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Russo-Ukrainian War: The Political Economy of the Present Balance of Forces
Get PDFThis paper examines the evolving political economy of the Russo-Ukrainian War, arguing that despite its asymmetric nature, the conflict has become more balanced due to Ukraine’s institutional resilience and consistent financial support from allies. Neither side currently has a viable path to total victory. Both economies have adopted forms of military Keynesianism, though in distinct ways shaped by regime type and external dependencies: Ukraine on allied funding, Russia on volatile oil rents. Ukraine has secured financing until 2027 and maintained monetary stability, while Russia faces growing economic risks, including a potential credit crunch and balance of payments crisis. War has reshaped both states’ capacity for autonomous organisation, central to mobilising resources and restructuring their economies. As global geopolitics fragment and protectionism rises, the prospects for peace are increasingly defined by economic pressures and shifting alliances. A ceasefire, if reached, is likely to be unstable, with Russia potentially maintaining a militarised economy. Ukraine, meanwhile, has shifted its focus from military breakthroughs to securing long-term security guarantees. The outcome of negotiations will hinge not only on military dynamics but also on the internal strains shaping each regime’s strategic calculus
Genomics of hybridisation in British native flowering plants
No full textNatural hybridisation can lead to various evolutionary consequences, from homogenising the differences between populations to generating phenotypic and genotypic novelty.
However, the majority of these phenomena are evaluated in isolated case studies, and how well their findings represent generalities of natural hybridisation remain unknown. To address this knowledge gap, it is important to have a comparative perspective on hybridisation by comparing multiple hybridising pairs from diverse taxonomic lineages. This thesis aims to explore the general outcomes of natural hybridisation in British native flowering plants using large-scale genomic sequencing and demographic inference.
The British flora is very well-studied with extensive records of species that hybridise, rendering it the ideal system for understanding hybridisation at a broad taxonomic scale. In Chapter 2, I first review hybridisation studies that use comparative approaches to identify correlates of hybrid formation and the amount of introgression. I then discuss the current state and future prospects for integrating comparative and genomic approaches to study hybridisation. In Chapter 3, I focus on five congeneric pairs of British native flowering plant species, namely Geum, Linaria, Primula, Viola, and Verbascum, to understand the factors impacting genetic diversity and differentiation. Using whole genome resequencing data, I find that mating system has a major impact on shaping species genetic diversity, LD patterns, and differentiation, with selfing species showing lower diversity, slower decay in LD, and greater intraspecific population structure. In Chapter 4, I evaluate the dynamics of introgression with respect to postzygotic reproductive isolation. The extent, direction, and timing of introgressive gene flow for each hybridising species pair are characterised using model-based demographic inference. Comparisons across five species pairs show that the extent of gene flow decreases in line with reduced hybrid F1 fertility. In Chapter 5, I then focus on introgression between Geum species, which have the strongest evidence of gene flow among all pairs, and ask where barriers to gene flow are located along the genome as well as whether barriers change across evolutionary time scales. Using demographically explicit scans, I find that genomic regions with reduced gene flow in sympatry are highly consistent with those found in allopatry, showing that most of the barriers to gene flow in the recent past persisted over generations in Geum species. In summary, this work shows the importance of integrating genomics, comparative perspectives, and natural history datasets to understand general hybridisation outcomes in the light of species evolutionary history and ecological context
Cardiac extracellular matrix metabolism: the roles of age and sex in collagen dynamics
Get PDFAging is a major risk factor for cardiovascular disease, making it crucial to understand physiological aging in the context of cardiovascular health. In the absence of pathology, aging leads to a reduction in cardiac output and increased heart rate variability, vascular stiffening, and cardiac fibrosis. This age-related cardiac fibrosis is characterized by increased myocardial stiffness due to excessive extracellular matrix (ECM) components like fibrillin and collagen. The mechanisms of cardiovascular aging are poorly understood, though inflammation, senescence, and oxidative stress are implicated. These factors result in adverse remodelling, collagen accumulation, cardiac stiffening, and reduced cardiac function. It remains unclear whether collagen accumulation stems from increased synthesis or reduced clearance. The overarching hypothesis of this project is that aging disrupts cardiac collagen metabolism, causing a decrease in collagen synthesis despite significant collagen accumulation, with higher rates of collagen synthesis and accumulation in males compared to females. Therefore, this thesis focuses on the effect of aging on cardiac collagen metabolism, particularly on collagen synthesis both in vivo and in vitro. It also examines the influence of sex on age-related collagen metabolism, as females are thought to be relatively protected from adverse collagen accumulation.
