Ewch i’r prif gynnwys

Mobility and Skills Award

Mae'r cynnwys hwn ar gael yn Saesneg yn unig.

The Mobility and Skills Award supports our early career researchers by enabling acquisition of new research skills, visits to external laboratories for small-scale data collection, secondments to industry, government or other key stakeholders and engagement training.

Principal Investigator: Dr Alan Parker
School of Medicine

The proposed visit will cement collaborative links between the Parker Lab at Cardiff University School of Medicine and the Borad lab at the Mayo Clinic, Arizona. Together, our laboratories form a logical and complementary research alliance, with the potential for significant synergistic collaborative benefit at both ends. Our laboratory specialises in basic and preclinical evaluation and manipulation of DNA viruses as therapeutic agents, yet lacks the capacity and capability to produce these agents in house to GMP grant and translate these agents into clinically relevant medicines.

Conversely, the Borad laboratory, based at the Mayo Clinic, Arizona, have great experience in taking virotherapies through to later stages of preclinical studies (eg POX mouse models), have facilities on site for the production of GMP grade clinical trials and specialise in leading early phase "first in man" clinical trials of novel biotherapeutics. As such there is clear synergistic benefit to both parties through collaboration. Cardiff University will be able to translate basic virotherapies through facilities and expertise to deliver first in man clinical trials using the Mayo pipeline, whilst in return we will provide in house training and expertise in molecular techniques required to manipulate viral genomes and function.

Principal Investigator: Dr David Stanton
School of Biosciences

We are in a period of rapid climate change, which is going to affect wild animal populations in many unforeseen ways. Some may go extinct, while others might greatly increase in number. It is important to be able to prepare for either of these circumstances. Many animals help to maintain our natural resources, which could be compromised if they were to go extinct. Other animals are reservoirs for diseases, which are more likely to spill over to the human population if those animal populations increase in size. If we knew how animals were going to respond to future climate change, this would allow us to implement management and conservation strategies that would help to identify any potential risks. Unfortunately these responses are very difficult to predict, however, one possible approach is to investigate how animals have responded to historical changes in climate.

This study aims to do this, by working in collaboration with the Swedish Natural History Museum in Stockholm. We will look at how different animal populations have responded to climate change in Europe over the past 40,000 years. We already know that there are some populations and species that survived historic cooling and warming, while others went extinct. This study will attempt to work out what the differences were between these climate change ‘success’ and ‘failure’ stories, so that we can learn from them and effectively manage the wildlife resources that we still have.

Principal Investigator: Dr Kristin Ladell
School of Medicine

Hyperlipidaemia (high fat in the blood stream) is a metabolic abnormality that has become increasingly prevalent in the UK due to peoples' sedentary lifestyle and poor diet. The increased lipids in the bloodstream lead to inflammation of the blood vessels and increase the risk of heart disease or stroke, the most prevalent causes of death worldwide. T cells are white blood cells that play a key role in inflammation. These cells are found in the plaques that clog the blood vessels in people with hyperlipidaemia. So far, no specific reagents have been available to study these cells in this condition.

Professor Rossjohn's laboratory has state-of-the-art infrastructure, protocols and technology established to generate novel biological tools to study these cells in detail. A better understanding of the role of these cells as well as the molecules that present fat to these cells in blood vessel inflammation has the potential for the development of new and specific treatments that could be applicable to all, as the presenting molecules are found in every individual. My plan is to learn how to make and load these presenting molecules in Professor Rossjohn's laboratory to identify and study these inflammatory T cells in patients in Cardiff.

Principal Investigator: Dr Tatyana Shelkovnikova
School of Biosciences

Amyotrophic lateral sclerosis (ALS, also known as motor neuron disease) is a severe neurological condition which results in the inability to move and eventually death from paralysis of respiratory muscles. Currently ALS has no cure, and this is mainly due to poor understanding of universal disease mechanisms in this aetiologically very diverse disorder. NEAT1 is a multifaceted regulatory molecule functioning in fine tuning of gene expression and cellular stress response. NEAT1 also serves as a scaffold molecule to build a specific structure in the cell nucleus termed the paraspeckle. NEAT1 and paraspeckles have been recently implicated in ALS and other related diseases affecting the nervous system. They have a potential to become the much-sought ‘universal’ therapeutic targets in ALS.

The team of Dr Fox in University of Western Australia are leading experts in research on NEAT1 and paraspeckles. Visiting this laboratory will enable me to learn an advanced imaging technique called superresolution microscopy which allows visualising fine structure of paraspeckles. Knowledge of this technique will substantially advance my studies into the role of NEAT1 and paraspeckles in ALS. This visit will also help enhance and develop an important collaborative link.

Principle Investigator: Dr Daniel Burley 
School of Psychology

Three quarters of psychiatric illnesses begin in childhood and, therefore, it is imperative that we study psychopathology as early as possible to inform our understanding of the aetiology, as well as how and when to intervene. I work in the Neurodevelopment Assessment Unit (NDAU) at Cardiff University, which is a unique research centre that collects broad phenotypic and genetic data in a large sample of young children with diverse neurodevelopmental problems. We intend to extend our assessments by including neuroimaging in these children, but Cardiff University needs to build developmental imaging expertise.

I propose to visit the developmental imaging research laboratory within the Murdoch Children’s Research Institute (MCRI), led by Dr Marc Seal, who is a world-leader in neuroimaging as applied to understand the developing brain. I will work within the AQUA project imaging children aged 7-8 years old. My learning outcomes are to develop an increased understanding within young children of how to set up a brain imaging session, techniques that are important for successful scanning, and methods for image processing and data quality control. Visiting MCRI will provide me with the neuroimaging knowledge foundation to support and enhance developmental imaging expertise at Cardiff University.

Principal Investigator: Dr Nicholas Clifton
School of Medicine

My research aims to understand the biological pathways affected during brain development that lead to the manifestation of psychiatric disorders such as schizophrenia. The research strengths afforded by the resources and expertise at Cardiff University allow for exceptional insight into the genetics of psychiatric disorders. The Lieber Institute for Brain Development is a World-leading laboratory for research into disease-related changes in biological pathways across the lifespan of brain development. By bringing these expertise together, I will have a unique opportunity to perform novel and exciting research within a mutually beneficial and sustainable collaboration, whilst greatly enhancing my scientific skillset.

Specifically, I will be guided through access and interpretation of a new post-mortem human brain database, generated by the Lieber Institute, enabling me to link it to patient genetic data hosted by Cardiff University and study the effects of harmful mutations on biological pathways active during particular developmental stages. I will be shown the most up-to-date methods for analysing this type of developmental data and learn how to integrate it with similar datasets.

Principal Investigator: Dr Namrata Rastogi
School of Medicine

Acute myeloid leukaemia (AML) is an aggressive form of blood cancer which occurs when the normal development of a blood cell is altered. Unfortunately, patients with this blood cancer continue to die from the disease and we are in need of new therapies. Growth and development of blood cells is a complex process, governed by several proteins. Understanding how abnormal expression of these proteins turn blood cells into cancerous cells will allow us to develop targeted therapy. We have previously identified cell development proteins that are abnormally changed in AML. One protein is known as Nuclear Factor I-C (NFIC) which also has high expression in many solid cancers, implying an important role in cancer development. However, little is known of the role of this protein in blood cell development.

I will artificially introduce NFIC into normal blood stem cells allowing me to then analyse several hundred individual cells expressing high levels of NFIC. I will determine what genes are switched on or off, which will help me identify how high levels of NFIC in stem cells could be responsible for blood cancer development and whether it can be targeted for effective AML therapy in the future.