Correlation between immunotherapy biomarker PD-L1 expression and genetic alteration in patients with non-small cell lung cancer.

Programmed death-ligand 1 (PD-L1) has been widely used in immunotherapy evaluation of patients with non-small cell lung cancer (NSCLC). However, the effect is not particularly ideal, and the association between PD-L1 and genetic alterations requires more exploration. Here, we performed targeted next-generation sequencing and PD-L1 immunohistochemistry (IHC) testing for PD-L1 expression on both tumor cells (TCs) and tumor-infiltrating immune cells (ICs) in 1549 patients. Our studies showed that surgical method of resection was positively correlated with IC+, and a low tumor mutation burden (TMB) was negatively correlated with TC+. Furthermore, we found that EGFR was mutually exclusive with both ALK and STK11. In addition, the features between PD-L1 expression status and genomic alterations were characterized. These results suggest that clinical characteristics and molecular phenotypes are associated with PD-L1 expression signatures, which may provide novel insights for improving the efficiency of immune checkpoint inhibitors (ICIs) in immunotherapy.

Genomic characterization of thymic epithelial tumors reveals critical genes underlying tumorigenesis and poor prognosis.

Thymic epithelial tumors (TETs) are rare mediastinal tumors whose tumorigenesis mechanism is poorly understood. Characterization of molecular alterations in TETs may contribute to a better understanding of tumorigenesis and prognosis. Hybrid capture-based next-generation sequencing was performed on tumor tissues from 47 TETs (39 thymomas and 8 thymic carcinomas) to detect mutations in 315 tumor-associated genes. In total, 178 nonsynonymous mutations were identified, with a median of 3.79 per tumor in 47 TETs. Higher tumor mutation burden (TMB) level was more common in older TET patients, and significantly associated with the more advanced pathological type, especially in thymic carcinomas (TC) patients. The gene mutation profiles of B1-3, A/AB, and TC patients varied greatly. In the actionable mutations analysis, we found 32 actionable mutations in 24 genes. Among them, NFKBIA and TP53 mutations was the most frequently, which were only identified in TCs. Additionally, TCGA database analysis found that the expression of NFKBIA mRNA in the TCs were significantly higher than thymomas. TET patients with high NFKBIA expression had shorter overall survival compared with patients with low/medium NFKBIA expression, thus providing insights to consider NFKBIA as a potential prognosis biomarker and therapeutic target in TETs.

Mechanistic study on the formation of the alkyl acrylates from CO2, ethylene and alkyl iodides over nickel-based catalyst.

The catalytic conversion of carbon dioxide (CO2) and olefins into acrylates has been a long standing target, because society attempts to synthesize commodity chemicals in a more economical and sustainable fashion. In this work, two alkylation reaction pathways were investigated to explore the role of methylene linkage (-CH2-) on the formation of alkyl acrylate from coupling of CO2 and ethylene, catalyzed by a nickel catalyst in the presence of different alkyl iodides. The energy barrier of Ni-O bond cleavage decreases with increasing methylene linkage of alkyl iodides, which may be due to NPA charge transfer of alkyl iodides. Meanwhile, the O1 (ester sp3 O atom) attack route leading to the formation of alkyl acrylate competes with the O2 (carboxylic sp2 O atom) attack route in terms of energy barriers. Further studies on the fluoro-substituted alkyl acrylates show that neither CF3I nor CF3CH2I is effective in releasing trifluoroalkyl acrylates from the nickellacycle, which explains why only negligible amounts of the desired product were detected in the experiment. In addition, we investigated the non-productive pathways leading to byproducts, such as propionic acid, propionates and ion pair complexes, etc. By comparing the results obtained with CH3I, the use of C2H5I as an electrophilic reagent may stabilize the non-productive intermediates. The methylene linkage has little effect on the main productive pathway. However, it has a significant influence on the side reactions, which is detrimental to the formation of alkyl acrylate in competing with the main productive pathway.

Recent Progress of Carbon Dots for Air Pollutants Detection and Photocatalytic Removal: Synthesis, Modifications, and Applications.

