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The selective catalytic reduction (SCR) of N2O with CH4 in the absence and presence of excess O2 has been studied over ion-exchanged Fe−BEA catalyst by the combination of an activity test with in-situ infrared spectroscopy to understand the nature of the surface species involved in the SCR of N2O with CH4. From the results of flow reaction studies, the Fe−BEA catalyst exhibited high activity in the SCR of N2O with CH4, even in the presence of excess oxygen, which demonstrates that the active Fe species for the SCR are formed on the ion-exchanged Fe−BEA catalyst. In the FTIR spectra of fresh catalysts, the OH band on Fe ion species (Fe−OH) was observed on the Fe−BEA catalyst, and the Fe−OH species can be involved in the SCR of N2O with CH4. Furthermore, the reaction intermediates of methoxy and formate species over the Fe−BEA catalyst were observed during the reaction. We measured the oxidation rates of these surface species with N2O and O2, and found that the methoxy species were oxidized with N2O more rapidly than O2, while the formate species were oxidized with both N2O and O2 at almost the same rate. On the basis of these results, we discuss the reaction mechanism of the SCR of N2O with CH4.

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Translocations of retinoic acid receptor-α (), typically , are a genetic hallmark of acute promyelocytic leukemia (APL). However, because a small fraction of APL lack translocations of, we focused here on APL cases without translocation to elucidate the molecular etiology of-negative APL. We performed whole-genome sequencing, PCR, and FISH for five APL cases without translocations. Four of five-negative APL cases had translocations involving retinoic acid receptor-β () translocations, and was identified as an in-frame fusion in three cases; one case had an rearrangement detected by FISH, although the partner gene could not be identified. When transduced in cell lines, homodimerized and diminished transcriptional activity for the retinoic acid receptor pathway in a dominant-negative manner. enhanced the replating capacity of mouse bone marrow cells and inhibited myeloid maturation of human cord blood cells as did. However, the response of APL with translocation to retinoids was attenuated compared with that of , an observation in line with the clinical resistance of-positive APL to ATRA. Our results demonstrate that the majority of -negative APL have translocations, thereby forming a novel, distinct subgroup of APL. as an oncogenic protein exerts effects similar to those of, underpinning the importance of retinoic acid pathway alterations in the pathogenesis of APL. These findings report a novel and distinct genetic subtype of acute promyelocytic leukemia (APL) by illustrating that the majority of APL without RARA translocations harbor RARB translocations. .