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In most of the world's building material industries, the control of flue gas pollutants mainly focuses on a single pollutant. However, given the large capacity and high contribution of China's building materials industry to global air pollution, the need to develop multi-pollutant emission reduction technology is urgent. Recently, China has focused on reducing the emissions of flue gas pollutants in the building materials industry, established many key research and development projects, and gradually implemented more stringent pollutant emission limits. This project focuses on the most recent advances in flue gas emission control technology in China's building materials industry, including denitration, dust removal, desulfurization, synergistic multi-pollutant emission reduction, and the construction of pilot research and demonstration projects for pollutant removal in several building material industries. On this basis, revised pollutant limits in flue gas emitted in China's building material industry are proposed.

To explore the genetic etiology of a patient with glycogen storage diseases.Clinical data of child and his parents were collected. The genes associated with glycogen storage diseases were subjected to high-throughput sequencing to screen the variants. Candidate variant was validated by Sanger sequencing. Pathogenicity of the variant was predicted by bioinformatic analysis.High-throughput sequencing results showed that the boy has carried a hemizygous c.749CT (p.S250L) variant of the PHKA2 gene. Sanger sequencing verified the results and confirmed that it was inherited from his mother. This variant was unreported previously and predicted to be pathogenic by bioinformatic analysis.The patient was diagnosed with glycogen storage disease type IXa due to a novel c.749CT (p.S250L) hemizygous variant of the PHKA2 gene. High-throughput sequencing can facilitate timely and accurate differential diagnosis of glycogen storage disease type IXa.

Catalytic combustion is an advanced technology to eliminate industrial volatile organic compounds such as toluene. In order to replace the expensive noble metal catalysts and avoid the aggregation phenomenon occurring in traditional heterogeneous interfaces, designing homogeneous interfaces can become an emerging methodology to enhance the catalytic combustion performance of metal oxide catalysts. A mesocrystalline CeO2 catalyst with abundant Ce-Ce homogeneous interfaces is synthesized via a self-flaming method which exhibits boosted catalytic performance for toluene combustion compared with traditional CeO2, leading to a ∼40 °C lower T90. The abundant Ce-Ce homogeneous interfaces formed by both highly ordered stacking and small grain size endow the CeO2 mesocrystal with superior redox property and oxygen storage capacity via forming various oxygen vacancies. Surface and bulk oxygen vacancies generate and activate crucial oxygen species, while interfacial oxygen vacancies further promote the reaction behavior of oxygen species (i.e., activation, regeneration, and migration), causing the splitting of redox property toward lower temperature. These properties facilitate aromatic ring decomposition, the important rate-determining step, thus contributing to toluene catalytic degradation to CO2. This work may shed insights into the catalytic effects of homogeneous interfaces in pollutant removal and provide a strategy of interfacial defect engineering for catalyst development.

Although the deregulation of lysine methyltransferase (su(var)-3–9, enhancer-of-zeste, trithorax) domain-containing protein 7/9 (SET7/9) has been identified in a variety of cancers, the potential role of SET7/9 and the molecular events in which it is involved in breast cancer remain obscure. Using the online Human Protein Atlas and GEO databases, the expression of SET7/9 was analyzed. Furthermore, we investigated the underlying mechanisms using chromatin immunoprecipitation-based deep sequencing (ChIP-seq) and quantitative ChIP assays. To explore the physiological role of SET7/9, functional analyses such as CCK-8, colony formation, and transwell assays were performed and a xenograft tumor model was generated with the human breast cancer cell lines MCF-7 and MDA-MB-231. Mass spectrometry, co-immunoprecipitation, GST pull-down, and ubiquitination assays were used to explore the mechanisms of SET7/9 function in breast cancer. We evaluated the expression of SET7/9 in different breast cancer cohorts and found that higher expression indicated worse survival times in these public databases. We demonstrated positive effects of SET7/9 on cell proliferation, migration, and invasion via the activation of Runt-related transcription factor 2 (RUNX2). We demonstrate that tripartite motif-containing protein 21 (TRIM21) physically associates with SET7/9 and functions as a major negative regulator upstream of SET7/9 through a proteasome-dependent mechanism and increased ubiquitination. Taken together, our data suggest that SET7/9 has a promoting role via the regulation of RUNX2, whereas TRIM21-mediated SET7/9 degradation acts as an anti-braking system in the progression of breast cancer.

