Role of low-molecular-weight organic compounds on photochemical formation of Mn(III)-ligands in aqueous systems: Implications for BPA removal.

Aqueous trivalent manganese [Mn(III)], an important reactive intermediate, is ubiquitous in natural surface water containing humic acid (HA). However, the effect of low-molecular-weight organic acids (LMWOAs) on the formation, stability and reactivity of Mn(III) intermediate is still unknown. In this study, six LMWOAs, including oxalic acid (Oxa), salicylic acid (Sal), catechol (Cat), caffeic acid (Caf), gallic acid (Gal) and ethylene diamine tetraacetic acid (EDTA), were selected to investigate the effects of LMWOAs on the degradation of BPA induced by in situ formed Mn(III)-L in the HA/Mn(II) system under light irradiation. The chromophoric constituents of HA could absorb light radiation and generate superoxide radical to promote the oxidation of Mn(II) to form Mn(III), which was further involved in transformation of BPA. Our results implied that different LMWOAs did significantly impact on Mn(III) production and its degradation of BPA due to their different functional group. EDTA, Oxa and Sal extensively increased the Mn(III) concentration from 50 to 100 µM compared to the system without LMWOAs, following the order of EDTA > Oxa > Sal, and also enhanced the degradation of BPA with the similar patterns. In contrast, Cat, Caf and Gal had an inhibitory effect on the formation of Mn(III), which is likely because they consumed the superoxide radicals generated from irradiated HA, resulting in the inhibition of Mn(II) oxidation and further BPA removal. The product identification and theoretical calculation indicated that a single electron transfer process occurred between Mn(III)-L and BPA, forming BPA radicals and subsequent self-coupling products. Our results demonstrated that the LMWOAs with different structures could alter the cycling process of Mn via complexation and redox reactions, which would provide new implications for the removal of organic pollutants in surface water.

W-N heteroatom-interface in melon carbon nitride/N-doped tungsten oxide Z-Scheme photocatalyst toward improved photocatalytic hydrogen generation activity.

The construction of heterointerface in photocatalyst is an efficient approach to boost the separation and utilization efficiency of charge carriers, which is challenging and crucial in photocatalysis. Here, the construction of melon-structured carbon nitride/N-doped WO3 (MCN/NWx) heterojunction photocatalyst was achieved by a method of prealcoholysis combined with thermal polymerization, where N-doping of WO3 was achieved in-situ in the formation of heterojunction. The promoted charge separation efficiency was realized through the charge transfer from the conduction band of N-doped WO3 to the valence band of the MCN. Density functional theory calculation results showed that the formation of the W-N heteroatom-interface led to the increase of density of states at the heterointerface and decrease of the band gap. The MCN/NWx nanocomposite featured a metallic band structure of the nanocomposite photocatalysts, resulting in the enhanced photocatalytic activity. The photocatalytic hydrogen evolution activity of the MCN/NW2 was enhanced about 2.5 times than that of MCN. This research provides a novel insight into the construction of a novel heteroatom-junction that boosts the separation efficiency of charge carriers, and thereby improves the photocatalytic activity.

Dysregulation of iron homeostasis by TfR-1 renders EZH2 wild type diffuse large B-cell lymphoma resistance to EZH2 inhibition.

