Tropospheric Airborne Meteorological Data Reporting (TAMDAR) Overview

This paper is an overview of the Tropospheric Airborne Meteorological Data Reporting (TAMDAR) project, giving some history on the project, various applications of the atmospheric data, and future ideas and plans. As part of NASA's Aviation Safety and Security Program, the TAMDAR project developed a small low-cost sensor that collects useful meteorological data and makes them available in near real time to improve weather forecasts. This activity has been a joint effort with FAA, NOAA, universities, and industry. A tri-agency team collaborated by developing a concept of operations, determining the sensor specifications, and evaluating sensor performance as reported by Moosakhanian et. al. (2006). Under contract with Georgia Tech Research Institute, NASA worked with AirDat of Raleigh, NC to develop the sensor. The sensor is capable of measuring temperature, relative humidity, pressure, and icing. It can compute pressure altitude, indicated and true air speed, ice accretion rate, wind speed and direction, peak and average turbulence, and eddy dissipation rate. The overall development process, sensor capabilities, and performance based on ground and flight tests is reported by Daniels (2002), Daniels et. al. (2004) and by Tsoucalas et. al. (2006). An in-service evaluation of the sensor was performed called the Great Lakes Fleet Experiment (GLFE), first reported by Moninger et. al. (2004) and Mamrosh et. al. (2005). In this experiment, a Mesaba Airlines fleet was equipped to collect meteorological data over the Great Lakes region during normal revenue-producing flights

Nuclear receptor LRH-1/NR5A2 is required and targetable for liver endoplasmic reticulum stress resolution

Chronic endoplasmic reticulum (ER) stress results in toxicity that contributes to multiple human disorders. We report a stress resolution pathway initiated by the nuclear receptor LRH-1 that is independent of known unfolded protein response (UPR) pathways. Like mice lacking primary UPR components, hepatic Lrh-1-null mice cannot resolve ER stress, despite a functional UPR. In response to ER stress, LRH-1 induces expression of the kinase Plk3, which phosphorylates and activates the transcription factor ATF2. Plk3-null mice also cannot resolve ER stress, and restoring Plk3 expression in Lrh-1-null cells rescues ER stress resolution. Reduced or heightened ATF2 activity also sensitizes or desensitizes cells to ER stress, respectively. LRH-1 agonist treatment increases ER stress resistance and decreases cell death. We conclude that LRH-1 initiates a novel pathway of ER stress resolution that is independent of the UPR, yet equivalently required. Targeting LRH-1 may be beneficial in human disorders associated with chronic ER stress

Nuclear receptor LRH-1/NR5A2 is required and targetable for liver endoplasmic reticulum stress resolution.

Chronic endoplasmic reticulum (ER) stress results in toxicity that contributes to multiple human disorders. We report a stress resolution pathway initiated by the nuclear receptor LRH-1 that is independent of known unfolded protein response (UPR) pathways. Like mice lacking primary UPR components, hepatic Lrh-1-null mice cannot resolve ER stress, despite a functional UPR. In response to ER stress, LRH-1 induces expression of the kinase Plk3, which phosphorylates and activates the transcription factor ATF2. Plk3-null mice also cannot resolve ER stress, and restoring Plk3 expression in Lrh-1-null cells rescues ER stress resolution. Reduced or heightened ATF2 activity also sensitizes or desensitizes cells to ER stress, respectively. LRH-1 agonist treatment increases ER stress resistance and decreases cell death. We conclude that LRH-1 initiates a novel pathway of ER stress resolution that is independent of the UPR, yet equivalently required. Targeting LRH-1 may be beneficial in human disorders associated with chronic ER stress. DOI: http://dx.doi.org/10.7554/eLife.01694.001