Early onset of ground-state deformation in the neutron-deficient polonium isotopes

In-source resonant ionization laser spectroscopy of the even-$A$ polonium isotopes $^{192-210,216,218}$Po has been performed using the $6p^37s$ $^5S_2$ to $6p^37p$ $^5P_2$ ($\lambda=843.38$ nm) transition in the polonium atom (Po-I) at the CERN ISOLDE facility. The comparison of the measured isotope shifts in $^{200-210}$Po with a previous data set allows to test for the first time recent large-scale atomic calculations that are essential to extract the changes in the mean-square charge radius of the atomic nucleus. When going to lighter masses, a surprisingly large and early departure from sphericity is observed, which is only partly reproduced by Beyond Mean Field calculations.Comment: As submitted to PR

CSF Protein Level of Neurotransmitter Secretion, Synaptic Plasticity, and Autophagy in PD and DLB

BACKGROUND: Molecular pathways associated with α-synuclein proteostasis have been detected in genetic studies and in cell models and include autophagy, ubiquitin-proteasome system, mitochondrial homeostasis, and synaptic plasticity. However, we lack biomarkers that are representative for these pathways in human biofluids. OBJECTIVE: The objective of this study was to evaluate CSF protein profiles of pathways related to α-synuclein proteostasis. METHODS: We assessed CSF protein profiles associated with neurotransmitter secretion, synapse plasticity, and autophagy in 2 monocentric cohorts with α-synucleinopathy (385 PD patients and 67 DLB patients). We included 80 PD patients and 17 DLB patients with variants in the glucocerebrosidase gene to serve as proxy for accelerated α-synuclein pathology with pronounced clinical trajectories. RESULTS: (1) Proteins associated with neurotransmitter secretion, synaptic plasticity, and endolysosomal autophagy were lower in PD and DLB patients compared with healthy controls. (2) These patterns were more pronounced in DLB than in PD patients, accentuated by GBA variant status in both entities. (3) CSF levels of these proteins were positively associated with CSF levels of total α-synuclein, with lower levels of proteostasis proteins related to lower levels of total α-synuclein. (4) These findings could be confirmed longitudinally. PD patients with low CSF profiles of proteostasis proteins showed lower CSF levels of α-synuclein longitudinally compared with PD patients with a normal proteostasis profile. CONCLUSION: CSF proteins associated with neurotransmitter secretion, synaptic plasticity, and endolysosomal autophagy might serve as biomarkers related to α-synuclein proteostasis in PD and DLB

Gamow-Teller decay population of 64Ni levels in the decay of 1+ 64Co

The 64Co β-decay feeding levels in the well-studied 64Ni nucleus were investigated. Whereas the previously known 64Co decay scheme merely contained 2 γ rays, the decay scheme established in this work contains 18, of which 5 are observed in this work and 6 were previously observed in an (n,γ) study but not placed in the 64Ni level scheme. Surprisingly, one additional level—placed at an excitation energy of 3578.7 keV—could be determined. The observed β-decay paths involve allowed νf5/2 → πf7/2 and νp1/2 → πp3/2 transitions. Three strongly fed levels around 4 MeV are interpreted to possess possible proton-intruder characterstatus: publishe

Nuclear Spins and Magnetic Moments of Cu-71,Cu-73,Cu-75: Inversion of pi 2p(3/2) and pi 1f(5/2) Levels in Cu-75

We report the first confirmation of the predicted inversion between the pi 2p(3/2) and pi 1f(5/2) nuclear states in the nu g(9/2) midshell. This was achieved at the ISOLDE facility, by using a combination of in-source laser spectroscopy and collinear laser spectroscopy on the ground states of Cu-71,Cu-73,Cu-75, which measured the nuclear spin and magnetic moments. The obtained values are mu(Cu-71)=+2.2747(8)mu(N), mu(Cu-73)=+1.7426(8)mu(N), and mu(Cu-75)=+1.0062(13)mu(N) corresponding to spins I=3/2 for Cu-71,Cu-73 and I=5/2 for Cu-75. The results are in fair agreement with large-scale shell-model calculations.status: publishe