Hierarchically Porous ZSM-5 Synthesized by Nonionic- and Cationic-Templating Routes and Their Catalytic Activity in Liquid-Phase Esterification

Hierarchically porous MFI zeolites (ZSM-5) have been synthesized by hydrothermal treatment in the presence of trialkoxysilylated-derivatives of nonionic poly(oxyethylene) alkyl ether or alkyl quaternary ammonium cation as mesopore-generating agent, along with tetrapropylammonium cation as zeolite structure-directing agent. Powder X-ray diffraction revealed that zeolites have been crystallized, and scanning electron microscopy showed rugged surface morphology that was quite different from conventional ZSM-5. The mesoporosity was confirmed by nitrogen adsorption-desorption measurement showing type IV isotherms with narrow distribution of mesopore diameters. The catalytic activity of these mesoporous ZSM-5 was tested in liquid-phase esterification of benzyl alcohol with hexanoic acid. The conversion of benzyl alcohol on mesoporous ZSM-5 prepared via cationic-templating route was almost 100%, being much higher than on mesoporous ZSM-5 prepared with silylated nonionic surfactant as well as on conventional ZSM-5 with no mesopores. The presence of Brønsted acid sites, together with the mesopores, was responsible for this catalytic conversion, as confirmed by pyridine adsorption monitored by in situ infrared and 27Al magic angle spinning nuclear magnetic resonance spectroscopy

Development of a New DNA Marker for Fusarium Yellows Resistance in Brassica rapa Vegetables

In vegetables of Brassica rapa L., Fusarium oxysporum f. sp. rapae (For) or F. oxysporum f. sp. conglutinans (Foc) cause Fusarium yellows. A resistance gene against Foc (FocBr1) has been identified, and deletion of this gene results in susceptibility (focbr1-1). In contrast, a resistance gene against For has not been identified. Inoculation tests showed that lines resistant to Foc were also resistant to For, and lines susceptible to Foc were susceptible to For. However, prediction of disease resistance by a dominant DNA marker on FocBr1 (Bra012688m) was not associated with disease resistance of For in some komatsuna lines using an inoculation test. QTL-seq using four F2 populations derived from For susceptible and resistant lines showed one causative locus on chromosome A03, which covers FocBr1. Comparison of the amino acid sequence of FocBr1 between susceptible and resistant alleles (FocBr1 and FocBo1) showed that six amino acid differences were specific to susceptible lines. The presence and absence of FocBr1 is consistent with For resistance in F2 populations. These results indicate that FocBr1 is essential for For resistance, and changed amino acid sequences result in susceptibility to For. This susceptible allele is termed focbr1-2, and a new DNA marker (focbr1-2m) for detection of the focbr1-2 allele was develope

Experimental determination and thermodynamic calculation of the phase equilibria in the Cu-In-Sn system

The phase equilibria of the Cu-In-Sn system were investigated by means of the diffusion couple method, differential scanning calorimetry (DSC) and metallography. The isothermal sections at 110-900 degreesC, as well as vertical sections at 10wt.%Cu-70wt.%Cu were determined. It was found that there are large solubilities of In in the epsilon (Cu3Sn), delta (Cu41Sn11), and eta phases in the Cu-Sn system, and large solubilities of Sn in the gamma, eta, and delta (Cu7In3) phases in the Cu-In system. The eta phase was found to continuously form from the Cu-In side to the Cu-Sn side, and a ternary compound (Cu2In3Sn) was found to exist at 110 degreesC. Thermodynamic assessment of the Cu-In-Sn system was also carried out based on experimental data of activity and phase equilibria using the CALPHAD method, in which the Gibbs energies of the liquid, fcc and bcc phases are described by the subregular solution model and that of compounds, including two ternary compounds, are represented by the sublattice model. The thermodynamic parameters for describing the phase equilibria were optimized, and agreement between the calculated and experimental results was obtained

Distorted wave impulse approximation analysis for spin observables in nucleon quasi-elastic scattering and enhancement of the spin-longitudinal response