The synthesis of high energy facets and tunable low energy facets was achieved in CeO2 films on a SrTiO3 substrate by pulsed laser deposition. Three different facets of CeO2 with distinctive morphologies appeared consecutively. Firstly, the (100) facet of CeO2, which is the highest energy surface, was grown on the SrTiO3 (STO) (100) substrate. The surface energy was decreased gradually with the increase of the laser pulse shots, and the (110) and (111) LEF appeared consecutively. The three different facets presented distinctive morphologies and the interface between each facet could be easily observed by the cross section of Transmission Electron Microscope (TEM) imaging. The interface between the (100) and (110) facet may exhibit excellent oxygen storage capacity, even better than the (100) facet.

Catalytic combustion is an advanced technology to eliminate industrial volatile organic compounds such as toluene. In order to replace the expensive noble metal catalysts and avoid the aggregation phenomenon occurring in traditional heterogeneous interfaces, designing homogeneous interfaces can become an emerging methodology to enhance the catalytic combustion performance of metal oxide catalysts. A mesocrystalline CeO

How chromatin dynamics is regulated to ensure efficient DNA repair remains to be understood. Here, we report that the ubiquitin-specific protease USP11 acts as a histone deubiquitinase to catalyze H2AK119 and H2BK120 deubiquitination. We showed that USP11 is physically associated with the chromatin remodeling NuRD complex and functionally involved in DNA repair process. We demonstrated that USP11-mediated histone deubiquitination and NuRD-associated histone deacetylation coordinate to allow timely termination of DNA repair and reorganization of the chromatin structure. As such, USP11 is involved in chromatin condensation, genomic stability, and cell survival. Together, these observations indicate that USP11 is a chromatin modifier critically involved in DNA damage response and the maintenance of genomic stability.

Metastasis-associated protein 2 (MTA2) is a core subunit of the nucleosome remodeling and deacetylating (NuRD) complex and functions by mediating chromatin remodeling and gene silencing. However, its biological actions and clinical significance in pancreatic ductal adenocarcinoma (PDAC) remain elusive. The aim of this study was to explore the function and regulation mechanism of MTA2 in PDAC. As shown in GEO, ICGC, and TCGA databases, a higher expression of MTA2 was noticed in the PDAC tissues than in the normal pancreatic tissues. Moreover, a higher expression level of MTA2 was associated with a shorter overall survival time in these public PDAC databases. We further investigated the underlying mechanisms of these observations by using a chromatin immunoprecipitation (ChIP)-based deep sequencing, luciferase reporter, and quantitative ChIP assays. We identified the repressive binding of MTA2 to the promoter of phosphatase and tensin homolog (PTEN). We also found that Snail recruited MTA2 and HDAC1 to suppress PTEN expression. Ectopic expression and knockdown of MTA2 were performed to evaluate the effects of this gene on PDAC cell proliferation, migration, and invasion. Using CCK-8, colony formation and transwell assays, and a xenograft tumor model, we revealed that MTA2 promoted PDAC cell proliferation, migration, and invasion in vitro and PDAC tumor growth in vivo by downregulation of PTEN. In benzyl isothiocyanate (BITC)-treated MIA Paca-2 cells and PANC-1 cells, MTA2 level decreased in a dose- and time-dependent manner with concomitant upregulation of PTEN level and downregulation of phosphorylated PI3K and AKT levels, providing evidence of the involvement of MTA2 and PTEN in the regulation of the PI3K/AKT pathway in BITC-mediated PDAC suppression. Collectively, these findings uncover a novel role for MTA2 in the regulation of PDAC progression and help to elucidate the mechanisms involved in this process.

