A Simple Targeting Procedure for Lunar Trans-Earth Injection

A simple targeting algorithm for trans-Earth injection is developed. The techniques presented in this paper build on techniques developed for the Apollo program and other lunar and interplanetary missions. Presently, more sophisticated algorithms exist for solving this problem, but the simplicity of this particular algorithm makes it well-suited for on-board use during contingency and abort operations. In order to support a return from any lunar orbit with available fuel on the spacecraft the algorithm chooses between one-, two-, or three-burn return scenarios. The one- and two-burn cases are based on existing theory. For the three-burn case however, the existing theory is modified in order to provide a simple solution. Rather than attempting to create fuel-optimal trajectories, the algorithm presented in this paper focuses on computing a trajectory from low lunar orbit to direct atmospheric Earth entry that does not violate a fuel constraint. The algorithm attempts to use a minimal number of impulses to execute trans-earth injection. The algorithm can also be used to quickly generate good initial guesses for other more sophisticated targeting algorithms that can be used to find minimal fuel trajectories or optimize other parameters. This algorithm has three principle phases. First, an estimate of the hyperbolic excess velocity at the Lunar sphere of influence is generated. Second, a maneuver is computed that will transfer the craft from a lunar circular orbit to the hyperbolic escape asymptote. Finally, the effects of perturbations are eliminated by using linear state transition matrix targeting

Activin enhances skin tumourigenesis and malignant progression by inducing a pro-tumourigenic immune cell response

Activin is an important orchestrator of wound repair, but its potential role in skin carcinogenesis has not been addressed. Here we show using different types of genetically modified mice that enhanced levels of activin in the skin promote skin tumour formation and their malignant progression through induction of a pro-tumourigenic microenvironment. This includes accumulation of tumour-promoting Langerhans cells and regulatory T cells in the epidermis. Furthermore, activin inhibits proliferation of tumour-suppressive epidermal γδ T cells, resulting in their progressive loss during tumour promotion. An increase in activin expression was also found in human cutaneous basal and squamous cell carcinomas when compared with control tissue. These findings highlight the parallels between wound healing and cancer, and suggest inhibition of activin action as a promising strategy for the treatment of cancers overexpressing this factor