Rapid industrialization has inevitably led to serious air pollution problems, thus it is urgent to develop detection and treatment technologies for qualitative and quantitative analysis and efficient removal of harmful pollutants. Notably, the employment of functional nanomaterials, in sensing and photocatalytic technologies, is promising to achieve efficient in situ detection and removal of gaseous pollutants. Among them, carbon dots (CDs) have shown significant potential due to their superior properties, such as controllable structures, easy surface modification, adjustable energy band, and excellent electron-transfer capacities. Moreover, their environmentally friendly preparation and efficient capture of solar energy provide a green option for sustainably addressing environmental problems. Here, recent advances in the rational design of CDs-based sensors and photocatalysts are highlighted. An overview of their applications in air pollutants detection and photocatalytic removal is presented, especially the diverse sensing and photocatalytic mechanisms of CDs are discussed. Finally, the challenges and perspectives are also provided, emphasizing the importance of synthetic mechanism investigation and rational design of structures.

Comparison of Gefitinib in the treatment of patients with non-small cell lung cancer and clinical effects of Osimertinib and EGFR Gene mutation.

Objectives: To compare the clinical effects of Osimertinib and Gefitinib in the treatment of non-small cell lung (NSCLC) complicated with epidermal growth factor receptor (EGFR) gene mutation. Methods: We retrospectively analyzed the clinical data of 102 patients with advanced NSCLC and EGFR gene mutations treated in the Chest Disease Diagnosis and Treatment Center of our hospital from January 2018 to January 2020. We divided the data based on the administered treatments into Osimertinib and Gefitinib groups. The disease control rate (DCR), progression free survival (PFS) and the incidence of adverse events in both groups were analyzed. Results: In the Osimertinib group, there was one patients with complete response (CR), 38 with partial response (PR), eight with stable disease (SD), and two with progressive disease (PD)/ The overall response rate (ORR) was 79.59% (39/49), and the disease control rate (DCR) was 95.92% (47/49). In the Gefitinib group, we found zero patients with CR, 37 patients with PR, 11 with SD, and five with PD. The ORR in the Gefitinib group was 69.80% (37/53) and DCR was 90.57% (48/53). There was no statistical significance between the two groups, ORR was Χ2=0.927 (P=0.336) and the DCR Χ2=0.221 (P=0.638). The median PFS of and Gefitinib groups was significantly higher in the oxitinib group, compared to the Gefitinib group (18.1 months (95% CI 15.4-20.7) and 10.7 months (95% CI 9.9-11.4), respectively, P<0.001). The incidence of adverse reactions in the Osimertinib group was 12.24% (6/49), which was significantly lower than 28.30% (15/53) in the Gefitinib group (P < 0.05). Conclusions: The clinical effect of oxitinib in the treatment of non-small cell lung cancer complicated with EGFR gene mutation is similar to that of Gefitinib. In patients with advanced NSCLC and EGFR gene mutations, oxitinib treatment is associated with significantly longer PFS and lower adverse reaction rate compared with Gefitinib treatment.

Potential mechanism of primary resistance to icotinib in patients with advanced non-small cell lung cancer harboring uncommon mutant epidermal growth factor receptor: A multi-center study.

