Reaction Pathway Investigation on the Selective Catalytic Reduction of NO with NH₃ over Cu/SSZ-13 at Low Temperatures

The mechanism of the selective catalytic reduction of NO with NH₃ was studied using Cu/SSZ-13. The adspecies of NO and NH₃ as well as the active intermediates were investigated using in situ diffuse reflectance infrared Fourier transform spectroscopy and temperature-programmed surface reaction. The results revealed that three reactions were possible between adsorbed NH₃ and NO_<i>x</i>. NO₂^– could be generated by direct formation or NO₃^– reduction via NO. In a standard selective catalytic reduction (SCR) reaction, NO₃^– was hard to form, because NO₂^– was consumed by ammonia before it could be further oxidized to nitrates. Additionally, adsorbed NH₃ on the Lewis acid site was more active than NH₄⁺. Thus, SCR mainly followed the reaction between Lewis acid site-adsorbed NH₃ and directly formed NO₂^–. Higher Cu loading could favor the formation of active Cu-NH₃, Cu-NO₂^–, and Cu-NO₃^–, improving the SCR activity at low temperature

Design Strategies for Development of SCR Catalyst: Improvement of Alkali Poisoning Resistance and Novel Regeneration Method

Based on the ideas of the additives modification and regeneration method update, two different strategies were designed to deal with the traditional SCR catalyst poisoned by alkali metals. First, ceria doping on the V₂O₅–WO₃/TiO₂ catalyst could promote the SCR performance even reducing the V loading, which resulted in the enhancement of the catalyst’s alkali poisoning resistance. Then, a novel method, electrophoresis treatment, was employed to regenerate the alkali poisoned V₂O₅–WO₃/TiO₂ catalyst. This novel technique could dramatically enhance the SCR activities of the alkali poisoned catalysts by removing approximately 95% K or Na ions from the catalyst and showed less hazardous to the environment. Finally, the deactivation mechanisms by the alkali metals were extensively studied by employing both the experimental and DFT theoretical approaches. Alkali atom mainly influences the active site V species rather than W oxides. The decrease of catalyst surface acidity might directly reduce the catalytic activity, while the reducibility of catalysts could be another important factor

Extraordinary Deactivation Offset Effect of Arsenic and Calcium on CeO₂–WO₃ SCR Catalysts

An extraordinary deactivation offset effect of calcium and arsenic on CeO₂–WO₃ catalyst had been found for selective catalytic reduction of NO with NH₃ (NH₃–SCR). It was discovered that the maximum NO_<i>x</i> conversion of As–Ca poisoned catalyst reached up to 89% at 350 °C with the gaseous hourly space velocity of 120 000 mL·(g·h)⁻¹. The offset effect mechanisms were explored with respect to the changes of catalyst structure, surface acidity, redox property and reaction route by XRD, XPS, H₂-TPR, O₂-TPD, NH₃-TPD and in situ Raman, in situ TG, and DRIFTS. The results manifested that Lewis acid sites and reducibility originating from CeO₂ were obviously recovered, because the strong interaction between cerium and arsenic was weakened when Ca and As coexisted. Meanwhile, the CaWO₄ phase generated on Ca poisoned catalyst almost disappeared after As doping together, which made for Brønsted acid sites reformation on catalyst surface. Furthermore, surface Ce⁴⁺ proportion and oxygen defect sites amount were also restored for two-component poisoned catalyst, which favored NH₃ activation and further reaction. Finally, the reasons for the gap of catalytic performance between fresh and As–Ca poisoned catalyst were also proposed as follows: (1) surface area decrease; (2) crystalline WO₃ particles generation; and (3) oxygen defect sites irreversible loss

Comparison of the Structures and Mechanism of Arsenic Deactivation of CeO₂–MoO₃ and CeO₂–WO₃ SCR Catalysts

The mechanism of arsenic poisoning of CeO₂–WO₃ (CW) and CeO₂–MoO₃ (CM) catalysts during the selective catalytic reduction (SCR) of NO_<i>x</i> with NH₃ was investigated. It was found that the ratio of activity loss of the CW catalyst decreases as the temperature increases, while the opposite tendency was observed for the CM catalyst. The fresh and poisoned catalysts were characterized using X-ray diffraction (XRD) temperature-programmed reduction with H₂ (H₂-TPR), X-ray photoelectron spectra (XPS), NH₃-temperature-programmed desorption (NH₃-TPD), in situ DRIFTS, and in situ Raman spectroscopy. The results indicate that arsenic oxide primarily destroys the structure of the surface CeOx species in the CM catalyst but prefers to interact with WO₃ in the CW catalyst. Additionally, the BET surface area, the number and stability of Lewis acid sites, and the NO_<i>x</i> adsorption for these two types of catalysts clearly decrease after deactivation. According to the DRIFTS and Raman investigations, at low temperatures, the greater number of sites with adsorbed NH₃ in the poisoned CM catalyst leads to less loss of activity than the poisoned CW catalyst. However, at high temperatures, the greater number of Lewis acid sites remaining in the poisoned CW catalyst may play an important role in maintaining the activity of this catalyst

Regeneration of Commercial SCR Catalysts: Probing the Existing Forms of Arsenic Oxide

