ABSTRACT
Nascent observations about the influence of kinetic instabilities on electron cyclotron emission (ECE) from runaway electrons (REs) have been detected and explored at the Aditya-Upgrade (Aditya-U) tokamak. The developed broadband ECE radiometer system offers wideband measurements by integrating several radio frequency units with a fixed intermediate frequency receiver with multiple channels, which is a novel approach to meet the needs of the localized measurements at various toroidal fields and extend the system dynamic range. The low density (ne ≤ 1 × 10-19 m-3) plasma discharges at Aditya-U are consistently accompanied by a 20%-40% increase in the ECE radiometer signal amplitude within 100 µs and sporadic step-like modulations. The Pitch Angle Scattering (PAS) of REs induced by kinetic instabilities is a potential candidate for their occurrence. This steep jump in the radiometer signals was detected due to its high temporal resolution of 10 µs. A "PREDICT" code that employs the relativistic test particle model validates these experimental findings of the radiometer diagnostic for the first time for Aditya-U tokamak. Preliminary observations of the ECE radiometer signals also show that additional gas puffs can be used to vary the trigger timings of such PAS events or even lead to their complete avoidance.
ABSTRACT
BACKGROUND: The obesity epidemic, recognized in developed nations for decades, is now a worldwide phenomenon. All age groups are affected, including women of childbearing age, fueling concern that maternal obesity before and during pregnancy and lactation impairs developmental establishment of body weight regulatory mechanisms in the fetus or infant, causing transgenerational amplification of obesity prevalence and severity. The biological mechanisms underlying such processes remain unknown. METHODS: We used agouti viable yellow (A(vy)) mice to test the hypothesis that maternal obesity induces transgenerational amplification of obesity. We passed the A(vy) allele through three generations of A(vy)/a females and assessed cumulative effects on coat color and body weight. By studying two separate but contemporaneous populations of mice, one provided a standard diet and the other a methyl-supplemented diet that induces DNA hypermethylation during development, we tested whether potential transgenerational effects on body weight might be mediated by alterations in epigenetic mechanisms including DNA methylation. RESULTS: The genetic tendency for obesity in A(vy) mice was progressively exacerbated when the A(vy) allele was passed through successive generations of obese A(vy) females. This transgenerational amplification of body weight was prevented by a promethylation dietary supplement. Importantly, the effect of methyl supplementation on body weight was independent of epigenetic changes at the A(vy) locus, indicating this model may have direct relevance to human transgenerational obesity. CONCLUSION: Our results show that in a population with a genetic tendency for obesity, effects of maternal obesity accumulate over successive generations to shift the population distribution toward increased adult body weight, and suggest that epigenetic mechanisms are involved in this process.
