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Farmed carnivores may become ‘disease reservoirs’ posing human health risk

Tue, 24/08/2021 - 16:03

Farming large numbers of carnivores, like mink, could allow the formation of undetected ‘disease reservoirs’, in which a pathogen could spread to many animals and mutate to become a risk to human health.

Research led by the University of Cambridge has discovered that carnivores have a defective immune system, which makes them likely to be asymptomatic carriers of disease-causing pathogens.

Three key genes in carnivores that are critical for gut health were found to have lost their function. If these genes were working, they would produce protein complexes called inflammasomes to activate inflammatory responses and fight off pathogens. The study is published today in the journal Cell Reports.

The researchers say that the carnivorous diet, which is high in protein, is thought to have antimicrobial properties that could compensate for the loss of these immune pathways in carnivores – any gut infection is expelled by the production of diarrhoea. But the immune deficiency means that other pathogens can reside undetected elsewhere in these animals.

“We’ve found that a whole cohort of inflammatory genes is missing in carnivores - we didn’t expect this at all,” said Professor Clare Bryant in the University of Cambridge’s Department of Veterinary Medicine, senior author of the paper. 

She added: “We think that the lack of these functioning genes contributes to the ability of pathogens to hide undetected in carnivores, to potentially mutate and be transmitted becoming a human health risk.”

Zoonotic pathogens are those that live in animal hosts before jumping to infect humans. The COVID-19 pandemic, thought to originate in a wild animal, has shown the enormous damage that can be wrought by a novel human disease. Carnivores include mink, dogs, and cats, and are the biggest carriers of zoonotic pathogens. 

Three genes appear to be in the process of being lost entirely in carnivores: the DNA is still present but it is not expressed, meaning they have become ‘pseudogenes’ and are not functioning. A third gene important for gut health has developed a unique mutation, causing two proteins called caspases to be fused together to change their function so they can no longer respond to some pathogens in the animal’s body.

“When you have a large population of farmed carnivorous animals, like mink, they can harbour a pathogen - like SARS-CoV-2 and others - and it can mutate because the immune system of the mink isn’t being activated. This could potentially spread into humans,” said Bryant.

The researchers say that the results are not a reason to be concerned about COVID-19 being spread by dogs and cats. There is no evidence that these domestic pets carry or transmit COVID-19. It is when large numbers of carnivores are kept together in close proximity that a large reservoir of the pathogen can build up amongst them, and potentially mutate.

This research was funded by Wellcome.

Reference
Digby, Z. et al: ‘Evolutionary loss of inflammasomes in the Carnivora and implications for the carriage of zoonotic infections.’ Cell Reports, August 2021. DOI: 10.1016/j.celrep.2021.109614

 

Carnivorous animals lack key genes needed to detect and respond to infection by pathogens, a study has found.

Infectious diseasesCOVID-19Clare BryantDepartment of Veterinary MedicineCambridge Infectious DiseasesDepartment of MedicineQueens' CollegeSchool of the Biological SciencesSchool of Clinical MedicineWe’ve found that a whole cohort of inflammatory genes is missing in carnivores Clare Bryant Oikeutta elaimille on FlickrFarmed mink


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Female scientists lead Cambridge success in Royal Society awards

Tue, 24/08/2021 - 13:00

Burnell is one of twelve former and current Cambridge researchers, including six women, to be recognised in 2021 for their exceptional research and outstanding contributions to science.

Dame Jocelyn has been honoured for her work on the discovery of pulsars in the 1960s while she was a postgraduate student at New Hall (now Murray Edwards College) carrying out research at Cambridge's Cavendish Laboratory.

Past winners of the Copley Medal have included Charles Darwin, Albert Einstein and Dorothy Crowfoot Hodgkin. Dame Jocelyn said: “I am delighted to be the recipient of this year’s Copley Medal, a prize which has been awarded to so many incredible scientists.

“With many more women having successful careers in science, and gaining recognition for their transformational work, I hope there will be many more female Copley winners in the near future.