To investigate the poisoning and regeneration of SCR catalysts, fresh and arsenic-poisoned commercial V₂O₅–WO₃/TiO₂ catalysts are researched in the context of deactivation mechanisms and regeneration technology. The results indicate that the forms of arsenic oxide on the poisoned catalyst are related to the proportion of arsenic (As) on the catalyst. When the surface coverage of (V+W+As) is lower than 1, the trivalent arsenic species (As^III) is the major component, and this species prefers to permeate into the bulk-phase channels. However, at high As concentrations, pentavalent arsenic species (As^IV) cover the surface of the catalyst. Although both arsenic species lower the NO_<i>x</i> conversion, they affect the formation of N₂O differently. In particular, N₂O production is limited when trivalent arsenic species predominate, which may be related to As₂O₃ clogging the pores of the catalyst. In contrast, the pentavalent arsenic oxide species (As₂O₅) possess several As–OH groups. These As–OH groups could not only enhance the ability of the catalyst to become reduced, but also provide several Brønsted acid sites with weak thermal stability that promote the formation of N₂O. Finally, although our novel Ca­(NO₃)₂-based regeneration method cannot completely remove As₂O₃ from the micropores of the catalyst, this approach can effectively wipe off surface arsenic oxides without a significant loss of the catalyst’s active components

Removal of Antimonite (Sb(III)) and Antimonate (Sb(V)) from Aqueous Solution Using Carbon Nanofibers That Are Decorated with Zirconium Oxide (ZrO₂)

Zirconium oxide (ZrO₂)-carbon nanofibers (ZCN) were fabricated and batch experiments were used to determine antimonite (Sb­(III)) and antimonate (Sb­(V)) adsorption isotherms and kinetics. ZCN have a maximum Sb­(III) and Sb­(V) adsorption capacity of 70.83 and 57.17 mg/g, respectively. The adsorption process between ZCN and Sb was identified to be an exothermic and follows an ion-exchange reaction. The application of ZCN was demonstrated using tap water spiked with Sb (200 μg/L). We found that the concentration of Sb was well below the maximum contaminant level for drinking water with ZCN dosages of 2 g/L. X-ray photoelectron spectroscopy (XPS) revealed that an ionic bond of Zr–O was formed with Sb­(III) and Sb­(V). Based on the density functional theory (DFT) calculations, Sb­(III) formed Sb–O and O–Zr bonds on the surface of the tetragonal ZrO₂ (t-ZrO₂) (111) plane and monoclinic ZrO₂ planes (m-ZrO₂) (111) plane when it adsorbs. Only an O–Zr bond was formed on the surface of t-ZrO₂ (111) plane and m-ZrO₂ (111) plane for Sb­(V) adsorption. The adsorption energy (<i>E</i>_ad) of Sb­(III) and Sb­(V) onto t-ZrO₂ (111) plane were 1.13 and 6.07 eV, which were higher than that of m-ZrO₂ (0.76 and 3.35 eV, respectively)

Down-regulation of endogenous AR expression by AR shRNA in prostate cancer cells

<p><b>Copyright information:</b></p><p>Taken from "A promoting role of androgen receptor in androgen-sensitive and -insensitive prostate cancer cells"</p><p></p><p>Nucleic Acids Research 2007;35(8):2767-2776.</p><p>Published online 10 Apr 2007</p><p>PMCID:PMC1885678.</p><p>© 2007 The Author(s)</p> () LNCaP cells were infected with either the GFP adenovirus or the different AR shRNA adenovirus at an MOI of 40. Whole-cell lysates were prepared after 48 h of viral infection, and then analyzed by western blotting. Specific antibodies used to detect protein expression are labeled in the figure. () Identical experiments performed in LAPC4 cells. () LNCaP cells were infected with either the GFP adenovirus or AR shRNA3 adenovirus at an MOI of 40. Cells were fixed and immunostained 72 h after viral infection. Representative confocal laser scanning microscopy images of cells are shown. () Identical experiments performed in LAPC4 cells

Reduction of AR expression inhibits tumor xenograft formation in athymic mice

<p><b>Copyright information:</b></p><p>Taken from "A promoting role of androgen receptor in androgen-sensitive and -insensitive prostate cancer cells"</p><p></p><p>Nucleic Acids Research 2007;35(8):2767-2776.</p><p>Published online 10 Apr 2007</p><p>PMCID:PMC1885678.</p><p>© 2007 The Author(s)</p> () LAPC4 cells were transduced with the AR shRNA or GFP lentiviruses at a MOI of 3 for 24 h. Cells were harvested, resuspended in PBS and mixed with an equal volume of Matrigel ECM. Here, 100 μl of cell suspension (1 × 10 cells/ml) was injected subcutaneously in opposite lateral flanks of 6–8-week-old athymic male mice. Mice were monitored twice weekly. Tumors were measured in two dimensions with calipers, and tumor volume (mm) was calculated with the formula  = (length × width)/2. ‘Asterisk’ indicates a significant difference

Investigation of the Poisoning Mechanism of Lead on the CeO₂WO₃ Catalyst for the NH₃–SCR Reaction via in Situ IR and Raman Spectroscopy Measurement

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 WO_<i>x</i> 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

Down-regulation of AR expression inhibits the growth of androgen-sensitive prostate cancer cells

<p><b>Copyright information:</b></p><p>Taken from "A promoting role of androgen receptor in androgen-sensitive and -insensitive prostate cancer cells"</p><p></p><p>Nucleic Acids Research 2007;35(8):2767-2776.</p><p>Published online 10 Apr 2007</p><p>PMCID:PMC1885678.</p><p>© 2007 The Author(s)</p> () LNCaP cells were seeded into 96-well plates in media with or without DHT after 3 h adenovirus infection at an MOI of 10. Cell growth was measured every other day by MTS assay. The data represent the mean ± SD of three independent experiments. () Identical experiments performed in LAPC4 cells. () LNCaP cells were seeded into 24-well plates at 400 cells/well after 3 h adenovirus infection at an MOI of 10. Cells were cultured with the media in the presence or absence of DHT for 14 days and colonies were fixed and stained with crystal violet. () Similar experiments performed in LAPC4 cells