1,708 research outputs found

    Hamilton Jacobi Bellman equations in infinite dimensions with quadratic and superquadratic Hamiltonian

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    We consider Hamilton Jacobi Bellman equations in an inifinite dimensional Hilbert space, with quadratic (respectively superquadratic) hamiltonian and with continuous (respectively lipschitz continuous) final conditions. This allows to study stochastic optimal control problems for suitable controlled Ornstein Uhlenbeck process with unbounded control processes

    Caveolin-1 expression and cavin stability regulate caveolae dynamics in adipocyte lipid store fluctuation

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    Adipocytes specialized in the storage of energy as fat are among the most caveolae-enriched cell types. Loss of caveolae produces lipodystrophic diabetes in humans, which cannot be reversed by endothelial rescue of caveolin expression in mice, indicating major importance of adipocyte caveolae. However, how caveolae participate in fat cell functions is poorly understood. We investigated dynamic conditions of lipid store fluctuations and demonstrate reciprocal regulation of caveolae density and fat cell lipid droplet storage. We identified caveolin-1 expression as a crucial step in adipose cell lines and in mice to raise the density of caveolae, to increase adipocyte ability to accommodate larger lipid droplets, and to promote cell expansion by increased glucose utilization. In human subjects enrolled in a trial of 8 weeks of overfeeding to promote fattening, adipocyte expansion response correlated with initial caveolin-1 expression. Conversely, lipid mobilization in cultured adipocytes to induce lipid droplet shrinkage led to biphasic response of cavin-1 with ultimate loss of expression of cavin-1 and -3 and EHD2 by protein degradation, coincident with caveolae disassembly. We have identified the key steps in cavin/caveolin interplay regulating adipocyte caveolae dynamics. Our data establish that caveolae participate in a unique cell response connected to lipid store fluctuation, suggesting lipid-induced mechanotension in adipocytes

    The lipoatrophic caveolin-1 deficient mouse model reveals autophagy in mature adipocytes

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    Adipose tissue lipoatrophy caused by caveolin gene deletion in mice is not linked to defective adipocyte differentiation. We show that adipose tissue development cannot be rescued by endothelial specific caveolin-1 re-expression, indicating primordial role of caveolin in mature adipocytes. Partial or total caveolin deficiency in adipocytes induced broad protein expression defects, including but not limited to previously described downregulation of insulin receptor. Global alterations in protein turnover, and accelerated degradation of long-lived proteins were found in caveolin-deficient adipocytes. Lipidation of endogenous LC3 autophagy marker and distribution of GFP-LC3 into aggregates demonstrated activated autophagy in the absence of caveolin-1 in adipocytes. Furthermore, electron microscopy revealed autophagic vacuoles in caveolin-1 deficient but not control adipocytes. Surprisingly, significant levels of lipidated LC3-II were found around lipid droplets of normal adipocytes, maintained in nutrient-rich conditions or isolated from fed mice, which do not display autophagy. Altogether, these data indicate that caveolin deficiency induce autophagy in adipocytes, a feature that is not a physiological response to fasting in normal fat cells. This likely resulted from defective insulin and lipolytic responses that converge in chronic nutrient shortage in adipocytes lacking caveolin-1. This is the first report of a pathological situation with autophagy as an adaptative response to adipocyte failure

    Caveolin-1 but not cavin overexpression produces “supersized” adipocytes with larger lipid droplets in adipocytes

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    Caveolin-1 cooperates with the recently described cavin protein family to form membrane caveolae structures, which are particularly abundant in adipocytes. Caveolin-1 is also present in adipocytes as a lipid droplet associated pool, whose function remains uncertain. Caveolin-1 deficiency leads to lipoatrophy in mice models and human subjects, suggesting a critical role in the storage of lipids. We report here on retroviral overexpression caveolin-1-RFP, cavin-1-GFP or cavin-3-GFP in 3T3-L1 adipocytes. All three cell lines differentiated normally, contained a higher number of caveolae, and displayed ameliorated maximal insulin response, which is known to occur in caveolae. Only caveolin-1 overexpressing adipocytes, but not cavin-1 or -3, accumulated significantly larger lipid droplets than control lines containing empty retroviral vectors. Also, when injected into nude mice, all cell lines induced the formation of newly generated fat pads, but those produced from caveolin-1-RFP preadipocytes contained larger adipocytes, indicating a specific impact of caveolin-1 but not other cavins on lipid storage in vivo. Together our data demonstrate a specific role of lipid droplet caveolin pool, independent of caveolae, to modulate lipid droplet expansibility

