377 research outputs found

    Damagnetization cooling of a gas

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    We demonstrate demagnetization cooling of a gas of ultracold 52^{52}Cr atoms. Demagnetization is driven by inelastic dipolar collisions which couple the motional degrees of freedom to the spin degree. By that kinetic energy is converted into magnetic work with a consequent temperature reduction of the gas. Optical pumping is used to magnetize the system and drive continuous demagnetization cooling. Applying this technique, we can increase the phase space density of our sample by one order of magnitude, with nearly no atom loss. This method can be in principle extended to every dipolar system and could be used to achieve quantum degeneracy via optical means.Comment: 10 pages, 5 figure

    Generation and physiological roles of linear ubiquitin chains

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    Ubiquitination now ranks with phosphorylation as one of the best-studied post-translational modifications of proteins with broad regulatory roles across all of biology. Ubiquitination usually involves the addition of ubiquitin chains to target protein molecules, and these may be of eight different types, seven of which involve the linkage of one of the seven internal lysine (K) residues in one ubiquitin molecule to the carboxy-terminal diglycine of the next. In the eighth, the so-called linear ubiquitin chains, the linkage is between the amino-terminal amino group of methionine on a ubiquitin that is conjugated with a target protein and the carboxy-terminal carboxy group of the incoming ubiquitin. Physiological roles are well established for K48-linked chains, which are essential for signaling proteasomal degradation of proteins, and for K63-linked chains, which play a part in recruitment of DNA repair enzymes, cell signaling and endocytosis. We focus here on linear ubiquitin chains, how they are assembled, and how three different avenues of research have indicated physiological roles for linear ubiquitination in innate and adaptive immunity and suppression of inflammation

    Physical Foundations of Landauer's Principle

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    We review the physical foundations of Landauer's Principle, which relates the loss of information from a computational process to an increase in thermodynamic entropy. Despite the long history of the Principle, its fundamental rationale and proper interpretation remain frequently misunderstood. Contrary to some misinterpretations of the Principle, the mere transfer of entropy between computational and non-computational subsystems can occur in a thermodynamically reversible way without increasing total entropy. However, Landauer's Principle is not about general entropy transfers; rather, it more specifically concerns the ejection of (all or part of) some correlated information from a controlled, digital form (e.g., a computed bit) to an uncontrolled, non-computational form, i.e., as part of a thermal environment. Any uncontrolled thermal system will, by definition, continually re-randomize the physical information in its thermal state, from our perspective as observers who cannot predict the exact dynamical evolution of the microstates of such environments. Thus, any correlations involving information that is ejected into and subsequently thermalized by the environment will be lost from our perspective, resulting directly in an irreversible increase in total entropy. Avoiding the ejection and thermalization of correlated computational information motivates the reversible computing paradigm, although the requirements for computations to be thermodynamically reversible are less restrictive than frequently described, particularly in the case of stochastic computational operations. There are interesting possibilities for the design of computational processes that utilize stochastic, many-to-one computational operations while nevertheless avoiding net entropy increase that remain to be fully explored.Comment: 42 pages, 15 figures, extended postprint of a paper published in the 10th Conf. on Reversible Computation (RC18), Leicester, UK, Sep. 201

    Adaptive remodeling of the bacterial proteome by specific ribosomal modification regulates Pseudomonas infection and niche colonisation

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    Post-transcriptional control of protein abundance is a highly important, underexplored regulatory process by which organisms respond to their environments. Here we describe an important and previously unidentified regulatory pathway involving the ribosomal modification protein RimK, its regulator proteins RimA and RimB, and the widespread bacterial second messenger cyclic-di-GMP (cdG). Disruption of rimK affects motility and surface attachment in pathogenic and commensal Pseudomonas species, with rimK deletion significantly compromising rhizosphere colonisation by the commensal soil bacterium P. fluorescens, and plant infection by the pathogens P. syringae and P. aeruginosa. RimK functions as an ATP-dependent glutamyl ligase, adding glutamate residues to the C-terminus of ribosomal protein RpsF and inducing specific effects on both ribosome protein complement and function. Deletion of rimK in P. fluorescens leads to markedly reduced levels of multiple ribosomal proteins, and also of the key translational regulator Hfq. In turn, reduced Hfq levels induce specific downstream proteomic changes, with significant increases in multiple ABC transporters, stress response proteins and non-ribosomal peptide synthetases seen for both ΔrimK and Δhfq mutants. The activity of RimK is itself controlled by interactions with RimA, RimB and cdG. We propose that control of RimK activity represents a novel regulatory mechanism that dynamically influences interactions between bacteria and their hosts; translating environmental pressures into dynamic ribosomal changes, and consequently to an adaptive remodeling of the bacterial proteome