This thesis employs a comprehensive approach to investigate the impact of aging and sex on collagen synthesis and metabolism across the heart through in vivo, in vitro, and ex vivo methods. A longitudinal Positron Emission Tomography (PET)/Computer Tomography (CT) imaging study in male (n=7-14) and female (n=7-14) Sprague-Dawley rats across five timepoints (1, 3, 6, 12, and 18 months) was carried out. Longitudinal characterization included survival analysis, body weight, and frailty measurements to assess age-related physiological changes. Cardiovascular health was evaluated using CT-derived cardiac volume measurements, tail-cuff plethysmography for blood pressure, and echocardiography at the final experimental timepoint. PET/CT imaging utilized cis-4-18F-fluoro-L-proline and trans-4-18F-fluoro-L-proline proline to measure unhydroxylated and hydroxylated collagen synthesis, respectively. Images were analysed using a cardiac template defining the four heart chambers. Additional groups were used for ex vivo tissue analysis included hydroxyproline, soluble, and insoluble assays for collagen content, advanced glycation end-product (AGEs) ELISA for crosslinking, and picrosirius red staining (PSR) staining for total collagen. In vitro studies examined age, sex, and drug effects of AGEs inhibitor ALT711/Algaebrium on cardiac fibroblast collagen synthesis and utilized radiotracer assays to assess collagen synthesis types.
Characterisation of the preclinical model of aging in Sprague Dawley rats identified that survival between males and females showed no difference but that mortality increased in both sexes following a year. Similarly, all animals showed significantly increased frailty at 18 months, suggesting that our cohort had advancing biological age. Rats had healthy cardiovascular systems, with cardiac dimensions, blood pressure, and ejection fraction all within normal ranges, indicating no obvious cardiac dysfunction and suggesting we were measuring physiological cardiovascular aging. However, 18-month-old males showed significantly lower cardiac ejection fraction and end-diastolic volume compared to their female counterparts. This suggests that aging causes a reduction in cardiac function in males compared to females, although males remain physiologically healthy.
Age and sex effects on cardiac collagen synthesis were studied in the left ventricle (LV) and right ventricle (RV). No sex differences were found in collagen synthesis types, and aging effects were assessed by collating male and female data. Hydroxylated collagen synthesis significantly declined in the LV at 12 months, as did unhydroxylated collagen synthesis. Histological analysis using PSR revealed peak total collagen in males at 12 months and in females at 6 months, with subsequent declines. Males showed increased soluble and insoluble collagen at 18 months compared to females. An AGEs crosslinking ELISA identified that males had a significant increase in crosslinking at 12 months which was not observed in female counterparts. In the RV, both hydroxylated and unhydroxylated collagen synthesis decreased with age, despite significant increases in total collagen at 6 and 12 months, followed by a decline at 18 months. These findings suggest that while collagen synthesis declines with age in both ventricles, males experience greater age-related collagen accumulation, contributing to increased cardiac stiffness and functional impairment compared to females.
Similarly, the effect of age and sex was assessed on atrial cardiac collagen synthesis and deposition. Hydroxylated and unhydroxylated collagen synthesis were measured in the left atria (LA) and right atria (RA) with no significant sex difference observed in either chamber. In the LA, hydroxylated collagen synthesis was increased at 3 months and at 18 months. Interestingly, unhydroxylated collagen synthesis showed an increase at 3 months but no other significant changes with age in LA, suggesting that collagen synthesis in the LA remains stable with age. Within the RA we observed that hydroxylated collagen synthesis increased with aging and this was also observed with unhydroxylated collagen synthesis. Interestingly, no increased deposition of collagen was identified in histological analysis.
