MARCO POLO: near earth object sample return mission

MARCO POLO is a joint European--Japanese sample return mission to a Near-Earth Object. This Euro-Asian mission will go to a primitive Near-Earth Object (NEO), which we anticipate will contain primitive materials without any known meteorite analogue, scientifically characterize it at multiple scales, and bring samples back to Earth for detailed scientific investigation. Small bodies, as primitive leftover building blocks of the Solar System formation process, offer important clues to the chemical mixture from which the planets formed some 4.6 billion years ago. Current exobiological scenarios for the origin of Life invoke an exogenous delivery of organic matter to the early Earth: it has been proposed that primitive bodies could have brought these complex organic molecules capable of triggering the pre-biotic synthesis of biochemical compounds. Moreover, collisions of NEOs with the Earth pose a finite hazard to life. For all these reasons, the exploration of such objects is particularly interesting and urgent. The scientific objectives of MARCO POLO will therefore contribute to a better understanding of the origin and evolution of the Solar System, the Earth, and possibly Life itself. Moreover, MARCO POLO provides important information on the volatile-rich (e.g. water) nature of primitive NEOs, which may be particularly important for future space resource utilization as well as providing critical information for the security of Earth. MARCO POLO is a proposal offering several options, leading to great flexibility in the actual implementation. The baseline mission scenario is based on a launch with a Soyuz-type launcher and consists of a Mother Spacecraft (MSC) carrying a possible Lander named SIFNOS, small hoppers, sampling devices, a re-entry capsule and scientific payloads. The MSC leaves Earth orbit, cruises toward the target with ion engines, rendezvous with the target, conducts a global characterization of the target to select a sampling site, and delivers small hoppers (MINERVA type, JAXA) and SIFNOS. The latter, if added, will perform a soft landing, anchor to the target surface, and make various in situ measurements of surface/subsurface materials near the sampling site. Two surface samples will be collected by the MSC using ``touch and go'' manoeuvres. Two complementary sample collection devices will be used in this phase: one developed by ESA and another provided by JAXA, mounted on a retractable extension arm. After the completion of the sampling and ascent of the MSC, the arm will be retracted to transfer the sample containers into the MSC. The MSC will then make its journey back to Earth and release the re-entry capsule into the Earth's atmosphere

Stroma-mediated dysregulation of myelopoiesis in mice lacking IkappaBalpha

Hematopoiesis occurs in the liver and the bone marrow (BM) during murine development. Newborn mice with a ubiquitous deletion of IκBα develop a severe hematological disorder characterized by an increase of granulocyte/erythroid/monocyte/macrophage colony-forming units (CFU-GEMM) and hypergranulopoiesis. Here, we report that this particular myeloproliferative disturbance is mediated by continuously deregulated perinatal expression of Jagged1 in IκBα-deficient hepatocytes. The result is a permanent activation of Notch1 in neutrophils. In contrast, in mice with a conditional deletion of IκBα only in the myeloid lineage (ikbaflox/flox × LysM-Cre) and in fetal liver cell chimeras (ikbaFLΔ/FLΔ), a cell-autonomous induction of the myeloproliferative disease was not observed. Coculture of IκBα-deficient hepatocytes with wild-type (wt) BM cells induced a Jagged1-dependent increase in CFUs. In summary, we show that cell-fate decisions leading to a premalignant hematopoietic disorder can be initiated by nonhematopoietic cells with inactive IκBα

Crosstalk between keratinocytes and adaptive immune cells in an IkappaBalpha protein-mediated inflammatory disease of the skin.

Inflammatory diseases at epithelial borders develop from aberrant interactions between resident cells of the tissue and invading immunocytes. Here, we unraveled basic functions of epithelial cells and immune cells and the sequence of their interactions in an inflammatory skin disease. Ubiquitous deficiency of the I?B? protein (Ikba?/?) as well as concomitant deletion of Ikba specifically in keratinocytes and T cells (IkbaK5?/K5? lck?/lck?) resulted in an inflammatory skin phenotype that involved the epithelial compartment and depended on the presence of lymphocytes as well as tumor necrosis factor and lymphotoxin signaling. In contrast, mice with selective ablation of Ikba in keratinocytes or lymphocytes showed inflammation limited to the dermal compartment or a normal skin phenotype, respectively. Targeted deletion of RelA from epidermal keratinocytes completely rescued the inflammatory skin phenotype of Ikba?/? mice. This finding emphasizes the important role of aberrant NF-?B activation in both keratinocytes and lymphocytes in the development of the observed inflammatory skin changes