EZH2 has been regarded as an efficient target for diffuse large B-cell lymphoma (DLBCL), but the clinical benefits of EZH2 inhibitors (EZH2i) are limited. To date, only EPZ-6438 has been approved by FDA for the treatment of follicular lymphoma and epithelioid sarcoma. We have discovered a novel EZH1/2 inhibitor HH2853 with a better antitumor effect than EPZ-6438 in preclinical studies. In this study we explored the molecular mechanism underlying the primary resistance to EZH2 inhibitors and sought for combination therapy strategy to overcome it. By analyzing EPZ-6438 and HH2853 response profiling, we found that EZH2 inhibition increased intracellular iron through upregulation of transferrin receptor 1 (TfR-1), ultimately triggered resistance to EZH2i in DLBCL cells. We demonstrated that H3K27ac gain by EZH2i enhanced c-Myc transcription, which contributed to TfR-1 overexpression in insensitive U-2932 and WILL-2 cells. On the other hand, EZH2i impaired the occurrence of ferroptosis by upregulating the heat shock protein family A (Hsp70) member 5 (HSPA5) and stabilizing glutathione peroxidase 4 (GPX4), a ferroptosis suppressor; co-treatment with ferroptosis inducer erastin effectively overrode the resistance of DLBCL to EZH2i in vitro and in vivo. Altogether, this study reveals iron-dependent resistance evoked by EZH2i in DLBCL cells, and suggests that combination with ferroptosis inducer may be a promising therapeutic strategy.

Effect of duloxetine on pain relief after total knee arthroplasty: A meta-analysis of randomized controlled trials.

BACKGROUND: Postoperative pain is one of the most feared complications of total knee arthroplasty. Recently, randomized controlled trials have compared the efficacy of duloxetine in patients undergoing total knee arthroplasty. However, there is no definite answer as to the efficacy and safety of duloxetine. METHODS: Randomized controlled trials about relevant studies were searched from PubMed (1996 to July 2022), Embase (1996 to July 2022), and Cochrane Library (CENTRAL, July 2022). RESULTS: Six high-quality studies containing 532 patients met the inclusion criteria. Results show patients in the duloxetine group had better performance in terms of visual analog scale (P < .05), equivalent morphine consumption (P < .05), and length of stay (P < .05). CONCLUSION: Duloxetine can be used to reduce pain after knee arthroplasty in selected patients.

Combined effects of fluoroquinolone antibiotics and organophosphate flame retardants on Microcystis aeruginosa.

As freshwater harmful algal blooms continue to rise in frequency and severity, increasing focus is made on the effects of mixed pollutants and the dominant cyanobacterial species Microcystis aeruginosa (M. aeruginosa). However, few studies have investigated whether M. aeruginosa has a synergistic relationship with two common pollutants, namely, organophosphate flame retardants (OPFRs) and fluoroquinolone antibiotics (FQs). In this paper, three FQs and three OPFRs commonly detected in freshwaters were selected to construct a ternary mixture of FQs, a ternary mixture of OPFRs, and a six-component mixture of OPFRs and FQs. The effects of single substance and mixture on the growth of M. aeruginosa were determined at 24, 48, 72, and 96 h, and the toxicities of the mixture were evaluated by concentration addition model and independent action model. The results showed that the mixture of FQs and the mixture of OPFRs do not show toxicological interaction. However, partial mixtures of OPFRs and FQs showed antagonism or synergism at different concentrations and times. This indicated that combined toxicities of OPFRs and FQs on M. aeruginosa were mixture ratio dependent, concentration dependent and time dependent. This study improves our understanding of the role of OPFRs and FQs in cyanobacterial outbreaks of Microcystis.

Histone deacetylase inhibitors promote breast cancer metastasis by elevating NEDD9 expression.

Histone deacetylase (HDAC) is a kind of protease that modifies histone to regulate gene expression, and is usually abnormally activated in tumors. The approved pan-HDAC inhibitors have demonstrated clinical benefits for patients in some hematologic malignancies. Only limited therapeutic success in breast cancer has been observed in clinical trials. In this study, we declare that pan-HDAC inhibitors targeting NEDD9-FAK pathway exacerbate breast cancer metastasis in preclinical models, which may severely impede their clinical success. NEDD9 is not an oncogene, however, it has been demonstrated recently that there are high level or activity changes of NEDD9 in a variety of cancer, including leukemia, colon cancer, and breast cancer. Mechanistically, pan-HDAC inhibitors enhance H3K9 acetylation at the nedd9 gene promoter via inhibition of HDAC4 activity, thus increase NEDD9 expression, and then activate FAK phosphorylation. The realization that pan-HDAC inhibitors can alter the natural history of breast cancer by increasing invasion warrants clinical attention. In addition, although NEDD9 has been reported to have a hand in breast cancer metastasis, it has not received much attention, and no therapeutic strategies have been developed. Notably, we demonstrate that FAK inhibitors can reverse breast cancer metastasis induced by upregulation of NEDD9 via pan-HDAC inhibitors, which may offer a potential combination therapy for breast cancer.

