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

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

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

Antivirals Reduce the Formation of Key Alzheimer's Disease Molecules in Cell Cultures Acutely Infected with Herpes Simplex Virus Type 1

Alzheimer's disease (AD) afflicts around 20 million people worldwide and so there is an urgent need for effective treatment. Our research showing that herpes simplex virus type 1 (HSV1) is a risk factor for AD for the brains of people who possess a specific genetic factor and that the virus causes accumulation of key AD proteins (β-amyloid (Aβ) and abnormally phosphorylated tau (P-tau)), suggests that anti-HSV1 antiviral agents might slow AD progression. However, currently available antiviral agents target HSV1 DNA replication and so might be successful in AD only if Aβ and P-tau accumulation depend on viral DNA replication. Therefore, we investigated firstly the stage(s) of the virus replication cycle required for Aβ and P-tau accumulation, and secondly whether antiviral agents prevent these changes using recombinant strains of HSV1 that progress only partly through the replication cycle and antiviral agents that inhibit HSV1 DNA replication. By quantitative immunocytochemistry we demonstrated that entry, fusion and uncoating of HSV1, are insufficient to induce Aβ and P-tau production. We showed also that none of the “immediate early” viral proteins is directly responsible, and that Aβ and P-tau are produced at a subsequent stage of the HSV1 replication cycle. Importantly, the anti-HSV1 antiviral agents acyclovir, penciclovir and foscarnet reduced Aβ and P-tau accumulation, as well as HSV1, with foscarnet being less effective in each case. P-tau accumulation was found to depend on HSV1 DNA replication, whereas Aβ accumulation was not. The antiviral-induced decrease in Aβ is attributable to the reduced number of new viruses, and hence the reduction in viral spread. Since antiviral agents reduce greatly Aβ and P-tau accumulation in HSV1-infected cells, they would be suitable for treating AD with great advantage unlike current AD therapies, only the virus, not the host cell, would be targeted

APP Processing Induced by Herpes Simplex Virus Type 1 (HSV-1) Yields Several APP Fragments in Human and Rat Neuronal Cells

Lifelong latent infections of the trigeminal ganglion by the neurotropic herpes simplex virus type 1 (HSV-1) are characterized by periodic reactivation. During these episodes, newly produced virions may also reach the central nervous system (CNS), causing productive but generally asymptomatic infections. Epidemiological and experimental findings suggest that HSV-1 might contribute to the pathogenesis of Alzheimer's disease (AD). This multifactorial neurodegenerative disorder is related to an overproduction of amyloid beta (Aβ) and other neurotoxic peptides, which occurs during amyloidogenic endoproteolytic processing of the transmembrane amyloid precursor protein (APP). The aim of our study was to identify the effects of productive HSV-1 infection on APP processing in neuronal cells. We found that infection of SH-SY5Y human neuroblastoma cells and rat cortical neurons is followed by multiple cleavages of APP, which result in the intra- and/or extra-cellular accumulation of various neurotoxic species. These include: i) APP fragments (APP-Fs) of 35 and 45 kDa (APP-F35 and APP-F45) that comprise portions of Aβ; ii) N-terminal APP-Fs that are secreted; iii) intracellular C-terminal APP-Fs; and iv) Aβ1-40 and Aβ1-42. Western blot analysis of infected-cell lysates treated with formic acid suggests that APP-F35 may be an Aβ oligomer. The multiple cleavages of APP that occur in infected cells are produced in part by known components of the amyloidogenic APP processing pathway, i.e., host-cell β-secretase, γ-secretase, and caspase-3-like enzymes. These findings demonstrate that HSV-1 infection of neuronal cells can generate multiple APP fragments with well-documented neurotoxic potentials. It is tempting to speculate that intra- and extracellular accumulation of these species in the CNS resulting from repeated HSV-1 reactivation could, in the presence of other risk factors, play a co-factorial role in the development of AD

Differential Release and Phagocytosis of Tegument Glycoconjugates in Neurocysticercosis: Implications for Immune Evasion Strategies

Neurocysticercosis (NCC) is an infection of the central nervous system (CNS) by the metacestode of the helminth Taenia solium. The severity of the symptoms is associated with the intensity of the immune response. First, there is a long asymptomatic period where host immunity seems incapable of resolving the infection, followed by a chronic hypersensitivity reaction. Since little is known about the initial response to this infection, a murine model using the cestode Mesocestoides corti (syn. Mesocestoides vogae) was employed to analyze morphological changes in the parasite early in the infection. It was found that M. corti material is released from the tegument making close contact with the nervous tissue. These results were confirmed by infecting murine CNS with ex vivo–labeled parasites. Because more than 95% of NCC patients exhibit humoral responses against carbohydrate-based antigens, and the tegument is known to be rich in glycoconjugates (GCs), the expression of these types of molecules was analyzed in human, porcine, and murine NCC specimens. To determine the GCs present in the tegument, fluorochrome-labeled hydrazides as well as fluorochrome-labeled lectins with specificity to different carbohydrates were used. All the lectins utilized labeled the tegument. GCs bound by isolectinB4 were shed in the first days of infection and not resynthesized by the parasite, whereas GCs bound by wheat germ agglutinin and concavalinA were continuously released throughout the infectious process. GCs bound by these three lectins were taken up by host cells. Peanut lectin-binding GCs, in contrast, remained on the parasite and were not detected in host cells. The parasitic origin of the lectin-binding GCs found in host cells was confirmed using antibodies against T. solium and M. corti. We propose that both the rapid and persistent release of tegumental GCs plays a key role in the well-known immunomodulatory effects of helminths, including immune evasion and life-long inflammatory sequelae seen in many NCC patients

Cross-Section Measurement of Virtual Photoproduction of Iso-Triplet Three-Body Hypernucleus, ⋀nn

Missing-mass spectroscopy with the 3H(e, e′K+) reaction was carried out at Jefferson Lab’s (JLab) Hall A in Oct–Nov, 2018. The differential cross section for the 3H(γ∗, K+)Λnn was deduced at ω = Ee − Ee′ = 2.102 GeV and at the forward K+-scattering angle (0° ≤ θγ∗K ≤ 5°) in the laboratory frame. Given typical predicted energies and decay widths, which are (BΛ, Γ) = (−0.25, 0.8) and (−0.55, 4.7) MeV, the cross sections were found to be 11.2 ± 4.8(stat.)+4.1−2.1(sys.) and 18.1 ± 6.8(stat.)+4.2−2.9(sys.) nb/sr, respectively. The obtained result would impose a constraint for interaction models particularly between Λ and neutron by comparing to theoretical calculations