“My career has not fitted a conventional – male – pattern. Being the first person to identify pulsars would be the highlight of any career; but I have also swung sledgehammers and built radio telescopes; set up a successful group of my own studying binary stars; and was the first female president of the Institute of Physics and of the Royal Society of Edinburgh.

“I hope that my work and presence as a senior woman in science continues to encourage more women to pursue scientific careers”.

The Copley Medal award includes a £25,000 gift which Dame Jocelyn will add to the Institute of Physics' Bell Burnell Graduate Scholarship Fund, which provides grants to graduate students from under-represented groups in physics.

Three female scientists currently working at Cambridge have been recognised in 2021. Professor Sadaf Farooqi from the MRC Metabolic Diseases Unit receives the Croonian Medal and Lecture, together with Sir Stephen O'Rahilly, for their seminal discoveries regarding the control of human body weight, resulting in novel diagnostics and therapies, which improve human health. 

Dr Serena Nik-Zainal from the MRC Cancer Unit has been awarded the Francis Crick Medal and Lecture, for her contributions to understanding the aetiology of cancers by her analyses of mutation signatures in cancer genomes, which is now being applied to cancer therapy.

Professor Anne Ferguson-Smith from the Department of Genetics and currently the University’s Pro-Vice-Chancellor for Research receives the Buchanan Medal, for her pioneering work in epigenetics, her interdisciplinary work on genomic imprinting, the interplay between the genome and epigenome, and how genetic and environmental influences affect development and human diseases.

Former Cavendish Laboratory Research Fellow, Professor Michelle Simmons, has won the Bakerian Medal and Lecture, for her seminal contributions to our understanding of nature at the atomic-scale by creating a sequence of world-first quantum electronic devices in which individual atoms control device behaviour. 

Professor Frances Kirwan, alumna and Honorary Fellow of Clare College, received the Sylvester Medal, for her research on quotients in algebraic geometry, including links with symplectic geometry and topology, which has had many applications.

Other current Cambridge researchers honoured include Dr Sjors Scheres from the MRC Laboratory of Molecular Biology. Scheres has been awarded the Leeuwenhoek Medal and Lecture for his ground-breaking contributions and innovations in image analysis and reconstruction methods in electron cryo-microscopy, enabling the structure determination of complex macromolecules of fundamental biological and medical importance to atomic resolution.

Emeritus Professor Michael Green from the Department of Applied Mathematics and Theoretical Physics has been awarded Royal Medal A for crucial and influential contributions to the development of string theory over a long period, including the discovery of anomaly cancellation.

The Royal Society’s President, Sir Adrian Smith, said: “Through its medals and awards the Royal Society recognises those researchers and science communicators who have played a critical part in expanding our understanding of the world around us.”

“From advancing vaccine development to catching the first glimpses of distant pulsars, these discoveries shape our societies, answer fundamental questions and open new avenues for exploration.”

Find the full list of 2021 Royal Society medal, award and prize winners here.

Professor Dame Jocelyn Bell Burnell has become only the second woman to be awarded the Royal Society’s prestigious Copley Medal, the world’s oldest scientific prize.

Royal SocietyWomen in STEMMJocelyn Bell BurnellAnne Ferguson-SmithStephen O’RahillySadaf FarooqiMichael GreenSerena Nik-ZainalSjors ScheresRoyal SocietyCavendish LaboratoryMRC Cancer UnitMRC Laboratory of Molecular BiologyDepartment of Applied Mathematics and Theoretical PhysicsMRC Metabolic Diseases UnitDepartment of GeneticsMurray Edwards CollegeChurchill CollegeSchool of the Physical SciencesSchool of the Biological SciencesI hope there will be many more female Copley winners in the near futureJocelyn Bell Burnellhttps://www.youtube.com/watchProfessor Dame Jocelyn Bell Burnell


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Hospital-acquired COVID-19 tends to be picked up from other patients, not from healthcare workers

Tue, 24/08/2021 - 08:00

The study provides previously unprecedented detail on how infections might spread in a hospital context, showing that a minority of individuals can cause most of the transmission.

