KING'S COLLEGE LONDON

UKRI Gateway to Research · FY 2027 · 2027-01

The remarkable idea that matter is comprised of discrete units, indiscernible to the eye, can be traced back to ancient Greece. In the centuries since, scientists have grappled with the myriad questions this atomic theory raises. This project is guided by one such question: How does matter, consisting of a multitude of interacting particles, exhibit such a rich array of patterns and structures? Over the past century, statistical physics has emerged to address precisely this question. The essence of the problem—understanding the relationship between order and disorder—is so fundamental that it is central to several scientific fields. During my Fellowship, I have demonstrated how tools and intuitions from statistical physics can be used to help solve longstanding problems in combinatorics, computer science, and geometry. These findings set the stage for an ambitious research programme for the future aiming to deepen understanding of these fields and strengthen the connections between them. This project begins with one of the most well-known problems in mathematics: the sphere packing problem. Dating back to Kepler in 1611, it asks: If you want to fit as many identical spheres into a box as possible, what is the best way to arrange them? Though simple to state, the problem hides deep mysteries that continue to challenge scientists. One aim of my FLF was to construct particularly dense sphere packings in high-dimensional space using ideas from combinatorics. In late 2023, we succeeded—our packings were the first to improve a classical construction due to Rogers from 1947 by more than a constant factor. In contrast to many constructions from the past century, our packings were disordered, lacking global crystalline structure. The existence of such dense, disordered packings was predicted by Parisi (Nobel Prize, Physics) and Zamponi, which inspired our work. One major objective of this project is to explore the sphere packing problem through the lenses of physics, combinatorics, and algorithms. A key step will be to rigorously confirm a prediction by Parisi and Zamponi about the entropy of sphere packings—a quantity that captures how plentiful packings are. This objective promises valuable insight into the rich and elusive structure of packings in high-dimensional space. The study of sphere packings led my collaborators and me to a significant advance on an old problem in Ramsey theory, a seemingly unrelated field. Ramsey theory, a cornerstone of combinatorics, is built on the idea that in any sufficiently large system, some form of order must emerge—total randomness is impossible. I aim to build on this unexpected connection to advance our understanding of both the sphere packing and Ramsey problems, and thereby strengthen the powerful emerging links between combinatorics and geometry. Another central aim of this project is to revisit classical problems in combinatorics through the lens of statistical physics and algorithms. Many combinatorial structures exhibit rich order–disorder phase transitions, yet traditional combinatorial tools often fail to capture this behaviour. Building on advances from my Fellowship, I aim to develop a toolkit, grounded in algorithms and statistical physics, to study these phenomena. A particular focus will be on what I believe is a deep and largely unexplored connection between the classical theory of large deviations and the framework of message-passing algorithms. Uniting these two powerful perspectives promises fresh insight into the emergence of structure in discrete systems.

UKRI Gateway to Research · FY 2027 · 2027-01

Politically engaged interwar women writers redefined the female citizen in the wake of 1928 electoral reform by interrogating her perceived intelligence. This research demonstrates that a study of this process reveals the origins of a new form of politics that influenced Britain: meritocracy. In partnership with external stakeholders, the project reframes knowledge of women’s role in meritocracy, educates potential new voters and illuminates how education informs democratic inclusion today. The 1928 Equal Franchise Act gave British women the vote on equal terms with men and removed the property qualification, newly enfranchising 5 million women. Public debate suggested that the new, female citizen was part of an imagined intelligent elite, implying that it was women’s intelligence that made them worthy voters. Interwar women writers troubled this idea. Against George Bernard Shaw’s The Intelligent Woman’s Guide to Socialism, Capitalism, Sovietism and Fascism (1928), Winifred Holtby defended a female voter who ‘seems stupid’ (10). Author-activists including Vera Brittain considered how the idea of female intelligence was used to restrict access to education, the professions and political participation. For Marie Stopes and Naomi Mitchison, intelligence was embedded in the eugenicist and biomedical. In their fictional and non-fictional works, these women showed how intelligence was a concept shrouded in gender, class and racial hierarchies, cast light on these prejudices, and negotiated women’s new relationship to the state. Previous work has examined interwar women in the private sphere as domestic citizens. This project focuses instead on how these women were activists in organisations that influenced women’s new identities as female citizens. Interwar women writers’ interrogation of the perceived intelligence of the female citizen demonstrates how women became a testing ground for Britain’s new political story: meritocracy. Meritocracy claimed to make a person’s mental ability, not their family background, shape their future. The intelligence test was first discussed as a tool for organising a secondary education system in 1924. Women’s new civic identity therefore coincided with a period of educational reform that promised to make meritocracy possible by offering a seemingly objective measurement of intelligence. The gender-based discrepancy in educational opportunities meant that codes of competition that define meritocracy were more pronounced for women than for men. The project shows that women writers were at the frontline of debates surrounding how far mental ability should determine access to the public sphere. In modern Britain, voting habits divide along educational lines and lowering the voting age to 16 is a matter of political debate and government strategy in the Elections Bill. Partnerships with the Pankhurst Centre and LSE Women’s Library will influence public understanding of how education shapes democratic participation. The project will enable both partners to reach new audiences and bring the research to beneficiaries in centenary exhibitions, schools’ workshops and teaching materials that meet criteria on the GCSE Citizenship and A-Level History curricula. Objectives: 1.     To demonstrate how women writers shaped new ideas of female intelligence in response to the 1928 Act, challenging the relationship between intelligence and citizenship. 2.     To demonstrate how gender, class and race shaped the public debate on female intelligence and to establish interwar women writers’ relationship to these debates. 3.     To explore democratic inclusion today through partnerships with heritage organisations, libraries and schools. 4.     To realise the societal relevance of an analysis of the historical origins of meritocracy through project partnerships.    

UKRI Gateway to Research · FY 2026 · 2026-09

The UK's globally leading creative economy is rapidly evolving, driven by advancements in immersive technologies and artificial intelligence (AI). Despite significant investment in creative R&D and lab infrastructure, two critical gaps hinder future growth: a skills gap in leveraging new technologies for audience engagement, and a diversity gap in both workforce and audience composition. Recent research underscores "a huge potential audience [...] currently attracting the smallest proportions of the population" (PEC, 2024: 5), highlighting the urgent need for innovative approaches to audience research and development. It also reveals that "the make-up of the workforce inform[s] the kind of work that is made, thereby likely affecting the composition of audiences" (Ibid.). This cyclical relationship between workforce and audience diversity presents both a challenge and an opportunity for the sector's growth and sustainability. Positioned in the AHRC 'Creative Economy' priority area ADAPT-AI addresses these interconnected gaps by training the next generation of diverse creative sector leaders as experts in analysing and diversifying audience participation in immersive experiences. This adaptive approach will harness UK creative intellectual property while addressing underrepresentation in both the doctoral community and creative sector workforce, combining AI and creative technologies as key tools for innovation. Our interdisciplinary training programme addresses the pressing needs for innovative methods to understand and engage diverse audiences, advanced digital skills, creative thinking, and entrepreneurial mindsets. ADAPT-AI will transcend traditional audience studies and reception analysis. While studying audience trends at an unprecedented scale, our ambitious vision is to identify, create, and shape audiences for emerging creative technologies. ADAPT-AI will develop a diverse cohort of experts proficient in using creative technologies and AI to analyse and diversify audience participation critically, creatively, ethically and responsibly. The doctoral training and development programme will deliver: Rigorous training in AI, including machine learning, machine vision alongside Extended Reality, Virtual Reality, Augmented Reality, and real-time technologies. Methods for ethical audience analysis: Equipping leaders with skills to map, track, and analyse audience patterns, behaviours, and attitudes in immersive experiences using novel methodologies. Innovative approaches for inclusive audience participation: Developing new methods for deep audience engagement driven by principles of equality and inclusion. Industry-academia collaboration: Engaging in knowledge sharing to develop new economic models of audience access, targeting untapped markets and underserved communities. Increased diversity in creative sector leadership: Boosting the proportion of doctoral students from underrepresented backgrounds and supporting their progression into leadership roles. ADAPT-AI is a diverse consortium of three highly interconnected and interdisciplinary research and innovation cultures - one Russell Group, one post-92 and one small specialist institution. It combines expertise in creative industries, digital humanities, media production, and performance practice. Working with world-class venues drawing millions of audience members annually, and leaders in immersive content creation, ADAPT-AI is uniquely positioned to contribute to an unparalleled evidence base. ADAPT-AI's London focus leverages the city's position as a global hub for creative industries and cultural innovation. Our partners' London-based facilities and audiences offer students access to cutting-edge technologies and diverse user groups, essential for comprehensive audience research and development. By developing expertise, innovating engagement methods, and fostering industry-academia collaboration, ADAPT-AI will empower the next generation of leaders to shape the future of arts, entertainment, and media landscapes. Our graduates will drive innovation, contribute to UK GDP growth and ensure the UK enhances its leading position in the global creative economy.

