Calibration of the whole body counter at PSI

Abstract. At the Paul Scherrer Institut (PSI), measurements with the whole body counter are routinely carried out for occupationally exposed persons and occasionally for individuals of the population suspected of radioactive intake. In total about 400 measurements are performed per year. The whole body counter is based on a p-type high purity germanium (HPGe) coaxial detector mounted above a canvas chair in a shielded small room. The detector is used to detect the presence of radionuclides that emit photons with energies between 50 keV and 2 MeV. The room itself is made of iron from old railway rails to reduce the natural background radiation to 24 nSv/h. The present paper describes the calibration of the system with the IGOR phantom. Different body sizes are realized by different standardized configurations of polyethylene bricks, in which small tubes of calibration sources can be introduced. The efficiency of the detector was determined for four phantom geometries (P1, P2, P4 and P6) simulating human bodies in sitting position of 12 kg, 24 kg, 70 kg and 110 kg, respectively. The measurements were performed serially using five different radionuclide sources ( Eu) within the phantom bricks. Based on results of the experiment, an efficiency curve for each configuration and the detection limits for relevant radionuclides were determined. For routine measurements, the efficiency curve obtained with the phantom geometry P4 was chosen. The detection limits range from 40 Bq to 1000 Bq for selected radionuclides applying a measurement time of 7 min. The proper calibration of the system, on the one hand, is essential for the routine measurements at PSI. On the other hand, it serves as a benchmark for the already initiated characterisation of the system with Monte Carlo simulations

Glucagon-Induced Acetylation of Foxa2 Regulates Hepatic Lipid Metabolism

Circulating levels of insulin and glucagon reflect the nutritional state of animals and elicit regulatory responses in the liver that maintain glucose and lipid homeostasis. The transcription factor Foxa2 activates lipid metabolism and ketogenesis during fasting and is inhibited via insulin-PI3K-Akt signaling-mediated phosphorylation at Thr156 and nuclear exclusion. Here we show that, in addition, Foxa2 is acetylated at the conserved residue Lys259 following inhibition of histone deacetylases (HDACs) class I-III and the cofactors p300 and SirT1 are involved in Foxa2 acetylation and deacetylation, respectively. Physiologically, fasting states and glucagon stimulation are sufficient to induce Foxa2 acetylation. Introduction of the acetylation-mimicking (K259Q) or -deficient (K259R) mutations promotes or inhibits Foxa2 activity, respectively, and adenoviral expression of Foxa2-K259Q augments expression of genes involved in fatty acid oxidation and ketogenesis. Our study reveals a molecular mechanism by which glucagon signaling activates a fasting response through acetylation of Foxa2