A Nexafs Study of Nitric Oxide Layers Adsorbed from a nitrite Solution onto a Pt(111) Surface

NO molecules adsorbed on a Pt(111) surface from dipping in an acidic nitrite solution are studied by near edge X-ray absorption fine structure spectroscopy (NEXAFS), X-ray photoelectron spectroscopy (XPS), low energy electron diffraction (LEED) and scanning tunnelling microscopy (STM) techniques. LEED patterns and STM images show that no long range ordered structures are formed after NO adsorption on a Pt(111) surface. Although the total NO coverage is very low, spectroscopic features in N K-edge and O K-edge absorption spectra have been singled out and related to the different species induced by this preparation method. From these measurements it is concluded that the NO molecule is adsorbed trough the N atom in an upright conformation. The maximum saturation coverage is about 0.3 monolayers, and although nitric oxide is the major component, nitrite and nitrogen species are slightly co-adsorbed on the surface. The results obtained from this study are compared with those previously reported in the literature for NO adsorbed on Pt(111) under UHV conditions

Role of the exchange and correlation potential into calculating the x-ray absorption spectra of half-metallic alloys: the case of Mn and Cu K-edge XANES in Cu2_2MnM (M = Al, Sn, In) Heusler alloys

This work reports a theoretical study of the x-ray absorption near-edge structure spectra at both the Cu and the Mn K-edge in several Cu$_2$MnM (M= Al, Sn and In) Heusler alloys. Our results show that {\it ab-initio} single-channel multiple-scattering calculations are able of reproducing the experimental spectra. Moreover, an extensive discussion is presented concerning the role of the final state potential needed to reproduce the experimental data of these half-metallic alloys. In particular, the effects of the cluster-size and of the exchange and correlation potential needed in reproducing all the experimental XANES features are discussed.Comment: 15 pages, 5 figure

Effects of N,N-dimethyltryptamine on electrically evoked responses in the cat visual system and modification by neuroleptic agents,

The effects of N,N-dimethyltryptamine on electrically evoked potentials in the visual system of the cat and the interaction of selected neuroleptic agents with dimethyltryptamine were studied. Dimethyltryptamine caused a dose-dependent decrease in the amplitude of the response evoked by stimulation of the optic chiasm as recorded in the lateral geniculate nucleus and the visual cortex. Dimethyltryptamine had no significant effect on antidromically evoked potentials in the lateral geniculate nucleus or potentials in the visual cortex produced by optic radiation stimulation. A dose-dependent biphasic effect was found in animals pretreated with various doses of chlorpromazine, haloperidol, thiothixene, molindone, methiothepin and octoclothepin. Methiothepin and octoclothepin were the most potent antagonists of dimethyltryptamine, while molindone was essentially ineffective. Low doses of the neuroleptics, with the exception of molindone, potentiated the inhibitory action of dimethyltryptamine on evoked responses.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/21690/1/0000081.pd

Influenza C virus NS1 protein counteracts RIG-I-mediated IFN signalling

The nonstructural proteins 1 (NS1) from influenza A and B viruses are known as the main viral factors antagonising the cellular interferon (IFN) response, inter alia by inhibiting the retinoic acid-inducible gene I (RIG-I) signalling. The cytosolic pattern-recognition receptor RIG-I senses double-stranded RNA and 5'-triphosphate RNA produced during RNA virus infections. Binding to these ligands activates RIG-I and in turn the IFN signalling. We now report that the influenza C virus NS1 protein also inhibits the RIG-I-mediated IFN signalling. Employing luciferase-reporter assays, we show that expression of NS1-C proteins of virus strains C/JJ/50 and C/JHB/1/66 considerably reduced the IFN-β promoter activity. Mapping of the regions from NS1-C of both strains involved in IFN-β promoter inhibition showed that the N-terminal 49 amino acids are dispensable, while the C-terminus is required for proper modulation of the IFN response. When a mutant RIG-I, which is constitutively active without ligand binding, was employed, NS1-C still inhibited the downstream signalling, indicating that IFN inhibitory properties of NS1-C are not necessarily linked to an RNA binding mechanism

Gene correction in hematopoietic progenitor cells by homologous recombination

Homologous recombination (gene targeting) has many desirable features for gene therapy, because it can precisely correct mutant genes and restore their normal expression, and random nonhomologous integration of DNA is infrequent in cells in which homologous recombination has occurred. There are, however, no reports of attempts to use homologous recombination to correct mutant genes in normal hematopoietic stem cells (HSCs), which are prime cells for therapy of a variety of hematological and other conditions, presumably because of their low abundance and uncertainty that homologous recombination can occur at a usable frequency in these cells. The experiments reported here encourage optimism in this respect by demonstrating targeted correction of a defective hypoxanthine phosphoribosyltransferase gene in hematopoietic progenitor cells that can form colonies in methylcellulose culture. These clonogenic cells are in the same lineage as HSCs but are more abundant and more mature and so less pluripotent. Corrected colonies were identified by their survival in selective medium after electroporation of correcting DNA into unfractionated mouse bone marrow cells and were confirmed by reverse transcription–PCR and sequencing. The observed frequency (4.4 ± 3.3 × 10−5 per treated clonogenic cell) is the same as in embryonic stem cells (2.3 ± 0.4 × 10−5) with the same DNA and mutation. These data suggest that gene targeting to correct mutant genes eventually will prove feasible in HSCs capable of long-term bone marrow reconstitution

Individual influenza A virus mRNAs show differential dependence on cellular NXF1/TAP for their nuclear export

The influenza A virus RNA-dependent RNA polymerase produces capped and polyadenylated mRNAs in the nucleus of infected cells that resemble mature cellular mRNAs, but are made by very different mechanisms. Furthermore, only two of the 10 viral protein-coding mRNAs are spliced: most are intronless, while two contain unremoved introns. The mechanism(s) by which any of these mRNAs are exported from the nucleus is uncertain. To probe the involvement of the primary cellular mRNA export pathway, we treated cells with siRNAs against NXF1, Aly or UAP56, or with the drug 5,6-dichloro-1-β-d-ribofuranosyl-benzimidazole (DRB), an inhibitor of RNA polymerase II phosphorylation previously shown to inhibit nuclear export of cellular mRNA as well as influenza virus segment 7 mRNAs. Depletion of NXF1 or DRB treatment had similar effects, inhibiting the nuclear export of several of the viral mRNAs. However, differing degrees of sensitivity were seen, depending on the particular segment examined. Intronless HA mRNA and spliced M2 or unspliced M1 transcripts (all encoding late proteins) showed a strong requirement for NXF1, while intronless early gene mRNAs, especially NP mRNA, showed the least dependency. Depletion of Aly had little effect on viral mRNA export, but reduction of UAP56 levels strongly inhibited trafficking and/or translation of the M1, M2 and NS1 mRNAs. Synthesis of NS2 from the spliced segment 8 transcript was, however, resistant. We conclude that influenza A virus co-opts the main cellular mRNA export pathway for a subset of its mRNAs, including most but not all late gene transcripts