The researchers analysed data from the first wave of the pandemic, between March and June 2020.  While a great deal of effort is made to prevent the spread of viruses within hospital by keeping infected and non-infected individuals apart, this task is made more difficult during times when the number of infections is high. The high level of transmissibility of the virus and the potential for infected individuals to be asymptomatic both make this task particularly challenging.

Looking back at data from the first wave, researchers identified five wards at Addenbrooke’s Hospital, part of Cambridge University Hospitals (CUH) NHS Foundation Trust, where multiple individuals, including patients and healthcare workers, tested positive for COVID-19 within a short space of time, suggesting that a local outbreak might have occurred.

Using new statistical methods that combine viral genome sequence data with clinical information about the locations of individuals, the researchers identified cases where the data were consistent with transmission occurring between individuals in the hospital. Looking in detail at these transmission events highlighted patterns in the data.

The results of the study, published today in eLife, showed that patients who were infected in the hospital were mostly infected by other patients, rather than by hospital staff. Out of 22 cases where patients were infected in hospital, 20 of these were the result of the virus spreading from patients to other patients

Dr Chris Illingworth, a lead author on the study, who carried out his research while at Cambridge’s MRC Biostatistics Unit, said: “The fact that the vast majority of infections were between patients suggests that measures taken by hospital staff to prevent staff transmitting the virus to patients, such as the wearing of masks, were likely to have been effective.

“But it also highlights why it is important that patients themselves are screened for COVID-19 regularly, even if asymptomatic, and wear face masks where possible.”

The study found contrasting results among healthcare workers, who were almost as likely to be infected by patients as they were by other healthcare workers. This was one piece of evidence that motivated the decision to upgrade the respiratory protection worn by healthcare workers in COVID-19 wards at CUH. A recent Cambridge study indicated that this resulted in staff being better protected against catching COVID-19.

The researchers also found a trend towards individuals either infecting no one else, or infecting multiple other people – just over a fifth of patients (21%) caused 80% of the infections. This phenomenon is sometimes called ‘superspreading’ and can make infection control very challenging. Whether or not an individual can be identified in advance as being more or less likely to pass on the virus is an ongoing topic of research.

Dr William Hamilton, an infectious diseases clinician at CUH and co-lead author on the study said: “Preventing new cases of hospital-based infection is a critical part of our work.  Here we have shown that analysing clinical and viral genome sequence data can produce insights that inform infection control measures, which are so important for protecting patients and healthcare workers alike.”

The research was funded by COG-UK, Wellcome, the Academy of Medical Sciences, the Health Foundation and the NIHR Cambridge Biomedical Research Centre.

Reference
Illingworth, CJR & Hamilton, WL et al. Superspreaders drive the largest outbreaks of hospital onset COVID-19 infections. eLife; 24 Aug 2021; DOI: 10.7554/eLife.67308

The majority of patients who contracted COVID-19 while in hospital did so from other patients rather than from healthcare workers, concludes a new study from researchers at the University of Cambridge and Addenbrooke’s Hospital.

COVID-19CoronavirusGenomicshealthcareChris IllingworthWilliam HamiltonWellcomeThe Academy of Medical SciencesHealth FoundationNIHR Cambridge Biomedical Research CentreSchool of Clinical MedicineCOVID-19 Genomics UK (COG-UK) ConsortiumAddenbrooke's HospitalCambridge University Hospitals NHS Foundation TrustDepartment of MedicineThe fact that the vast majority of infections were between patients suggests that measures taken by hospital staff to prevent staff transmitting the virus to patients, such as the wearing of masks, were likely to have been effectiveChris Illingworth Preventing hospital acquired Covid-19 infection | Estée Torok outsideclickCoronavirus


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10,000 autistic people to take part in the UK’s largest study of autism

Tue, 24/08/2021 - 00:01

Spectrum 10K is led by researchers at the world-leading Autism Research Centre (ARC), the University of Cambridge, together with the Wellcome Sanger Institute and University of California Los Angeles (UCLA) and will study how biological and environmental factors impact on the wellbeing of autistic individuals.