In vitro, sex and age at the time of cell explantation appeared to have much clearer effects on collagen synthesis with male fibroblasts producing significantly more unhydroxylated collagen synthesis than female cardiac fibroblasts. We observed similar trends with hydroxylated collagen synthesis however this was not statistically significant. Aging was a key driver of both hydroxylated and unhydroxylated collagen synthesis with aged male cells having significantly higher uptake of both tracers. Interestingly, collagen deposition analysis suggested a disruption in collagen metabolism with aged cells producing significantly lower amounts of insoluble collagen compared to younger counterparts. Drug treatment with ALT711/Algaebrium showed no effect on collagen synthesis or deposition, potentially due to suboptimal dosage or that the drug only impacted directly the established crosslinking and no other part of the collagen cascade.
In summary, this study found that aging significantly impacts cardiac collagen metabolism. For the first time collagen synthesis has been longitudinally assessed and evaluated in each cardiac chamber, revealing region specific dynamic changes. Males showed more pronounced age-related collagen accumulation and potential cardiac stiffness compared to females. In both the left and right ventricles, collagen synthesis had overall significant declines with aging.
Contrastingly, in the atria, hydroxylated collagen synthesis increased significantly with age, but without corresponding increases in collagen deposition. All these findings point to a disruption in the homeostatic control of collagen turnover and suggest that synthesis is not directly responsible for collagen accumulation in aging, proving our hypothesis
Role of RamA on biofilm formation of Klebsiella variicola
No full textKlebsiella variicola (Kv) is a bacterium which occupies diverse natural niches, colonising different hosts, including humans. Initially isolated from plants and the broader environment, Kv is now considered as an emerging pathogen causing human infections with a high mortality rate. One of the main microbiological features of Kv, allowing it to survive in the environment, is biofilm formation. In the human host, biofilm-associated infections are hard to treat as they display high resistance to immune cells and antibiotics. It is, therefore, vital to determine the factors involved in the biofilm formation mechanisms. Aspects regarding Kv’s biofilm formation and virulence traits remain to be elucidated. RamA is an AraC-transcriptional protein regulator described in Klebsiella pneumoniae, responsible for bacterial multidrug resistance and virulence. Studies in Salmonella and Klebsiella pneumoniae show that RamA can also influence the expression of genes involved in biofilm formation. Despite the genetic similarity between Klebsiella variicola and Klebsiella pneumoniae, the regulatory role of RamA in Klebsiella variicola is not fully characterised. Our hypothesis is that the RamA plays a role in the biofilm formation in Kv. To test this hypothesis, our aim was to determine the possible role of RamA in biofilm formation of Kv. We compared the biofilm formation between strains presenting with different levels of RamA, both using the crystal violet staining technique and by growing strains on Congo Red plates. We found that the ramA expression levels were inversely correlated with biofilm formation. We also found that RamA altered biofilm formation independent of the mrk operon and capsule (wcaJ) in Kv. We undertook transcriptomic analyses, to establish the genes necessary for biofilm formation. Transcriptomic analyses allowed us to identify pspA & pspG as genes participating to this RamA-dependant variations in biofilm formation. In conclusion, our work showed that RamA plays a role in the biofilm formation of Kv independently of the mrk operon
Germline influences on processes that contribute to colorectal carcinogenesis
No full textColorectal cancer (CRC) is one of the most common causes of cancer-related death in the
world with incidence rising particularly in younger individuals in the West. Understanding of
the genetic causes underlying CRC has increased greatly in recent years as a result of work
on familial CRC syndromes, which has identified rarer but more impactful genetic mutations,
and CRC genome-wide association studies (GWAS), which have identified more common
forms of DNA variation. The common variants from CRC GWAS are less impactful individually
but when combined have a non-trivial effect on CRC risk. However, there are still many gaps
of knowledge in terms of CRC genetics, with one notable example being the mechanisms
through which variants are affecting CRC risk. This project aimed to contribute to this area by
first expanding the existing GWAS meta-analysis dataset through the addition of 2,356 CRC
patients and 14,162 CRC-free control patients from the 100,000 Genomes Project (100kGP).