UKRI Gateway to Research · FY 2026 · 2026-09

The challenge: Schizophrenia is a top cause of global disability and costs are ~100 billion Euros per year in Europe alone. Cognitive impairment is a leading contributor to the disability of the disorder, and there is no licensed drug treatment for it. Consequently, cognitive impairment is a major unmet need in schizophrenia. Moreover, focus groups involving people with schizophrenia and carers were unanimous that identifying treatment targets for cognitive impairment is a top priority. Aim: to test a mechanism thought to underlie cognitive impairment in schizophrenia and validate a potential biological target for treatment. Context: Brain cells have high energy needs. The first step in cellular energy production requires mitochondrial protein complex 1 (MC1) to catalyse electron transfer from NADH (producing NAD+), which is required for ATP synthesis. Multiple lines of genetic, cellular and post-mortem evidence indicate that schizophrenia is associated with impaired MC1 levels and function. In vivo brain imaging data show that people with schizophrenia have lower NAD+/NADH ratios and less MC1 in the frontal part of their brains than healthy people, and that lower MC1 levels are related to lower brain activity during cognitive tasks and poorer cognitive function. These data indicate that lower MC1 levels in schizophrenia could impair brain function to underlie cognitive impairments in the disorder. Our proposed project will provide a crucial test of this mechanism. Our hypothesis is that bypassing MC1 will increase NAD+/NADH ratios and restore brain activity in schizophrenia. We will use methylene blue as a mechanistic probe. This drug transfers electrons from NADH to the next step in ATP synthesis, bypassing MC1. If our hypothesis is correct, administering this drug will increase NAD+/NADH ratios and neural activity and so improve cognitive function in schizophrenia. We will test the effect of methylene blue on NAD+/NADH and brain activity using magnetic resonance imaging measures of brain activity and cognitive performance during a cognitive task in people with schizophrenia. Timeliness: the new lines of genetic, cellular and PET evidence for MC1 alterations in schizophrenia mean it is timely to test this target. Moreover, a number of pharmaceutical companies are developing drugs that could target MC1. Applications and benefits: The findings will benefit researchers in the field by providing a key test of whether MC1 dysfunction underlies altered neural activity in schizophrenia and could result in a paradigm shift in the understanding of schizophrenia by providing the first in vivo evidence of a molecular mechanism underlying cognitive impairments. Findings will also be relevant to other disorders where MC1 has been implicated (e.g. Alzheimer’s disease, bipolar disorder) Impact: the study could identify MC1 as a treatment target with the potential to lead to the first medicine for a major unmet need in schizophrenia, benefiting people with schizophrenia, healthcare systems and society in general. It could also inform the development of treatments targeting this approach for other disorders with cognitive impairments.

UKRI Gateway to Research · FY 2026 · 2026-08

In the 21st century, scientific advances have fundamentally challenged the view that an individual’s health and well-being is written into their genes. Human development and health are now understood as profoundly shaped by early life environmental conditions. There have been significant public health investments in developing interventions during pregnancy and early childhood, particularly for decreasing obesity and non-communicable disease in the next generation. Recent evidence shows that interventions in pregnancy for decreasing obesity risk is of limited efficacy, and scientists are turning to the period before conception as a window of opportunity to shape intergenerational health. Testing this theory requires clinical trials that start before pregnancy and measure outcomes in the next generation. These new scientific approaches raise important questions that require urgent consideration given their possible societal impacts. The 'preconception' focus could productively emphasise the wide range of social determinants of health, but also has the potential for a loss of gains in reproductive rights and gender equality, and diminished attention to the social drivers of health inequities. This timely program of research meets the urgent need for (1) Social science attention to the social and ethical implications of research and intervention in the 'preconception period', including how preconception trials are conducted, the assumptions underpinning this research, and what this means for global public health policy; (2) Innovative qualitative methodologies for studying the social factors that shape life trajectories. To do this, Trajectories hosted at King's College London is partnered with the Developmental Pathways for Health Research Unit at the University of the Witwatersrand in South Africa, the Geneva Graduate Institute and the Healthy Life Trajectories Initiative (HeLTI) study. HeLTI is hosted by the World Health Organisation and has cohorts in Canada, India, China and South Africa. HeLTI recruits approximately 20,000 women to assess the effects of a four-phase complex intervention from preconception to childhood on early childhood development outcomes and child obesity risk at age 5. Drawing on an excellent interdisciplinary team of anthropologists, bioethicists and public health researchers, Trajectories works with HeLTI to produce the first ethnography of a life course intervention trial and the first qualitative longitudinal study of a cohort of this kind, tracking sixty women enrolled in the HeLTI-South Africa trial to trace the interaction of the social and biological factors that shape health outcomes - from preconception to early childhood, and across the life course. Trajectories will advance our theory and understanding of the social contexts of early life development and obesity risk; document key scientific lessons from HeLTI; and create a space for public dialogue on the implications of new scientific knowledge for how we understand patterns of intergenerational health and disease. This unprecedented collaboration will offer rich insights into how life course interventions can work most effectively to decrease health inequities and will build the interdisciplinary research capacity needed to achieve this aim.  

