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- Regan, P H, et al.
(author)
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Vibrational and rotational sequences in Mo-101 and Ru-103,Ru-4 studied via multinucleon transfer reactions
- 2005
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In: Acta Physica Polonica B. - 0587-4254 .- 1509-5770. ; 36:4, s. 1313-1322
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Journal article (peer-reviewed)abstract
- The near-yrast states of Mo-101(42)59 and Ru-103,4(44)59,60 have been studied following their population via heavy-ion multinucleon transfer reactions between a Xe-136 beam and a thin, self-supporting Mo-100 target. The ground state sequence in Ru-104 can be understood as demonstrating a simple evolution from a quasi-vibrational structure at lower spins to statically deformed, quasi-rotational excitation involving the population of a pair of low-Omega h(11/2) neutron orbitals. The effect of the decoupled h(11/2) orbital on this vibration-to-rotational evolution is demonstrated by an extension of the "E-GOS" prescription to include odd-A nuclei. The experimental results are also compared with self-consistent Total Routhian Surface calculations which also highlight the polarising role of the highly aligned neutron h(11/2) orbital in these nuclei.
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3. |
- Stacey, D, et al.
(author)
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Elucidating mechanisms of genetic cross-disease associations at the PROCR vascular disease locus
- 2022
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In: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 13:1, s. 1222-
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Journal article (peer-reviewed)abstract
- Many individual genetic risk loci have been associated with multiple common human diseases. However, the molecular basis of this pleiotropy often remains unclear. We present an integrative approach to reveal the molecular mechanism underlying the PROCR locus, associated with lower coronary artery disease (CAD) risk but higher venous thromboembolism (VTE) risk. We identify PROCR-p.Ser219Gly as the likely causal variant at the locus and protein C as a causal factor. Using genetic analyses, human recall-by-genotype and in vitro experimentation, we demonstrate that PROCR-219Gly increases plasma levels of (activated) protein C through endothelial protein C receptor (EPCR) ectodomain shedding in endothelial cells, attenuating leukocyte–endothelial cell adhesion and vascular inflammation. We also associate PROCR-219Gly with an increased pro-thrombotic state via coagulation factor VII, a ligand of EPCR. Our study, which links PROCR-219Gly to CAD through anti-inflammatory mechanisms and to VTE through pro-thrombotic mechanisms, provides a framework to reveal the mechanisms underlying similar cross-phenotype associations.
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