902 research outputs found

    Twin CWG systems Final report

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    Construction, operation, and maintenance of twin control moment gyroscope system for space vehicle motion simulato

    Scaling laws to understand tidal dissipation in fluid planetary regions and stars I - Rotation, stratification and thermal diffusivity

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    Tidal dissipation in planets and stars is one of the key physical mechanisms driving the evolution of star-planet and planet-moon systems. Several signatures of its action are observed in planetary systems thanks to their orbital architecture and the rotational state of their components. Tidal dissipation inside the fluid layers of celestial bodies are intrinsically linked to the dynamics and the physical properties of the latter. This complex dependence must be characterized. We compute the tidal kinetic energy dissipated by viscous friction and thermal diffusion in a rotating local fluid Cartesian section of a star/planet/moon submitted to a periodic tidal forcing. The properties of tidal gravito-inertial waves excited by the perturbation are derived analytically as explicit functions of the tidal frequency and local fluid parameters (i.e. the rotation, the buoyancy frequency characterizing the entropy stratification, viscous and thermal diffusivities) for periodic normal modes. The sensitivity of the resulting possibly highly resonant dissipation frequency-spectra to a control parameter of the system is either important or negligible depending on the position in the regime diagram relevant for planetary and stellar interiors. For corresponding asymptotic behaviors of tidal gravito-inertial waves dissipated by viscous friction and thermal diffusion, scaling laws for the frequencies, number, width, height and contrast with the non-resonant background of resonances are derived to quantify these variations. We characterize the strong impact of the internal physics and dynamics of fluid planetary layers and stars on the dissipation of tidal kinetic energy in their bulk. We point out the key control parameters that really play a role and demonstrate how it is now necessary to develop ab-initio modeling for tidal dissipation in celestial bodies.Comment: 24 pages, 14 figures, accepted for publication in Astronomy & Astrophysic

    Impact of the frequency dependence of tidal Q on the evolution of planetary systems

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    Context. Tidal dissipation in planets and in stars is one of the key physical mechanisms that drive the evolution of planetary systems. Aims. Tidal dissipation properties are intrisically linked to the internal structure and the rheology of studied celestial bodies. The resulting dependence of the dissipation upon the tidal frequency is strongly different in the cases of solids and fluids. Methods. We compute the tidal evolution of a two-body coplanar system, using the tidal quality factor's frequency-dependencies appropriate to rocks and to convective fluids. Results. The ensuing orbital dynamics comes out smooth or strongly erratic, dependent on how the tidal dissipation depends upon frequency. Conclusions. We demonstrate the strong impact of the internal structure and of the rheology of the central body on the orbital evolution of the tidal perturber. A smooth frequency-dependence of the tidal dissipation renders a smooth orbital evolution while a peaked dissipation can furnish erratic orbital behaviour.Comment: Accepted for publication as a letter in Astronomy And Astrophysic

    Scaling laws to understand tidal dissipation in fluid planetary layers and stars

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    Tidal dissipation is known as one of the main drivers of the secular evolution of planetary systems. It directly results from dissipative mechanisms that occur in planets and stars' interiors and strongly depends on the structure and dynamics of the bodies. This work focuses on the mechanism of viscous friction in stars and planetary layers. A local model is used to study tidal dissipation. It provides general scaling laws that give a qualitative overview of the different possible behaviors of fluid tidal waves. Furthermore, it highlights the sensitivity of dissipation to the tidal frequency and the roles played by the internal parameters of the fluid such as rotation, stratification, viscosity and thermal diffusivity that will impact the spins/orbital architecture in planetary systems.Comment: 4 pages, 3 figures, IAU 310 symposium proceedings, Complex planetary system

    Evolution des recouvrements forestiers et de l'Occupation des sols entre 1964 et 2002 dans la haute vallée des Ait Bouguemez (Haut Atlas Central, Maroc). Impact des modes de gestion.