UKRI Gateway to Research · FY 2026 · 2026-04

Detection of severe fetal structural disease usually occurs at the 20-week anomaly ultrasound scan, meaning that for the 3000 patients every year in the UK who choose termination of pregnancy following this diagnosis, this procedure is performed late, increasing clinical risk and impacting long-term psychological wellbeing. However, these diseases could actually be picked up at the 12-week scan, as seen in a few highly expert specialist centres. This is technically challenging because of the small size of the fetus at this stage, resulting in poorly resolved anatomical features. This proposal aims to bridge a key gap that could unlock future research on artificial intelligence (AI) to transform fetal health screening by bringing the diagnosis forward to 12 weeks across all centres. Detecting problems this early would give parents and clinicians more time to plan care, arrange genetic testing, and make informed choices. It also allows any interventions such as termination of pregnancy to happen in a safer, less distressing way. Over a 10-year research programme, our team has already created advanced AI tools that assist with the 20-week ultrasound scan. Our tools can automatically identify which part of the fetus is being scanned (the “standard plane”), measure growth, and support the diagnosis of structural abnormalities. In the world’s first randomised controlled trial of AI in fetal ultrasound, these tools were shown to reduce scan time and sonographer workload while maintaining diagnostic accuracy. The technology has since been commercialised through a university spin-out company, Fraiya Ltd, and is now CE-marked as a medical device. To enable AI-assisted diagnosis at an early stage of pregnancy, we have recently collected an unprecedented prospective dataset of entire screening scan videos performed at 12 weeks. However, we cannot yet use this dataset to train disease detection models, because the data are unstructured, and not labelled for anatomical view. This project proposes to bridge this gap between unstructured data and structured, usable data, by developing an AI model that can automate this process. We can do this because of our previous work, meaning we have a highly accurate 20-week anatomical classifier that could be retrained for 12 weeks using transfer learning methods, coupled with this new, unique dataset. Training a 12-week anatomical classifier is a high-risk and complex step, as the size of the fetus is extremely small at that stage. However, if successful, this project will remove a key barrier that currently limits research and innovation in early pregnancy screening. It will unlock the development of future AI models for 12-week anomaly detection and could ultimately transform prenatal care worldwide. By bringing diagnosis significantly forward in gestation, this work has the potential to improve outcomes for thousands of families, reduce emotional stress, and make screening more efficient and equitable within the NHS and beyond.

UKRI Gateway to Research · FY 2026 · 2026-04

Background and importance: The essential role of the adaptive immune system is to provide long-term protection against pathogens via the production of antibodies. To combat the complexity of pathogens in the environment, our immune system has evolved the capacity to produce a vast diversity of antibodies from a relatively small set of genes. This diversity is primarily achieved through somatic hypermutation (SHM), during which mutations are introduced into the antibody-encoding genes in B lymphocytes, a specialized type of white blood cell. These mutations subtly alter the "shape" of antibodies, affecting their binding strength, or affinity, towards the pathogen or vaccine. However, in the case of some pathogens, notably HIV-1, protective antibodies are difficult to elicit, highlighting the need for a deeper understanding of the mutational pathways and the molecular principles that govern the mutation reaction to design more effective vaccination regimens. Aims and objectives: Despite the importance of SHM, we still lack a thorough understanding of how it works, particularly the exact mutagenic pathways and mechanisms that lead to the evolution of the desired protective antibodies. Understanding these pathways is crucial for improving our ability to design effective vaccines and therapies. To address these gaps in our knowledge, our research aims to systematically study how SHM generates potent, anti-viral antibodies in a controlled setting using a specialized human B cell system that we have engineered and optimized for this purpose. Specifically, we will focus on identifying how antibodies are diversified via SHM to target two major viruses, human immunodeficiency virus-1 (HIV-1) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agents for AIDS and COVID-19, respectively. By tracking the mutations that occur across multiple timepoints (referred to as a longitudinal analysis), we aim to map and study the mutational trajectories that lead to the production of potent, neutralizing antibodies against these viruses. Additionally, we will investigate how neighbouring DNA sequences influence, either positively or negatively, the occurrence of higher affinity-conferring mutations in the antibody genes and thereby gain mechanistic insights into the rules and principles guiding the evolution of the mature antibodies. Potential benefits and relevance: Understanding the development of HIV-1 and SARS-CoV-2 broadly neutralizing antibodies (i.e. antibodies that can neutralize the majority of viral variants) can guide the design of vaccines that could trigger these potent antibodies. By identifying the most probable mutational pathways that can generate the desired protective antibodies, we can pinpoint the best targets for vaccine development. This is especially important for current strategies where vaccines are crafted to gradually activate and mature specific B cells in a systematic, stepwise manner that enables them to produce the desired protective antibodies over time. Additionally, since SHM can also contribute to cancer (due to undesired mutation of cancer-causing oncogenes), deciphering the rules governing the mutation process will be of direct relevance towards understanding the genesis of B cell cancers. Another potential benefit of our research is the discovery of new neutralizing antibodies against HIV-1 and SARS-CoV-2. Finally, and more generally, our experimental system could we used as a template for studying antibody maturation against a range of pathogens.  

UKRI Gateway to Research · FY 2026 · 2026-03

This proposal will be entirely hold in probability theory, as a domain of pure mathematics. It is, however, related to classical models in statistical physics. How to predict the trajectory of particles in a fluid, the movements of an animal searching for food in a changing environment, or the variation of stock prices in an fluctuating market? Modelling dynamic systems straddle several branches of mathematics. Because of the high complexity of real-world instances, using randomness is crucial to make computations tractable, and to focus on essential properties rather than contingent details. In probability theory, random walks are a generic class of models describing a sequence of random steps. Studies often focus on random walks in static environments, and there is today a rich literature since seminal papers by Kestlen, Kozlov, Sinai and Spitzer in the 1970s. However, most of the classical techniques break down when making the environment dynamic - which is problematic if one has realistic applications in mind, but also poses challenging questions from a purely mathematical perspective. In the past two decades, probabilists have intensively investigated random walks in dynamic environments, notably when the later are particle systems. A popular instance is the exclusion process (in which particles move independently under the condition of not superposing, a natural model for a fluid). However, little is still known due to heavy space-time correlations. This makes such models very hard to handle, while giving hope to observe intriguing phenomena such as non-diffusive fluctuations. The aim of this proposal is to deliver pioneering results on random walks on the exclusion process, and to develop powerful tools to understand similar environments. The model is as follows: on top of the environment, which is a one-dimensional symmetric exclusion process, a random walker moves with a bias to the right (resp. to the left) when sitting on a particle (resp. an empty site). I will take advantage of the novel techniques developed in a recent work, where my coauthors and myself show that increasing the density of particles leads to a positive speed increase for the walker. My main objectives are: 1) Investigating the critical density where the speed could be zero: is the speed defined and continuous? What are the fluctuations of the random walker? 2) Adding a current flow: the particles themselves now have a drift. Does the random walker still have a speed? The current complicates the space-time correlations, but our techniques can bypass that. 3) Cooling of the environment: if the activity rate of the particles goes to zero with time, do we start seeing effects from static environments, where the random walker can spend most of its time into traps which now take long to dissolve? 4) Higher dimensions: in dimensions above one, the loss of monotonicity makes the study especially difficult. However, I believe that in dimension at least five, particles get ‘dissipated’ quickly after meeting the walker, so that one can control the correlations to prove a law of large numbers for the walker’s displacement.   The findings will hugely advance the understanding of random walks on various dynamic environments. They will also benefit neighbouring areas in probability theory such as percolation or mixing times, where the techniques developed in the proposal will apply. Finally, the results will also deliver valuable insights on conjectures from statistical physics.

