Optical tracking of deep-space spacecraft in Halo L2 orbits and beyond: the Gaia mission as a pilot case

We tackle the problem of accurate optical tracking of distant man-made probes, on Halo orbit around the Earth-Sun libration point L2 and beyond, along interplanetary transfers. The improved performance of on-target tracking, especially when observing with small-class telescopes is assessed providing a general estimate of the expected S/N ratio in spacecraft detection. The on-going Gaia mission is taken as a pilot case for our analysis, reporting on fresh literature and original optical photometry and astrometric results. The probe has been located, along its projected nominal path, within 0.13 +/- 0.09 arcsec, or 0.9 +/- 0.6 km. Spacecraft color appears to be red, with (V-R_c) = 1.1 +/- 0.2 and a bolometric correction to the R_c band of (Bol-R_c) = -1.1 +/- 0.2. The apparent magnitude, R_c = 20.8 +/- 0.2, is much fainter than originally expected. These features lead to suggest a lower limit for the Bond albedo a = 0.11 +/- 0.05 and confirm that incident Sun light is strongly reddened by Gaia through its on-board MLI blankets covering the solar shield. Relying on the Gaia figures, we found that VLT-class telescopes could yet be able to probe distant spacecraft heading Mars, up to 30 million km away, while a broader optical coverage of the forthcoming missions to Venus and Mars could be envisaged, providing to deal with space vehicles of minimum effective area Aeff >= 10^6 cm^2. In addition to L2 surveys, 2m-class telescopes could also effectively flank standard radar-ranging techniques in deep-space probe tracking along Earth's gravity-assist maneuvers for interplanetary missions.Comment: In press for Advances in Space Research (w/ 15 colour figures and 1 table

Natural and sail-displaced doubly-symmetric Lagrange point orbits for polar coverage

This paper proposes the use of doubly-symmetric, eight-shaped orbits in the circular restricted three-body problem for continuous coverage of the high-latitude regions of the Earth. These orbits, for a range of amplitudes, spend a large fraction of their period above either pole of the Earth. It is shown that they complement Sun-synchronous polar and highly eccentric Molniya orbits, and present a possible alternative to low thrust pole-sitter orbits. Both natural and solar-sail displaced orbits are considered. Continuation methods are described and used to generate families of these orbits. Starting from ballistic orbits, other families are created either by increasing the sail lightness number, varying the period or changing the sail attitude. Some representative orbits are then chosen to demonstrate the visibility of high-latitude regions throughout the year. A stability analysis is also performed, revealing that the orbits are unstable: it is found that for particular orbits, a solar sail can reduce their instability. A preliminary design of a linear quadratic regulator is presented as a solution to stabilize the system by using the solar sail only. Finally, invariant manifolds are exploited to identify orbits that present the opportunity of a ballistic transfer directly from low Earth orbit

The 1:1 resonance in Extrasolar Systems: Migration from planetary to satellite orbits

We present families of symmetric and asymmetric periodic orbits at the 1/1 resonance, for a planetary system consisting of a star and two small bodies, in comparison to the star, moving in the same plane under their mutual gravitational attraction. The stable 1/1 resonant periodic orbits belong to a family which has a planetary branch, with the two planets moving in nearly Keplerian orbits with non zero eccentricities and a satellite branch, where the gravitational interaction between the two planets dominates the attraction from the star and the two planets form a close binary which revolves around the star. The stability regions around periodic orbits along the family are studied. Next, we study the dynamical evolution in time of a planetary system with two planets which is initially trapped in a stable 1/1 resonant periodic motion, when a drag force is included in the system. We prove that if we start with a 1/1 resonant planetary system with large eccentricities, the system migrates, due to the drag force, {\it along the family of periodic orbits} and is finally trapped in a satellite orbit. This, in principle, provides a mechanism for the generation of a satellite system: we start with a planetary system and the final stage is a system where the two small bodies form a close binary whose center of mass revolves around the star.Comment: to appear in Cel.Mech.Dyn.Ast