Regulation of CCL2 by EZH2 affects tumor-associated macrophages polarization and infiltration in breast cancer.

Tumor associated macrophages (TAMs) play an important role in tumorigenesis, development and anti-cancer drug therapy. However, very few epigenetic compounds have been elucidated to affect tumor growth by educating TAMs in the tumor microenvironment (TME). Herein, we identified that EZH2 performs a crucial role in the regulation of TAMs infiltration and protumoral polarization by interacting with human breast cancer (BC) cells. We showed that EZH2 inhibitors-treated BC cells induced M2 macrophage polarization in vitro and in vivo, while EZH2 knockdown exhibited the opposite effect. Mechanistically, inhibition of EZH2 histone methyltransferase alone by EZH2 inhibitors in breast cancer cells could reduce the enrichment of H3K27me3 on CCL2 gene promoter, elevate CCL2 transcription and secretion, contributing to the induction of M2 macrophage polarization and recruitment in TME, which reveal a potential explanation behind the frustrating results of EZH2 inhibitors against breast cancer. On the contrary, EZH2 depletion led to DNA demethylation and subsequent upregulation of miR-124-3p level, which inhibited its target CCL2 expression in the tumor cells, causing arrest of TAMs M2 polarization. Taken together, these data suggested that EZH2 can exert opposite regulatory effects on TAMs polarization through its enzymatic or non-enzymatic activities. Our results also imply that the effect of antitumor drugs on TAMs may affect its therapeutic efficacy, and the combined application with TAMs modifiers should be warranted to achieve great clinical success.

Carbon nitride-based Z-scheme heterojunctions for solar-driven advanced oxidation processes.

Solar-driven advanced oxidation processes (AOPs) via direct photodegradation or indirect photocatalytic activation of typical oxidants, such as hydrogen peroxide (H2O2), peroxymonosulfate (PMS), and peroxydisulfate (PDS), have been deemed to be an efficient technology for wastewater remediation. Artificial Z-scheme structured materials represent a promising class of photocatalysts due to their spatially separated charge carriers and strong redox abilities. Herein, we summarize the development of metal-free graphitic carbon nitride (g-C3N4, CN)-based direct and indirect Z-scheme photocatalysts for solar-driven AOPs in removing organic pollutants from water. In the work, the classification of AOPs, definition and validation of Z-schemes are summarized firstly. The innovative engineering strategies (e.g., morphology and dimensionality control, element doping, defect engineering, cocatalyst loading, and tandem Z-scheme construction) over CN-based direct Z-scheme structure are then examined. Rational design of indirect CN-based Z-scheme systems using different charge mediators, such as solid conductive materials and soluble ion pairs, is further discussed. Through examining the relationship between the Z-scheme structure and activity (charge transfer and separation, light absorption, and reaction kinetics), we aim to provide more insights into the construction strategies and structure modification on CN-based Z-schemes towards improving their catalytic performances in AOPs. Lastly, limitations, challenges, and perspectives on future development in this emerging field are proposed.

The HDAC inhibitor GCJ-490A suppresses c-Met expression through IKKα and overcomes gefitinib resistance in non-small cell lung cancer.