UKRI Gateway to Research · FY 2026 · 2026-03

We have developed and patented HYDROGIT, a novel transformative self-expanding and biodegradable hydrogel technology for dilation and delivery of drugs to tubular mucosa of the gastrointestinal tract. This project will bridge the gap between the novel hydrogel technology that we have developed and its applicability for clinical translation. The device underwent design development, in vitro, ex vivo studies in rats. However, the anatomy, dimensions and mechanical interaction in human is vastly different to rodents. This proposal seeks funding to provide in vivo proof of concept data for a human version of HYDROGIT in large animals (pigs). The outcomes will generate a go/no-go in vivo data to pave the way for first-in-human studies. This will enable progressing the technology to the translational phase towards clinical application. We have identified oesophageal strictures as the target first indication; the data will unlock other opportunities by establishing the viability of the technology for oral delivery of large biologics. Current treatments for oesophageal strictures, such as endoscopic dilation and stent placement, can be invasive and may not always provide long-term relief, necessitating multiple hospital visits and repeated risk-burden of interventions each time. Our technology employs smart highly expanding and degradable hydrogel based interpenetrate polymeric network of gelatine and polyacrylate. The device has tubular architecture with built-in microneedles (HYDROGIT) to align with tubular organs e.g. oesophagus, avoid gastrointestinal blockage and interact with gastrointestinal mucosa. The device can expand up to 5-fold its diameter and enhance the permeation of biologics. Through the dissolution of its soluble component (gelatine), the device can be engineered to collapse following deployment at a preset time. We have provided a proof of concept using rat animal model. The specific objective of this in vivo study is to demonstrate in vivo proof-of-concept by obtaining pharmacokinetic profile in porcine model. HYDROGIT is a multidisciplinary project based on collaboration of experts in oral drug delivery, engineering in King’s College London and clinical researchers in Gastroenterology, Upper GI and Endoscopy Department at King's College Hospital as well as experts in large animal studies with a particular focus on porcine models in Griffin Institute. The strategic integration of these findings and expertise will drive the translation of the HYDROGIT prototype into a human-ready platform and accelerate its development and regulatory approval for the treatment of oesophageal strictures and oral delivery of biologics.

UKRI Gateway to Research · FY 2026 · 2026-03

This research project seeks to investigate a wide range of political, military, and business archival sources held at the Library of Congress. It plans to utilise historical source analysis to extract information relating to the international armaments sector from 1870 through to 1918. More specifically, it looks to trace the movement of arms technology and products between America and Great Britain. In so doing, it will assess the complex and evolving connection that both nations had with weapons manufacturers and the role which armaments increasingly played in relations between them. Covering periods of both peacetime and war, international trends will be extracted which can then be contrasted against domestic military-industrial interactions.

UKRI Gateway to Research · FY 2026 · 2026-03

The AHRC Doctoral Landscape Hub for London and the East of England will bring together twelve HEIs across the region, each of which has been awarded studentships through the AHRC's Doctoral Landscape scheme. The Hub, led by King's College London, will provide skills training, cohort events and development opportunities for all the students funded by the Landscape Awards across the member institutions. Our vision for the London and East of England Hub is to build a thriving cohort of doctoral scholars across the unique constellation of institutions that make it up. Drawing on our diverse resources, we will work together to equip all our students with the tools for success in their research and in future careers, responding to identified skills gaps and to student need. We will provide a high quality, distinctive, accessible, responsive programme of training, enabling our students to make meaningful impacts in a rapidly changing world. Our aims are fully aligned with the emphasis on the creative industries in the UK government’s recently published industrial strategy, in that they focus on developing the high-level skills and knowledge that will be needed for success in those domains. Our Hub is made up of diverse institutions, including large, multi-faculty universities and smaller, more specialized institutions. Our disciplinary spread is comprehensive, encompassing practice-led research and rapidly evolving disciplines such as Digital Humanities, alongside more traditional humanities fields. Many of our member HEIs work closely with their local and regional communities, as well as with national and international partners. Our students will be diverse in terms of their backgrounds, motivations, interests and career aspirations. Many will be working at or across disciplinary boundaries, including with the social sciences and STEM subjects, and many will be working with partners beyond HE, whether in formal CDA arrangements or other kinds of collaboration. By drawing effectively on the rich resources of knowledge across the Hub partners, we will give all our students access to expertise, dialogue and development opportunities beyond their own institutional and disciplinary locations, allowing them to form a rich understanding of the different contexts in which research takes place, and how their own research can have an impact beyond their field. The Hub will be led by King's, with a management committee comprising representatives from each of the partner HEIs. Training will be programmed in response to known skills gaps and to student need, as revealed by Training Needs Analyses and student feedback. A Hub-led core programme of training will be provided, maximising the offer by sharing existing training already available through members, in addition to new training activities to be commissioned by the Hub. Alongside this we will encourage the co-creation of training by students and supervisors, though a responsive fund to which they can apply. In addition to these training opportunities, the Hub will offer several cohort events each year to bring students together across institutions and disciplines, fostering networks and a sense of community. Equity, diversity and inclusivity will be embedded in all our activities, with a nominated lead ensuring that our training serves the needs of all students and is underpinned by core EDI principles. The Hub will serve to share good practice among supervisors, students and partners, working with other doctoral training programmes to maximise student opportunities and make creative use of our shared resources.

UKRI Gateway to Research · FY 2026 · 2026-03

Please see Oxford application (APP70417)

UKRI Gateway to Research · FY 2026 · 2026-03

Migraine and endometriosis are both common and disabling conditions that cause chronic pain and disrupt normal body functions in similar ways. While migraine is more frequent in women and endometriosis exclusively affects them, both diseases tend to peak in pain during menstruation. Despite affecting around 20% of women, endometriosis remains underdiagnosed and under-researched in Europe. Clinical and preclinical evidence suggests that both conditions share common biological mechanisms, particularly involving pain-related molecules, hormones, and immune cells. We believe that it is the interaction between these three elements—especially the hormonally regulated cross-talk between immune cells and neurons—that drives pain in both diseases. However, how exactly these components influence one another is still unclear. To fill this knowledge gap, we have assembled an international, multidisciplinary team within MiNE, bringing together experts in clinical pain neurology, gynecology, endometriosis, chronic pain models, human sensory neurons, organ donor tissue, neuro-immune interactions, and statistical genomics. Our research will focus on three main areas: understanding how pain-related molecules and hormones affect immune cells; examining how these immune cells, once influenced by hormones, affect pain-sensing neurons; and exploring ways to interrupt this harmful interaction in order to reduce nerve sensitivity and pain behaviors. These studies will use both human cells and animal models and will guide the development of better treatments. We hope this will ultimately lead to clinical trials, the discovery of new painkillers, and the possibility of repurposing existing drugs. By deeply comparing migraine and endometriosis, MiNE aims to uncover shared causes of pain and open new paths toward better care for the millions of women suffering from these chronic, painful conditions.

UKRI Gateway to Research · FY 2026 · 2026-03

To understand the origin of life, demonstrating the organic chemistry that produced the first biomolecules is necessary. This is a goal of prebiotic chemistry: to reveal the chemical processes that led to nascent biology on early Earth. Enzymes are life’s principal catalysts, but their structures are of such overwhelming complexity that it is unimaginable how they self-assembled on early Earth. There was probably an intermediary phase comprising of simpler catalysts that preceded enzymes. However, the functional range of these simple catalysts was likely limited in the same way that enzyme catalysis is restricted by a lack in diversity of the twenty amino acids. Despite billions of years of evolution, enzymes still require low-molecular weight ‘helper’ molecules called ‘coenzymes’ to expand their catalytic repertoire. This strongly suggests that early catalysts also depended on coenzymes, so chemical pathways to coenzymes need to be found. A major hypothesis for the origin of life is that biomolecules necessary for the first cell were produced from hydrogen cyanide. The chemistry emanating from cyanide produces an array of complex products: ribonucleotides, peptides, and lipids. This reaction network initially lacked pathways for coenzyme formation until we very recently produced the catalytic core of coenzyme A. However, coenzyme A alone is not enough for onward progression towards metabolic networks. We need more coenzymes, and we think thiamine is one of them. Thiamine pyrophosphate is one of nature’s most unique and essential coenzymes. It reverses the natural polarity (‘umpolung’) of organic molecules to allow otherwise impossible biochemical reactions to proceed. Our aim is to demonstrate prebiotic syntheses of thiamine precursors (‘proto-thiamines’) using cyanide chemistry. These syntheses will feature organocatalysis for selective bond formations, dehydration reactions in water, and reaction cascades to rapidly generate structural complexity. Upcycling of waste is of enormous benefit in environments with limited resources, so we will convert by-products of proto-thiamine syntheses into amino acids in ways that sidestep the challenges associated with biomimetic reductive aminations. The production of thiamines through shared pathways already producing essential biomolecules would greatly support an origin of life starting from cyanide. It will motivate the exploration of catalytic prebiotic umpolung chemistry, and increase the possibilities of simple chemical ensembles undergoing rapid expansion towards reaction networks under catalytic control. This proposal will have broad appeal: origins of life researchers will reconsider coenzymes as plausible prebiotic substrates; geochemists will constrain environmental boundaries of life’s earliest habitat; enzymologists will be informed of prebiotic pathways for coenzymes that preceded extant biosynthetic processes. Our approach for the rapid onset of molecular complexity in water fits well with the EPSRC’s priority for sustainable green chemistry sought by synthetic and industrial chemists that are cheap, atom-efficient, and scalable. By recreating ancient predecessors of intermediary metabolism, we will contribute towards the bottom-up approach to synthetic biology. This is recognised by the UK government as one of the great new technologies in science. As the international quest to discover life beyond our planet intensifies, our findings will inform physicists and astronomers on key biosignatures to search for across the solar system. Finally, the question of life’s origin holds unique appeal for people of all ages and backgrounds, each of whom bring their own perspectives on our beginnings. An insight into the origins of life enriches our understanding of our shared ancestry and deepens our connection to the natural world.  