A series of Cu-SAPO-34 zeolites with different Cu contents were prepared by one-pot synthesis method. The NH3-SCR performance and the oxidation of elemental mercury (Hg0) efficiency over the Cu-SAPO-34 samples were tested respectively. With the increase of Cu loadings, the amount of Cu2+ and CuO were both increased, wherein the former promoted SCR reaction and the latter accelerated the Hg0 oxidation. What's more, the ratio of Cu2+/CuO was also increased. The NO conversion rate and Hg0 removal efficiency could be over 80% on the high Cu catalyst at 150–300 °C.

MnO

The scope and variety of the metabolic intermediates from the mitochondrial tricarboxylic acid (TCA) cycle that are engaged in epigenetic regulation of the chromatin function in the nucleus raise an outstanding question about how timely and precise supply/consumption of these metabolites is achieved in the nucleus. We report here the identification of a nonclassical TCA cycle in the nucleus (nTCA cycle). We found that all the TCA cycle-associated enzymes including citrate synthase (CS), aconitase 2 (ACO2), isocitrate dehydrogenase 3 (IDH3), oxoglutarate dehydrogenase (OGDH), succinyl-CoA synthetase (SCS), fumarate hydratase (FH), and malate dehydrogenase 2 (MDH2), except for succinate dehydrogenase (SDH), a component of electron transport chain for generating ATP, exist in the nucleus. We showed that these nuclear enzymes catalyze an incomplete TCA cycle similar to that found in cyanobacteria. We propose that the nTCA cycle is implemented mainly to generate/consume metabolic intermediates, not for energy production. We demonstrated that the nTCA cycle is intrinsically linked to chromatin dynamics and transcription regulation. Together, our study uncovers the existence of a nonclassical TCA cycle in the nucleus that links the metabolic pathway to epigenetic regulation.

Obstetric antiphospholipid syndrome (OAPS) is an autoimmune disorder with severe life-threatening complications shown during pregnancy. It has been reported that the increase in CD16+CD56dim natural killer (NK) cells in peripheral blood are risk factors for recurrent miscarriages, but this expression of CD16+CD56dim NK cells in OAPS patients has not been reported, and the mechanism is not clearly illustrated. In this study, we compared the distributional profiles of different NK cell subsets and the expressions of NK cell-activating receptors in peripheral blood of patients with OAPS and healthy women. Our results showed significantly increased NKG2A-NKG2D+ subset and decreased NKG2A+NKG2D- subset in CD3- CD16+CD56dim NK cells, CD3-CD16-CD56bright NK cells and CD56+T cells in OAPS patients compared with those in healthy control women. The CD27-CD11b+ subset significantly increased in CD3-CD16+CD56dim NK cells in OAPS patients compared with those in healthy control women. In addition, the NKG2A-NKG2D+ subset in CD3-CD16+CD56dim NK subset in triple positivity was higher than single positivity OAPS patients. At the optimal diagnostic threshold established by ROC analysis, using the cut-off of NKG2A-NKG2D+ and CD27-CD11b+ subset in CD3-CD16+CD56dim NK cells is 10.10% and 92.75%, the sensitivity of NKG2A-NKG2D+ and CD27-CD11b+ to detect patients with OAPS compared with healthy control results was 94.1% and 60.8%, and specificity was 84.2% and 89.5%, respectively, with an area under the curve (AUC) of 0.903 and 0.829, respectively. The NKG2A-NKG2D+ subset in CD3-CD16+CD56dim NK cells was positively correlated with the antiphospholipid antibodies lg anti-aCL IgG, lg anti-aCL IgM, lg anti-aCL IgA, lg anti-β2GP1 IgM and Complement 4(C4), while the CD27+CD11b+ subset in CD3-CD16+CD56dim NK cells was correlated with lg anti-β2GP1 IgG and lg anti-β2GP1 IgA. These results suggested that the NK cytotoxic function enhanced in OAPS patients and unbalanced of NK activating receptors and inhibiting receptors may contribute to the immune pathogenesis of OAPS.

