Design of structured H∞ flight controllers: Passive fault-tolerant versus observer-based structures.

This article presents the structured H∞ design and validation of two types of flight controller architectures: a passive fault-tolerant controller for the longitudinal motion and an active observer-based fault-tolerant controller for the lateral-directional motion. In the first, the controller follows the conventional Stability/Control Augmentation System (SCAS) structure, and its gains are obtained in continuous-time with the hinfstruct command by considering a set of elevator Loss-Of-Efficiency (LOE) faults. For the second, the conventional Luenberger observer-based controller structure is used, and the design aims to monitor the health of the aileron and rudder actuators in addition to provide active tolerance against LOE faults. Two different discrete-time designs are obtained for the latter, one focused on control performance optimization (using also the hinfstruct command), and the other on simultaneous control and observer performance optimization (using the systune command and under a slightly relaxed control performance constraint). For the two types of architectures, unmodeled dynamics are represented by uncertain bounded time delays modeled as pure delays or first-order Padé approximations. The resulting controllers are implemented on-board JAXA's research airplane MuPAL-α, and not only is their practicality demonstrated but also control performance is validated via Aircraft-In-the-Loop (AIL) testing under gust-free and realistic gusty conditions. This demonstration is at a Technological Readiness Level (TRL) of 7-8, resulting in a high-level of confidence in the validity of the proposed flight control structures.

Serotonin Improves High Fat Diet Induced Obesity in Mice.

There are two independent serotonin (5-HT) systems of organization: one in the central nervous system and the other in the periphery. 5-HT affects feeding behavior and obesity in the central nervous system. On the other hand, peripheral 5-HT also may play an important role in obesity, as it has been reported that 5-HT regulates glucose and lipid metabolism. Here we show that the intraperitoneal injection of 5-HT to mice inhibits weight gain, hyperglycemia and insulin resistance and completely prevented the enlargement of intra-abdominal adipocytes without having any effect on food intake when on a high fat diet, but not on a chow diet. 5-HT increased energy expenditure, O2 consumption and CO2 production. This novel metabolic effect of peripheral 5-HT is critically related to a shift in the profile of muscle fiber type from fast/glycolytic to slow/oxidative in soleus muscle. Additionally, 5-HT dramatically induced an increase in the mRNA expression of peroxisome proliferator-activated receptor coactivator 1α (PGC-1α)-b and PGC-1α-c in soleus muscle. The elevation of these gene mRNA expressions by 5-HT injection was inhibited by treatment with 5-HT receptor (5HTR) 2A or 7 antagonists. Our results demonstrate that peripheral 5-HT may play an important role in the relief of obesity and other metabolic disorders by accelerating energy consumption in skeletal muscle.

Peripheral serotonin enhances lipid metabolism by accelerating bile acid turnover.

Serotonin is synthesized by two distinct tryptophan hydroxylases, one in the brain and one in the periphery. The latter is known to be unable to cross the blood-brain barrier. These two serotonin systems have apparently independent functions, although the functions of peripheral serotonin have yet to be fully elucidated. In this study, we have investigated the physiological effect of peripheral serotonin on the concentrations of metabolites in the circulation and in the liver. After fasting, mice were ip injected with 1 mg serotonin. The plasma glucose concentration was significantly elevated between 60 and 270 min after the injection. In contrast, plasma triglyceride, cholesterol, and nonesterified fatty acid concentrations were decreased. The hepatic glycogen synthesis and concentrations were significantly higher at 240 min. At the same time, the hepatic triglyceride content was significantly lower than the basal levels noted before the serotonin injection, whereas the hepatic cholesterol content was significantly higher by 60 min after the injection. Furthermore, serotonin stimulated the contraction of the gallbladder and the excretion of bile. After the serotonin injection, there was a significant induction of apical sodium-dependent bile acid transporter expression, resulting in a decrease in the concentration of bile acids in the feces. Additionally, data are presented to show that the functions of serotonin are mediated through diverse serotonin receptor subtypes. These data indicate that peripheral serotonin accelerates the metabolism of lipid by increasing the concentration of bile acids in circulation.