Easily retrievable objects among the NEO population

Asteroids and comets are of strategic importance for science in an effort to understand the formation, evolution and composition of the Solar System. Near-Earth Objects (NEOs) are of particular interest because of their accessibility from Earth, but also because of their speculated wealth of material resources. The exploitation of these resources has long been discussed as a means to lower the cost of future space endeavours. In this paper, we consider the currently known NEO population and define a family of so-called Easily Retrievable Objects (EROs), objects that can be transported from accessible heliocentric orbits into the Earth’s neighbourhood at affordable costs. The asteroid retrieval transfers are sought from the continuum of low energy transfers enabled by the dynamics of invariant manifolds; specifically, the retrieval transfers target planar, vertical Lyapunov and halo orbit families associated with the collinear equilibrium points of the Sun-Earth Circular Restricted Three Body problem. The judicious use of these dynamical features provides the best opportunity to find extremely low energy Earth transfers for asteroid material. A catalogue of asteroid retrieval candidates is then presented. Despite the highly incomplete census of very small asteroids, the ERO catalogue can already be populated with 12 different objects retrievable with less than 500 m/s of Δv. Moreover, the approach proposed represents a robust search and ranking methodology for future retrieval candidates that can be automatically applied to the growing survey of NEOs

Localization of Putative Stem Cells in Dental Epithelium and Their Association with Notch and Fgf Signaling

The continuously growing mouse incisor is an excellent model to analyze the mechanisms for stem cell lineage. We designed an organ culture method for the apical end of the incisor and analyzed the epithelial cell lineage by 5-bromo-2′-deoxyuridine and DiI labeling. Our results indicate that stem cells reside in the cervical loop epithelium consisting of a central core of stellate reticulum cells surrounded by a layer of basal epithelial cells, and that they give rise to transit-amplifying progeny differentiating into enamel forming ameloblasts. We identified slowly dividing cells among the Notch1-expressing stellate reticulum cells in specific locations near the basal epithelial cells expressing lunatic fringe, a secretory molecule modulating Notch signaling. It is known from tissue recombination studies that in the mouse incisor the mesenchyme regulates the continuous growth of epithelium. Expression of Fgf-3 and Fgf-10 were restricted to the mesenchyme underlying the basal epithelial cells and the transit-amplifying cells expressing their receptors Fgfr1b and Fgfr2b. When FGF-10 protein was applied with beads on the cultured cervical loop epithelium it stimulated cell proliferation as well as expression of lunatic fringe. We present a model in which FGF signaling from the mesenchyme regulates the Notch pathway in dental epithelial stem cells via stimulation of lunatic fringe expression and, thereby, has a central role in coupling the mitogenesis and fate decision of stem cells

Role of Notch signaling in cell-fate determination of human mammary stem/progenitor cells

INTRODUCTION: Notch signaling has been implicated in the regulation of cell-fate decisions such as self-renewal of adult stem cells and differentiation of progenitor cells along a particular lineage. Moreover, depending on the cellular and developmental context, the Notch pathway acts as a regulator of cell survival and cell proliferation. Abnormal expression of Notch receptors has been found in different types of epithelial metaplastic lesions and neoplastic lesions, suggesting that Notch may act as a proto-oncogene. The vertebrate Notch1 and Notch4 homologs are involved in normal development of the mammary gland, and mutated forms of these genes are associated with development of mouse mammary tumors. METHODS: In order to determine the role of Notch signaling in mammary cell-fate determination, we have utilized a newly described in vitro system in which mammary stem/progenitor cells can be cultured in suspension as nonadherent 'mammospheres'. Notch signaling was activated using exogenous ligands, or was inhibited using previously characterized Notch signaling antagonists. RESULTS: Utilizing this system, we demonstrate that Notch signaling can act on mammary stem cells to promote self-renewal and on early progenitor cells to promote their proliferation, as demonstrated by a 10-fold increase in secondary mammosphere formation upon addition of a Notch-activating DSL peptide. In addition to acting on stem cells, Notch signaling is also able to act on multipotent progenitor cells, facilitating myoepithelial lineage-specific commitment and proliferation. Stimulation of this pathway also promotes branching morphogenesis in three-dimensional Matrigel cultures. These effects are completely inhibited by a Notch4 blocking antibody or a gamma secretase inhibitor that blocks Notch processing. In contrast to the effects of Notch signaling on mammary stem/progenitor cells, modulation of this pathway has no discernable effect on fully committed, differentiated, mammary epithelial cells. CONCLUSION: These studies suggest that Notch signaling plays a critical role in normal human mammary development by acting on both stem cells and progenitor cells, affecting self-renewal and lineage-specific differentiation. Based on these findings we propose that abnormal Notch signaling may contribute to mammary carcinogenesis by deregulating the self-renewal of normal mammary stem cells