133 research outputs found

    Adsorption and reaction of CO on (Pd–)Al2O3 and (Pd–)ZrO2: vibrational spectroscopy of carbonate formation

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    γ-Alumina is widely used as an oxide support in catalysis, and palladium nanoparticles supported by alumina represent one of the most frequently used dispersed metals. The surface sites of the catalysts are often probed via FTIR spectroscopy upon CO adsorption, which may result in the formation of surface carbonate species. We have examined this process in detail utilizing FTIR to monitor carbonate formation on γ-alumina and zirconia upon exposure to isotopically labelled and unlabelled CO and CO2. The same was carried out for well-defined Pd nanoparticles supported on Al2O3 or ZrO2. A water gas shift reaction of CO with surface hydroxyls was detected, which requires surface defect sites and adjacent OH groups. Furthermore, we have studied the effect of Cl synthesis residues, leading to strongly reduced carbonate formation and changes in the OH region (isolated OH groups were partly replaced or were even absent). To corroborate this finding, samples were deliberately poisoned with Cl to an extent comparable to that of synthesis residues, as confirmed by Auger electron spectroscopy. For catalysts prepared from Cl-containing precursors a new CO band at 2164 cm−1 was observed in the carbonyl region, which was ascribed to Pd interacting with Cl. Finally, the FTIR measurements were complemented by quantification of the amount of carbonates formed via chemisorption, which provides a tool to determine the concentration of reactive defect sites on the alumina surface

    Structure of Metaphase Chromosomes: A Role for Effects of Macromolecular Crowding

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    In metaphase chromosomes, chromatin is compacted to a concentration of several hundred mg/ml by mechanisms which remain elusive. Effects mediated by the ionic environment are considered most frequently because mono- and di-valent cations cause polynucleosome chains to form compact ∼30-nm diameter fibres in vitro, but this conformation is not detected in chromosomes in situ. A further unconsidered factor is predicted to influence the compaction of chromosomes, namely the forces which arise from crowding by macromolecules in the surrounding cytoplasm whose measured concentration is 100–200 mg/ml. To mimic these conditions, chromosomes were released from mitotic CHO cells in solutions containing an inert volume-occupying macromolecule (8 kDa polyethylene glycol, 10.5 kDa dextran, or 70 kDa Ficoll) in 100 µM K-Hepes buffer, with contaminating cations at only low micromolar concentrations. Optical and electron microscopy showed that these chromosomes conserved their characteristic structure and compaction, and their volume varied inversely with the concentration of a crowding macromolecule. They showed a canonical nucleosomal structure and contained the characteristic proteins topoisomerase IIα and the condensin subunit SMC2. These observations, together with evidence that the cytoplasm is crowded in vivo, suggest that macromolecular crowding effects should be considered a significant and perhaps major factor in compacting chromosomes. This model may explain why ∼30-nm fibres characteristic of cation-mediated compaction are not seen in chromosomes in situ. Considering that crowding by cytoplasmic macromolecules maintains the compaction of bacterial chromosomes and has been proposed to form the liquid crystalline chromosomes of dinoflagellates, a crowded environment may be an essential characteristic of all genomes

    Elevated Proteasome Capacity Extends Replicative Lifespan in Saccharomyces cerevisiae

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    Aging is characterized by the accumulation of damaged cellular macromolecules caused by declining repair and elimination pathways. An integral component employed by cells to counter toxic protein aggregates is the conserved ubiquitin/proteasome system (UPS). Previous studies have described an age-dependent decline of proteasomal function and increased longevity correlates with sustained proteasome capacity in centenarians and in naked mole rats, a long-lived rodent. Proof for a direct impact of enhanced proteasome function on longevity, however, is still lacking. To determine the importance of proteasome function in yeast aging, we established a method to modulate UPS capacity by manipulating levels of the UPS–related transcription factor Rpn4. While cells lacking RPN4 exhibit a decreased non-adaptable proteasome pool, loss of UBR2, an ubiquitin ligase that regulates Rpn4 turnover, results in elevated Rpn4 levels, which upregulates UPS components. Increased UPS capacity significantly enhances replicative lifespan (RLS) and resistance to proteotoxic stress, while reduced UPS capacity has opposing consequences. Despite tight transcriptional co-regulation of the UPS and oxidative detoxification systems, the impact of proteasome capacity on lifespan is independent of the latter, since elimination of Yap1, a key regulator of the oxidative stress response, does not affect lifespan extension of cells with higher proteasome capacity. Moreover, since elevated proteasome capacity results in improved clearance of toxic huntingtin fragments in a yeast model for neurodegenerative diseases, we speculate that the observed lifespan extension originates from prolonged elimination of damaged proteins in old mother cells. Epistasis analyses indicate that proteasome-mediated modulation of lifespan is at least partially distinct from dietary restriction, Tor1, and Sir2. These findings demonstrate that UPS capacity determines yeast RLS by a mechanism that is distinct from known longevity pathways and raise the possibility that interventions to promote enhanced proteasome function will have beneficial effects on longevity and age-related disease in humans