In the UK, there are approximately 700,000 autistic individuals. The level of support needed by autistic individuals varies considerably. Many autistic people have additional physical health conditions such as epilepsy, or mental health conditions such as anxiety or depression.

It is unclear what gives rise to the diversity within the autism spectrum or why some autistic people have better outcomes than others. The project aims to answer this question and to identify what support works best for each individual.

Professor Simon Baron-Cohen, leading Spectrum 10K and Director of the ARC, explained: “There is an urgent need to better understand the wellbeing of autistic individuals. Spectrum 10K hopes to answer questions such as why some autistic people have epilepsy or poor mental health outcomes and others do not.”

Individuals of all ages, genders, ethnicities and intellectual capacities will take part in Spectrum 10K. Eligible participants join by completing an online questionnaire and providing a DNA saliva sample by post. Autistic participants involved in Spectrum 10K can also invite their biological relatives (autistic or otherwise) to participate. Information collected from the questionnaire and DNA saliva sample, and information from health records will be used to increase knowledge and understanding of wellbeing in autism.

Dr James Cusack, CEO of the autism research charity Autistica and an autistic person, said: “We are delighted to support Spectrum 10K. This project enables autistic people to participate in and shape autism research to build a future where support is tailored to every individual’s needs.”

The Spectrum 10K team views autism as an example of neurodiversity and is opposed to eugenics or looking for a cure for preventing or eradicating autism itself.  Instead, their research aims to identify types of support and treatment which alleviate unwanted symptoms and co-occurring conditions that cause autistic people distress.

The Spectrum 10K team collaborates with an Advisory Panel consisting of autistic individuals, parents of autistic children, clinicians, and autism charity representatives to ensure Spectrum 10K is designed in a way that best serves the autistic community. 27 specialist NHS sites around the UK are also helping with recruitment for Spectrum 10K.

Dr Venkat Reddy, Consultant Neurodevelopmental Paediatrician in the Community Child Health Services at Cambridgeshire and Peterborough NHS Foundation Trust, said: “There is a need to conduct further research into autism and co-occurring conditions to enable researchers and clinicians to build a better understanding of autism. I would encourage autistic individuals and their families to consider taking part in Spectrum 10K.”

Chris Packham, naturalist and TV presenter who is also autistic, said: “I’m honoured to be an ambassador of Spectrum 10K because I believe in the value of science to inform the support services that autistic kids and adults will need.”

Paddy McGuinness, actor, comedian, television presenter, and father of three autistic children, said: “As a parent of three autistic children, I am really excited to support Spectrum 10K. This research is important to help us understand what makes every autistic person different, and how best to support them.”

Dr Anna and Alastair Gadney, parents of a teenager with autism and learning difficulties: “We have been exploring, over many years, how to implement the best support for our son. We wholeheartedly endorse Spectrum 10K and hope our involvement can help increase understanding of autism and in-turn support many families out there.”

Recruitment for Spectrum 10K is now open. Autistic children under the age of 16 must be registered by their parent or legal guardian. Autistic adults who lack the capacity to consent by themselves must be registered by a carer/or family member. To register, participants should visit www.spectrum10k.org

An ambitious new research project, Spectrum 10K, launches today and will recruit 10,000 autistic individuals, as well as their relatives, living in the UK.