    Dense active matter model of motion patterns in confluent cell monolayers

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    Epithelial cell monolayers show remarkable displacement and velocity correlations over distances of ten or more cell sizes that are reminiscent of supercooled liquids and active nematics. We show that many observed features can be described within the framework of dense active matter, and argue that persistent uncoordinated cell motility coupled to the collective elastic modes of the cell sheet is sufficient to produce swirl-like correlations. We obtain this result using both continuum active linear elasticity and a normal modes formalism, and validate analytical predictions with numerical simulations of two agent-based cell models, soft elastic particles and the self-propelled Voronoi model together with in-vitro experiments of confluent corneal epithelial cell sheets. Simulations and normal mode analysis perfectly match when tissue-level reorganisation occurs on times longer than the persistence time of cell motility. Our analytical model quantitatively matches measured velocity correlation functions over more than a decade with a single fitting parameter.Comment: updated version accepted for publication in Nat. Com

    Search for the W-exchange decays B0 --> Ds(*)- Ds(*)+

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    We report a search for the decays B0DsDs+B^{0} \to D_{s}^{-} D_{s}^{+}, B0DsDs+B^{0} \to D_{s}^{*-} D_{s}^{+}, B0DsDs+B^{0} \to D_{s}^{*-} D_{s}^{*+} in a sample of 232 million Υ(4S)\Upsilon(4S) decays to \BBb ~pairs collected with the \babar detector at the PEP-II asymmetric-energy e+ee^+ e^- storage ring. We find no significant signal and set upper bounds for the branching fractions: B(B0DsDs+)<1.0×104,B(B0DsDs+)<1.3×104{\cal B}(B^{0} \to D_{s}^{-} D_{s}^{+}) < 1.0 \times 10^{-4}, {\cal B}(B^{0} \to D_{s}^{*-} D_{s}^{+}) < 1.3 \times 10^{-4} and B(B0DsDs+)<2.4×104{\cal B}(B^{0} \to D_{s}^{*-} D_{s}^{*+}) < 2.4 \times 10^{-4} at 90% confidence level.Comment: 8 pages, 2 figures, submitted to PRD-R

    Evidence for the η_b(1S) Meson in Radiative Υ(2S) Decay

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    We have performed a search for the η_b(1S) meson in the radiative decay of the Υ(2S) resonance using a sample of 91.6 × 10^6 Υ(2S) events recorded with the BABAR detector at the PEP-II B factory at the SLAC National Accelerator Laboratory. We observe a peak in the photon energy spectrum at E_γ = 609.3^(+4.6)_(-4.5)(stat)±1.9(syst) MeV, corresponding to an η_b(1S) mass of 9394.2^(+4.8)_(-4.9)(stat) ± 2.0(syst) MeV/c^2. The branching fraction for the decay Υ(2S) → γη_b(1S) is determined to be [3.9 ± 1.1(stat)^(+1.1)_(-0.9)(syst)] × 10^(-4). We find the ratio of branching fractions B[Υ(2S) → γη_b(1S)]/B[Υ(3S) → γη_b(1S)]= 0.82 ± 0.24(stat)^(+0.20)_(-0.19)(syst)

    Measurement of Branching Fractions and Rate Asymmetries in the Rare Decays B -> K(*) l+ l-

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    In a sample of 471 million BB events collected with the BABAR detector at the PEP-II e+e- collider we study the rare decays B -> K(*) l+ l-, where l+ l- is either e+e- or mu+mu-. We report results on partial branching fractions and isospin asymmetries in seven bins of di-lepton mass-squared. We further present CP and lepton-flavor asymmetries for di-lepton masses below and above the J/psi resonance. We find no evidence for CP or lepton-flavor violation. The partial branching fractions and isospin asymmetries are consistent with the Standard Model predictions and with results from other experiments.Comment: 16 pages, 14 figures, accepted by Phys. Rev.
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