The incidence of epidermal growth factor receptor uncommon mutation (EGFRum) is relatively low and patients harboring EGFRum are resistant to the first-generation tyrosine kinase inhibitors (TKI). However, the mechanism of primary resistance remains unclear. Medical records of 98 patients who had never been treated by TKI and who accepted icotinib treatment were collected and followed. The circulating tumor DNA (ctDNA) were detected and analyzed using the next-generation sequencing (NGS) platform after progression on icotinib. The potential primary resistance mechanism of icotinib was explored. A total of 21 (21.4%) and 48 (49%) patients developed primary and acquired resistance to icotinib, respectively. The median progression-free survival (PFS) of primary resistance patients was 1.8 months (0.5-2.3, 95% CI = 1.50-2.10). Before treatment, 52.4% (11/21) of patients carried S768I, 23.8% (5/21) L861Q, 14.3% (3/21) G719X and 14.3% (3/21) exon 20-ins mutations. Approximately 23.8% (5/21) of patients harbored the combined pattern mutations and 76.2% (16/21) of patients harbored the single pattern mutations. The combined pattern with EGFR classical mutation (EGFRcm) had worse PFS than the combined with EGFRum and single pattern (P < .05). There were 6 (28.57%) patients with acquired EGFR extracellular domain mutation, 5 (23.81%) with BCL2L11 loss (BIM deletion polymorphism), 3 (14.29%) with MET amplification, 1 (4.76%) with ERBB2 amplification, 1 (4.76%) with MYC amplification, 1 (4.76%) with PTEN mutation, 1 (4.76%) with PIK3CA mutation and 3 (14.29%) with unknown status. EGFR extracellular domain mutation, BCL2L11 loss, PI3K-AKT-mTOR signaling pathway (PTEN and PIK3CA mutations), MET amplification, ERBB2 amplification or MYC amplification might contribute to molecular mechanisms of primary resistance to icotinib in patients with advanced non-small cell lung cancer harboring uncommon mutant epidermal growth factor receptor. Combined targeted therapy or chemotherapy should be considered in this population.

Simultaneous Detection of Gene Fusions and Base Mutations in Cancer Tissue Biopsies by Sequencing Dual Nucleic Acid Templates in Unified Reaction.

BACKGROUND: Targeted next-generation sequencing is a powerful method to comprehensively identify biomarkers for cancer. Starting material is currently either DNA or RNA for different variations, but splitting to 2 assays is burdensome and sometimes unpractical, causing delay or complete lack of detection of critical events, in particular, potent and targetable fusion events. An assay that analyzes both templates in a streamlined process is eagerly needed. METHODS: We developed a single-tube, dual-template assay and an integrated bioinformatics pipeline for relevant variant calling. RNA was used for fusion detection, whereas DNA was used for single-nucleotide variations (SNVs) and insertion and deletions (indels). The reaction chemistry featured barcoded adaptor ligation, multiplexed linear amplification, and multiplexed PCR for noise reduction and novel fusion detection. An auxiliary quality control assay was also developed. RESULTS: In a 1000-sample lung tumor cohort, we identified all major SNV/indel hotspots and fusions, as well as MET exon 14 skipping and several novel or rare fusions. The occurrence frequencies were in line with previous reports and were verified by Sanger sequencing. One noteworthy fusion event was HLA-DRB1-MET that constituted the second intergenic MET fusion ever detected in lung cancer. CONCLUSIONS: This method should benefit not only a majority of patients carrying core actionable targets but also those with rare variations. Future extension of this assay to RNA expression and DNA copy number profiling of target genes such as programmed death-ligand 1 may provide additional biomarkers for immune checkpoint therapies.

Upregulation of miR-219a-5p Decreases Cerebral Ischemia/Reperfusion Injury In Vitro by Targeting Pde4d.

BACKGROUND: Ischemic stroke is the leading cause of disability and death globally. Micro-RNAs (miRNAs) have been reported to play important roles in the development and pathogenesis of the nervous system. However, the exact function and mechanism of miRNAs have not been fully elucidated about brain damage caused by cerebral ischemia/reperfusion (I/R). METHODS: In this study, we explored the neuroprotective effects of miR-219a-5p on brain using an in vitro ischemia model (mouse neuroblastoma N2a cells treated with oxyglucose deprivation and reperfusion), and in vivo cerebral I/R model in mice. Western blot assay and Reverse Transcription-Polymerase Chain Reaction were used to check the expression of molecules involved. Flow cytometry and cholecystokinin were used to examine cell apoptosis, respectively. RESULTS: Our research shows that miR-219a-5p gradually decreases in cerebral I/R models in vivo and in vitro. In vitro I/R, we find that miR-219a-5p mimics provided evidently protection for cerebral I/R damage, as shown by increased cell viability and decreased the release of LDH and cell apoptosis. Mechanically, our findings indicate that miR-219a-5p binds to cAMP specific 3', 5'-cyclic phosphodiesterase 4D (PDE4D) mRNA in the 3'-UTR region, which subsequently leads to a decrease in Pde4d expression in I/R N2a cells. CONCLUSIONS: Our results provide new ideas for the study of the mechanism of cerebral ischemia/reperfusion injury, and lay the foundation for further research on the treatment of brain I/R injury. Upregulation of miR-219a-5p decreases cerebral ischemia/reperfusion injury by targeting Pde4d in vitro.

