44 research outputs found
Decay spectroscopy of Cd-129
Excited states of In populated following the -decay of
Cd were experimentally studied with the GRIFFIN spectrometer at the
ISAC facility of TRIUMF, Canada. A 480-MeV proton beam was impinged on a
uranium carbide target and Cd was extracted using the Ion Guide Laser
Ion Source (IG-LIS). - and -rays following the decay of
Cd were detected with the GRIFFIN spectrometer comprising the plastic
scintillator SCEPTAR and 16 high-purity germanium (HPGe) clover-type detectors.
%, along with the -particles were detected with SCEPTAR. From the
-- coincidence analysis, 32 new transitions and 7 new
excited states were established, expanding the previously known level scheme of
In. The values deduced from the -feeding intensities
suggest that some of the high-lying states were populated by the allowed Gamow-Teller (GT) transition, which
indicates that the allowed GT transition is more dominant in the Cd
decay than previously reported. Observation of fragmented Gamow-Teller
strengths is consistent with theoretical calculations.Comment: 13 pages, 9 figures, to be published in Physical Review
Cornelia-de Lange syndrome-associated mutations cause a DNA damage signalling and repair defect
Cornelia de Lange syndrome is a multisystem developmental disorder typically caused by mutations in the gene encoding the cohesin loader NIPBL. The associated phenotype is generally assumed to be the consequence of aberrant transcriptional regulation. Recently, we identified a missense mutation in BRD4 associated with a Cornelia de Lange-like syndrome that reduces BRD4 binding to acetylated histones. Here we show that, although this mutation reduces BRD4-occupancy at enhancers it does not affect transcription of the pluripotency network in mouse embryonic stem cells. Rather, it delays the cell cycle, increases DNA damage signalling, and perturbs regulation of DNA repair in mutant cells. This uncovers a role for BRD4 in DNA repair pathway choice. Furthermore, we find evidence of a similar increase in DNA damage signalling in cells derived from NIPBL-deficient individuals, suggesting that defective DNA damage signalling and repair is also a feature of typical Cornelia de Lange syndrome