Compound-Nucleus and Doorway-State Decays of β-Delayed Neutron Emitters ^{51,52,53}K.

We investigated decays of ^{51,52,53}K at the ISOLDE Decay Station at CERN in order to understand the mechanism of the β-delayed neutron-emission (βn) process. The experiment quantified neutron and γ-ray emission paths for each precursor. We used this information to test the hypothesis, first formulated by Bohr in 1939, that neutrons in the βn process originate from the structureless "compound nucleus.

Metabolic Bypass Rescues Aberrant S-nitrosylation-Induced TCA Cycle Inhibition and Synapse Loss in Alzheimer's Disease Human Neurons.

In Alzheimer's disease (AD), dysfunctional mitochondrial metabolism is associated with synaptic loss, the major pathological correlate of cognitive decline. Mechanistic insight for this relationship, however, is still lacking. Here, comparing isogenic wild-type and AD mutant human induced pluripotent stem cell (hiPSC)-derived cerebrocortical neurons (hiN), evidence is found for compromised mitochondrial energy in AD using the Seahorse platform to analyze glycolysis and oxidative phosphorylation (OXPHOS).

Deformation versus Sphericity in the Ground States of the Lightest Gold Isotopes.

The changes in mean-squared charge radii of neutron-deficient gold nuclei have been determined using the in-source, resonance-ionization laser spectroscopy technique, at the ISOLDE facility (CERN). From these new data, nuclear deformations are inferred, revealing a competition between deformed and spherical configurations. The isotopes ^{180,181,182}Au are observed to possess well-deformed ground states and, when moving to lighter masses, a sudden transition to near-spherical shapes is seen in the extremely neutron-deficient nuclides, ^{176,177,179}Au.

^{133}In: A Rosetta Stone for Decays of r-Process Nuclei.

The β decays from both the ground state and a long-lived isomer of ^{133}In were studied at the ISOLDE Decay Station (IDS). With a hybrid detection system sensitive to β, γ, and neutron spectroscopy, the comparative partial half-lives (logft) have been measured for all their dominant β-decay channels for the first time, including a low-energy Gamow-Teller transition and several first-forbidden (FF) transitions. Uniquely for such a heavy neutron-rich nucleus, their β decays selectively populate only a few isolated neutron unbound states in ^{133}Sn.

S-Nitrosylation-mediated dysfunction of TCA cycle enzymes in synucleinopathy studied in postmortem human brains and hiPSC-derived neurons.

A causal relationship between mitochondrial metabolic dysfunction and neurodegeneration has been implicated in synucleinopathies, including Parkinson disease (PD) and Lewy body dementia (LBD), but underlying mechanisms are not fully understood. Here, using human induced pluripotent stem cell (hiPSC)-derived neurons with mutation in the gene encoding α-synuclein (αSyn), we report the presence of aberrantly S-nitrosylated proteins, including tricarboxylic acid (TCA) cycle enzymes, resulting in activity inhibition assessed by carbon-labeled metabolic flux experiments. This inhibition principally affects α-ketoglutarate dehydrogenase/succinyl coenzyme-A synthetase, metabolizing α-ketoglutarate to succinate.