17 research outputs found

    Liquid Phase Hydrogenation of MIBK over M/CsPW (M = Ag, Ru, Pt, and Pd)

    No full text
    Four different metal nanoparticles (metal = Ag, Ru, Pt, or Rh) were impregnated on the acidic cesium salt of tungstophosphoric acid Cs2.5H0.5PW12O40 (CsPW) with a loading amount of 2 wt%. The prepared catalysts were characterized by using X-ray diffraction (XRD), Fourier transform-infrared spectroscopy (FTIR), N2 sorption measurements, scanning electron microscopy (SEM), and energy-dispersive X-ray spectroscopy (EDX). Results confirmed the formation of highly distributed metallic nanoparticle centres over the acidic CsPW. The catalytic activity of the prepared catalysts were evaluated in the liquid phase hydrogenation of methyl isobutyl ketone (MIBK) to 2-methylpentane (2-MP) at 453 K. Pd-CsPW showed the highest activity compared to other catalysts, where 10% conversion was obtained with 91% selectivity after 4 h’s reaction time

    Identification of a negative response element in the human inducible nitric-oxide synthase (hiNOS) promoter: The role of NF-κB-repressing factor (NRF) in basal repression of the hiNOS gene

    Get PDF
    Although nuclear factor (NF)-κB plays a central role in mediating cytokine-stimulated human inducible nitric-oxide synthase (hiNOS) gene transcription, very little is known about the factors involved in silencing of the hiNOS promoter. NF-κB-repressing factor (NRF) interacts with a specific negative regulatory element (NRE) to mediate transcriptional repression of certain NF-κB responsive genes. By sequence comparison with the IFN-β and IL-8 promoters, we identified an NRE in the hiNOS promoter located at −6.7 kb upstream. In A549 and HeLa human cells, constitutive NRF mRNA expression is detected by RT-PCR. Gel shift assay showed constitutive NRF binding to the hiNOS NRE. Mutation of the −6.7-kb NRE site in the hiNOS promoter resulted in loss of NRF binding and increased basal but not cytokine-stimulated hiNOS transcription in promoter transfection experiments. Interestingly, overexpression of NRF suppressed both basal and cytokine-induced hiNOS promoter activity that depended on an intact cis-acting NRE motif. By using stably transformed HeLa cells with the tetracycline on/off expression system, reduction of cellular NRF by expressing antisense NRF increased basal iNOS promoter activity and resulted in constitutive iNOS mRNA expression. These data demonstrate that the transacting NRF protein is involved in constitutive silencing of the hiNOS gene by binding to a cis-acting NRE upstream in the hiNOS promoter

    Reactive oxygen signaling and MAPK activation distinguish Epstein–Barr Virus (EBV)-positive versus EBV-negative Burkitt's lymphoma

    No full text
    Burkitt's lymphoma (BL) is an aggressive B cell neoplasm, which is one of the most common neoplasms of childhood. It is highly widespread in East Africa, where it appears in endemic form associated with Epstein–Barr virus (EBV) infection, and around the world in a sporadic form in which EBV infection is much less common. In addition to being the first human neoplasm to be associated with EBV, BL is associated with a characteristic translocation, in which the Ig promoter is translocated to constitutively activate the c-myc oncogene. Although many BLs respond well to chemotherapy, a significant fraction fails to respond to therapy, leading to death. In this article, we demonstrate that EBV-positive BL expresses high levels of activated mitogen-activated protein kinase and reactive oxygen species (ROS), and that ROS directly regulate NF-κB activation. EBV-negative BLs exhibit activation of phosphoinositol 3-kinase, but do not have elevated levels of ROS. Elevated reactive oxygen may play a role in diverse forms of viral carcinogenesis in humans, including cancers caused by EBV, hepatitis B, C, and human T cell lymphotropic virus. Our findings imply that inhibition of ROS may be useful in the treatment of EBV-induced neoplasia

    Additional file 4: of Exome sequencing in routine diagnostics: a generic test for 254 patients with primary immunodeficiencies

    No full text
    Table S4. (A) The number of patients with isolated or combined infections, and (B) the number of patients with isolated or combined immunophenotypes, and the percentage for which we have reported a genetic diagnosis. (XLSX 11 kb
    corecore