UKRI Gateway to Research · FY 2026 · 2026-02

Unhousing Restitution (henceforth UNREST) is a two-year interdisciplinary project that researches, refines and disseminates practice-oriented and Africa-led solutions to African loss of audiovisual heritage. Co-produced with cultural partners by researchers from film studies, African history and digital humanities, UNREST recasts restitution as a collaborative endeavour co-led with international partners and rooted in shared knowledge production and cultural renewal. The project’s framing term, ‘unhousing’, derives from Sudanese artist-filmmaker Hussein Shariffe. Writing in exile from Sudanese dictatorship, Shariffe described the depredations, but also the ‘unhoused energies’ released by states of dislocation. UNREST harnesses those energies by working with archives born in states of dislocation and retrieved by independent archivists working at a tangent to nation-state practice. The research context is one of radical archival loss. Only eight African states boast national film archives. UNESCO concluded in 2021 that African cinema’s ‘best surviving elements’ are ‘almost never found in Africa’. Shared historical narratives are silenced and cultural imaginaries diminished by this loss. Yet public debate and restitutionary action remain sparse. AHRC-funded research on film and Empire has revealed UK film archives replete with colonial-era collections. The BFI, however, records only one successful instance of colonial film restitution (to Trinidad and Tobago). The lack of available models presents urgent challenges in a current context of global geopolitical realignment, and long-delayed demands for restitution of Global South heritage. European moves to meet those demands accelerated with French President Emmanuel Macron’s 2017 declaration of the moral rights of formerly colonised peoples to cultural heritage restitution. Sarr and Savoy’s foundational 2020 follow-up report outlined first principles for restitution of African cultural heritage. The challenge remains, however, to find flexible restitution modes that meet ethical demands for reparatory justice, while overcoming obstacles including budgetary constraints, Global South infrastructure deficits, inflexible legal frameworks, and postcolonial socio-political volatility. UNREST responds with a collaborative project that combines historical enquiry, digital archive development and creative research on two African case studies: Sudan and Ghana. Our aim is to move restitution debates from a focus on the politics of return, to practices of shared transnational history-making, infrastructure development and creative renewal. The project emerges from extensive prior work. PI Carter and Co-I Abdelrahman have led development of a prototype digital archive housing the document collection of Hussein Shariffe. Co-I Hodgkinson worked with Ghanaian partners during a 3-year Leverhulme Fellowship to chart possibilities of archival retrieval for Nkrumah-era films. UNREST brings the three researchers together for a comparative project exploring shared problematics and solutions. It engages a partner network spanning Cairo, Accra, Tamale, Berlin, Khartoum and London. The common aim is, through collaboration with Global South archivists, researchers, artists, filmmakers and technical specialists, to develop and test new approaches to audiovisual heritage restitution including collaborative historical research; community digital archiving; digital repatriation based on shared governance; and creative projects where restitution becomes a democratic practice of reclamation by dispossessed communities. Objectives include digital repatriation of two internationally significant screen heritage collections—the Shariffe and Hesse Collections, the latter named after Kwame Nkrumah’s personal cameraman and UNREST Advisory Board member Chris Hesse; and the development and dissemination of transferable and scalable methodologies for audiovisual heritage restitution in Global South locales. The research has potential applications across the audiovisual heritage sector but will particularly benefit displaced and/or marginalised young filmmakers building creative livelihoods in precarious locales.

UKRI Gateway to Research · FY 2026 · 2026-02

Filamentous actin (F-actin) is an essential dynamic and modular cytoskeletal polymer serving diverse functions in cell motility, morphogenesis and signalling. Responsive architecture modifications of single filaments and their arrangement into higher-order networks of multiple filaments underlie function, driven by the association of F-actin binding proteins (ABPs). Drebrin is a key vertebrate ABP with diverse functions in multiple cell types and is implicated in pathological processes including opioid addiction, epilepsy, Down Syndrome, Alzheimer’s disease and normal aging. Drebrin has best known functions in neurons. In adult neurons, drebrin is localised at the dendritic post-synapse and is important in synaptic plasticity underlying learning and memory. In developing neurons, drebrin is a key modulator of developmental migration, projection outgrowth and connective pathfinding via its localisation and action at the leading-edge growth cone. Drebrin achieves these functions through binding F-actin and coincident single filament and downstream network modification, yet the mechanism of binding is unknown, or how binding translates into modifications of F-actin or higher-order networks. There is some evidence drebrin modifies the architecture of single F-actin filaments directly and modifies their stability. Drebrin F-actin association has been hypothesised to further regulate higher-order networks in cells by displacing other organiser ABPs either via rendering an incompatible F-actin architecture or by directly outcompeting for ABP-binding surfaces on F-actin. The core goal of this project is to reveal how drebrin interacts with F-actin and how this drives its modification both at the single filament and network level. We will first use cutting-edge cryo-electron microscopy (cryo-EM) to detail the interaction of drebrin with F-actin at near-atomic resolution. This objective will also reveal how drebrin modifies filament architecture and competes with ABPs. We will test our models by assessing the F-actin association-dependent ability of structure-based designed drebrin mutants to induce cellular filopodia. Filopodia are an important cell projection in motility and signal sensing formed and maintained by F-actin reorganisation. Secondly, we will determine how drebrin induces filopodia in cells. Nano-scale F-actin architecture reorganisation in drebrin-induced filopodia will be described using in situ cryo-electron tomography (cryo-ET). The possible roles of ABPs in drebrin-mediated filopodial induction will then be analysed by knockdown or overexpression of various ABPs. Furthermore, to analyse if they are displaced by drebrin, their relocalisation after drebrin overexpression will be assessed using immunofluorescence microscopy. Finally, we will determine how drebrin influences F-actin architectures in the neuronal growth cone, where it is concentrated at particular subregions; the transition zone (T-zone) and the base of filopodia. Using cryo-ET, the nano-scale F-actin architectures of these subregions where drebrin is concentrated will be revealed, comparing basal conditions with drebrin overexpression or removal. The potential relocalisation of ABPs from their normal localisations after drebrin overexpression or knockdown will also be assessed using immunofluorescence microscopy. This proposal will unveil the mechanisms of a fundamental regulator of the vertebrate F-actin cytoskeleton with important roles in neurons and numerous other cell types. In addition to advancing our basic understanding of fundamental biology, given drebrin’s implication in a variety of pathologies, this research promises auxiliary biomedical impact. The utilisation and development of cutting edge cryo-EM/cryo-ET techniques in this research will have supplemental impact in advancing the competitiveness of the UK scientific workforce.