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    Les espaces forestiers montagnards mĂ©diterranĂ©ens sont souvent fortement dĂ©gradĂ©s. La cause principale est la surexploitation des ressources. Au cours de l'histoire, la raretĂ© des ressources a probablement incitĂ© les hommes Ă  mettre en place des formes de contrĂŽle coutumiĂšres (ou « traditionnelles ») des espaces forestiers et pastoraux. Ces rĂ©gimes perdurent dans le Haut Atlas marocain sous le nom d'agdal, terme qui dĂ©signe un territoire sylvopastoral collectif soumis Ă  des mises en dĂ©fens temporaires. Ce travail vise Ă  Ă©valuer l'impact de cette gestion coutumiĂšre sur les dynamiques des formations boisĂ©es dans une zone de montagne, la vallĂ©e des Ait Bouguemez, Ă  travers une analyse diachronique basĂ©e sur la comparaison de documents anciens (photographies aĂ©riennes de 1964) avec des documents rĂ©cents (image satellitaire Spot 5 Ă  trĂšs haute rĂ©solution). La mĂ©thodologie adoptĂ©e repose sur la photointerprĂ©tation visuelle des documents prĂ©citĂ©s en se basant sur une charte commune d'estimation du recouvrement arborĂ©. Deux cartes de recouvrement ont Ă©tĂ© produites pour 1964 et 2002, dont le croisement a permis d'obtenir une carte de la dynamique des peuplements. Les rĂ©sultats obtenus soulignent de fortes disparitĂ©s dans les dynamiques forestiĂšres selon le statut agdal ou non-agdal de la forĂȘt. La surface forestiĂšre a diminuĂ© de 21 % en 38 ans, et le recouvrement arborĂ© moyen sur la zone forestiĂšre chute globalement de 20 % Ă  18 % pendant cette pĂ©riode. On observe un maintien du couvert boisĂ© en zone agdal et sa forte dĂ©gradation hors agdal dans un contexte de forte croissance dĂ©mographique

    Nanodisc-cell fusion: Control of fusion pore nucleation and lifetimes by SNARE protein transmembrane domains

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    The initial, nanometer-sized connection between the plasma membrane and a hormone- or neurotransmitter-filled vesicle-the fusion pore- can flicker open and closed repeatedly before dilating or resealing irreversibly. Pore dynamics determine release and vesicle recycling kinetics, but pore properties are poorly known because biochemically defined single-pore assays are lacking. We isolated single flickering pores connecting v-SNARE-reconstituted nanodiscs to cells ectopically expressing cognate, "flipped" t-SNAREs. Conductance through single, voltage-clamped fusion pores directly reported sub-millisecond pore dynamics. Pore currents fluctuated, transiently returned to baseline multiple times, and disappeared ∌6 s after initial opening, as if the fusion pore fluctuated in size, flickered, and resealed. We found that interactions between v- and t-SNARE transmembrane domains (TMDs) promote, but are not essential for pore nucleation. Surprisingly, TMD modifications designed to disrupt v- and t-SNARE TMD zippering prolonged pore lifetimes dramatically. We propose that the post-fusion geometry of the proteins contribute to pore stability.Fil: Wu, Zhenyong. University of Yale; Estados Unidos. University of Yale. School of Medicine; Estados UnidosFil: Auclair, Sarah M.. University of Yale. School of Medicine; Estados Unidos. University of Yale; Estados UnidosFil: Bello, Oscar Daniel. University of Yale. School of Medicine; Estados Unidos. University of Yale; Estados Unidos. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas. Centro CientĂ­fico TecnolĂłgico Conicet - Mendoza. Instituto de HistologĂ­a y EmbriologĂ­a de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias MĂ©dicas. Instituto de HistologĂ­a y EmbriologĂ­a de Mendoza Dr. Mario H. Burgos; ArgentinaFil: Vennekate, Wensi. University of Yale. School of Medicine; Estados Unidos. University of Yale; Estados UnidosFil: Dudzinski, Natasha R.. University of Yale; Estados Unidos. University of Yale. School of Medicine; Estados UnidosFil: Krishnakumar, Shyam S.. University of Yale. School of Medicine; Estados Unidos. University of Yale; Estados UnidosFil: Karatekin, Erdem. University of Yale; Estados Unidos. University of Yale. School of Medicine; Estados Unidos. Universite Paris Descartes; Francia. Centre National de la Recherche Scientifique; Franci