OBJECTIVE: The novel compound GCJ-490A has been discovered as a pan-histone deacetylase (HDAC) inhibitor that exerts potent inhibitory activity against HDAC1, HDAC3, and HDAC6. Because of the important roles of HDACs in lung cancer development and the high distribution of GCJ-490A in lung tissue, we explored the anti-tumor potency of GCJ-490A against non-small cell lung cancer (NSCLC) in vitro and in vivo in this study. METHODS: The in vitro effects of GCJ-490A alone or combined with the EGFR inhibitor gefitinib against NSCLC were measured with proliferation, apoptosis, and colony formation assays. NSCLC xenograft models were used to investigate the efficacy of GCJ-490A combined with gefitinib for the treatment of NSCLC in vivo. Western blot assays, luciferase reporter assays, chromatin immunoprecipitation assays, quantitative real time-PCR, immunohistochemistry, and transcription factor activity assays were used to elucidate possible mechanisms. RESULTS: GCJ-490A effectively inhibited NSCLC cell proliferation and induced apoptosis in vitro and in vivo. Interestingly, inhibition of HDAC1 and HDAC6 by GCJ-490A increased histone acetylation at the IKKα promoter and enhanced IKKα transcription, thus decreasing c-Met. Moreover, this c-Met downregulation was found to be essential for the synergistic anti-tumor activity of GCJ-490A and gefitinib. CONCLUSIONS: These findings highlight the promising potential of HDAC inhibitors in NSCLC treatment and provide a rational basis for the application of HDAC inhibitors in combination with EGFR inhibitors in clinical trials.

Synergy of Oxygen Vacancies and Acid Sites on N-Doped WO3 Nanobelts for Efficient C-C Coupling Synthesis of Benzoin Isopropyl Ether.

The surface property of a photocatalyst, including surface acid sites and oxygen vacancies, plays a pivotal role in photocatalytic organic synthesis reactions. Benzoin isopropyl ether (BIE) is usually produced via polycondensation of benzaldehyde and catalyzed with highly toxic cyanide. Here, we report a green photocatalytic approach for the selective synthesis of BIE over WO3 driven by a green-light-emitting diode. The improved photocatalytic activity can be attributed to the synergy of oxygen vacancies (VOs) and acid sites over N-doped WO3 nanobelts. The results revealed that reactant molecules were predominantly adsorbed and activated on surface oxygen vacancies (VOSs) and the Brønsted acid promoted the etherification reaction; the introduction of VOs and nitrogen altered the band structure and electronic properties, resulting in improved photocatalytic activity. Our work provides an efficient approach to the selective photocatalytic synthesis of organics over photocatalysts with finely tuned surface properties and band structures via defect and doping engineering.

Improved transfer efficiency of supercharged 36 + GFP protein mediate nucleic acid delivery.

The potential of nucleic acid therapeutics to treat diseases by targeting specific cells has resulted in its increasing number of uses in clinical settings. However, the major challenge is to deliver bio-macromolecules into target cells and/or subcellular locations of interest ahead in the development of delivery systems. Although, supercharged residues replaced protein 36 + GFP can facilitate itself and cargoes delivery, its efficiency is still limited. Therefore, we combined our recent progress to further improve 36 + GFP based delivery efficiency. We found that the penetration efficacy of 36 + GFP protein was significantly improved by fusion with CPP-Dot1l or treatment with penetration enhancer dimethyl sulfoxide (DMSO) in vitro. After safely packaged with plasmid DNA, we found that the efficacy of in vitro and in vivo transfection mediated by 36 + GFP-Dot1l fusion protein is also significantly improved than 36 + GFP itself. Our findings illustrated that fusion with CPP-Dot1l or incubation with DMSO is an alternative way to synergically promote 36 + GFP mediated plasmid DNA delivery in vitro and in vivo.

The Novel RET Inhibitor SYHA1815 Inhibits RET-Driven Cancers and Overcomes Gatekeeper Mutations by Inducing G1 Cell-Cycle Arrest through c-Myc Downregulation.

