Grants

ULTRA-LOWD will explore the development of a new table-top light source utilising gas-filled hollow-core fibre that will enable us to track the evolution of elementary excitations in low-dimensional materials using pump-probe and ultimately photoelectron spectroscopies. For example, we will be able to observe and optically control the modulation of the bandgap in semiconducting thin-films on ultrafast time-scales and generate single-burst electron bunches, accelerated to record-high energies for an optically driven system. This will have a significant impact on advancing the field of ultrafast laser science, while enriching our understanding of electron interactions in an important class of material system for next-generation semiconducting devices, moving us closer to an era of high-speed THz electronics. Finally, this project lays foundations on the path to momentum-resolved measurements of electron dynamics in low-dimensional materials using THz pumped photoelectron spectroscopy.

Bacteria have intricate social lives. Interactions occur within and between species, and when they take place inside the human body complexity increases. Our microbiome composition is dynamic, and while some changes are implicated in disease development less is known about how interactions within the microbiome affect community composition and host health. To address this I propose to use an interdisciplinary Evolutionary Medicine approach, which seeks to implement evolutionary theory to tackle health challenges. With a focus on the human stomach bacterium Helicobacter pylori, which can both cause and protect against disease, I will use mouse models to explore how interactions within and between species affect host health. I will test the hypothesis that intra- and interspecies interactions shape symbiont traits that are involved in host manipulation, and affect host health. As such, my Research Program will open new horizons in how we study and manage our microbial associates.

With a prevalence of 20% to 45%, fatty liver disease has reached epidemic proportions. However, only a subset of those with hepatic steatosis, the first stage of the disorder, go on to develop severe liver diseases such as cirrhosis and hepatocellular carcinoma. We currently lack effective methods to identify these ‘progressors’ early, before they reach an irreversible disease stage. We hypothesize that genetic factors play a key role in fatty liver disease progression. The aims of this study are to: 1) identify and characterize new genetic risk factors for fatty liver disease, 2) combine the individual genetic factors into a risk score, and 3) test if a higher genetic risk score predicts disease progression. We will utilize four cohorts from the UK, US, and Denmark totalling >600,000, including >1,000 patients with various stages of fatty liver disease. The study may open new avenues to the prediction and prevention of fatty liver disease progression.