    Dilation of fusion pores by crowding of SNARE proteins

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    Hormones and neurotransmitters are released through fluctuating exocytotic fusion pores that can flicker open and shut multiple times. Cargo release and vesicle recycling depend on the fate of the pore, which may reseal or dilate irreversibly. Pore nucleation requires zippering between vesicle-associated v-SNAREs and target membrane t-SNAREs, but the mechanisms governing the subsequent pore dilation are not understood. Here, we probed the dilation of single fusion pores using v-SNARE-reconstituted ~23-nm-diameter discoidal nanolipoprotein particles (vNLPs) as fusion partners with cells ectopically expressing cognate, ’flipped’ t-SNAREs. Pore nucleation required a minimum of two v-SNAREs per NLP face, and further increases in v-SNARE copy numbers did not affect nucleation rate. By contrast, the probability of pore dilation increased with increasing v-SNARE copies and was far from saturating at 15 v-SNARE copies per face, the NLP capacity. Our experimental and computational results suggest that SNARE availability may be pivotal in determining whether neurotransmitters or hormones are released through a transient (’kiss and run’) or an irreversibly dilating pore (full fusion).Fil: Wu, Zhenyong. University of Yale; Estados Unidos. University of Yale. School of Medicine; Estados UnidosFil: Bello, Oscar Daniel. University of Yale. School of Medicine; Estados Unidos. University of Yale; Estados Unidos. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas. Centro CientĂ­fico TecnolĂłgico Conicet - Mendoza. Instituto de HistologĂ­a y EmbriologĂ­a de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias MĂ©dicas. Instituto de HistologĂ­a y EmbriologĂ­a de Mendoza Dr. Mario H. Burgos; ArgentinaFil: Thiyagarajan, Sathish. Columbia University; Estados UnidosFil: Auclair, Sarah Marie. University of Yale. School of Medicine; Estados Unidos. University of Yale; Estados UnidosFil: Vennekate, Wensi. University of Yale; Estados Unidos. University of Yale. School of Medicine; Estados UnidosFil: Krishnakumar, Shyam S. University of Yale; Estados Unidos. University of Yale. School of Medicine; Estados UnidosFil: O'Shaughnessy, Ben. Columbia University; Estados UnidosFil: Karatekin, Erdem. University of Yale; Estados Unidos. Universite Paris Descartes; Francia. University of Yale. School of Medicine; Estados Unido

    The Multifunctional Sorting Protein PACS-2 Regulates SIRT1-Mediated Deacetylation of p53 to Modulate p21-Dependent Cell-Cycle Arrest

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    SIRT1 regulates the DNA damage response by deacetylating p53, thereby repressing p53 transcriptional output. Here, we demonstrate that the sortingprotein PACS-2 regulates SIRT1-mediated deacetylation of p53 to modulate the DNA damage response. PACS-2 knockdown cells failed to efficiently undergo p53-induced cell-cycle arrest in response to DNA damage. Accordingly, p53 acetylation was reduced both in PACS-2 knockdown cells and thymocytes from Pacs-2-/- mice, thereby blunting induction of the cyclin-dependent kinase inhibitor p21 (CDKN1A). The SIRT1 inhibitor EX-527 or SIRT1 knockdown restored p53 acetylation and p21 induction as well as p21-dependent cell-cycle arrest in PACS-2 knockdown cells. Traffickingstudies revealed that cytoplasmic PACS-2 shuttled to the nucleus, where it interacted with SIRT1 andrepressed SIRT1-mediated p53 deacetylation. Correspondingly, invitro assays demonstrated that PACS-2 directly inhibited SIRT1-catalyzed p53 deacetylation. Together, these findings identify PACS-2 as an invivo mediator of the SIRT1-p53-p21 axis that modulates the DNA damage response
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