Optimal Propellant Maneuver Flight Demonstrations on ISS

In this paper, first ever flight demonstrations of Optimal Propellant Maneuver (OPM), a method of propulsive rotational state transition for spacecraft controlled using thrusters, is presented for the International Space Station (ISS). On August 1, 2012, two ISS reorientations of about 180deg each were performed using OPMs. These maneuvers were in preparation for the same-day launch and rendezvous of a Progress vehicle, also a first for ISS visiting vehicles. The first maneuver used 9.7 kg of propellant, whereas the second used 10.2 kg. Identical maneuvers performed without using OPMs would have used approximately 151.1kg and 150.9kg respectively. The OPM method is to use a pre-planned attitude command trajectory to accomplish a rotational state transition. The trajectory is designed to take advantage of the complete nonlinear system dynamics. The trajectory choice directly influences the cost of the maneuver, in this case, propellant. For example, while an eigenaxis maneuver is kinematically the shortest path between two orientations, following that path requires overcoming the nonlinear system dynamics, thereby increasing the cost of the maneuver. The eigenaxis path is used for ISS maneuvers using thrusters. By considering a longer angular path, the path dependence of the system dynamics can be exploited to reduce the cost. The benefits of OPM for the ISS include not only reduced lifetime propellant use, but also reduced loads, erosion, and contamination from thrusters due to fewer firings. Another advantage of the OPM is that it does not require ISS flight software modifications since it is a set of commands tailored to the specific attitude control architecture. The OPM takes advantage of the existing ISS control system architecture for propulsive rotation called USTO control mode1. USTO was originally developed to provide ISS Orbiter stack attitude control capability for a contingency tile-repair scenario, where the Orbiter is maneuvered using its robotic manipulator relative to the ISS. Since 2005 USTO has been used for nominal ISS operations

Phosphomimetic Modulation of eNOS Improves Myocardial Reperfusion and Mimics Cardiac Postconditioning in Mice

Objective: Myocardial infarction resulting from ischemia-reperfusion injury can be reduced by cardiac postconditioning, in which blood flow is restored intermittently prior to full reperfusion. Although key molecular mechanisms and prosurvival pathways involved in postconditioning have been identified, a direct role for eNOS-derived NO in improving regional myocardial perfusion has not been shown. The objective of this study is to measure, with high temporal and spatial resolution, regional myocardial perfusion during ischemia-reperfusion and postconditioning, in order to determine the contribution of regional blood flow effects of NO to infarct size and protection. Methods and Results: We used myocardial contrast echocardiography to measure regional myocardial blood flow in mice over time. Reperfusion after myocardial ischemia-reperfusion injury is improved by postconditioning, as well as by phosphomimetic eNOS modulation. Knock-in mice expressing a phosphomimetic S1176D form of eNOS showed improved myocardial reperfusion and significantly reduced infarct size. eNOS knock-out mice failed to show cardioprotection from postconditioning. The size of the no-reflow zone following ischemia-reperfusion is substantially reduced by postconditioning and by the phosphomimetic eNOS mutation. Conclusions and Significance: Using myocardial contrast echocardiography, we show that temporal dynamics of regional myocardial perfusion restoration contribute to reduced infarct size after postconditioning. eNOS has direct effects on myocardial blood flow following ischemia-reperfusion, with reduction in the size of the no-reflow zone. These results have important implications for ongoing clinical trials on cardioprotection, because the degree of protective benefit may be significantly influenced by the regional hemodynamic effects of eNOS-derived NO.American Heart Association (Predoctoral Fellowship)National Institutes of Health (U.S.) (R01 NS33335)National Institutes of Health (U.S.) (R01 HL57818