Characterizing quantum chaoticity of kicked spin chains.

Quantum many-body systems are commonly considered as quantum chaotic if their spectral statistics, such as the level spacing distribution, agree with those of random matrix theory (RMT). Using the example of the kicked Ising chain we demonstrate that even if both level spacing distribution and eigenvector statistics agree well with random matrix predictions, the entanglement entropy deviates from the expected RMT behavior, i.e., the Page curve. To explain this observation we propose a quantity that is based on the effective Hamiltonian of the kicked system. Specifically, we analyze the distribution of the strengths of the effective spin interactions and compare them with analytical results that we obtain for circular ensembles. Thereby we group the effective spin interactions corresponding to the number k of spins which contribute to the interaction. By this the deviations of the entanglement entropy can be attributed to significantly different behavior of the k-spin interactions compared with RMT.

Entanglement in coupled kicked tops with chaotic dynamics.

The entanglement of eigenstates in two coupled, classically chaotic kicked tops is studied in dependence of their interaction strength. The transition from the noninteracting and unentangled system toward full random matrix behavior is governed by a universal scaling parameter. Using suitable random matrix transition ensembles we express this transition parameter as a function of the subsystem sizes and the coupling strength for both unitary and orthogonal symmetry classes. The universality is confirmed for the level spacing statistics of the coupled kicked tops and a perturbative description is in good agreement with numerical results. The statistics of Schmidt eigenvalues and entanglement entropies of eigenstates is found to follow a universal scaling as well. Remarkably, this is not only the case for large subsystems of equal size but also if one of them is much smaller. For the entanglement entropies a perturbative description is obtained, which can be extended to large couplings and provides very good agreement with numerical results. Furthermore, the transition of the statistics of the entanglement spectrum toward the random matrix limit is demonstrated for different ratios of the subsystem sizes.

Induction of suicidal erythrocyte death by novobiocin.

BACKGROUND: Novobiocin, an aminocoumarin antibiotic, interferes with heat shock protein 90 and hypoxia inducible factor dependent gene expression and thus compromises cell survival. Similar to survival of nucleated cells, erythrocyte survival could be disrupted by eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and by phospholipd scrambling of the cell membrane with phosphatidylserine translocation to the erythrocyte surface. Triggers of eryptosis include increase of cytosolic Ca(2+)-activity ([Ca(2+)]i). The Ca(2+) sensitivity of phospholipid scrambling is enhanced by ceramide. The present study explored, whether novobiocin elicits eryptosis. METHODS: [Ca(2+)]i was estimated from Fluo3-fluorescence, ceramide abundance utilizing fluorescent antibodies, cell volume from forward scatter, phosphatidylserine-exposure from annexin V binding. RESULTS: A 48 hours exposure to novobiocin (500 µM) was followed by a significant increase of [Ca(2+)]i, decrease of forward scatter, increase of annexin-V-binding and enhanced ceramide formation. Removal of extracellular Ca(2+) virtually abrogated the increase of annexin-V-binding following novobiocin exposure. CONCLUSIONS: Novobiocin stimulates eryptosis, an effect at least in part due to entry of extracellular Ca(2+) and formation of ceramide.

Tannic acid induced suicidal erythrocyte death.

BACKGROUND: The polyphenol tannic acid with antioxidant and antimicrobial potency may trigger suicidal death of nucleated cells or apoptosis and thus may counteract tumor growth. In analogy to apoptosis of nucleated cells, erythrocytes may undergo eryptosis, a suicidal death characterized by cell shrinkage and cell membrane scrambling with appearance of phosphatidylserine at the erythrocyte surface. A major trigger of eryptosis is increase of cytosolic Ca(2+)-activity ([Ca(2+)]i). Erythrocytes could be sensitized to the eryptotic effect of cytosolic Ca(2+) by ceramide. METHODS: Cell volume has been estimated from forward scatter, phosphatidylserine abundance at the erythrocyte surface from annexin V binding, hemolysis from hemoglobin release, [Ca(2+)]i from Fluo3-fuorescence and ceramide utilizing fluorescent antibodies. RESULTS: A 48 h treatment with tannic acid was followed by significant decrease of forward scatter (≥ 1 µg/ml) and significant increase of annexin-V-binding (≥ 10 µg/ml). Tannic acid did not significantly modify [Ca(2+)]i (up to 50 µM) but significantly increased ceramide formation (50 µM). The annexin-V-binding following tannic acid treatment (50 µM) was significantly blunted in the nominal absence of extracellular Ca(2+). CONCLUSIONS: Tannic acid stimulates eryptosis, an effect at least partially due to ceramide formation with subsequent sensitization of erythrocytes to cytosolic Ca(2+).

Effect of honokiol on erythrocytes.

Honokiol ((3,5-di-(2-propenyl)-1,1-biphenyl-2,2-diol), a component of Magnolia officinalis, stimulates apoptosis and is thus considered for the treatment of malignancy. In analogy to apoptosis of nucleated cells, erythrocytes may enter eryptosis, a suicidal death characterized by cell shrinkage and by breakdown of cell membrane phosphatidylserine asymmetry with phosphatidylserine-exposure at the erythrocyte surface. Eryptosis may be triggered following increase of cytosolic Ca(2+)-activity ([Ca(2+)]i). The present study explored, whether honokiol elicits eryptosis. Cell volume has been estimated from forward scatter, phosphatidylserine-exposure from annexin V binding, hemolysis from hemoglobin release, [Ca(2+)]i from Fluo3-fluorescence, and ceramide from fluorescent antibodies. As a result, a 48 h exposure to honokiol was followed by a slight but significant increase of [Ca(2+)]i (15 µM), significant decrease of forward scatter (5 µM), significant increase of annexin-V-binding (5 µM) and significant increase of ceramide formation (15 µM). Honokiol further induced slight, but significant hemolysis. Honokiol (15 µM) induced annexin-V-binding was significantly blunted but not abrogated in the nominal absence of extracellular Ca(2+). In conclusion, honokiol triggers suicidal erythrocyte death or eryptosis, an effect at least in part due to stimulation of Ca(2+) entry and ceramide formation.