Commissioning of inline ECE system within waveguide based ECRH transmission systems on ASDEX upgrade

A CW capable inline electron cyclotron emission (ECE) separation system for feedback control, featuring oversized corrugated waveguides, is commissioned on ASDEX upgrade (AUG). The system is based on a combination of a polarization independent, non-resonant, Mach-Zehnder diplexer equipped with dielectric plate beam splitters [2, 3] employed as corrugated oversized waveguide filter, and a resonant Fast Directional Switch, FADIS [4, 5, 6, 7] as ECE/ECCD separation system. This paper presents an overview of the system, the low power characterisation tests and first high power commissioning on AUG

Toward Male Individualization with Rapidly Mutating Y-Chromosomal Short Tandem Repeats

Peer reviewe

Longitudinal in vivo bioimaging of hepatocyte transcription factor activity following cholestatic liver injury in mice

© The Author(s) 2017.Molecular mechanisms regulating liver repair following cholestatic injury remain largely unknown. We have combined a mouse model of acute cholestatic liver injury, partial bile duct ligation (pBDL), with a novel longitudinal bioimaging methodology to quantify transcription factor activity during hepatic injury and repair. We administered lentiviral transcription factor activated luciferase/eGFP reporter (TFAR) cassettes to neonatal mice enabling longitudinal TFAR profiling by continued bioimaging throughout the lives of the animals and following pBDL in adulthood. Neonatal intravascular injection of VSV-G pseudotyped lentivirus resulted in almost exclusive transduction of hepatocytes allowing analysis of hepatocyte-specific transcription factor activity. We recorded acute but transient responses with NF-? B and Smad2/3 TFAR whilst our Notch reporter was repressed over the 40 days of evaluation post-pBDL. The bipotent hepatic progenitor cell line, HepaRG, can be directed to differentiate into hepatocytes and biliary epithelia. We found that forced expression of the Notch inhibitor NUMB in HepaRG resulted in enhanced hepatocyte differentiation and proliferation whereas over-expressing the Notch agonist JAG1 resulted in biliary epithelial differentiation. In conclusion, our data demonstrates that hepatocytes rapidly upregulate NF-? B and Smad2/3 activity, whilst repressing Notch signalling. This transcriptional response to cholestatic liver injury likely promotes partial de-differentiation to allow pro-regenerative proliferation of hepatocytes