Catalytic combustion technology is one of the effective methods to remove VOCs such as toluene from industrial emissions. The decomposition of an aromatic ring via catalyst oxygen vacancies is usually the rate-determining step of toluene oxidation into CO

The precise molecular mechanism of hepatocellular carcinoma (HCC) remains ambiguous. Isocitrate dehydrogenase 3A (IDH3A) is known as a subunit of the IDH3 heterotetramer. To the best of our knowledge, the biological effect of IDH3A in malignant tumors is unclear. Here, we report that IDH3A is significantly upregulated in HCC tissues; moreover, high expression of IDH3A is strongly associated with tumor size and the clinicopathologic stage of HCC. RNA-seq revealed that depletion of IDH3A affects the expression of metastasis associated 1 (MTA1), an oncogene which is related to the progression of numerous cancer types to the metastasis stage. Cell transfection was used to upregulate and downregulate the expression of IDH3A in HCC cells. The migration activity of HCC cells was assessed using wound healing assays. While transwell assays were carried out to detect the invasion of HCC cells. RNA-seq, RT-qPCR and western blot were used to validate MTA1 as a potential target gene. The present study suggested that IDH3A can upregulate MTA1 expression and promote epithelial-mesenchymal transition (EMT) in HCC by inducing MTA1 expression, thereby facilitating cell migration and invasion of HCC cells. Here, we demonstrated the importance of IDH3A in HCC progression. The identification of the IDH3A axis provides novel insight into the pathogenesis of HCC, and the IDH3A axis might represent a novel target for the treatment of HCC.

A dual-functional MnO 2 /La 0.6 Sr 0.4 MnO 3 composite catalyst was prepared and tested for the oxidation of elemental mercury (Hg 0 ) present in the coal-derived flue gas. The thus derived Hg 2+ can then be removed from the flue gas via current pollution control devices. The MnO 2 appears as the active component for the oxidation of elemental mercury, whereas the superior magnetic property of La 0.6 Sr 0.4 MnO 3 catalytic component makes the catalyst recoverable from the fly-ash mixture. The Hg 0 oxidation efficiency was found larger than 80% in the temperature range of 150–300 °C and at a GHSV of 120,000 mL/ (g h), whereas the catalytic efficiency could be further increased to >95% in the presence of 5 ppm HCl in the flue gas.

MnO2 catalysts have been widely studied for catalytic gaseous ozone decomposition. However, their poor moisture resistance often leads to undesirable catalytic effects in the presence of high humidity. In this study, a novel catalyst with γ-like MnO2 was synthesized using the selective dissolution method on LaMnO3 perovskites. The as-prepared catalyst exhibited quite stable ozone conversion of ~90% within 12 h under 75% relative humidity (400–800 ppm of ozone, 30 °C, 150 000 mL·g−1·h−1 of WHSV). In contrast, traditional γ-MnO2 catalyst showed deficient resistance to H2O and sensitivity to space velocity. Detailed characterizations showed that the larger number of oxygen vacancies induced by structure reconstruction of the γ-like MnO2 and residual La3+ cations facilitated ozone decomposition in humid atmosphere. Finally, the reaction rate of ozone decomposition was proposed by a kinetic study, which further proved that the amount and hydrophilicity of oxygen vacancies are the determinants of the first-order reaction rate constant.

A series of Sm-doped Co3O4 catalysts for the N2O direct catalytic decomposition were synthesized by the sol–gel method using citric acid as a chelating agent and urea as a combustion agent. The doping of Sm significantly altered the activity of N2O decomposition on the Co3O4 catalyst. Sm was incorporated into the Co3O4 matrix, leading to the distortion of Co3O4 lattice with the spinel configuration maintained. Sm-doping can effectively promote the oxygen vacancy generation, and the electron interaction between Co and Sm species occurred as the Co3+ + Sm2+ ↔ Co2+ + Sm3+ redox cycle. Combined with in situ Raman and in situ NAP-XPS results proposed that this redox cycle is the main reason that the Sm-doping accelerates the high-efficiency N2O decomposition.