Inclusion of 100kGP data led to the identification of eight novel CRC risk loci but also called
into question six previously identified loci. This modest net gain of CRC risk loci indicates that
substantial expansion of GWAS cohorts (perhaps the addition of > 100,000 patients) may be
needed for meaningful improvements in understanding common causes of CRC. Several risk
loci identified by CRC GWAS highlight genomic regions where the target gene may not be
affecting CRC predisposition through effects on the colorectal epithelium, but instead via an
intermediate phenotype. The project explored two of these potential intermediate
phenotypes: blood cell traits and the microbiome. For blood cell traits, genetic fine-mapping
of a locus at 12q24.12 was first conducted to identify whether pan-haematopoietic regulator
SH2B3 was the CRC causal risk gene, but these results were not conclusive. Work was then
expanded to examine the phenotype generally, initially by using Mendelian randomisation
(MR) to establish whether causal links existed between blood cell trait variation and CRC
risk. A modified PCA-based GWAS and MR approach was then used to try and mitigate the
high levels of horizontal pleiotropy that are apparent in haematopoietic genetics. These
results showed indications of red blood cell and platelet variation affecting CRC risk but were
not definitive and require further investigation. For the microbiome, fine-mapping was
conducted on four risk loci, where the possible CRC causal genes (GALNT12, B3GNT8, FUT2,
FUT3, and FUT6) play roles in oligosaccharide modification processes such as glycosylation
and fucosylation in the colon, thereby potentially affecting susceptibility to microbial
infections and subsequent CRC risk. The previous study of rare variants in GALNT12
specifically has raised the question as to whether it is a moderate CRC risk gene; this
hypothesis was tested using the larger 100kGP cohort, which suggested that it is not a
moderate risk gene, and then expanded to include the other four potential microbiome CRC
genes. Once again, work was then extended from individual loci to the overall mechanism.
First, MR was conducted using reported variants from existing microbiome association
studies performed in disease-free individuals to test whether there are causal links between
levels of bacterial taxa and CRC risk. This analysis suggested that variation in the
Escherichia/Shigella, Fusobacterium, Streptococcus, and Bifidobacterium genera may be
causal for CRC risk. A new complementary approach running GWAS in CRC patients
specifically using the 100kGP cohort was performed, with relative abundance of bacterial
genera and species, counts from toxin-producing bacterial strains, as well as global bacterial
measures taken from the tumour directly used as phenotypes. Variants identified from these
GWAS were then used in MR analyses to see whether causality between bacterial measures
derived from CRC patients and CRC risk could be established. This analysis instead suggested
causal associations for Oscillibacter and Blautia genera, Bacteroides fragilis and
Ruminococcus faecis species, and bacterial count per human cell. In summary, this project
has contributed to the understanding of the genetics of CRC carcinogenesis using methods
that are, in large part, based on the intrinsic robustness of genetic data. The challenges
encountered in this project are common in the field, namely (i) the weakness of most
genetic associations with both CRC and its risk factors and (ii) confounding and pleiotropic
effects of genes and other unobserved factors. My work provides insight into common
genetic variation in CRC, as well as interesting clues for the role of blood cell levels and gut
bacteria in CRC risk
Developing an array of field emitters as a stationary digital tomosynthesis source
No full textIn a world with a dynamic, growing, and ageing population, a new generation of medical imaging devices is needed to meet the demands of early preventive diagnosis, sustainability, and mobility. Static Digital Tomosynthesis offers low-dose 3D imaging with small tumour detection, low power consumption, minimal maintenance, and a compact, mobile form. The core enabling technology is field emission, where a strong electric field (F > 1 GV/m) at a high aspect ratio tip induces quantum electron emission (see Chapter 1).
For medical imaging, the emitter must deliver large currents (I > 100 μA), but in this regime, heating effects (Joule and Nottingham) can cause emitter failure via vacuum breakdown. This thesis focuses on identifying a material that withstands high current, temperature, and electric fields, while remaining compatible with cleanroom mass production for use by an industrial partner.