UKRI Gateway to Research · FY 2026 · 2026-02

Mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP1) plays a crucial role in the regulation of immune responses and the body’s defence mechanisms against infections.  MKP1 is involved in modulating the activity of MAPKs, which are vital for transducing signals from microbial pathogens.  During infection, MKP1 acts as a ‘regulatory brake’ on the inflammatory response, as excessive or prolonged inflammation can lead to tissue damage and chronic inflammatory diseases.  MKP1 fine-tune’s this response by deactivating MAPKs, thereby reducing the production of pro-inflammatory cytokines.  This action is critical for preventing tissue damage and promoting resolution of inflammation, demonstrating a dual role for MKP1 in infections acting as a critical modulator of the immune response.  While the functional role of MKP1 has been studied in bacterial infections, no studies have investigated its role in fungal infections. Fungi kill ~2.5 million individuals each year, five times more than malaria or influenza, and are deadlier than most bacterial infections.  Candida spp. cause ~1 million deaths from invasive/bloodstream infections and >150 million mucosal infections annually.  As such, Candida infections are a serious medical problem and an immense burden to human health.  Given this, the World health Organisation recently cited C. albicans in the ‘critical’ group (highest) in the ‘fungal priority pathogens’ list.  Thus, identifying biological and immunological mechanisms that advance our understanding of C. albicans infection and lead to disease prevention is now a recognised priority. MKP1 is strongly activated in epithelial cells and neutrophils during C. albicans infection.  Importantly, using a MKP1 knockout (KO) mouse, MKP1 deletion resulted in protection against mucosal and systemic C. albicans infection.  These findings are in stark contrast to bacterial studies, where the MKP1 KO dramatically increases morbidity and mortality.  This dichotomy between fungal and bacterial responses is highly intriguing and highlights the complexity of MKP1's role in immune regulation.  Therefore, our objectives are twofold. First, to determine why MKP1 deletion is protective in fungal disease but detrimental in bacterial disease. Second, to determine the cell-type specific functional role of MKP1 in C. albicans infection, which will reveal new mechanisms by which fungal diseases outcome could be improved through targeted immunostimulatory therapy.  The work will considerably enhance our understanding of immune regulation during fungal and bacterial infection and will identify new therapeutic opportunities that may arise from manipulating MKP1 pathways to improve microbial infection resolution, especially as adjunctive therapy during antimicrobial resistance. This work will have multiple academic beneficiaries in the fields of general and innate immunology, fungal and bacterial pathogenesis, cellular signalling, and host-pathogen interactions.  An integral part of this research proposal involves the creation of conditional MKP1 knockout mouse models, which will create invaluable and powerful research tools that will enhance the impact and significance of this research proposal and be of considerable value to the wider scientific community (broader ranging infection studies, immunology, MAPK biology).  In addition, this proposal has potential commercial beneficiaries, as our findings could be exploited at several levels in the longer term to improve human health and quality of life.

UKRI Gateway to Research · FY 2026 · 2026-02

Introduction: Acne is the 8th most prevalent disease in the world and peaks in prevalence in adolescence when it impacts confidence, academic performance and quality of life. Understanding the key components of acne development is essential for developing effective treatment strategies. Acne arises due to a complex interplay between a genetic predisposition to follicular hyperkeratinization, or blocked pores, and inflammation driven by the bacteria Cutibacterium acnes, hormones and other environmental factors. Challenge the project addresses: Genome-wide association studies (GWAS) have uncovered the genetic basis of acne vulgaris, which indicate that cellular programs governing the maintenance of hair follicle and skin formation, are central to its development. Acne has been linked to environmental triggers such as hormonal and dietary factors in epidemiological studies, where large populations have been surveyed. However, clear causality and mechanisms that explain why certain exposures are linked to acne remain lacking. Therefore, treatment strategies aimed at targeting modifiable exposures are limited and lack evidence-base. Our project aims to leverage insights from our recent genome-wide association meta-analysis of acne, which has identified genes that are implicated in acne, to identify causal circulating factors using Mendelian randomisation (MR), an analytical approach which uses understanding of genetic variants to identify causes of disease. We will then identify pathogenic cell types in which genetic mechanisms of acne are enriched and generate an lab-based in vitro model system for acne in which can be used to validate the impact of genetic and environmental perturbations. Aim: To characterise gene-environment interactions in acne vulgaris. Objectives: Identification of causal serum biomarkers of acne vulgaris using bidirectional Mendelian Randomisation (MR) approaches Identification of cell-type specific genetic perturbations through the integration of GWAS and single-cell RNA sequencing data Generation of an in vitro model of acne informed by identified genetic and environmental factors, which will provide both functional validation and a model system for future studies. Potential applications and benefits: This approach will add both specificity and detail to our understanding of both genetics as well as environmental factors in acne pathogenesis. Identification of circulating factors has two benefits; firstly, these circulating factors could represent new treatment targets. Secondly, new circulating factors or 'biomarkers' could be used clinically to help distinguish sub-types of acne vulgaris, which could be treated using different approaches. And finally, we aim to leverage our knowledge of genetic and environmental factors to develop an in vitro culture model of acne, which will functionally validate these genetic discoveries as well as provide a lab-based model system for future studies in acne vulgaris, which is currently lacking

UKRI Gateway to Research · FY 2026 · 2026-02

Catalysis is central to a wide range of endeavours within industry and academia. Estimated to be worth $433M to the UK economy in 2021 (which enables $188B of revenue in downstream sectors), it is an essential aspect in the pursuit of a sustainable society. Whilst the term 'catalysis' is a broad term that includes for example, the heterogeneous converters in cars, the purification of water, and carbon dioxide capture, a significant part of this field are the homogenous catalyst systems that can provide new ways of creating molecules that have never been made before. Some of these molecules are particularly challenging to make because the only difference between them is that they are mirror images that cannot be superimposed (such as the left and right hands). This phenomenon, known as chirality, has the consequence that differently handed molecules will interact with molecules within the body - which themselves are handed - with different efficacies or effects; think how easy it is to shake someone's right hand (the "biological receptor") with your own right hand (the correctly handed molecule) vs your left hand (the incorrectly handed molecule). This concept within chemistry is specifically known as "asymmetric catalysis" and has clearly an important role in the manufacture of safe and effective pharmaceuticals (an endeavour identified in the 2021 Innovate UK report as being a core benefit of investment). However, the discovery of catalyst systems can be a long process, because they are generally designed to be specific to a single, often fairly niche, reaction process. Many catalytic systems use relatively small molecules to help discriminate between left and right hands of a particular target. Successful catalyst optimisation relies on being able to derivatise those small molecules, which can be severely limited by their molecular structure - often these libraries are very small because there is only one position within the molecule where changes in the molecule can be made. Certainly the functionality within these small molecules - often derived from natural products - cannot be changed easily in either its position or its nature (for example an amine to a carboxylic acid). This proposal seeks to address this by generating highly preorganised catalysts that are modular in nature. There are two very important aspects to that design which give us confidence that this approach will speed up the catalyst discovery process beyond it existing cul-de-sac. First that these catalysts are helical. This means that they are intrinsically "handed" (the mirror image of helices are also non-superimposable) and that the orchestration of reaction processes around them will be highly defined in three-dimensional space (and thus the origin of asymmetry). The second important aspect is that the modularity of these helical scaffolds allows us to swap functionality with ease to whatever is required by the reaction we are trying to catalyse. Half of these modules are amino acids, which make up all of the proteins in our body and thus have a huge range of functionality. For example, we can swap an amine for a carboxylic acid as above by just changing one of the amino acids. We can also modify other aspects of the system very easily, such as the distances between functionalities. This approach will enable vast libraries to be made and will thus impact the catalysis industry in a groundbreaking way.

