Power Consumption in Carbon Capture and Storage Systems (CCS) and Possibilities to Reduce Power Consumption with Variable Speed Drives

The aim of this master´s thesis is to study which processes increase the auxiliary power consumption in carbon capture and storage processes and if it is possible to reduce the auxiliary power consumption with variable speed drives. Also the cost of carbon capture and storage is studied. Data about auxiliary power consumption in carbon capture is gathered from various studies and estimates made by various research centres. Based on these studies a view is presented how the power auxiliary power consumption is divided between different processes in carbon capture processes. In a literary study, the operation of three basic carbon capture systems is described. Also different methods to transport carbon dioxide and carbon dioxide storage options are described in this section. At the end of the thesis processes that consume most of the auxiliary power are defined and possibilities to reduce the auxiliary power consumption are evaluated. Cost of carbon capture, transport and storage are also evaluated at this point and in the case that the carbon capture and storage systems are fully deployed. According to the results, it can be estimated what are the processes are where variable speed drives can be used and what kind of cost and power consumption reduction could be achieved. Results also show how large a project carbon capture and storage is if it is fully deployed.

Transgenic mice overexpressing neuropeptide Y: An experimental model of metabolic and cardiovascular diseases

Neuropeptide Y (NPY) is an abundant neurotransmitter in the brain and sympathetic nervous system (SNS). Hypothalamic NPY is known to be a key player in food intake and energy expenditure. NPY’s role in cardiovascular regulation has also been shown. In humans, a Leucine 7 to Proline 7 single nucleotide polymorphism (p.L7P) in the signal peptide of the NPY gene has been associated with traits of metabolic syndrome. The p.L7P subjects also show increased stress-related release of NPY, which suggests that more NPY is produced and released from SNS. The main objective of this study was to create a novel mouse model with noradrenergic cell-targeted overexpression of NPY, and to characterize the metabolic and vascular phenotype of this model. The mouse model was named OE-NPY^DBH mouse. Overexpression of NPY in SNS and brain noradrenergic neurons led to increased adiposity without significant weight gain or increased food intake. The mice showed lipid accumulation in the liver at young age, which together with adiposity led to impaired glucose tolerance and hyperinsulinemia with age. The mice displayed stress-related increased mean arterial blood pressure, increased plasma levels of catecholamines and enhanced SNS activity measured by GDP binding activity to brown adipose tissue mitochondria. Sexual dimorphism in NPY secretion pattern in response to stress was also seen. In an experimental model of vascular injury, the OE-NPY^DBH mice developed more pronounced neointima formation compared with wildtype controls. These results together with the clinical data indicate that NPY in noradrenergic cells plays an important role in the pathogenesis of metabolic syndrome and related diseases. Furthermore, new insights on the role of the extrahypothalamic NPY in the process have been obtained. The OE-NPY^DBH model provides an important tool for further stress and metabolic syndrome-related studies.