ROS1-ADGRG6: a case report of a novel ROS1 oncogenic fusion variant in lung adenocarcinoma and the response to crizotinib.

BACKGROUND: ROS1 rearrangements are validated drivers in lung cancer, which have been identified in a small subset (1-2%) of patients with non-small cell lung cancer (NSCLC). To date, 18 fusion genes of ROS1 have been identified in NSCLC. The ALK inhibitor (crizotinib) exhibits therapeutic effect against ROS1-rearranged NSCLC. Next-generation sequencing (NGS) technology represents a novel tool for ROS1 detection that covers many fusion genes. CASE PRESENTATION: A 55-year-old female with EGFR mutation (L858R) was diagnosed with lung adenocarcinoma, who was responsive to first-generation EGFR-tyrosine kinase inhibitor (TKI). Afterwards, she developed acquired resistance accompanied with a ROS1 rearrangement. A NGS assay showed that the tumor had a novel ROS1-ADGRG6 rearrangement generated by the fusion of exons of 1-33 of ROS1 on chr6: q22.1 to exons of 2-26 of ADGRG6 on chr6: q24.2. The patient was obviously responsive to crizotinib. CONCLUSION: We firstly identified ROS1-ADGRG6 fusion variant in NSCLC by NGS, which should be considered in further ROS1 detecting assays.

Effect of SCR Atmosphere on the Removal of Hg0 by a V2O5-CeO2/AC Catalyst at Low Temperature.

A series of V2O5-xCeO2/AC (noted as V-Ce/AC) catalysts were synthesized by the impregnation method, which combined the advantage of AC and V-Ce. The effects of SCR atmosphere on Hg0 removal were systematically investigated at low temperature. The experimental results indicated that NO had a positive effect on Hg0 removal. In addition, an interesting experimental phenomenon was found that NH3 also showed a positive effect on Hg0 removal, which is different from many studies that have reported a negative effect of NH3 on Hg0 removal by other catalysts. NH3-TPD experiment showed that there was no apparent competition between NH3 and Hg0. An FT-IR gas analyzer and in situ DRIFTS were used to study the mechanism for the effect of NH3 on the catalyst surface and found that a small part of NH3 was overoxidized to NO2 in this catalytic system. O2 acted as a promoter in the whole process of NO and Hg0 removal. However, H2O showed an inhibiting effect on Hg0 and NO removal over V-Ce/AC catalysts, which may be caused by the competitive adsorption of H2O and pollutants (NO and Hg0). Additionally, 1 V-8Ce/AC catalyst exhibited high stability ( EHg = 87.6%, ENO = 82.84%) after 72 h reaction in SCR atmosphere at 150 °C.

Ginsenoside compound K inhibits growth of lung cancer cells via HIF-1α-mediated glucose metabolism.

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths. Compound K, an active metabolite of ginsenosides, is reported to exhibit anti-cancer property in various types of human malignancies. The present study investigated the role of compound K on glucose metabolism in NSCLC cells and its underlying mechanism. Our study found that compound K dose-dependently inhibited the cell viability of NSCLC cells. Moreover, administration with compound K decreased glucose uptake and lactate secretion under normoxic and hypoxic conditions. Consistently, the expression of key enzymes (HK II, PDK1 and LDHA) involved in glucose metabolism were inhibited in compound K-treated tumor cells. In addition, compound K inhibited the expression of HIF-1α and its downstream gene GLUT1. On the contrary, overexpression of HIF-1α elevated metabolic reactions and partly attenuated the inhibitory role of compound K on NSCLC cell growth. These results demonstrate that compound K suppresses NSCLC cell growth via HIF-1α mediated metabolic alteration, contributing to novel anticancer therapy by targeting glucose metabolism.

