71 research outputs found

    FRW Quantum Cosmology with a Generalized Chaplygin Gas

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    Cosmologies with a Chaplygin gas have recently been explored with the objective of explaining the transition from a dust dominated epoch towards an accelerating expansion stage. We consider the hypothesis that the transition to the accelerated period involves a quantum mechanical process. Three physically admissible cases are possible. In particular, we identify a minisuperspace configuration with two Lorentzian sectors, separated by a classically forbidden region. The Hartle-Hawking and Vilenkin wave functions are computed, together with the transition amplitudes towards the accelerating epoch. Furthermore, it is found that for specific initial conditions, the parameters characterizing the generalized Chaplygin gas become related through an expression involving an integer nn. We also introduce a phenomenological association between some brane-world scenarios and a FRW minisuperspace cosmology with a generalized Chaplygin gas. The aim is to promote a discussion and subsequent research on the quantum creation of brane cosmologies from such a perspective. Results suggest that the brane tension would become related with generalized Chaplygin gas parameters through another expression involving an integer.Comment: 13 pages, 3 figures, RevTeX

    Cerebral Cavernous Malformation severity is impacted by distinct forms of Hyaluronic acid in the vascular microenvironment

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    ABSTRACTCerebral Cavernous Malformations (CCMs) are vascular lesions that predominantly form in blood vessels of the central nervous system (CNS) upon loss of the CCM multimeric protein complex. The endothelial cells (ECs) within CCM lesions are characterised by overactive MEKK3 kinase and KLF2/4 transcription factor signalling, leading to pathological changes such as increased EC spreading and reduced junctional integrity. Concomitant to aberrant EC signalling, non-autonomous signals from the extracellular matrix (ECM) have also been implicated in CCM lesion growth and these factors might explain why CCM lesions mainly develop in the CNS. Here, we adapted a three dimensional (3D) microfluidic system to examine CCM1 deficient human micro-vessels in distinctive ECMs. We validate that EC pathological hallmarks are maintained in this 3D model. We further show that key genes responsible for homeostasis of Hyaluronic Acid (HA), a major ECM component of the CNS, are dysregulated in CCM. Supplementing the ECM in our model with forms of HA that are predicted to be reduced, inhibits CCM cellular phenotypes, independent of KLF2/4. This study thereby provides a proof-of-principle that ECM embedded 3D microfluidic models are ideally suited to identify how changes in ECM structure and signalling impact vascular malformations.</jats:p
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