UKRI Gateway to Research · FY 2026 · 2026-02

Context Depression is a common condition that affects people around the world and causes serious problems in their lives. However, current treatments do not work well for 1 in 3 people. Psilocybin, or "magic mushrooms”, are a new medication that might help when other treatments fail. Psilocybin changes how people think and feel, creating a dreamlike state. However, we do not fully understand how it works. There are three main ideas about how psilocybin helps: Expectation: People might feel better because they expect the drug to work. This is called the placebo effect. The excitement around psychedelics might make this effect stronger. Meaningful experiences: The dreamlike state caused by psilocybin can be powerful. It may help people make changes that improve their mood. Brain changes: Psilocybin may cause changes in the brain, like growing new brain cells. The Challenge To test medication, researchers usually hide whether people get a drug or inactive pill. This does not work with Psilocybin because its effects are obvious. This makes it hard to understand why psilocybin works. Giving psilocybin to people while they sleep might solve this problem as sleeping people may not notice the effects of the drug. People also may not have the same meaningful experiences when asleep. A small study in the U.S. tested this by giving psilocybin through a vein to sleeping people. Participants woke up unless they were also given clonidine, a sedative medication. When given both psilocybin and clonidine people did not know if they got a drug or a placebo. We do not know if combining these changes how psilocybin works. Making psilocybin to give through a vein is slow and expensive. We also understand less about psilocybin given through a vein than as a tablet. A tablet would be cheaper and easier to use which could make larger studies possible. Therefore, we want to test if using a tablet is possible. We will used a delayed release tablet taken just before going to sleep. Aims and Objectives Find out how quickly delayed-release psilocybin works. Figure out the best way to give psilocybin to people while keeping them asleep. Understand if combining sedatives and psilocybin changes how psilocybin works. Test if people can tell if they got psilocybin or an inactive pill while asleep. Create a guide for other researchers to use this method in future studies. Potential Applications and Benefits Understanding how psilocybin works is very important. This method would be used to help study this in the future. Currently, there is uncertainty about how much "expectation" affects medications like psilocybin. This uncertainty has made some governments cautious to approve medications like these. Learning more about this could help these medications become available to people sooner. We have also talked to both people with depression and participants in past trials. They believe it is very important to understand why psilocybin works. This knowledge could help patients better understand their treatment. Understanding how psilocybin works would also guide researchers who are developing new medications based on psilocybin. Some other drugs have obvious effects, making them hard to test using regular methods. This method could also be used to help test these other drugs.

UKRI Gateway to Research · FY 2026 · 2026-02

Microplastics are recognised as a globally ubiquitous contaminant found in all marine and terrestrial environments. Defined as plastic particles smaller than 5 mm in diameter, they are suspected of posing a health risk to humans and impact all biotic food chains and ecosystems as vectors of harmful microbes and chemical pollutants. The transport and deposition of microplastics by water in fluvial and marine environments is extensively studied, but we currently have very little insight into the movement of microplastics by wind in coastal and semi-arid environments around the world, even though airborne pathways are a – if not the – major entry into ecosystems and agriculture here. Artificial laboratory wind tunnel studies have shown that they are more easily transported by the airflow than mineral sand grains, but we have no real-world quantifications or theoretical models of how microplastics are potentially released or eroded by wind from the subaerial beach or the soil, how they are moved over a distance (whether by rolling, creep, hopping, partial-suspension?), how they interact with regular wind-blown sediments and the underlying bed surface during this transport (mid-air collisions, impact, rebound, splash?), and how they are ultimately deposited and/or buried inside coastal dunes or croplands (gravity separation, grain fall, kinetic sieving?). Since the weekend of 8-9 November 2025, a severe pollution incident has been unfolding on the beach at Camber Sands, East Sussex. Hundreds of millions of small, lightweight, plastic pellets have been washing up along the entire 3km long coastline, deposited at the high-tide wrack line and mixing with the sand. The 4mm-size microplastic pellets are so-called ‘bio-beads’, accidentally released into the sea from a nearby wastewater treatment works. Despite immediate clean-up efforts the latest evidence shows that the pellets have thoroughly mixed with the sand matrix across the entire inter-tidal zone of the beach surface and will be impossible to fully remove. Over the course of spring-summer 2026 these pellets will be blown by dry onshore winds from the beach into the adjacent coastal dunes (a nature conservation area and Site of Special Scientific Interest) where they will pose a hazard to plants and wildlife as the toxic heavy metal contaminants they contain leach out into the environment. This incident has created an unfortunate but unique ‘natural experiment’: an opportunity to investigate the wind-blown movement of these well-defined microplastic pellets from the beach into the coastal dunes under natural conditions. The research we propose here aims to establish unprecedented empirical insights into the fundamental physical mechanisms of erosion, transport, and deposition of microplastics, yielding a quantitative transport model. This is pursued by conducting an intense programme of repeated field sampling and laboratory analyses of the microplastics/sand mixture over beach-dune gradients, and field work campaigns on windy days to directly measure, on a particle scale, the real-time microplastics transport process over the dry beach and into the dunes with an array of high-resolution electronic instrumentation. The resulting transport model for the mixture of microplastic pellets and sand will greatly broaden our fundamental understanding of particle transport by fluids over a spectrum of environments and density ratios, also applicable to other planetary environments. Extrapolating these insights will furthermore inform the design of effective methods for intercepting wind-blown microplastics in general, serving mitigation efforts to reduce their harmful effects in coastal and semi-arid environments.  

UKRI Gateway to Research · FY 2026 · 2026-01

Peripheral arterial disease (PAD) is a common circulatory condition that affects over 200 million people worldwide, especially those over the age of 50. It reduces blood flow to the legs, often causing pain during walking - a condition known as intermittent claudication (IC). While medications, lifestyle changes, and supervised exercise programmes can help, up to 30% of patients do not improve and remain at risk of worsening symptoms, progression to limb threatening ischaemia, and eventual limb amputation. Invasive limb revascularisation by bypass surgery/angioplasty/stenting is costly and associated with complications that include limb loss. There is demand, in the UK and internationally,  for developing regenerative treatments for patients with IC to address this area of unmet clinical need and reduce the burden on health services. The challenge the project addresses Current treatments for IC do not effectively reverse the underlying arterial insufficiency and invasive options are not routinely recommended due to their risk profile and poor long-term durability. There are no approved therapies that stimulate clinically effective vascular remodelling or prevent progression to chronic limb-threatening ischaemia (CLTI). The key challenge is to develop a safe, scalable and disease-modifying therapy that promotes natural blood vessel regeneration in patients who have exhausted standard medical therapy. Aims and objectives This project will evaluate MON002, an autologous cell therapy using monocytes which are primed with clinical-grade mesenchymal stem cells towards a vascular remodelling functional phenotype, in a first-in-kind Phase 1b/2a clinical trial in patients with IC. The specific objectives are to: Scale up GMP manufacturing of MON002 - leukapheresis-isolated monocytes from patients, engineered to express a pro-angio/arteriogenic phenotype by co-culture with mesenchymal stem cells; Test the safety, tolerability, and optimal dosing of MON002 with an adaptive, randomised, placebo-controlled trial in patients with IC; Assess early signals of efficacy including 6-minute walking distance, blood flow (ankle:brachial pressure index; ABPI), quality of life, and relevant biological markers; Engage with regulatory bodies to define a clear path towards later-phase trials and clinical use. Potential applications and benefits If successful, MON002 could offer the first regenerative, minimally invasive treatment for patients with intermittent claudication - an intervention that will help patients regain mobility, reduce symptoms, prevent progression to CLTI and avoid major surgery or future amputation. It may reduce hospital admissions and healthcare costs, while enhancing patient quality of life. The platform also has broader relevance to other conditions involving ischaemic tissues, including the ischaemic myocardium. In the longer term, MON002 could help integrate cell-based therapies into routine vascular care, contributing to the UK's ambition of becoming a global leader in advanced cell and gene therapies.

