Bifurcation structures and transient chaos in a four-dimensional Chua model

A four-dimensional four-parameter Chua model with cubic nonlinearity is studied applying numerical continuation and numerical solutions methods. Regarding numerical solution methods, its dynamics is characterized on Lyapunov and isoperiodic diagrams and regarding numerical continuation method, the bifurcation curves are obtained. Combining both methods the bifurcation structures of the model were obtained with the possibility to describe the {\it shrimp}-shaped domains and their endoskeletons. We study the effect of a parameter that controls the dimension of the system leading the model to present transient chaos with its corresponding basin of attraction being riddled.Comment: 9 figures, to appear in PL

Tunnel and thermal c-axis transport in BSCCO in the normal and pseudogap state

We consider the problem of c-axis transport in double-layered cuprates, in particular with reference to Bi$_{2}$Sr$_{2}$CaCu$_{2}$O$_{8+\delta}$ compounds. We exploit the effect of the two barriers on the thermal and tunnel transport. The resulting model is able to describe accurately the normal state c-axis resistivity in Bi$_{2}$Sr$_{2}$CaCu$_{2}$O$_{8+\delta}$, from the underdoped side up to the strongly overdoped. We extend the model, without introducing additional parameters, in order to allow for the decrease of the barrier when an external voltage bias is applied. The extended model is found to describe properly the c-axis resistivity for small voltage bias above the pseudogap temperature $T^{*}$, the c-axis resistivity for large voltage bias even below $T_c$, and the differential $dI/dV$ curves taken in mesa structures.Comment: 12 pages, 6 figures. Submitted to Superconductor Science and Technolog

ETosis: A Microbicidal Mechanism beyond Cell Death

Netosis is a recently described type of neutrophil death occurring with the release to the extracellular milieu of a lattice composed of DNA associated with histones and granular and cytoplasmic proteins. These webs, initially named neutrophil extracellular traps (NETs), ensnare and kill microorganisms. Similarly, other cell types, such as eosinophils, mast cells, and macrophages, can also dye by this mechanism; thus, it was renamed as ETosis, meaning death with release of extracellular traps (ETs). Here, we review the mechanism of NETosis/etosis, emphasizing its role in diseases caused by protozoan parasites, fungi, and viruses