Association between BIM polymorphism and lung cancer outcomes: a meta-analysis.

Accumulating evidences have indicated that BIM expression largely decides the development of lung cancer and outcome of EGFR-mutant lung cancers after TKI treatments. BIM polymorphism is a 2,903-bp deletion in the second exon. To clarify the relationship between this BIM polymorphism and clinical outcomes of lung cancers, we conducted this meta-analysis and observed the survival and responses to TKIs. Sixteen cohort studies, covering 4393 WT and 916 BIM deletion patients were included. Overall, BIM deletion polymorphism was associated with significantly shorter progression-free survival (PFS) and slightly shorter overall survival (OS), compared to the WT group. Moreover, patients with BIM deletion polymorphism showed significantly inferior response to EGFR TKIs. In conclusion, our analysis confirmed that lung cancer patients harboring the BIM deletion have inferior survival and TKI responses. Examination of the novel biomarker BIM deletion in lung cancer patients, especially for the EGFR mutant cohort, could provide some prognostic utility.

A meta-analysis of association between serum iron levels and lung cancer risk.

Many studies conducted on the relationship between serum iron levels and lung cancer risk had produced inconsistent results. We therefore conducted a meta-analysis to determine whether serum iron levels were lower in lung cancer patients compared to those in controls.A literature survey was conducted by searching the PubMed, WanFang, CNKI, and SinoMed databases for articles published as of Mar 1, 2018. Standard mean differences (SMD) with the corresponding 95% confidence intervals (CI) were executed by Stata 12.0 software. A total of 13 publications involving 1118 lung cancer patients and 832 controls were included in our study. The combined results showed that serum iron levels in lung cancer cases had no significantly lower when compared to those in controls [summary SMD = -0.125, 95%CI= -0.439, 0.189, Z = 0.78, p for Z test= 0.435], with high heterogeneity (I2= 89.9%, P< 0.001) found. In the stratified analysis by geographic locations, consistent results were found for serum iron levels between lung cancer patients and controls both in Asian populations [summary SMD = -0.113, 95%CI= -0.471, 0.245] and European populations [summary SMD = -0.215, 95%CI= -0.835, 0.404]. Publication bias was not found when evaluated by Begg's funnel plot and Egger's regression asymmetry test.In summary, the current study showed that serum iron levels had no significant association on lung cancer risk.

Combined detection of CEA and CA125 for the diagnosis for lung cancer: A meta-analysis.

This study aimed to systematically evaluate the value of combined detection of serum CEA and CA125 concentrations for the diagnosis of lung cancer. Related studies regarding the diagnosis of lung cancer were searched in PubMed, Embase, CNKI, and Wanfang using a computer. The number of patients who were true-positive, false-positive, false-negative, and true-negative were extracted from each study. Meta-analysis was performed using the Meta-Disc l.4, RevMan 5.3. Seven studies involving 2,216 cases were finally included. Regarding the diagnosis of lung cancer, the sensitivity, specificity, and diagnostic odds ratio of combined CEA and CA125 detection were higher than those of CEA detection alone. The area under the curve (AUC) of combined detection was 0.90, whereas the independently detected AUC was 0.73. Combined CEA and CA125 detection has higher diagnostic efficiency for lung cancer than CEA detection alone. The significance of combined serum CEA and CA125 detection in lung cancer is confirmed.

Comparison of Rearranged During Transfection (RET) Gene Rearrangements in Primary Versus Metastatic Non-Small Cell Lung Cancer (NSCLC).

