ORCID Profile
0000-0001-5652-1516
Current Organisation
University of Sydney
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Publisher: American Astronomical Society
Date: 04-2022
Abstract: We reassess the 65 As(p, γ ) 66 Se reaction rates based on a set of proton thresholds of 66 Se, S p ( 66 Se), estimated from the experimental mirror nuclear masses, theoretical mirror displacement energies, and full p f -model space shell-model calculation. The self-consistent relativistic Hartree–Bogoliubov theory is employed to obtain the mirror displacement energies with much reduced uncertainty, and thus reducing the proton-threshold uncertainty up to 161 keV compared to the AME2020 evaluation. Using the simulation instantiated by the one-dimensional multi-zone hydrodynamic code, K epler , which closely reproduces the observed GS 1826−24 clocked bursts, the present forward and reverse 65 As(p, γ ) 66 Se reaction rates based on a selected S p ( 66 Se) = 2.469 ± 0.054 MeV, and the latest 22 Mg( α ,p) 25 Al, 56 Ni(p, γ ) 57 Cu, 57 Cu(p, γ ) 58 Zn, 55 Ni(p, γ ) 56 Cu, and 64 Ge(p, γ ) 65 As reaction rates, we find that though the GeAs cycles are weakly established in the rapid-proton capture process path, the 65 As(p, γ ) 66 Se reaction still strongly characterizes the burst tail end due to the two-proton sequential capture on 64 Ge, not found by the Cyburt et al. sensitivity study. The 65 As(p, γ ) 66 Se reaction influences the abundances of nuclei A = 64, 68, 72, 76, and 80 up to a factor of 1.4. The new S p ( 66 Se) and the inclusion of the updated 22 Mg( α ,p) 25 Al reaction rate increases the production of 12 C up to a factor of 4.5, which is not observable and could be the main fuel for a superburst. The enhancement of the 12 C mass fraction alleviates the discrepancy in explaining the origin of the superburst. The waiting point status of and two-proton sequential capture on 64 Ge, the weak-cycle feature of GeAs at a region heavier than 64 Ge, and the impact of other possible S p ( 66 Se) are also discussed.
Publisher: American Chemical Society (ACS)
Date: 15-04-2019
DOI: 10.1021/ACSCHEMNEURO.9B00143
Abstract: Post-translational modifications (PTMs) of proteins are becoming the focus of intense research due to their implications in a broad spectrum of neurodegenerative diseases. Various PTMs have been identified to alter the toxic profiles of proteins which play critical roles in disease etiology. In Alzheimer's disease (AD), dysregulated phosphorylation is reported to promote pathogenic processing of the microtubule-associated tau protein. Among the PTMs, the enzymatic addition of N-acetyl-d-glucosamine (GlcNAc) residues to Ser/Thr residues is reported to deliver protective effects against the pathogenic processing of both amyloid precursor protein (APP) and tau. Modification of tau with as few as one single O-GlcNAc residue inhibits its toxic self-assembly. This modification also has the same effect on the assembly of the Parkinson's disease (PD) associated α-synuclein (ASyn) protein. In fact, O-GlcNAcylation ( O-linked GlcNAc modification) affects the processing of numerous proteins implicated in AD, PD, amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD) in a similar manner. As such, manipulation of a protein's O-GlcNAcylation status has been proposed to offer therapeutic routes toward addressing multiple neurodegenerative pathologies. Here we review the various effects that O-GlcNAc modification, and its modulated expression, have on pathogenically significant proteins involved in neurodegenerative disease.
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Liu Zi-Xin.