UKRI Gateway to Research · FY 2026 · 2026-01

In the vertebrate brain and spinal cord, cells called "oligodendrocytes" construct a fatty insulating layer around "axons" - long filamentous extensions of "neurons", the electrically excitable cells. This insulation, called "myelin", greatly speeds up the electrical signals sent by nerve cells as well as providing energetic support to neurons and their axons. Recently it has been demonstrated that oligodendrocytes and the myelin that they make also help the brain to adapt to new experiences, contributing to learning and memory formation. How exactly myelin influences learning is still not well understood. Our hypothesis is that oligodendrocytes can sense the neurons that are activated by specific behaviours, resulting in the formation or remodelling of myelin on those active neurons. We predict that this process will fine-tune electrical signals and alter the connectivity of the active neurons leading to the development of new neuronal circuits responsible for new behaviours. In this project we will train mice to learn a new motor skill (running on a wheel with irregularly spaced rungs) and observe how the myelin on activated neurons changes with learning. We will then use a number of different genetic manipulations to disrupt pathways that may enable oligodendrocytes to sense neuronal activity and determine if these mice maintain the ability to learn motor skills. We will also disrupt the formation and maintenance of new myelin that is formed during skill learning to ask how this process changes neuronal connectivity. Our experiments will help illuminate the general mechanisms underpinning one of the fundamental functions of the brain - the ability to adapt - and may provide insights into how better to maintain cognitive ability during healthy aging, or to aid recovery of brain function following disease or injury.

UKRI Gateway to Research · FY 2026 · 2026-01

Healthcare nanotechnology has recently delivered highly impactful products such as the Pfizer & Moderna COVID-19 vaccines (20 million lives saved) and Vyxeos® (first anticancer drug co-delivering two complementary drugs). In addition, novel therapies such as radionuclide therapy and Theranostics –where imaging is used to guide therapy– create new exciting opportunities to exploit the unique properties of healthcare nanomaterials (HN). To further develop future HN we need a deeper understanding of their in vivo behaviour, to answer questions such as: Where do nanomaterials go inside the human body? How long do they stay inside, and how are they excreted? Do they reach the intended tissues (for example, tumours)? Do they accumulate in unwanted organs as recent data suggests causing unexpected side effects?. Most of our knowledge in this area comes from animal studies, using same sex and nearly genetically identical subjects. This has provided invaluable information but does not fully represent the diversity of human and disease physiology and pathology. The ambition of this programme is to address these knowledge gaps to accelerate and optimise the safe clinical translation and application of novel HN products, thanks to the advent of a new clinical imaging technique: total-body positron emission tomography (TB-PET). TB-PET allows quantitative imaging the whole human body simultaneously with unprecedented sensitivity. We will develop methods to label HN with very small amounts of radioactivity (radiolabelling), endowing them with both real-time tracking and therapeutic properties. With our innovative chemistry, we will leverage TB-PET to image the biodistribution and pharmacokinetics of HN in humans using unprecedented low amounts of radioactivity and nanomaterial, overcoming the radiotoxicity barriers that have limited imaging of HN previously, allowing effective identification of the most impactful and safe nanomedicines of the future. To do this we will focus our efforts into four themes: Th1: Image-guided diagnosis and drug delivery, to guide development of nanoparticulate-delivery systems for sensitive cargoes (mRNAs/vaccines), and novel diagnostic approaches; Th2: Radionuclide Therapy, exploiting the large radionuclide loading capacity and tumour targeting properties of nanoparticles to treat and image cancer; Th3: Image-guided Surgery, exploiting synergies within multimodal imaging nanomaterials to guide surgical procedures; and Th4: Combination Therapies, exploiting the unique properties of HN that synergise with complementary novel therapies (cell immunotherapy, advanced radiotherapy). Themes will be supported by interdependent cross-cutting work packages (WPs), 4 core research WPs and 3 management, advocacy, engagement and technical support WPs: WP1: Synthesis and Characterisation will develop and scale up the synthesis of nanomaterials. WP2: In vitro toxicology and radiobiological evaluation, allowing selection of the best candidates from each theme for in vivo evaluation. WP3: Preclinical imaging and therapy, utilizing state-of-the-art preclinical imaging and radiotherapy facilities at QMUL/KCL. WP4: Clinical translation for first-in-human evaluation using our clinical TB-PET. Core research WPs will be supported by WP5, providing management, external networking, advocacy and sustainability, WP6 providing Technical and Health & Safety support, and WP7 leading patient and public involvement and engagement (PPIE) to inform our research based on patient and community feedback and communicate our results effectively. To achieve this we have assembled a diverse, collaborative and highly experienced multidisciplinary team from King’s College London, the University of Leeds and Queen Mary University of London with a world-leading track record and facilities portfolio at the forefront of nanomedicine chemistry, physics, biology, and preclinical and clinical medicine (including two clinical TB-PET scanners).

UKRI Gateway to Research · FY 2026 · 2026-01

This proposal addresses the fundamental ‘rules of life’ remit of the BBSRC, specifically: How our body is formed and what happens if this process goes awry? Embryonic development starts from a fertilised egg and will ultimately result in the formation of the adult anatomy. Obviously, this entails an increase in cell number, but an essential feature of this process is that it involves making group of cells different from each other, in space and time, so they do different things. This is underpinned by stereotypical use of instructive signals, and alterations to the usual sequence of events can lead to different outcomes. A morphogen is a special class of signalling molecule that acts during embryonic development to generate a variety of cell states. In response to distinct threshold levels of morphogen signalling, cells follow different fates and form different structures. Therefore, within a given territory, a single morphogen can generate multiple outcomes. While the significance of morphogen activity is widely appreciated, we still do not have a clear understanding of how morphogens work and, more specifically, how their activity can be modulated during embryonic development to modify the shape and form of the anatomical structures they generate. This is an issue, both within a species, in the formation of different structures, and during evolution, in the generation of morphological diversity across different species. Disruption of normal morphogen activity is also associated with congenital birth defects and can be responsible for structures not forming or additional elements being present, such as supernumerary (additional) digits in the hand. Our aim is to study the parameters of morphogen action by modulating physiological morphogen signalling levels in space and time and to understand the consequences of these manipulations for the allocation of different cells states/fate and the later morphology of the limbs. This is important as morphogens act in both a concentration and time dependent manner. Cells respond differently to a morphogen depending on the concentration of the signalling molecule they have been exposed to and the length of exposure. We will create experimental situations in which cells of the limb bud are exposed to low, intermediate, or high physiological levels of the morphogen, SHH, and modulate the length of time cells are exposed to these levels of signalling. This study will advance understanding of how a single type of signalling molecule can generate different anatomical structures and how this property can be employed within a developing organism to generate features such as the different digits of the hand and feet. This study will also fruther develop an experimental methodology in the chick model organism that will contribute to the objectives of the NC3Rs.