In the effort to develop a high-power field emitter GETELEC (General Tool for Electron Emission Calculations) has been expanded to include the physics of field emission from semiconductors (see Chapter 2). To provide the inputs to GETELEC-2.0, a finite element method Multiphysics model has been developed. This model solves self consistently all the required differential equations, taking GETELEC-2.0 outputs as boundary conditions, to compute the electric field, the temperature, the band structure, and the emitted current. To the knowledge of the author this is the first full self-consistent 3D model for thermal-field emission from semiconductors (see Chapter 2). With this new model, it is predicted that 4H-SiC should be able to withstand from ×4 to ×10 more current than Si (reference material). In order to validate the theoretical predictions, three types of emitters have been fabricated both in Si and 4H-SiC, keeping the same geometry but changing the material - emitter twins – (see Chapter 3). The experimental data obtained from each emitter type shows that 4H-SiC emitters yield currents between ×3.5 and ×9.5 higher than those from their Si twins (see Chapter 4).
The theoretical and experimental evidence gathered over the course of this PhD research supports the idea that 4H-SiC is a material that can be used to meet the current needs that medical imaging devices require. Improvements on the emitter cleaning protocol (e.g., thermal treatment or laser treatment) and taking the emitter to ultra-high vacuum conditions (P<10-9 Torr) is likely to improve the performance the emitters; and yet these have yield up to ×12 more current (in DC mode) than any other SiC reported emitters to the knowledge of the author (caution when comparing field emission experiments is to be reminded). These results are sufficient justification for the industrial partner of this PhD research to start the development of 4H-SiC field emitters for their high current devices
LGI4 and ADAM22: a Schwann cell-neuronal interaction that gets myelin on your nerves
No full textMyelin is a highly ordered, lipid-rich lamellar structure that ensheathes axons and is produced by dedicated neuroglial cells, oligodendrocytes in the central nervous system and Schwann Cells (SCs) in the peripheral nervous system (PNS). SC in the PNS are the essential support cells vital for peripheral nerve structure, health, and function. Neuronal axons are reliant on SC for trophic support and the production and maintenance of myelin while SC rely on axons for cues that drive their survival and differentiation.
One essential interaction is SC secreted Lgi4 (Leucine-rich glioma inactivated 4) binding to neuronal Adam22 (A disintegrin and metalloproteinase 22). This interaction is required for axonal sorting and myelination. Dysfunction in Lgi4 signalling has been shown to cause hypomyelination and arthrogryposis multiplex congenita, a developmental disorder characterised by congenital postural abnormalities involving the major joints in both mice and humans. The downstream mechanism of LGI4-ADAM22 signalling that drives myelination is yet to be elucidated. Furthermore, Lgi1, the evolutionary ancestor to Lgi4, has been demonstrated to dimerise when interacting with Adam22. This may suggest a mechanism through which Lgi4 acts to drive myelination. We propose three potential mechanisms: 1) extracellular trans-interaction with the Schwann cell 2) Extracellular cis interaction with axon 3) Intracellular transduction via Adam22 intracellular domain. Based on the initial hypothesises my thesis followed three broad aims. Firstly, to elucidate the downstream interactions post LGI4-ADAM22 binding. Secondly, to identify the domains of ADAM22 that make it promyelinating. Thirdly, to determine if dimerisation is functionally relevant to LGI4-ADAM22 driven myelination.
Using primary rat SC cultures, I showed that ADAM22 does not interact with the SC in the presence or absence of LGI4 (first aim 1). Using Dorsal root ganglia (DRG):SC cocultures derived from ADAM22 knockout mice and a lentiviral based expression system we were able to show that both the metalloprotease and disintegrin domains of ADAM22 contribute to myelination, though this was inefficient compared to wildtype (second aim). Finally, using DRG:SC cocultures from claw paw mice (a model with no in vitro Lgi4 expression) and a retroviral expression system we were able to determine that dimerisation was functionally relevant for LGI4-ADAM22 mediated myelination (third aim) and that disruption of dimerisation significantly impacted the efficiency of myelination.
