1,717 research outputs found

    Self-Screening Hawking Atmosphere in the Presence of a Bulk Viscosity

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    The recent theory of 't Hooft [ Nucl. Phys. Suppl. {\bf 68}, 174 (1998)] models the black hole as a system endowed with an envelope of matter that obeys an equation of state in the form p=(γ1)ρ p=(\gamma -1)\rho, and acts as a source in Einstein's equations. The present paper generalizes the 't Hooft theory so as to take into account a bulk viscosity ζ\zeta in the fluid. It is shown that even a slight positive value of ζ\zeta will suffice to yield complete agreement with the Hawking formula for the entropy of the black hole, if the value of the constant γ\gamma takes a value that is slightly less than 4/3. The value γ=4/3\gamma=4/3 corresponds to a radiation fluid.Comment: 12 pages, LaTeX, no figures, minor extensions of the discussion. To appear in PR

    Exact solution of scalar field cosmology with exponential potentials and transient acceleration

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    We show that the general solution of scalar field cosmology in dd dimensions with exponential potentials for flat Robertson-Walker metric can be found in a straightforward way by introducing new variables which completely decouple the system. The explicit solution shows the region of parameters where the expansion has eternal acceleration, transient periods of acceleration, or no period of acceleration at all. In the cases of transient acceleration, the energy density exhibits a plateau during the accelerated expansion, where pρp\cong -\rho, due to dominance of potential energy. We determine the interval of accelerated expansion in terms of a simple formula. In particular, it shows that the period of accelerated expansion decreases in higher dimensions.Comment: 6 pages, latex, 1 figure, references adde

    Quercetin as an Emerging Anti-Melanoma Agent: A Four-Focus Area Therapeutic Development Strategy

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    Replacing current refractory treatments for melanoma with new prevention and therapeutic approaches is crucial in order to successfully treat this aggressive cancer form. Melanoma develops from neural crest cells, which express tyrosinase -- a key enzyme in the pigmentation pathway. The tyrosinase enzyme is highly active in melanoma cells and metabolizes polyphenolic compounds; tyrosinase expression thus makes a feasible a target for polyphenol-based therapies. For example, quercetin (3,3′,4′,5,7-pentahydroxyflavone) is a highly ubiquitous and well-classified dietary polyphenol found in various fruits, vegetables and other plant products including onions, broccoli, kale, oranges, blueberries, apples, and tea. Quercetin has demonstrated anti-proliferative and pro-apoptotic activity in various cancer cell types. Quercetin is readily metabolized by tyrosinase into various compounds that promote anti-cancer activity; additionally, given that tyrosinase expression increases during tumorigenesis, and its activity is associated with pigmentation changes in both early- and late-stage melanocytic lesions, it suggests that quercetin can be used to target melanoma. In this review we explore the potential of Quercetin as an anti-melanoma agent utilizing and extrapolating on evidence from previous in vitro studies in various human malignant cell lines and propose a four-focus area strategy to develop quercetin as a targeted anti-melanoma compound for use as either a preventative or therapeutic agent. The four areas of focus include utilizing quercetin to i) modulate cellular bioreduction potential and associated signaling cascades, ii) affect transcription of relevant genes, iii) regulate epigenetic processes, and iv) develop effective combination therapies and delivery modalities/protocols. In general, quercetin could be used to exploit tyrosinase activity to prevent, and/or treat, melanoma with minimal additional side effects

    Grd19/Snx3p functions as a cargo-specific adapter for retromer-dependent endocytic recycling

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    Amajor function of the endocytic system is the sorting of cargo to various organelles. Endocytic sorting of the yeast reductive iron transporter, which is composed of the Fet3 and Ftr1 proteins, is regulated by available iron. When iron is provided to iron-starved cells, Fet3p–Ftr1p is targeted to the lysosome-like vacuole and degraded. In contrast, when iron is not available, Fet3p–Ftr1p is maintained on the plasma membrane via an endocytic recycling pathway requiring the sorting nexin Grd19/Snx3p, the pentameric retromer complex, and the Ypt6p Golgi Rab GTPase module. A recycling signal in Ftr1p was identified and found to bind directly to Grd19/Snx3p. Retromer and Grd19/Snx3p partially colocalize to tubular endosomes, where they are physically associated. After export from the endosome, Fet3p–Ftr1p transits through the Golgi apparatus for resecretion. Thus, Grd19/Snx3p, functions as a cargo-specific adapter for the retromer complex, establishing a precedent for a mechanism by which sorting nexins expand the repertoire of retromer-dependent cargos

    The GAP activity of Msb3p and Msb4p for the Rab GTPase Sec4p is required for efficient exocytosis and actin organization

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    Polarized growth in Saccharomyces cerevisiae is thought to occur by the transport of post-Golgi vesicles along actin cables to the daughter cell, and the subsequent fusion of the vesicles with the plasma membrane. Previously, we have shown that Msb3p and Msb4p genetically interact with Cdc42p and display a GTPase-activating protein (GAP) activity toward a number of Rab GTPases in vitro. We show here that Msb3p and Msb4p regulate exocytosis by functioning as GAPs for Sec4p in vivo. Cells lacking the GAP activity of Msb3p and Msb4p displayed secretory defects, including the accumulation of vesicles of 80–100 nm in diameter. Interestingly, the GAP activity of Msb3p and Msb4p was also required for efficient polarization of the actin patches and for the suppression of the actin-organization defects in cdc42 mutants. Using a strain defective in polarized secretion and actin-patch organization, we showed that a change in actin-patch organization could be a consequence of the fusion of mistargeted vesicles with the plasma membrane
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