Monolithic Ni‐Al2O3/Ni‐foam catalyst is developed by modified wet chemical etching of Ni‐foam, being highly active/selective and stable in strongly exothermic CO2 methanation process. The as‐prepared catalysts are characterized by x‐ray diffraction scanning electron microscopy, inductively coupled plasma atomic emission spectrometry, and H2‐temperature programmed reduction‐mass spectrometry. The results indicate that modified wet chemical etching method is working efficiently for one‐step creating and firmly embedding NiO‐Al2O3 composite catalyst layer (∼2 μm) into the Ni‐foam struts. High CO2 conversion of 90% and high CH4 selectivity of >99.9% can be obtained and maintained for a feed of H2/CO2 (molar ratio of 4/1) at 320°C and 0.1 MPa with a gas hourly space velocity of 5000 h−1, throughout entire 1200 h test over 10.2 mL such monolithic catalysts. Computational fluid dynamics calculation and experimental measurement consistently confirm a dramatic reduction of “hotspot” temperature due to enhanced heat transfer. © 2015 American Institute of Chemical Engineers AIChE J, 61: 4323–4331, 2015

Peroxisomes play important roles in metabolisms of eukaryotes and infection of plant fungal pathogens. These organelles proliferate by de novo formation or division in response to environmental stimulation. Although the assembly of peroxisomes was documented in fungal pathogens, their division and its relationship to pathogenicity remain obscure. In present work, we analyzed the roles of three Pex11 family members in peroxisomal division and pathogenicity of the rice blast fungus Magnaporthe oryzae. Deletion of MoPEX11A led to fewer but enlarged peroxisomes, and impaired the separation of Woronin bodies from peroxisomes, while deletion of MoPEX11B or MoPEX11C put no evident impacts to peroxisomal profiles. MoPEX11A mutant exhibited typical peroxisome related defects, delayed conidial germination and appressoria formation, and decreased appressorial turgor and host penetration. As a result, the virulence of MoPEX11A mutant was greatly reduced. Deletion of MoPEX11B and MoPEX11C did not alter the virulence of the fungus. Further, double or triple deletions of the three genes were unable to enhance the virulence decrease in MoPEX11A mutant. Our data indicated that MoPEX11A is the main factor modulating peroxisomal division and is required for full virulence of the fungus.

The present study explored the association between KRAS proto-oncogene GTPase (KRAS), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α (PIK3CA) and tumor protein p53 (TP53) mutations, and the clinical features and survival prognosis in 50 patients with non-small cell lung cancer (NSCLC). The most common concurrent single gene mutation was TP53, followed by KRAS and PIK3CA . Co-existing mutations were found in 17 patients. KRAS, PIK3CA and TP53 mutations were associated with carbohydrate antigen 19-9 expression, invasive growth, vacuolar signs and margin lobulation on chest CT. The incidence of distant metastasis (bone and adrenal) with KRAS and TP53 mutations was greater than that of local metastasis (pleura). Patients with the wild-type genes experienced longer progression-free survival (PFS) times than those with KRAS, TP53, KRAS/TP53 or PIK3CA/TP53 mutations. Patients with KRAS/TP53 or PIK3CA/TP53 mutations experienced shorter PFS times than those with a single KRAS or TP53 mutation. KRAS, PIK3CA and TP53 mutations were associated with distant metastases and a poor prognosis. Patients with NSCLC should receive routine KRAS, PIK3CA and TP53 gene sequencing to determine mutations for the analysis of clinical characteristics and prognosis .