Rearranged during transfection (RET), an oncogenic driver, has been found in multiple tumor types and is thus a promising anticancer therapeutic target. Novel selective RET inhibitors (RETi) that can overcome V804 gatekeeper mutations, endowing resistance to multikinase inhibitors (MKI) and, in particular, achieving KDR selectivity, are needed. In addition, the mechanisms underlying RET-inhibition-induced antiproliferative effects in the context of RET addiction are incompletely understood. This study describes a novel selective RETi, SYHA1815, which inhibited the kinase activity of RET wild type and V804 mutant with an IC50 in the subnanomolar to nanomolar range. Notably, SYHA1815 exhibited approximately 20-fold selectivity for RET over KDR, almost equivalent to that of the launched selective inhibitor pralsetinib. SYHA1815 had only a marginal inhibitory effect on cellular KDR signaling at a high (200 nmol/L) concentration, confirming the selectivity over KDR. In addition, SYHA1815 exhibited a favorable selectivity profile, with greater than 100-fold selectivity for RET over 347 other kinases. It exhibited potent antitumor efficacy and overcame V804 mutations in vitro and in vivo by targeting RET. Then, using SYHA1815 as a probe, we found that RET inhibition suppressed RET-driven cell proliferation via G1 cell-cycle arrest through downregulating c-Myc. Furthermore, disruption of c-Myc upon Brd4 inhibitor treatment led to G1 cell-cycle arrest and overrode RET-driven cell proliferation. Moreover, consistent with the marked in vivo efficacy of RET inhibition, the intratumoral c-Myc level was significantly decreased. In summary, SYHA1815 is a promising RETi for RET-aberrant cancer treatment that is currently in a phase I trial.

SAF-189s, a potent new-generation ROS1 inhibitor, is active against crizotinib-resistant ROS1 mutant-driven tumors.

The ROS1 fusion kinase is an attractive antitumor target. Though with significant clinical efficacy, the well-known first-generation ROS1 inhibitor (ROS1i) crizotinib inevitably developed acquired resistance due to secondary point mutations in the ROS1 kinase. Novel ROS1is effective against mutations conferring secondary crizotinib resistance, especially G2032R, are urgently needed. In the present study, we evaluated the antitumor efficacy of SAF-189s, the new-generation ROS1/ALK inhibitor, against ROS1 fusion wild-type and crizotinib-resistant mutants. We showed that SAF-189s potently inhibited ROS1 kinase and its known acquired clinically resistant mutants, including the highly resistant G2032R mutant. SAF-189s displayed subnanomolar to nanomolar IC50 values against ROS1 wild-type and mutant kinase activity and a selectivity vs. other 288 protein kinases tested. SAF-189s blocked cellular ROS1 signaling, and in turn potently inhibited the cell proliferation in HCC78 cells and BaF3 cells expressing ROS1 fusion wild-type and resistance mutants. In nude mice bearing BaF3/CD74-ROS1 or BaF3/CD74-ROS1G2032R xenografts, oral administration of SAF-189s dose dependently suppressed the growth of both ROS1 wild-type- and G2032R mutant-driven tumors. In a patient-derived xenograft model of SDC4-ROS1 fusion NSCLC, oral administration of SAF-189s (20 mg/kg every day) induced tumor regression and exhibited notable prolonged and durable efficacy. In addition, SAF-189s was more potent than crizotinib and comparable to lorlatinib, the most advanced ROS1i known against the ROS1G2032R. Collectively, these results suggest the promising potential of SAF-189s for the treatment of patients with the ROS1 fusion G2032R mutation who relapse on crizotinib. It is now recruiting both crizotinib-relapsed and naive ROS1-positive NSCLC patients in a multicenter phase II trial (ClinicalTrials.gov Identifier: NCT04237805).

Green and efficient degradation of cefoperazone sodium by Bi4O5Br2 leading to the production of non-toxic products: Performance and degradation pathway.