BACKGROUND RET rearrangements have been reported in 30% of papillary thyroid carcinomas and 1-2% of non-small cell lung cancer (NSCLC). In these tumors, RET gene fusion product provides a constitutively active tyrosine kinase (TKR), leading to uncontrolled cellular proliferation, differentiation, and migration. In this investigation we assessed the positivity rate of RET gene rearrangement in primary and metastatic non-small cell lung cancer and explored their relationships. MATERIAL AND METHODS Between January 2013 and May 2015, we collected 384 cases of primary metastatic non-small cell lung cancer, which included 246 matched metastatic tumors cases from multiple centers. The RET rearrangement uniformity in metastatic lymph nodes and tumor specimens were contrasted and the relationships between RET rearrangement and patients' clinical features were investigated. RESULTS For those 384 cases, 7 (1.82%) cases had tumors with identified RET rearrangement. Among the 246 paired cases, 3 (1.22%) cases of primary tumor had identified RET rearrangement and 2 (0.81%) cases of metastases had identified RET rearrangement. The sensitivity was 66.67% (2/3) and the specificity was 100% (243/243). CONCLUSIONS The results of this research indicate that the metastases of non-small cell lung cancer can predict RET rearrangement of the primary tumor tissue in the majority of cases. Testing for RET rearrangement in metastases can be used as an alternative to testing of primary tumor tissue if it is inaccessible.

Sequential separation of critical metals from lithium-ion batteries based on deep eutectic solvent and electrodeposition.

The rise and development of electric vehicles have brought much attention to the recycling of lithium-ion batteries (LIBs). However, the recovery of critical metals from LiNixCoyMn1-x-yO2 (NCM) is a challenge, especially for the nickel and cobalt, which have similar chemical properties. Here, a novel ternary deep eutectic solvent (DES) composed of choline chloride, ethylene glycol, and tartaric acid was proposed. Our protocol of DES synthesis, nickel separation, and leaching of cobalt and manganese were integrated into one step, which significantly simplified the recovery process. The crystallization occurring during DES leaching was subjected to detailed investigation. The lithium, nickel, and cobalt were sequentially separated as Li2CO3, NiO, and Co(OH)2 by anterior formic acid leaching and posterior electrodeposition. After electrodeposition, DES was reused. This work provides new ideas for the sequential separation of critical metals from NCM and has great application prospects.

A prognostic signature for lung adenocarcinoma by five genes associated with chemotherapy in lung adenocarcinoma.

BACKGROUND: Lung adenocarcinoma (LUAD) is one of the most common subtypes of lung cancer. Finding prognostic biomarkers is helpful in stratifying LUAD patients with different prognosis. METHODS: We explored the correlation of LUAD prognosis and genes associated with chemotherapy in LUAD and obtained data of LUAD patients from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Drug sensitivity data were acquired from the Genomics of Drug Sensitivity in Cancer (GDSC) database. Differential and enrichment analyses were used to screen the target genes utilizing limma and "clusterProfiler" packages. Then univariate and LASSO Cox analyses were used to select the prognosis-related genes. Survival analysis was used to estimate the overall survival (OS) of different groups. RESULTS: Twenty-three differentially expressed genes (DEGs) were screened between LUAD samples and healthy samples, and BTK, FGFR2, PIM2, CHEK1, and CDK1 were selected to construct a prognostic signature. The OS of patients in the high-risk group (risk score higher than 0.69) was worse than that in the low-risk group (risk score lower than 0.69). CONCLUSION: The risk score model constructed by five genes is a potential prognostic biomarker for LUAD patients.

Life quality improvement of patients with non-small cell lung cancer undergoing targeted therapy: A case study of continuous care.

