If the mass excess of neutron-deficient nuclei and their neutron-rich mirror partners are both known, it can be shown that deviations of the Isobaric Mass Multiplet Equation (IMME) in the form of a cubic term can be probed. Such a cubic term was probed by using the atomic mass of neutron-rich magnesium isotopes measured using the TITAN Penning trap and the recently measured proton-separation energies of 29 Cl and 30 Ar. The atomic mass of 27 Mg was found to be within 1.6σ of the value stated in the Atomic Mass Evaluation. The atomic masses of 28,29 Mg were measured to be both within 1σ, while being 7 and 33 times more precise, respectively. Using the 29 Mg mass excess and previous measurements of 29 Cl we uncovered a cubic coefficient of d = 28 (7) keV, which is the largest known cubic coefficient of the IMME. This departure, however, could also be caused by experimental data with unknown systematic errors. Hence there is a need to confirm the mass excess of 28 S and the one-neutron separation energy of 29 Cl, which have both come from a single measurement. Finally, our results were compared to ab initio calculations from the valence-space in-medium similarity renormalization group, resulting in a good agreement.
Cell crawling on flat substrates stems from intracellular flows of the actin cytoskeleton that are driven by both actin polymerization at the front and myosin contractility at the back. Optogenetics makes it experimentally possible to spatially control contraction and possibly cell migration too. Here we theoretically analyze this situation using a one-dimensional active gel model that reflects the property of myosin II to assemble into minifilaments. Our model predicts bistability between sessile and motile solutions when cell adhesion and contractility are sufficiently large and in balance. We show that one can switch between the different states at realistic parameter values via optogenetic activation or inhibition of contractility, in agreement with recent experiments performed for neutrophils in microchannels. We predict the required activation strengths and initiation times, compare the effects of local and global increases of myosin II levels, and show that actin polymerization alone can affect a switch in direction only at high strength.
Cell crawling on flat substrates is based on intracellular flows of the actin cytoskeleton that are driven by both actin polymerization at the front and myosin contractility at the back. The new experimental tool of optogenetics makes it possible to spatially control contraction and thereby possibly also cell migration. Here we analyze this situation theoretically using a one-dimensional active gel model in which the excluded volume interactions of myosin and their aggregation into minifilaments is modeled by a supercritical van der Waals fluid. This physically simple and transparent, but nonlinear and thermodynamically rigorous model predicts bistability between sessile and motile solutions. We then show that one can switch between these two states at realistic parameter ranges via optogenetic activation or inhibition of contractility, in agreement with recent experiments. We also predict the required activation strengths and initiation times.
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