Abstract: The properties of the shape memory behaviour of Ni-rich binary NiTi are strongly dependant on the thermal history of the material. In this respect the changing of transformation temperatures of the underlying martensitic transformation and the occurrence of multiple step transformations are the most important phenomena. Part of the explanation is found in the presence of Ni4Ti3 precipitates in the B2 matrix after particular heat treatments. The formation of these precipitates changes the Ni concentration of the matrix and induces a strain field, with both of these aspects expected to be of importance. In this work atomic resolution and analytical TEM (transmission electron microscopy) techniques are used to obtain quantitative information concerning these two main features. Furthermore, the known structure of Ni4Ti3 is refined by a least squares optimization of quantitative electron diffraction data. The high-resolution TEM results show that there are strains up to 2% in the matrix surrounding the precipitates and they gradually increase until a maximum is reached when moving away from the interface. Analytical results reveal a global decrease of Ni content in the matrix when sufficient precipitates are present and a gradient in their close vicinity. The refinement of the structure shows atomic displacements, thereby increasing our understanding of the shrinking of the precipitate lattice with respect to the matrix.

Abstract: Recent technological advances resulted in high-quality superconducting metallic nanofilms and nanowires. The physical properties of such nanostructures are governed by the size-quantization of the transverse electron spectrum. This has a substantial impact on the basic superconducting characteristics, e.g., the order parameter, the critical temperature and the critical magnetic field. In the present paper we give an overview of our theoretical results on this subject. Based on a numerical self-consistent solution of the Bogoliubov-de Gennes equations, we investigate how the superconducting properties are modified in the quantum-size regime.

Abstract: Reactive oxygen and nitrogen species (RONS) generated by cold atmospheric plasma (CAP) can activate discrete signaling transduction pathways or disrupt redox cellular homeostasis, depending on their concentration. This makes that CAP possesses therapeutic potential towards wound healing, cancer, and other diseases. In order to effectively use CAP in the clinic, a clear understanding of the interaction of RONS with biomolecules (lipids, proteins and nucleic acids) from the atomic to the macro scale, and their biological significance, is needed. In this work, I have therefore studied the dual role of CAP-derived RONS, i.e., (i) in the signaling pathways involved in wound healing, and (ii) in their reaction with biomolecules to cause oxidation-mediated damage. I performed computer simulations to provide fundamental insight about the occurring processes that are difficult or even impossible to obtain experimentally. Furthermore, next to computational studies, I used both 2D and 3D tissue cultures. 3D model allows proliferation in a more physiologically relevant geometry that stimulates the production of extracellular matrix proteins. I investigated the treatment of human gingival fibroblasts with low doses of CAP-generated RONS. This treatment demonstrated that it can inhibit colony formation but does not induce cell death, induce the expression of metalloprotease proteins, induce extracellular matrix degradation, and promote cell migration, which could result in enhanced wound healing. In contrast, at high concentrations, RONS can disrupt the cell membrane integrity and induce cancer cell death through oxidative stress-mediated pathways. I discovered how oxidation of the cell membrane (lipid-peroxidation) can facilitate the access of a drug (Melittin) into cancer cells, and in this way, reduce the required therapeutic dose of Melittin in melanoma and breast cancer cells (demonstrated using in vitro, in ovo and in silico approaches). Furthermore, I studied how excessive lipid-oxidation in chemoresistant pancreatic cancer cells promotes ferroptotic cell death. This was due to the stimulation of the iron-dependent Fenton reaction by targeting a redox specific signaling network. However, upon oxidative stress, cells protect themselves via a sophisticated intracellular antioxidant system that involves the regulation of glutathione/glutathione peroxidase 4 (lipid repair enzyme). Cancer cells exhibited increased levels of intracellular RONS due to their hyper metabolism, leading to high expression of anti-oxidant systems. I therefore focus on the effect of reactive species on the intracellular anti-oxidant system and corresponding DNA damages in both temozolomide-sensitive as well as temozolomide-resistant glioblastoma spheroids, in a 3-dimensional tumor model with a more complex tumor microenvironment than cell monolayers.