8 research outputs found
Second T = 3/2 state in B and the isobaric multiplet mass equation
Recent high-precision mass measurements and shell model calculations~[Phys.
Rev. Lett. {\bf 108}, 212501 (2012)] have challenged a longstanding explanation
for the requirement of a cubic isobaric multiplet mass equation for the lowest
isospin quartet. The conclusions relied upon the choice of the
excitation energy for the second state in B, which had two
conflicting measurements prior to this work. We remeasured the energy of the
state using the reaction and significantly disagree
with the most recent measurement. Our result supports the contention that
continuum coupling in the most proton-rich member of the quartet is not the
predominant reason for the large cubic term required for nuclei
Isospin mixing and the cubic isobaric multiplet mass equation in the lowest <i>T</i>=2, <i>A</i>=32 quintet
The isobaric multiplet mass equation (IMME) is known to break down in the
first T = 2, A = 32 isospin quintet. In this work we combine high-resolution
experimental data with state-of-the-art shell-model calculations to investigate
isospin mixing as a possible cause for this violation. The experimental data
are used to validate isospin-mixing matrix elements calculated with newly
developed shell-model Hamiltonians. Our analysis shows that isospin mixing with
nonanalog T = 1 states contributes to the IMME breakdown, making the
requirement of an anomalous cubic term inevitable for the multiplet
Histone deacetylase modulators provided by Mother Nature
Protein acetylation status results from a balance between histone acetyltransferase and histone deacetylase (HDAC) activities. Alteration of this balance leads to a disruption of cellular integrity and participates in the development of numerous diseases, including cancer. Therefore, modulation of these activities appears to be a promising approach for anticancer therapy. Histone deacetylase inhibitors (HDACi) are epigenetically active drugs that induce the hyperacetylation of lysine residues within histone and non-histone proteins, thus affecting gene expression and cellular processes such as protein–protein interactions, protein stability, DNA binding and protein sub-cellular localization. Therefore, HDACi are promising anti-tumor agents as they may affect the cell cycle, inhibit proliferation, stimulate differentiation and induce apoptotic cell death. Over the last 30 years, numerous synthetic and natural products, including a broad range of dietary compounds, have been identified as HDACi. This review focuses on molecules from natural origins modulating HDAC activities and presenting promising anticancer activities