To investigate the improvement effect of targeted therapy on non-small cell carcinoma patients life quality after the continuous nursing intervention. 104 non-small cell lung cancer patients in our hospital from July 2017 to November 2019 were allocated evenly and randomly into the control group (C) and the study group (S). By using clinical baseline data, quality of life questionnaire core 30 for cancer patients, evaluation of patient compliance behavior, the MOS item short-form health survey (SF-36), self rating depression scale (SDS), self rating anxiety scale (SAS), Overall Survival (OS) progression-free survival and adverse reaction symptoms were evaluated for the life quality of patients. There was comparability between the 2 sets of basic data. There was no significant difference in quality of life questionnaire core 30, SF-36, SAS, or SDS scores before treatment. After 3 months, there was a significant difference in the scores of various scales before treatment. At the same time, there was significant statistical significance before and after treatment in Group S. Their compliance rates were 84.62% and 98.08%. Adverse reactions incidence in Group S was lower. Taking a 2-year follow-up period as an example, significant statistical differences existed in OS and progression-free survival rates between adenocarcinoma and squamous carcinoma. SDS and SAS had high consistency in scoring with QLQ-30 and SF-36 scales. Targeted treatment for non-small cell carcinoma patients significantly improves their life quality and reduces the incidence of adverse reactions after continuous nursing intervention.

Tunning active oxygen species for boosting Hg0 removal and SO2-resistance of Mn-Fe oxides supported on (NH4)2S2O8 doping activated coke.

Active oxygen species (AOS) play an essential role in modulating the activity of activated coke (AC) based samples. In this paper, AC was endowed with abundant AOS by modifying with (NH4)2S2O8 and MnOx-FeOx for Hg0 removal. (NH4)2S2O8 treatment induced abundant micropores and oxygen-containing functional groups, and thus provided more anchoring sites for the dispersion of MnOx-FeOx. The synergy of MnOx-FeOx and interaction between MnOx-FeOx and NAC support contributed to a larger surface area, highly-dispersed active components, stronger reducibility, and more metal ions with high valence of MnFe/NAC. The optimal MnFe/NAC exhibited superior Hg0 removal efficiency above 90% at 120∼180 â„ƒ, as well as excellent performance for simultaneous removal of Hg0 and NO, and 600 ppm SO2 and 8 vol.% H2O addition led to a slight deterioration. XPS and Hg-TPD revealed that mercury adsorbed on MnFe/NAC included phy-Hg, C=O-Hg, COO-Hg, and OL-HgO. Besides, the priority of AOS for Hg0 chemisorption was C=O > COO- > OL, and Hg2+ was also detected in the outlet. Moreover, the SO2-poisoning effect was ascribed to the sulfation of MnOx and the occupation of COO- and C=O, and FeOx incorporation enhanced the SO2-resistance through weakening SO2 adsorption on C=O and COO-. The motivation of O2 mainly contributed to the regeneration of AOS, especially OL. The excellent regeneration performance and stability further affirmed the application potential of MnFe/NAC for Hg0 capture from coal-fired flue gas.

Interface engineering of Mn3O4/Co3O4 S-scheme heterojunctions to enhance the photothermal catalytic degradation of toluene.

Transition metal oxides have high photothermal conversion capacity and excellent thermal catalytic activity, and their photothermal catalytic ability can be further improved by reasonably inducing the photoelectric effect of semiconductors. Herein, Mn3O4/Co3O4 composites with S-scheme heterojunctions were fabricated for photothermal catalytic degradation of toluene under ultraviolet-visible (UV-Vis) light irradiation. The distinct hetero-interface of Mn3O4/Co3O4 effectively increases the specific surface area and promotes the formation of oxygen vacancies, thus facilitating the generation of reactive oxygen species and migration of surface lattice oxygen. Theoretical calculations and photoelectrochemical characterization demonstrate the existence of a built-in electric field and energy band bending at the interface of Mn3O4/Co3O4, which optimizes the photogenerated carriers' transfer path and retains a higher redox potential. Under UV-Vis light irradiation, the rapid transfer of electrons between interfaces promotes the generation of more reactive radicals, and the Mn3O4/Co3O4 shows a substantial improvement in the removal efficiency of toluene (74.7%) compared to single metal oxides (53.3% and 47.5%). Moreover, the possible photothermal catalytic reaction pathways of toluene over Mn3O4/Co3O4 were also investigated by in situ DRIFTS. The present work offers valuable guidance toward the design and fabrication of efficient narrow-band semiconductor heterojunction photothermal catalysts and provides deeper insights into the mechanism of photothermal catalytic degradation of toluene.