| Summary: | <p>Liver fibrosis, a consequence of most chronic liver diseases, is characterised by collagen deposition. Collagen has a short-T<sub>2</sub><sup>*</sup> signal that is undetectable with conventional magnetic resonance (MR) sequences. However, collagen signal is measurable with the ultrashort echo time (UTE) sequence, which can achieve an echo time of less than 1 ms. This thesis explored the modelling of the short-T<sub>2</sub><sup>*</sup> signal in the liver with UTE.</p>
<p>Given the implication of collagen in liver disease, MR signal properties, including the R<sub>2</sub><sup>*</sup> and resonant frequency shift, were investigated in oriented collagen. Ex vivo measurements were performed at 3 T in tendon, an example of oriented collagen. Furthermore, the R<sub>2</sub><sup>*</sup> of collagen was investigated in phantoms in vitro.</p>
<p>The UTE sequence was optimised for in vivo imaging on the Siemens Trio 3-T and Prisma 3-T scanners. On the Trio, optimisations included reduced gradient spoiling, the use of a double-echo vs. a single-echo acquisition and the use of spatial saturation. Calibrations were performed on the Prisma for the bandwidth, radiofrequency coil and minimum TE.</p>
<p>From the R<sub>2</sub><sup>*</sup> and resonant frequency shift of tendon, an R<sub>2</sub><sup>*</sup> model was developed for describing isotropic collagen and free water in the liver. Other exponential models were also considered, accounting for short-T<sub>2</sub><sup>*</sup> signal. UTE acquisitions were performed to measure R<sub>2</sub><sup>*</sup> signal in the liver from healthy subjects and liver-disease patients in vivo. The models were used to fit the R<sub>2</sub><sup>*</sup> signal and the most appropriate model was selected. Subsequently, the repeatability and reproducibility of the short-T<sub>2</sub><sup>*</sup> signal fraction were evaluated. Comparisons of the short-T2* signal fraction were made between healthy subjects and patients.</p>
<p>Given the selected model for the short-T<sub>2</sub><sup>*</sup> signal in the liver, potential sources of short-T<sub>2</sub><sup>*</sup> signal were discussed. Future work involves the identification of the constituent(s) giving rise to the short-T<sub>2</sub><sup>*</sup> signal in the liver.</p>
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