Probabilistic Modeling of Space Shuttle Debris Impact

On Feb 1, 2003, the Shuttle Columbia was lost during its return to Earth. As a result of the conclusion that debris impact caused the damage to the left wing of the Columbia Space Shuttle Vehicle (SSV) during ascent, the Columbia Accident Investigation Board recommended that an assessment be performed of the debris environment experienced by the SSV during ascent. A flight rationale based on probabilistic assessment is used for the SSV return-to-flight. The assessment entails identifying all potential debris sources, their probable geometric and aerodynamic characteristics, and their potential for impacting and damaging critical Shuttle components. A probabilistic analysis tool, based on the SwRI-developed NESSUS probabilistic analysis software, predicts the probability of impact and damage to the space shuttle wing leading edge and thermal protection system components. Among other parameters, the likelihood of unacceptable damage depends on the time of release (Mach number of the orbiter) and the divot mass as well as the impact velocity and impact angle. A typical result is visualized in the figures below. Probability of impact and damage, as well as the sensitivities thereof with respect to the distribution assumptions, can be computed and visualized at each point on the orbiter or summarized per wing panel or tile zone

Phosphorylation of TXNIP by AKT Mediates Acute Influx of Glucose in Response to Insulin

Growth factors, such as insulin, can induce both acute and long-term glucose uptake into cells. Apart from the rapid, insulin-induced fusion of glucose transporter (GLUT)4 storage vesicles with the cell surface that occurs in muscle and adipose tissues, the mechanism behind acute induction has been unclear in other systems. Thioredoxin interacting protein (TXNIP) has been shown to be a negative regulator of cellular glucose uptake. TXNIP is transcriptionally induced by glucose and reduces glucose influx by promoting GLUT1 endocytosis. Here, we report that TXNIP is a direct substrate of protein kinase B (AKT) and is responsible for mediating AKT-dependent acute glucose influx after growth factor stimulation. Furthermore, TXNIP functions as an adaptor for the basal endocytosis of GLUT4 in vivo, its absence allows excess glucose uptake in muscle and adipose tissues, causing hypoglycemia during fasting. Altogether, TXNIP serves as a key node of signal regulation and response for modulating glucose influx through GLUT1 and GLUT4