    A Mechanism for Chronic Filarial Hydrocele with Implications for Its Surgical Repair

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    Chronic hydrocele is the accumulation of fluid around the testis leading to an increase in the volume of the scrotal contents. Depending on the volume of fluid, hydrocele can be disfiguring and even incapacitating. Chronic hydrocele has multiple etiologies, but irrespective of the cause, surgery is the standard form of treatment and this can be done using different surgical techniques. The prevalence of chronic hydrocele in bancroftian filariasis endemic areas—a parasitic disease transmitted by mosquito—is very high and represents the most common clinical manifestation of bancroftosis, following by swollen legs of lower limbs or lymphedema among women. In Greater Recife, northeastern, Brazil, a bancroftian filariasis endemic area, a pioneering, prospective surgical study proposes a new mechanism for filarial-induced hydrocele and presents evidence that the filarial hydrocele fluid may damage the testis. Thus, based on the findings presented, the authors propose that in bancroftian filariasis endemic areas hydrocele patients should be operated on using a specific surgical technique in order to avoid recurrence of the disease, and consequently, additional damage to the testicle

    Impact of protein supplementation during endurance training on changes in skeletal muscle transcriptome

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    Background: Protein supplementation improves physiological adaptations to endurance training, but the impact on adaptive changes in the skeletal muscle transcriptome remains elusive. The present analysis was executed to determine the impact of protein supplementation on changes in the skeletal muscle transcriptome following 5- weeks of endurance training. Results: Skeletal muscle tissue samples from the vastus lateralis were taken before and after 5-weeks of endurance training to assess changes in the skeletal muscle transcriptome. One hundred and 63 genes were differentially expressed after 5-weeks of endurance training in both groups (q-value 0.05). Endurance training primarily affected expression levels of genes related to extracellular matrix and these changes tended to be greater in PRO than in CON. Conclusions: Protein supplementation subtly impacts endurance training-induced changes in the skeletal muscle transcriptome. In addition, our transcriptomic analysis revealed that the extracellular matrix may be an important factor for skeletal muscle adaptation in response to endurance training. This trial was registered at clinicaltrials.gov as NCT03462381, March 12, 201

    Search for Charged Higgs Bosons in e+e- Collisions at \sqrt{s} = 189 GeV

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    A search for pair-produced charged Higgs bosons is performed with the L3 detector at LEP using data collected at a centre-of-mass energy of 188.6 GeV, corresponding to an integrated luminosity of 176.4 pb^-1. Higgs decays into a charm and a strange quark or into a tau lepton and its associated neutrino are considered. The observed events are consistent with the expectations from Standard Model background processes. A lower limit of 65.5 GeV on the charged Higgs mass is derived at 95 % confidence level, independent of the decay branching ratio Br(H^{+/-} -> tau nu)

    Search for the standard model Higgs boson at LEP

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    Joint Binding of OTX2 and MYC in Promotor Regions Is Associated with High Gene Expression in Medulloblastoma

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    Both OTX2 and MYC are important oncogenes in medulloblastoma, the most common malignant brain tumor in childhood. Much is known about MYC binding to promoter regions, but OTX2 binding is hardly investigated. We used ChIP-on-chip data to analyze the binding patterns of both transcription factors in D425 medulloblastoma cells. When combining the data for all promoter regions in the genome, OTX2 binding showed a remarkable bi-modal distribution pattern with peaks around −250 bp upstream and +650 bp downstream of the transcription start sites (TSSs). Indeed, 40.2% of all OTX2-bound TSSs had more than one significant OTX2-binding peak. This OTX2-binding pattern was very different from the TSS-centered single peak binding pattern observed for MYC and other known transcription factors. However, in individual promoter regions, OTX2 and MYC have a strong tendency to bind in proximity of each other. OTX2-binding sequences are depleted near TSSs in the genome, providing an explanation for the observed bi-modal distribution of OTX2 binding. This contrasts to the enrichment of E-box sequences at TSSs. Both OTX2 and MYC binding independently correlated with higher gene expression. Interestingly, genes of promoter regions with multiple OTX2 binding as well as MYC binding showed the highest expression levels in D425 cells and in primary medulloblastomas. Genes within this class of promoter regions were enriched for medulloblastoma and stem cell specific genes. Our data suggest an important functional interaction between OTX2 and MYC in regulating gene expression in medulloblastoma
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