This dissertation is an experimental study of laser-generated, atmospheric pressure, transient toroidal helium plasmas.The formation mechanism of these toroidal plasmas is identified and an... Show moreThis dissertation is an experimental study of laser-generated, atmospheric pressure, transient toroidal helium plasmas.The formation mechanism of these toroidal plasmas is identified and an estimate of their main plasma parameters is obtained. Furthermore, preliminary experiments are presented, aimed at heating these plasmas by absorption of microwave radiation, in order to counteract their transient nature.Through a tomographic reconstruction, cross-sectional images of the toroidal plasma are obtained, visualising the fluid flow responsible for the generation of the toroidal structure. The origin of the flow is traced back to the structure of the plasma kernel. The shocks generated by this kernel interact akin to a Mach reflection and generate a low pressure region whose replenishment transforms the plasma into a toroid. Schlieren imaging, complemented with a novel scanning-probe technique, and thermodynamic modelling, as well as deliberately breaking the flow symmetry, confirm the formation mechanism. A high-power, sub-microsecond rise time, pulsed magnetron source has been designed for the microwave heating experiments. Its detailed design and the effect of the microwave pulse on the plasma are discussed.This work is part of a larger study on self-organising knotted magnetic structures in plasma, which may find their application in nuclear fusion and astrophysical research. Show less
Several cellular processes and pathways were altered both by fluid shear stress and Pkd1 gene disruption in renal epithelial cells. Many of these signaling pathways are implicated in ADPKD as... Show moreSeveral cellular processes and pathways were altered both by fluid shear stress and Pkd1 gene disruption in renal epithelial cells. Many of these signaling pathways are implicated in ADPKD as well. However, more than 20 years after the discovery of PKD1 and PKD2 as genetic cause of ADPKD, the exact cellular function of the polycystins still remains unclear. Our data indicate that polycystin-1 is not a direct mechano-sensor, but it restrains shear stress induced gene expression via an unknown mechanism. Additional research is required to identify the cellular function of polycystins and the mechanism of mechanotransduction. This is needed to refine the mechanism of cyst formation in ADPKD and other ciliopathies, which could identify potential targets for therapy. Nevertheless, we showed that inhibition of activin signaling is a promising therapy to slow cyst progression in Pkd1del mice. Although other treatment strategies have been tested successfully to reduce PKD progression in pre-clinical studies, the efficacy in human patients is sometimes minimal or absent. Therefore, it has been suggested to target multiple signaling pathways affected in ADPKD. These combined therapies should reestablish the balance in cellular signaling of renal epithelial cells and maintain cellular homeostasis within physiological boundaries. Show less