Catalytic combustion is a well-established way to remove the pollution of volatile organic compounds (VOCs), and the highly active catalyst is the key issue of this process. Herein, a series of sponge-like ternary mixed oxide were prepared by a facile surfactant modified coprecipitation approach. The structure properties were characterized via BET, XRD, Raman, TEM, EDS, H2-TPR, and XPS techniques. It was found that the Cu content significantly influences the catalytic activity in toluene combustion. The CMC-2 (Cu:Mn:Ce = 1:5:5) showed the best catalytic performance under the air atmosphere, and the complete conversion of toluene was achieved at 240 °C. The characterization reveals that a proper amount of Cu facilitates the incorporation of highly reducible Mn4+ into ceria lattice to form sponge-like MnCeOx solid solution structures. Such promotion effect of copper can improve the redox behavior, produce large amounts of Oα at the interface of CuOx/MnCeOx, both of which benefit the toluene combustion at low temperature. The findings of this work highlight the importance of Cu in preparation of the active MnOx−CeO2 catalyst for VOCs combustion.

The synthesis of high energy facets and tunable low energy facets was achieved in CeO

Mn-based heterostructure catalysts show great potential for catalytic oxidation of toluene owing to the unique properties of their hetero-interfaces. Herein, we tailored the MnO2 heteroepitaxy over Mn2O3 to achieve well-defined morphology and constructed clean MnO2-Mn2O3 heterostructure interfaces by H+/KMnO4 treatment. The T-0.5 catalyst (treating duration of 0.5 h) gave the highest activity and good stability. The interface enhanced the reducibility and oxygen storage capacity compared with pure Mn2O3. Surface reconstruction and metastable facets exposure were observed after the H+/KMnO4 treatment, leading to the easy-release of lattice oxygen. Additionally, abundant oxygen vacancies and redundant coordination lattice oxygen were observed at the MnO2 and Mn2O3 sides of the hetero-interface, respectively. These features provided ample oxygen adspecies and increased lattice oxygen mobility. The interface-related oxygen vacancies facilitated methyl dehydrogenation and demethylation of adsorbed toluene. The redundant coordination lattice oxygen contributed to the enhanced aromatic ring breakage capability.

The in situ IR and Raman spectroscopy measurements were conducted to investigate lead poisoning on the CeO2-WO3 catalysts. The deactivation mechanisms were studied with respect to the changes of surface acidity, redox property, nitrate/nitrite adsorption behaviors, and key active sites (note that the results of structure-activity relationship of CeO2-WO3 were based on our previous research). (1) Lewis acid sites originated from CeO2 and crystalline WO3, whereas Brønsted acid sites originated from Ce2(WO4)3. The poisoned catalysts exhibited a lower surface acidity than the fresh catalysts: the number of acid sites decreased, and their thermal stability weakened. (2) The reducibility of catalysts and the amount of active oxygen exhibited a smaller influence after poisoning because lead preferred to bond with surface WOx species rather than CeO2. (3) The quantity of active nitrate species decreased due to the lead coverage on the catalyst and the partial bridged-nitrate species induced by lead exhibited a low degree of activity at 200 °C. (4) Crystalline WO3 and Ce2(WO4)3 originated from the transformation of polytungstate sites. These sites were the key active sites during the SCR process. The formation temperatures of polytungstate on the poisoned catalysts were higher than those on the fresh catalysts.

Deactivation and regeneration of arsenic are studied on novel CeO2–WO3/TiO2 for selective catalytic reduction (SCR) of NOx with NH3. It is found that the activity and N2 selectivity of poisoned catalyst are inhibited immensely at the entire temperature range. The fresh, poisoned and regenerated catalysts are characterized using XRD, BET, XPS, H2-TPR, NH3-TPD, NO + O2-TPD, in situ Raman and in situ DRIFTS. The characterization results indicate that the poisoning of arsenic decrease BET surface area, surface Ce3+ concentration and the amount of Lewis acid sites and adsorbed NOx species but increase the reducibility and number of chemisorbed oxygen species. According to the in situ DRIFTS investigations, the adsorption of surface-adsorbed NH3 and NOx species is suppressed at low temperature, while the reactivity between surface-adsorbed NH3 and NO is prohibited at high temperature. A novel H2 reduction regeneration not only effectively removes arsenic from the poisoned catalysts, but promotes surface Ce3+/Ce4+ ratio and form new NOx adsorptive sites. However, it also affects the chemical properties of catalyst such as crystalline Ce2(WO4)3 forming, surface active oxygen species raise and loss of Bronsted acid sites.

