Anti-Humanin polyclonal antibody

Past evaluations of airport surface operations automation technologies have focused on capacity utilization, delay mitigation and fuel efficiency impacts. Predictability, while recognized as an important operational performance goal, has received little attention. One reason could be that applicable predictability metrics have not been developed in the context of airport surface operations management. This research fills the gap by proposing metrics for predictability performance evaluation. Using results from a SARDA humanin-the-loop simulation conducted at NASA Ames' Future Flight Central, we present a comprehensive assessment of the predictability impacts of airport surface automation. A wide range of the impacts is considered, which includes variability in taxi-out time, predictability of take-off time and take-off sequence, entropy of the airfield state, and perceived predictability from users. (C) 2014 Elsevier Ltd. All rights reserved.

Humanin (HN) was originally identified as an endogenous peptide that protects neuronal cells from apoptosis induced by various types of Alzheimers disease-related insults. We have previously indicated that HN increases cellular ATP levels and speculated that this peptide may rescue energy-deficient cells in mitochondrial disorders. Here, we report, for the first time, increased HN expression in skeletal muscles from patients with mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS). HN was strongly positive in all ragged-red fibers (RRFs) and some non-RRFs, and most of them were type 1 fibers generally requiring higher energy than type 2 fibers. HN in these fibers was localized in mitochondria. HN expression was also increased in small arteries that strongly reacted for succinate dehydrogenase. Our experiments on muscular TE671 cells indicated the possibility that synthesized HN increases cellular ATP levels by directly acting on mitochondria. From these in vivo and in vitro findings, we propose that HN expression might be induced in response to the energy crisis within affected fibers and vessels in MELAS muscles and further be a possible therapeutic candidate for MELAS.