Overall, the data generated from in vitro co-culture systems and primary cell lines greatly enhance our understanding of the interactions between LGI4 and ADAM22 and begin to unravel the mechanisms downstream of LGI4-ADAM22 signalling
Ge Hong's Dao: locating the Baopuzi Neipian within the contexts of Early Medieval China
No full textThis thesis examines Ge Hong’s 葛洪 (283–343) Baopuzi neipian 抱朴子內篇 (Inner Chapters
of the Master Who Embraces Simplicity), a pivotal early fourth-century text on transcendence
(xian 仙). By situating the Neipian within its intellectual, social, and political contexts, this
study sheds light on how Ge Hong integrated intellectual concerns into Daoist traditions,
thereby constructing in the Neipian a close and dynamic interaction with both earlier and
contemporary scholarly discourses. Chapter I analyses Ge Hong’s construction of his
framework for advocating transcendence by responding to anti-transcendence discourses in
early scholarly writings. It explores how Ge Hong addressed scepticism towards transcendence
by establishing a robust intellectual defence that positioned this pursuit as a legitimate and
attainable goal. Chapter II examines the broader intellectual and social motivations behind the
Neipian. By situating Ge Hong’s critiques of misinterpretations of Lao-Zhuang thought within
his contemporary intellectual trends, particularly within the so-called “Mystery Learning”
(Xuanxue 玄學) tradition, it highlights how the Neipian sought to correct what it regarded as
basic interpretive errors , addressing their detrimental impact on social and scholarly norms as
a consequence of their misunderstandings about the true meaning of dao 道. Chapter III uses a
case study of Ge Hong’s discussion of Laozi 老子 to delve deeper into how the Neipian
engaged with key intellectual debates of its time. This chapter reveals how Ge Hong employed
transcendence as a means of engaging in dialogue with broader intellectual and social
discourses, thus positioning the ideas of Daoist traditions as a relevant intellectual force.
Chapter IV explores how Ge Hong redefined “lineage of dao” (daojia 道 家 ) through
advocating the correct understanding of transcendence and dao. By linking daojia to early
Daoist traditions, Ge Hong emphasised its authority as the teachings of sages, elevating daojia
to a position comparable to lineage of ru 儒. This connection also served as an active
engagement with the intellectual debates of his time. This study challenges the reductive
“religious/philosophical” dichotomy in past Neipian research by recontextualising it within its
historical setting, Daoist development, and Ge Hong’s broader works. By offering a more
integrated interpretation, this research repositions the Neipian as a key text for understanding
Daoism’s formation during early medieval China
Use of mutational signatures and spectra to determine the extent to which prior therapy drives the onset of colorectal and endometrial cancer
Get PDFThe mutagenic effects of genotoxic damage, caused from DNA-damaging chemotherapy (CT) and radiotherapy (RT), has been a long-term concern of anticancer treatment. Accumulating epidemiological evidence suggests there is a small increase of secondary cancers, including colorectal (CRC) and endometrial cancer (EC), a period after receiving genotoxic treatment for a first malignancy. CRC is the 4th most common cancer within the UK and is the 2nd biggest cancer killer; EC is the most commonly diagnosed gynaecological cancer, resulting in ~1,370 deaths per year. Recent advances in sequencing technology means established mutational signatures within a genome can now be identified and used to determine the extent in which prior genotoxic therapy drives the onset of cancer. Therefore, this study utilized next-generation (NGS) and whole genome sequencing (WGS) technologies, to identify both mutational signatures and unique CRC/EC driver gene mutations which may have originated from therapy exposure.
This was investigated within the 100K genomes project, and CORGI (Colorectal Tumour Gene Identification) cohorts. Variant callers strelka2 and smCounter2 produced VCFs (for unique driver mutation identification), and signatures within both cohorts were produced by inputting these VCFs into SigProfilerExtractor tool. Within the CORGI cohort, signature analysis identified de novo decomposed signature SBS96A, composed of SBS5, SBS87 and SBS54 COSMIC signatures – clock-like, thiopurine CT treatment, and possible sequencing artefact respectively. Additionally, driver gene analysis identified a handful of uncommon and/or rare pathogenic mutations in AT rich regions – primarily within APC, in a T>A C>T context, reflective of an alkylating agent. Within the GEL (Genomics England Limited) 100KGP cohort two signatures of interest were identified within RT groups: SBS58 and SBS89 – an artefact signature and unknown aetiology respectively. In EC, a significant increase of DBS were identified within the CT 10 year group. Conclusively, the above findings provide molecular evidence for the role of prior genotoxic therapy in the growth +/ onset of subsequent cancers. However, both GEL and CORGI cohorts lack power, because of their small size and limited clinical data, weakening the strength of these hypotheses. Consequently, observations could be due to a confounding variable. It is likely sample size and power will increase in future, as more genomes are sequenced as part of the personalised medicine drive within the NHS. With this additional supporting evidence, these preliminary findings may be enhanced and theoretically confirm genotoxic therapy’s influence in the onset of secondary cancer in latter life
Implications of realistic non-steady environments for tidal turbine performance evaluation and mechanical load characterisation
Get PDFDecarbonising human life is core to sustainability, and many facets of our existence
will need to be carbon-neutral in the future. The energy sector, specifically
electricity generation, is at the forefront of this green transition globally. One of
the challenges in this context is a shift from on-demand generation provided by
burning hydrocarbons to the often intermittent nature of harnessing renewable
resources. This is especially significant when addressing the need for consistent,
reliable base loads. One answer to this challenge, and the focus of this thesis,
comes in the form of tidal energy.
