responsive skeleton of ZIF-8 to release the encapsulated CeO2. The released CeO2 exerts its catalase-like activity to relieve hypoxia by generating oxygen via the decomposition of H2O2 highly expressed in the inflammatory sites. Thus, the constructed CZP composite can treat RA through NIR-photothermal/ROS-scavenging/oxygen-enriched combinative therapy and show good regression of pro-inflammatory cytokines and hypoxia-inducible factor-1α (HIF-1α) in vitro and promising therapeutic effect on RA in rat models. The multimodal nano-platform reported herein is expected to shed light on the design of synergistic therapeutic nanomedicine for effective RA therapy.

Synergistic photothermal-photodynamic-chemotherapy toward breast cancer based on a liposome-coated core-shell AuNS@NMOFs nanocomposite encapsulated with gambogic acid.

A multifunctional nanoplatform with core-shell structure was constructed in one-pot for the synergistic photothermal, photodynamic, and chemotherapy against breast cancer. In the presence of gambogic acid (GA) as the heat-shock protein 90 (HSP90) inhibitor and the gold nanostars (AuNS) as the photothermal reagent, the assembly of Zr4+ with tetrakis (4-carboxyphenyl) porphyrin (TCPP) gave rise to the nanocomposite AuNS@ZrTCPP-GA (AZG), which in turn, further coated with PEGylated liposome (LP) to enhance the stability and biocompatibility, and consequently the antitumor effect of the particle. Upon cellular uptake, the nanoscale metal - organic framework (NMOF) of ZrTCPP in the resulted AuNS@ZrTCPP-GA@LP (AZGL) could be slowly degraded in the weak acidic tumor microenvironment to release AuNS, Zr4+, TCPP, and GA to exert the synergistic treatment of tumors via the combination of AuNS-mediated mild photothermal therapy (PTT) and TCPP-mediated photodynamic therapy (PDT). The introduction of GA serves to reduce the thermal resistance of the cell to re-sensitize PTT and the constructed nanoplatform demonstrated remarkable anti-tumor activity in vitro and in vivo. Our work highlights a facile strategy to prepare a pH-dissociable nanoplatform for the effective synergistic treatment of breast cancer.

Tumor Suppressor Role and Clinical Significance of the FEV Gene in Prostate Cancer.

Background: In our previous research, we developed a 32-gene risk index model that may be utilized as a robust prognostic method for predicting prostate cancer (PCa) recurrence after surgery. Among the 32 genes, the Fifth Ewing Variant (FEV) gene was one of the top downregulated genes in relapsed PCa. However, current understanding of the FEV gene and its involvement in PCa is limited. Methods: FEV mRNA expression was analyzed and correlated to clinical outcomes in PCa patients who underwent prostatectomy at the Massachusetts General Hospital. Specimens from tissue microarray (TMA) including 102 prostate cancer patients were analysis for the expression of FEV. Meanwhile, FEV expression profiles were also assessed in PCa cell lines and in BPH-1 prostate epithelial cells using western blotting and quantitative reverse transcription-PCR (qRT-PCR). Furthermore, we transfected LNCaP and PC-3 cells with either an empty vector or full-length FEV gene and performed in vitro cell functional assays. The part FEV plays in tumor xenograft growth was also assessed in vivo. Results: Of the 191 patients included in this study base on the DASL dataset, 77 (40.3%) and 24 (13.6%), respectively, developed prostate-specific antigen (PSA) relapse and metastasis postradical prostatectomy. Significant FEV downregulation was observed in PCa patients showing PSA failure and metastasis. The protein expression of FEV was significantly negatively correlated with the Gleason score and pathological stage in prostate cancer tissues. Similarly, FEV expression significantly decreased in all PCa cell lines relative to BPH-1 (all P < 0.05). Functional assays revealed that FEV expression markedly inhibited PCa cell growth, migration, and invasion, which in turn significantly repressed the growth of tumor xenografts in vivo. Conclusion: The results of this study suggest an association between downregulated FEV expression and PSA relapse in PCa patients. In addition, FEV may act as a tumor suppressor in PCa.

The sarcopenia index is an effective predictor for malnutrition in patients with liver cirrhosis.

AIM: Reliable and valid predictors of malnutrition in patients with cirrhosis remain scarce, especially easily accessible blood indicators. Thus, this study aimed to investigate the validity of the sarcopenia index (serum creatinine/serum cystatin C × 100) as a tool in assessing the nutritional status of patients with cirrhosis. METHODS: This prospective cohort study included 109 patients with cirrhosis who were hospitalised in Renmin Hospital of Wuhan University from August 2020 to June 2021. Malnutrition was diagnosed by the Global Leadership Initiative on Malnutrition criteria. Multivariable logistic regression was used to examine the relationship between sarcopenia index and malnutrition. The area under the receiver operating characteristic curve was used to evaluate the diagnostic performance of sarcopenia index. By contrast, we evaluated the subjective global assessment and traditional nutrition-related indicators. RESULTS: Of the 109 included patients, 71 (65.1%) were diagnosed with malnutrition. The sarcopenia index was significantly lower in malnourished patients (56.39 ± 15.23) compared with well-nourished patients (74.95 ± 13.18, p < 0.001). In addition, the sarcopenia index was independently correlated with malnutrition (p < 0.001). The sarcopenia index was a good tool to predict malnutrition (area under curve = 0.833), which performed better than the subjective global assessment (area under curve = 0.782) and cholinesterase (area under curve = 0.812). A low sarcopenia index indicated longer hospital stay and higher risk of 90-day re-hospitalisation. CONCLUSION: Malnutrition is highly prevalent in this population. The sarcopenia index seems to be a good predictor in nutritional assessment of patients with cirrhosis.

Integrated constructed wetland and bioelectrochemistry system approach for simultaneous enhancment of p-chloronitrobenzene and nitrogen transformations performance.

Constructed wetlands (CWs) integrated with the bioelectrochemical system (BES-CW) to stimulate bio-refractory compounds removal holds particular promise, owing to its inherent greater scale and well-recognized environmentally benign wastewater advanced purification technology. However, the knowledge regarding the feasibility and removal mechanisms, particularly the potential negative effects of biorefractory compounds on nitrogen removal performance for the CWs is far insufficient. This study performed a critical assessment by using BES-CW (ECW) and conventional CW (CW) to investigate the effects of p-Chloronitrobenzene (pCNB) on nitrogen transformations in CWs. The results showed that low concentration (1 mg·L-1) of pCNB would inhibit the ammonia oxidation in CWs, while ECW could improve its tolerance to pCNB to a certain level (8 mg·L-1) due to the high pCNB degradation efficiencies (2.5 times higher than CWs), accordingly, much higher TN and nitrate removal efficiencies were observed in ECWs, 81.71% - 96.82% (TN) higher than CWs, further leading to a lower N2O emission from ECWs than CWs. The main intermediate of pCNB degradation was p-Chloroaniline (pCAN) and the genera Geobacter and Propionimicrobium were consider to be the responsible pCNB degradation bacteria in the present study. However, too high concentration (20 mg·L-1) of pCNB would have a huge impact on ECW and CW, especially microbial biomass. Nevertheless, ECW could improve the 1.87 times higher microbial biomass than CW on the substrate. Accordingly, considerably higher functional gene abundance was observed in ECW. Therefore, the introduction of BES has great potential to ensure CW stability when treating industrial wastewater containing bio-refractory compounds.