We present a formalism of distorted wave impulse approximation (DWIA) for analyzing spin observables in nucleon inelastic and charge exchange reactions leading to the continuum. It utilizes response functions calculated by the continuum random phase approximation (RPA), which include the effective mass, the spreading widths and the \Delta degrees of freedom. The Fermi motion is treated by the optimal factorization, and the non-locality of the nucleon-nucleon t-matrix by an averaged reaction plane approximation. By using the formalism we calculated the spin-longitudinal and the spin-transverse cross sections, ID_q and ID_p, of 12C, 40Ca (\vec{p},\vec{n}) at 494 and 346 MeV. The calculation reasonably reproduced the observed ID_q, which is consistent with the predicted enhancement of the spin-longitudinal response function R_L. However, the observed ID_p is much larger than the calculated one, which was consistent with neither the predicted quenching nor the spin-transverse response function R_T obtained by the (e,e') scattering. The Landau-Migdal parameter g'_N\Delta for the N\Delta transition interaction and the effective mass at the nuclear center m^*(r=0) are treated as adjustable parameters. The present analysis indicates that the smaller g'_{N\Delta}(\approx 0.3) and m^*(0) \approx 0.7 m are preferable. We also investigate the validity of the plane wave impulse approximation (PWIA) with the effective nucleon number approximation for the absorption, by means of which R_L and R_T have conventionally been extracted.Comment: RevTex 3, 29 pages, 2 tables, 8 figure

A novel method, digital genome scanning detects KRAS gene amplification in gastric cancers: involvement of overexpressed wild-type KRAS in downstream signaling and cancer cell growth

<p>Abstract</p> <p>Background</p> <p>Gastric cancer is the third most common malignancy affecting the general population worldwide. Aberrant activation of KRAS is a key factor in the development of many types of tumor, however, oncogenic mutations of <it>KRAS </it>are infrequent in gastric cancer. We have developed a novel quantitative method of analysis of DNA copy number, termed digital genome scanning (DGS), which is based on the enumeration of short restriction fragments, and does not involve PCR or hybridization. In the current study, we used DGS to survey copy-number alterations in gastric cancer cells.</p> <p>Methods</p> <p>DGS of gastric cancer cell lines was performed using the sequences of 5000 to 15000 restriction fragments. We screened 20 gastric cancer cell lines and 86 primary gastric tumors for <it>KRAS </it>amplification by quantitative PCR, and investigated <it>KRAS </it>amplification at the DNA, mRNA and protein levels by mutational analysis, real-time PCR, immunoblot analysis, GTP-RAS pull-down assay and immunohistochemical analysis. The effect of <it>KRAS </it>knock-down on the activation of p44/42 MAP kinase and AKT and on cell growth were examined by immunoblot and colorimetric assay, respectively.</p> <p>Results</p> <p>DGS analysis of the HSC45 gastric cancer cell line revealed the amplification of a 500-kb region on chromosome 12p12.1, which contains the <it>KRAS </it>gene locus. Amplification of the <it>KRAS </it>locus was detected in 15% (3/20) of gastric cancer cell lines (8–18-fold amplification) and 4.7% (4/86) of primary gastric tumors (8–50-fold amplification). <it>KRAS </it>mutations were identified in two of the three cell lines in which <it>KRAS </it>was amplified, but were not detected in any of the primary tumors. Overexpression of KRAS protein correlated directly with increased <it>KRAS </it>copy number. The level of GTP-bound KRAS was elevated following serum stimulation in cells with amplified wild-type <it>KRAS</it>, but not in cells with amplified mutant <it>KRAS</it>. Knock-down of <it>KRAS </it>in gastric cancer cells that carried amplified wild-type <it>KRAS </it>resulted in the inhibition of cell growth and suppression of p44/42 MAP kinase and AKT activity.</p> <p>Conclusion</p> <p>Our study highlights the utility of DGS for identification of copy-number alterations. Using DGS, we identified <it>KRAS </it>as a gene that is amplified in human gastric cancer. We demonstrated that gene amplification likely forms the molecular basis of overactivation of KRAS in gastric cancer. Additional studies using a larger cohort of gastric cancer specimens are required to determine the diagnostic and therapeutic implications of <it>KRAS </it>amplification and overexpression.</p