    Test of lepton universality in bs+b \rightarrow s \ell^+ \ell^- decays

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    The first simultaneous test of muon-electron universality using B+K++B^{+}\rightarrow K^{+}\ell^{+}\ell^{-} and B0K0+B^{0}\rightarrow K^{*0}\ell^{+}\ell^{-} decays is performed, in two ranges of the dilepton invariant-mass squared, q2q^{2}. The analysis uses beauty mesons produced in proton-proton collisions collected with the LHCb detector between 2011 and 2018, corresponding to an integrated luminosity of 9 fb1\mathrm{fb}^{-1}. Each of the four lepton universality measurements reported is either the first in the given q2q^{2} interval or supersedes previous LHCb measurements. The results are compatible with the predictions of the Standard Model.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-046.html (LHCb public pages

    Precision measurement of CP\it{CP} violation in the penguin-mediated decay Bs0ϕϕB_s^{0}\rightarrow\phi\phi

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    A flavor-tagged time-dependent angular analysis of the decay Bs0ϕϕB_s^{0}\rightarrow\phi\phi is performed using pppp collision data collected by the LHCb experiment at % at s=13\sqrt{s}=13 TeV, the center-of-mass energy of 13 TeV, corresponding to an integrated luminosity of 6 fb^{-1}. The CP\it{CP}-violating phase and direct CP\it{CP}-violation parameter are measured to be ϕssˉs=0.042±0.075±0.009\phi_{s\bar{s}s} = -0.042 \pm 0.075 \pm 0.009 rad and λ=1.004±0.030±0.009|\lambda|=1.004\pm 0.030 \pm 0.009 , respectively, assuming the same values for all polarization states of the ϕϕ\phi\phi system. In these results, the first uncertainties are statistical and the second systematic. These parameters are also determined separately for each polarization state, showing no evidence for polarization dependence. The results are combined with previous LHCb measurements using pppp collisions at center-of-mass energies of 7 and 8 TeV, yielding ϕssˉs=0.074±0.069\phi_{s\bar{s}s} = -0.074 \pm 0.069 rad and lambda=1.009±0.030|lambda|=1.009 \pm 0.030. This is the most precise study of time-dependent CP\it{CP} violation in a penguin-dominated BB meson decay. The results are consistent with CP\it{CP} symmetry and with the Standard Model predictions.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2023-001.html (LHCb public pages

    Observation of a resonant structure near the Ds+DsD_s^+ D_s^- threshold in the B+Ds+DsK+B^+\to D_s^+ D_s^- K^+ decay

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    An amplitude analysis of the B+Ds+DsK+B^+\to D_s^+ D_s^- K^+ decay is carried out to study for the first time its intermediate resonant contributions, using proton-proton collision data collected with the LHCb detector at centre-of-mass energies of 7, 8 and 13 TeV. A near-threshold peaking structure, referred to as X(3960)X(3960), is observed in the Ds+DsD_s^+ D_s^- invariant-mass spectrum with significance greater than 12 standard deviations. The mass, width and the quantum numbers of the structure are measured to be 3956±5±103956\pm5\pm10 MeV, 43±13±843\pm13\pm8 MeV and JPC=0++J^{PC}=0^{++}, respectively, where the first uncertainties are statistical and the second systematic. The properties of the new structure are consistent with recent theoretical predictions for a state composed of ccˉssˉc\bar{c}s\bar{s} quarks. Evidence for an additional structure is found around 4140 MeV in the Ds+DsD_s^+ D_s^- invariant mass, which might be caused either by a new resonance with the 0++0^{++} assignment or by a J/ψϕDs+DsJ/\psi \phi\leftrightarrow D_s^+ D_s^- coupled-channel effect.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-018.html (LHCb public pages

    Measurement of the Λb0Λ(1520)μ+μ\Lambda_{b}^{0}\to \Lambda(1520) \mu^{+}\mu^{-} differential branching fraction

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    The branching fraction of the rare decay Λb0Λ(1520)μ+μ\Lambda_{b}^{0}\to \Lambda(1520) \mu^{+}\mu^{-} is measured for the first time, in the squared dimuon mass intervals, q2q^2, excluding the J/ψJ/\psi and ψ(2S)\psi(2S) regions. The data sample analyzed was collected by the LHCb experiment at center-of-mass energies of 7, 8, and 13 TeV, corresponding to a total integrated luminosity of $9\ \mathrm{fb}^{-1}.Theresultinthehighest. The result in the highest q^{2}interval, interval, q^{2} >15.0\ \mathrm{GeV}^2/c^4$, where theoretical predictions have the smallest model dependence, agrees with the predictions.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-050.html (LHCb public pages

    Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

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    In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field
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