Photocatalytic process represents a promising approach to overcome the pollution challenge associated with the antibiotics-containing wastewater. This study provides a green, efficient and novel approach to remove cephalosporins, particularly cefoperazone sodium (CFP). Bi4O5Br2 was chosen for the first time to systematically study its degradation for CFP, including the analysis of material structure, degradation performance, the structure and toxicity of the transformation products, etc. The degradation rate results indicated that Bi4O5Br2 had an excellent catalytic activity leading to 78% CFP removal compared with the pure BiOBr (38%) within 120 min of visible light irradiation. In addition, the Bi4O5Br2 presents high stability and good organic carbon removal efficiency. The effects of the solution pH (3.12 - 8.75) on catalytic activity revealed that CFP was mainly photocatalyzed under acidic conditions and hydrolyzed under alkaline conditions. Combined with active species and degradation product identification, the photocatalytic degradation pathways of CFP by Bi4O5Br2 was proposed, including hydrolysis, oxidation, reduction and decarboxylation. Most importantly, the identified products were all hydrolysis rather than oxidation byproducts transformed from the intermediate of ß-lactam bond cleavage in CFP molecule, quite different from the mostly previous studies. Furthermore, the final products were demonstrated to be less toxic through the toxicity analysis. Overall, this study illustrates the detailed mechanism of CFP degradation by Bi4O5Br2 and confirms Bi4O5Br2 to be a promising material for the photodegradation of CFP.

Hydrothermal synthesis of m-BiVO4/t-BiVO4 heterostructure for organic pollutants degradation: Insight into the photocatalytic mechanism of exposed facets from crystalline phase controlling.

A series of BiVO4 photocatalysts were prepared by a co-precipitation followed hydrothermal synthesis method for the photodegradation of Rhodamine B (RhB) and 2,4-Dichlorophenol (2,4-DCP). The crystalline phase ratio of the heterostructured BiVO4 (m-BiVO4/t-BiVO4) between monoclinic and tetragonal could be easily controlled at different pH and hydrothermal time. Interestingly, the as-prepared heterostructured BiVO4 photocatalyst at pH = 7 for 24 h (BiVO4-7-24) showed the highest photocatalytic activities for the degradation of RhB, while the best photodegradation of 2,4-DCP was obtained at pH = 0.5 for 24 h (BiVO4-0.5-24). The photocatalytic mechanism can be explained by the different charge carrier transfer pathways and active oxidation species in the m-BiVO4/t-BiVO4 heterostructure. More importantly, the exposed facets originated from crystalline phase controlling in BiVO4-0.5-24 and BiVO4-7-24 photocatalyst is an essential reason for the different photocatalytic activity. The proposed energy band alignments of BiVO4-0.5-24 and BiVO4-7-24 photocatalyst provide insights into the photocatalytic mechanism of the m-BiVO4/t-BiVO4 heterostructure.

Design, Synthesis, and Biological Evaluation of HSP90 Inhibitor-SN38 Conjugates for Targeted Drug Accumulation.

Herein, a series of HSP90 inhibitor-SN38 conjugates through ester and carbamate linkage in the 20-OH and 10-OH positions of SN38 were developed for improving the tumor-specific penetration and accumulation of SN38 via extracellular HSP90 (eHSP90)-mediated endocytosis. Mechanistic analyses confirmed that these novel conjugates could bind to eHSP90 and be selectively internalized into the tumor cells, which led to prolonged tumor regression in multiple models of cancer. Among all studied conjugates, compound 18b showed excellent in vitro activities, including acceptable HSP90α affinity and potent antitumor activity. Moreover, compound 18b exhibited superior antitumor activity and low toxicity in HCT116 and Capan-1 xenograft models. Pharmacokinetic analyses in HCT116 and Capan-1 xenografts further confirmed that compound 18b treatment could lead to effective cleavage and extended SN38 exposure at tumor sites. All these encouraging data indicate that this compound is a promising new candidate for cancer therapy and merits further chemical and biological evaluation.

Antitumor activity of a novel Aurora A/B kinases inhibitor TY-011 against gastric cancer by inducing DNA damage.