Tidal stream turbine technology has advanced over the past few decades but is
still in its relative infancy. At this early stage in tidal turbine development, there
is a clear lack of in-service learning to draw from, so numerical and experimental
research is driving developments. Advancements in tidal turbine technology rely
on a better understanding of the interaction between turbine rotors and the environment.
The non-steady nature of tidal flows adds complexity to understanding
rotor loading. The inclusion of strongly sheared currents, turbulence and surface
waves all contribute to a unique operating environment.
The primary focus of this thesis is the mechanical performance of tidal turbine
rotors. Initially, research is undertaken to evaluate current methods for performance
benchmarking by assessing the classical performance indicators CP and
CT, or more specifically, scrutinising the normalising velocities used in constructing
these indicators. Two tank test data sets are analysed, one from IFREMER
and another from FloWave at the University of Edinburgh. On analysing onset
flow datasets from FloWave, it is shown that CP and CT can be biased by as
much as 22.44% and 15.58% respectively. The analysis of calibration data at the
IFREMER flume reveals that the method used to characterise a rotor plane area
(in the absence of a turbine) can introduce up to 12.04% change in CP and 7.88%
change in CT. These analyses highlight a significant challenge to benchmarking
rotors against each other. This leads to the recommendation at the FloWave
facility that performance benchmarking should be done using calibration flow
measurements rather than synchronous flow measurements. Additionally, these
calibration measurements should account for spatial variations in terms of transverse
shear in addition to the already specified vertical shear in IECTS62600-
200.
Next, considering dynamic mechanical performance, the effects of realistic,
complex ocean environments on rotor performance are studied. A novel numerical
model is developed on the OpenFOAM framework, which includes a twophase
fluid solver (water and air) that simulates surface waves, shear currents
and turbulence. An actuator line model is embedded within this to solve the
rotor loading. The model is scaled to a 1.5 MW machine, and by varying wave
configuration as well as rotor position in the water column, sensitivities in hub
loading are investigated in terms of torque and thrust, but also with regard to the
out-of-plane hub moment, which is hypothesised to be important when considering
turbine damage. A new metric, the maximum load span (MLS), is developed
in this thesis to describe the form of the out-of-plane hub moment. The MLS
was found to increase with both hub height and wave height. The MLS also
shows dependence on wave period, which changed the cyclic form of the out-ofplane
moment patterns, leading to what has been referred to as “wave-driven
moment-type dominance”. Longer wave periods resulted in moment loading
that was dominated by a yaw response, while shorter period waves resulted in a
predominantly pitching moment response.
The dynamic mechanical rotor loading characteristics uncovered in the numerical
simulations are verified experimentally. An experimental campaign was
undertaken as part of this research to further highlight the rotor loading in response
to surface waves. Complete validation of the out-of-plane load forms
was unachievable experimentally due to the challenge of maintaining a tightly
controlled constant speed of the University of Edinburgh turbine. However, applied
to tidal turbine rotors for the first time, a “load-loop” analysis approach
is used and verifies the changing form of the out-of-plane hub moment under
wave loading. The experimental campaign highlights a wave-driven moment-type
dominance dependent on both wave height and period, in slight contrast to the
numerical work, which only identifies wave period as the driving variable
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