MOx/ABO3 is a promising catalyst for the high-efficiency removal of volatile organic compounds. However, this catalyst is limited on practical applications due to its complex synthesis procedure and high cost. In this work, the MnO2/LaMnO3 catalyst was prepared in situ using a facile one-step method for the first time, in which partial La cations were selectively removed from three dimensionally chain-like ordered macroporous (3DOM) LaMnO3 material. After selective removal, the obtained MnO2/LaMnO3 sample expressed an excellent catalytic performance on toluene oxidation. Toluene could be completely oxidized into CO2 and H2O at 290 °C over the MnO2/LaMnO3 catalyst with a toluene/oxygen molar ratio of 1/100 and a space velocity of 120 000 mL/(g h). In addition, the apparent activation energy value of MnO2/LaMnO3 was 57 kJ/mol, which was lower than those of other metal oxides catalysts. According to O2-TPD and XPS results, it is concluded that the high catalytic performance of MnO2/LaMnO3 was mainly associated with the large amount of oxygen species and the excellent lattice oxygen mobility. MnO2/LaMnO3 is a promising catalyst for the practical removal of volatile organic compounds due to its high efficiency, good stability, low cost, and convenient preparation.

The mechanisms of arsenic poisoning on MoO3- and WO3-doped V2O5/TiO2 catalysts are studied and the poisoning resistance effect of MoO3 are revealed. The arsenic at certain amount (above 10% of arsenic from XPS) decreases the surface area and the number of active sites where reduction takes place. From the results of DRIFTS and DFT, arsenic lowers the surface acidity by decreasing the quantity of Lewis acid sites and the stability of Bronsted acid sites. We also found newly formed As–OH groups of poisoned catalysts (at 1440 cm−1) have quite low activity at high temperature. MoO3 provides better activity on poisoned catalysts than WO3 does on V2O5/TiO2 catalysts. This may be due to the good dispersion of MoO3 on the support. The reactivity of surface W–O–W and W = O groups is considerably lower than the corresponding Mo–O–Mo and Mo = O groups from the DFT calculations models. This could be one of the explanations on the decrease of surface acidity of poisoned catalysts.

Sn-doped rutile TiO2 supports (SnxTi1−xO2, X = 0.1, 0.2, 0.5) were designed and V2O5/SnxTi1−xO2 catalysts were synthesized by incipient wetness impregnation. The V2O5/Sn0.2Ti0.8O2 exhibited higher low-temperature SCR activity and better H2O and SO2 resistance than the traditional V2O5/TiO2 (anatase) catalyst. In situ DRIFTs, XPS, H2-TPR and NH3/NO+O2-TPD results showed that Sn doping improved the redox property, NH3/NO adsorption and the amount of surface chemisorbed oxygen. The kinetic study indicated that Sn doping had little effect on SCR reaction pathways, but promoted SCR reaction, mainly through Eley-Rideal mechanism. More importantly, the V2O5/Sn0.2Ti0.8O2 showed better thermal stability than V2O5/TiO2. For V2O5/TiO2, the aggregation and sintering of the catalyst occurred, and the surface area decreased significantly after thermal aging. The monomeric vanadyl species partially transferred to crystalline V2O5. But for V2O5/Sn0.2Ti0.8O2, the surface area did not decrease as much as that for V2O5/TiO2, and the monomeric vanadyl species partially transferred to the polymeric vanadyl species.