TY-011, a novel Aurora A/B kinases inhibitor, was found in our previous study to exhibit prominent inhibitory effects on growth of gastric cancer, both in vitro and in vivo. To clarify the mechanisms of TY-011 in inhibiting proliferation of gastric cancer cells, the effects of TY-011 on mitosis, cell cycle, apoptosis and cellular DNA were checked in the present study. Our results showed that TY-011 treatment induced aberrant mitosis, G2/M phase arrest and apoptosis. Importantly, TY-011 induced evident DNA damage in MGC-803 and MKN-45 human gastric cancer cells, which was further characterized as DNA double-strand break. Furthermore, cells treated with TY-011 appeared to generate multiple spindle fibers emanating from several spindle poles, leading to poly-merotelic kinetochore. These results suggested that TY-011 induced abnormal microtubule-kinetochores attachment and thus DNA damage, apoptosis and finally inhibition of cell proliferation of human gastric cancer cells.

Preliminary study on the electrocatalytic performance of an iron biochar catalyst prepared from iron-enriched plants.

Eichhornia crassipes is a hyperaccumulator of metals and has been widely used to remove metal pollutants from water, but disposal of contaminated plants is problematic. Biochar prepared from plants is commonly used to remediate soils and sequester carbon. Here, the catalytic activity of biochar prepared from plants enriched with iron was investigated as a potentially beneficial use of metal-contaminated plants. In a 30-day hydroponic experiment, E. crassipes was exposed to different concentrations of Fe(III) (0, 4, 8, 16, 32 and 64 mg/L), and Fe-biochar (Fe-BC) was prepared by pyrolysis of the plant roots. The biochar was characterized using X-ray diffraction (XRD), scanning electron microscopy (SEM), energy dispersive X-ray spectrometry (EDS), Brunauer-Emmett-Teller (BET) analysis, X-ray photoelectron spectroscopy (XPS) and atomic absorption spectrometry (AAS). The original root morphology was visible and iron was present as γ-Fe2O3 and Fe3O4. The biochar enriched with Fe(III) at 8 mg/L (8-Fe-BC) had the smallest specific surface area (SSA, 13.54 m2/g) and the highest Fe content (27.9 mg/g). Fe-BC catalytic activity was tested in the electrocatalytic reduction of H2O2 using cyclic voltammetry (CV). The largest reduction current (1.82 mA/cm2) was displayed by 8-Fe-BC, indicating the highest potential catalytic activity. We report here, for the first time, on the catalytic activity of biochar made from iron-enriched plants and demonstrate the potential for reusing metal-contaminated plants to produce a biochar catalyst.

Synergetic effects of defects and acid sites of 2D-ZnO photocatalysts on the photocatalytic performance.

Regulation of defects and surface acidic sites of photocatalysts is an efficient approach to improve the photocatalytic activity. Ultrathin 2D-ZnO photocatalysts were prepared to uncover the synergetic effects of defects and surface acidic sites on the photocatalytic activity. The reaction constant for photocatalytic degradation of MB upon ZnO-S is 2.26, 2.82, 12.2 times higher than that of SH-500, SO-500, and ZnO-R, respectively. The results revealed that the surface defects, hydroxyl group and chemisorbed water played pivotal roles in the generation of reactive oxygen species (ROS). Although the limited improvement of visible absorption was achieved after introduction of oxygen vacancy (VO), the overall photocatalytic activity decreased due to the reduced ROS production capacity shown by density functional theory (DFT) calculations. Hydroxyl radical is the key ROS in degradation of organics, and electron contributes a little bigger than hole in the generation of hydroxyl radical. Importantly, the decrease in surface acidic sites resulted in the decreased photocatalytic activity, proven by the dynamics of photoinduced carriers. This study reveals that the improved photocatalytic activity of 2D-ZnO photocatalysts can be attributed to the synergetic effects of surface defects and acidic sites rather than the enhanced visible absorption resulted from the VO introduction.