991 research outputs found

    Strangeness Enhancement in p+Ap+A and S+AS+A Interactions at SPS Energies

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    The systematics of strangeness enhancement is calculated using the HIJING and VENUS models and compared to recent data on pp\,pp\,, pA\,pA\, and AA\,AA\, collisions at CERN/SPS energies (200AGeV200A\,\, GeV\,). The HIJING model is used to perform a {\em linear} extrapolation from pppp to AAAA. VENUS is used to estimate the effects of final state cascading and possible non-conventional production mechanisms. This comparison shows that the large enhancement of strangeness observed in S+AuS+Au collisions, interpreted previously as possible evidence for quark-gluon plasma formation, has its origins in non-equilibrium dynamics of few nucleon systems. % Strangeness enhancement %is therefore traced back to the change in the production dynamics %from pppp to minimum bias pSpS and central SSSS collisions. A factor of two enhancement of Λ0\Lambda^{0} at mid-rapidity is indicated by recent pSpS data, where on the average {\em one} projectile nucleon interacts with only {\em two} target nucleons. There appears to be another factor of two enhancement in the light ion reaction SSSS relative to pSpS, when on the average only two projectile nucleons interact with two target ones.Comment: 29 pages, 8 figures in uuencoded postscript fil

    HDAC8 and STAT3 Repress BMF Gene Activity in Colon Cancer Cells

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    Histone deacetylase (HDAC) inhibitors are undergoing clinical trials as anticancer agents, but some exhibit resistance mechanisms linked to anti-apoptotic Bcl-2 functions, such as BH3-only protein silencing. HDAC inhibitors that reactivate BH3-only family members might offer an improved therapeutic approach. We show here that a novel seleno-α-keto acid triggers global histone acetylation in human colon cancer cells and activates apoptosis in a p21-independent manner. Profiling of multiple survival factors identified a critical role for the BH3-only member Bcl-2-modifying factor (Bmf). On the corresponding BMF gene promoter, loss of HDAC8 was associated with signal transducer and activator of transcription 3 (STAT3)/specificity protein 3 (Sp3) transcription factor exchange and recruitment of p300. Treatment with a p300 inhibitor or transient overexpression of exogenous HDAC8 interfered with BMF induction, whereas RNAi-mediated silencing of STAT3 activated the target gene. This is the first report to identify a direct target gene of HDAC8 repression, namely, BMF. Interestingly, the repressive role of HDAC8 could be uncoupled from HDAC1 to trigger Bmf-mediated apoptosis. These findings have implications for the development of HDAC8-selective inhibitors as therapeutic agents, beyond the reported involvement of HDAC8 in childhood malignancy

    Generative models of the human connectome

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    The human connectome represents a network map of the brain's wiring diagram and the pattern into which its connections are organized is thought to play an important role in cognitive function. The generative rules that shape the topology of the human connectome remain incompletely understood. Earlier work in model organisms has suggested that wiring rules based on geometric relationships (distance) can account for many but likely not all topological features. Here we systematically explore a family of generative models of the human connectome that yield synthetic networks designed according to different wiring rules combining geometric and a broad range of topological factors. We find that a combination of geometric constraints with a homophilic attachment mechanism can create synthetic networks that closely match many topological characteristics of individual human connectomes, including features that were not included in the optimization of the generative model itself. We use these models to investigate a lifespan dataset and show that, with age, the model parameters undergo progressive changes, suggesting a rebalancing of the generative factors underlying the connectome across the lifespan.Comment: 38 pages, 5 figures + 19 supplemental figures, 1 tabl

    Interplay between residual protease activity in commercial lactases and the subsequent digestibility of β-casein in a model system

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    One of the conventional ways to produce lactose-hydrolyzed (LH) milk is via the addition of commercial lactases into heat-treated milk in which lactose is hydrolyzed throughout storage. This post-hydrolysis method can induce proteolysis in milk proteins due to protease impurities remaining in commercial lactase preparations. In this work, the interplay between lactose hydrolysis, proteolysis, and glycation was studied in a model system of purified β-casein (β-CN), lactose, and lactases using peptidomic methods. With a lactase presence, the proteolysis of β-CN was found to be increased during storage. The protease side-activities mainly acted on the hydrophobic C-terminus of β-CN at Ala, Pro, Ile, Phe, Leu, Lys, Gln, and Tyr positions, resulting in the formation of peptides, some of which were N-terminal glycated or potentially bitter. The proteolysis in β-CN incubated with a lactase was shown to act as a kind of “pre-digestion”, thus increasing the subsequent in vitro digestibility of β-CN and drastically changing the peptide profiles of the in vitro digests. This model study provides a better understanding of how the residual proteases in commercial lactase preparations affect the quality and nutritional aspects of β-CN itself and could be related to its behavior in LH milk

    Calculating Dilepton Rates from Monte Carlo Simulations of Parton Production

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    To calculate dilepton rates in a Monte Carlo simulation of ultrarelativistic heavy ion collisions, one usually scales the number of similar QCD processes by a ratio of the corresponding differential probabilities. We derive the formula for such a ratio especially for dilepton bremsstrahlung processes. We also discuss the non-triviality of including higher order corrections to direct Drell-Yan process. The resultant mass spectra from our Monte Carlo simulation are consistent with the semi-analytical calculation using dilepton fragmentation functions.Comment: 14 pages in RevTex, 3 figures in uuencoded files, LBL-3466
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