Zinc-figure protein 217 (ZNF217) is a C2H2 zinc finger transcription factor that works as a pivotal effector stimulating embryonic immortalization as well as oncogenicity during multiple cancer processes. Nevertheless, the expression of ZNF217 in hepatocellular carcinoma (HCC) and the underlying specific molecular mechanisms remains elusive. In the present study, we aimed to explore the potential role of ZNF217 in HCC cell proliferation and invasion, as well as the underlying mechanism. Here, we demonstrated that the expression of ZNF217 was higher in HCC patients and indicated worse overall survival times, which was confirmed by Oncomine datasets and The Cancer Genome Atlas (TCGA) HCC cohorts. Further research discovered that knockdown of ZNF217 inhibited the proliferation of HCC cells in vitro and in vivo. Enforced expression of ZNF217 could promote Epithelial-mesenchymal transition and thus the invasion of HCC cells. Mechanistically, we identified ZNF217 interacted with LSD1 in vivo and in vitro. Knockdown of ZNF217 was accompanied by a parallel increase in di-methyl histone 3 lysine4 levels on CDH1 promoter, which indicated ZNF217 could recruit LSD1 to affect CDH1 epigenetic expression from transcription level. Of note, bioinformatics analyses, a dual luciferase reporter assay, RT-qPCR and western blot analysis demonstrated that microRNA-101 (miR-101), a well-known tumor suppressor in HCC, acted as a negative regulator of ZNF217. The inhibition of HCC progression by miR-101 was counteracted by ZNF217 overexpression. Taken together, our study presents the regulation mechanism of miR-101/ZNF217/CDH1 axis for the first time and provides new evidences of ZNF217 as a potential therapeutic target for HCC patients.

Chlorobenzene (CB) inhibits SCR activity of V-based catalysts at low temperature, though the adsorption amount is small. NH3 adsorption increases due to the break in the C-Cl bond during CB oxidation. The dissociated Cl- ions provide extra Bronsted acid sites, leading to the formation of inactive NH4Cl. Ce and Mn improve dechlorination, forming more NH4Cl on the catalyst surface.

The deactivation of catalysts by potassium and the promotion of cerium on MnO x /TiO 2 for selective catalytic reduction (SCR) of NO with NH 3 are investigated by both experiments and DFT calculations. Catalyst poisoning by K is due to the decrease of surface acidity, the loss of reducibility and the improvement of stable nitrite/nitrate species. When the catalyst is modified by CeO 2 , SCR activities of both fresh and poisoned catalysts are improved. Cerium provides new Lewis acid sites for NH 3 adsorption, which does not seem to be influenced by K. The Ce 4f orbitals of poisoned surfaces are nearly unaffected, which preserve reducibility of catalyst for NH 3 activation. Stable, inactive nitrite species do not build up and the reactive nitrate species are still present on the surface. These advantages can be attributed to the unique active sites, the [–O–Ce–O–Mn–O–] units . These active sites induce the movement of alkali metals to assemble together, leaving more surface active sites for SCR reaction.

Deactivation of alkali metals and arsenic and regeneration methods are studied on commercial V 2 O 5 –WO 3 /TiO 2 for the SCR reaction using experiments and DFT calculations. The poisoning of alkali metals is found to decrease the amount of Bronsted acid sites and the reducibility of active V 5+ sites. Arsenic decreases the amount of Lewis acid sites and the stability of Bronsted acid sites and increases N 2 O formation. After the catalysts are poisoned by both alkali metals and arsenic, the activity and N 2 selectivity are significantly suppressed. Diluted H 2 SO 4 effectively removes alkali metals from the poisoned catalysts. Half of the amount of arsenic can be removed using a 4% H 2 O 2 solution; however, some V 2 O 5 and surface sulfates are also eliminated from the catalysts. The activity of the regenerated catalysts is almost recovered at high temperatures. From the DFT results on the V 2 O 5 /TiO 2 (0 0 1) plane, potassium and arsenic significantly alter the electronic structures of the V orbitals and broaden the band gap of the models. Interactions between potassium and arsenic are also found. Potassium covers the active sites of the models that are constructed by V 2 O 5 and As 2 O 5 , which further decreases the number of acid sites. Potassium causes V and As orbitals to move to lower energies and inhibits the reactivity of the model.