Non-Markovian dynamics and quantum information probes

This Thesis discusses the phenomenology of the dynamics of open quantum systems marked by non-Markovian memory effects. Non-Markovian open quantum systems are the focal point of a flurry of recent research aiming to answer, e.g., the following questions: What is the characteristic trait of non-Markovian dynamical processes that discriminates it from forgetful Markovian dynamics? What is the microscopic origin of memory in quantum dynamics, and how can it be controlled? Does the existence of memory effects open new avenues and enable accomplishments that cannot be achieved with Markovian processes? These questions are addressed in the publications forming the core of this Thesis with case studies of both prototypical and more exotic models of open quantum systems. In the first part of the Thesis several ways of characterizing and quantifying non-Markovian phenomena are introduced. Their differences are then explored using a driven, dissipative qubit model. The second part of the Thesis focuses on the dynamics of a purely dephasing qubit model, which is used to unveil the origin of non-Markovianity for a wide class of dynamical models. The emergence of memory is shown to be strongly intertwined with the structure of the spectral density function, as further demonstrated in a physical realization of the dephasing model using ultracold quantum gases. Finally, as an application of memory effects, it is shown that non- Markovian dynamical processes facilitate a novel phenomenon of timeinvariant discord, where the total quantum correlations of a system are frozen to their initial value. Non-Markovianity can also be exploited in the detection of phase transitions using quantum information probes, as shown using the physically interesting models of the Ising chain in a transverse field and a Coulomb chain undergoing a structural phase transition.

Ultrastructural changes of Fusobacterium nucleatum as a defense mechanism against human neutrophil peptide-1 - A Transmission Electron Microscopy (TEM) study

Aims: The aim of this work was to assess the ultrastructural changes, cellular proliferation, and the biofilm formation ability of F. nucleatum as defense mechanisms against the effect of HNP-1. Materials and methods: The type strain of F. nucleatum (ssp. nucleatum ATCC 25586) and two clinical strains (ssp. polymorphum AHN 9910 and ssp. nucleatum AHN 9508) were cultured and incubated with four different test concentrations of recombinant HNP-1 (1, 5, 10 and 20 µg/ml) and one control group (0 µg/ml). Bacterial pellets from each concentration were processed for TEM imaging. Planktonic growth was assessed and colony forming units (CFU) were measured to determine the cellular proliferation. Scrambled HNP-1 was used for confirmation. Results: TEM analyses revealed a decrease in the outer membrane surface corrugations and roughness of the strain AHN 9508 with increasing HNP-1 concentrations. In higher concentrations of HNP-1, the strain AHN 9910 showed thicker outer membranes with a number of associated rough vesicles attached to the outer surface. For ATCC 25586, the treated bacterial cells contained higher numbers of intracellular granules with increasing the peptide concentration. Planktonic growth of the two clinical strains were significantly enhanced (P<0.001) with gradually increased concentrations of HNP-1. None of the planktonic growth results of the 3 strains incubated with the scrambled HNP-1 was statistically significant. HNP-1 decreased the biofilm formation of the two clinical strains, AHN 9910 and 9508, significantly (P<0.01 and P<0.001; respectively). Conclusions: The present in vitro study demonstrates that F. nucleatum has the ability to withstand the lethal effects of HNP-1 even at concentrations simulating the diseased periodontium in vivo. The increase in planktonic growth could act as defense mechanisms of F. nucleatum against HNP-1.