Spotlight on neuroscienceautismgeneticsSimon Baron-CohenWellcome Sanger InstituteUniversity of California Los AngelesSchool of Clinical MedicineAutism Research CentreDepartment of PsychiatryThere is an urgent need to better understand the wellbeing of autistic individuals. Spectrum 10K hopes to answer questions such as why some autistic people have epilepsy or poor mental health outcomes and others do notSimon Baron-CohenSpectrum 10kSpectrum 10k image


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Integrated conservation strategies could simultaneously meet biodiversity, climate, and water objectives

Mon, 23/08/2021 - 16:02

To halt the decline of nature and meet Paris Agreement objectives, strategies must be designed and implemented to better manage land use for agriculture, infrastructure, biodiversity conservation, climate change mitigation and adaptation, water provision, and other needs.

A new paper by the Nature Map consortium, published today in the journal Nature Ecology and Evolution, presents an approach for spatial planning to support such integrated conservation strategies.

The study demonstrates that by jointly considering biodiversity, carbon, and water, synergies can be gained from conservation efforts compared to placing emphasis on any individual asset alone. Through strategic action in selected locations, significant benefits can be achieved across all three dimensions. However, conservation efforts need to be greatly scaled-up to meet global biodiversity and climate objectives. 

The paper sets out to determine areas of global importance to manage for conservation that would simultaneously protect the greatest number of species from extinction, conserve vulnerable terrestrial carbon stocks, and safeguard freshwater resources. 

This work is the first of its kind to truly integrate biodiversity, carbon, and water conservation within a common approach and a single global priority map. 

“To implement post-2020 biodiversity strategies such as the Global Biodiversity Framework, policymakers and governments need clarity on where resources and conservation management could bring the greatest potential benefits to biodiversity,” said lead author Martin Jung, a researcher in the IIASA Biodiversity, Ecology, and Conservation Research Group.

He added: “Biodiversity should not be looked at in isolation. Other aspects such as conserving carbon stocks within natural ecosystems should also be considered, so that synergies and trade-offs can be evaluated when pursuing multiple objectives.” 

“This type of approach can support decision makers in prioritising locations for conservation efforts, and shows just how much both people and nature could gain,” said Lera Miles, Principal Technical Specialist – Planning for Places, UN Environment Programme World Conservation Monitoring Centre.

She added “To be successful long-term, these areas must be managed effectively and equitably. That includes respecting the rights of, and empowering indigenous peoples and local communities.” 

“Maps for integrated land use planning can accelerate progress towards climate and biodiversity objectives and have many important additional policy uses, including helping to generate finance for natural climate solutions, improving carbon markets, and greening supply chains,” said Guido Schmidt-Traub, an author of the paper who has also written a related commentary in the same issue of Nature Ecology and Evolution.

The global priority maps can be explored interactively on the UN Biodiversity lab to support decision makers and generate insight and impact for conservation and sustainable development.

Reference
Jung, M., et al.: Areas of global importance for conserving terrestrial biodiversity, carbon, and water. Nature Ecology and Evolution. August 2021. DOI: 10.1038/s41559-021-01528-7

Adapted from a press release by The International Institute for Applied Systems Analysis (IIASA).
 

Managing a strategically chosen 30% of land for conservation could safeguard 70% of all terrestrial plant and vertebrate animal species, while simultaneously conserving around two-thirds of the world’s vulnerable carbon and clean water, according to a new study carried out by the Nature Map Consortium, involving the University of Cambridge. 

Biodiversity conservationSustainable EarthMatt LewisThe International Institute for Applied Systems AnalysisDepartment of ZoologySchool of the Biological SciencesThis type of approach can support decision makers in prioritising locations for conservation effortsLera MilesAdam Islaam | International Institute for Applied Systems Analysis (IIASA)Global areas of importance for terrestrial biodiversity, carbon and water (dark blue = highest priority, dark orange = lowest priority)


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Worsening GP shortages in disadvantaged areas likely to widen health inequalities

Wed, 18/08/2021 - 08:43

In a study published today in the BJGP Open, a team from the University of Cambridge looked at the relationship between shortages in the healthcare workforce and levels of deprivation. The team found significantly fewer full time equivalent (FTE) GPs per 10,000 patients in practices within areas of higher levels of deprivation. This inequality has widened slightly over time. By December 2020, there were on average 1.4 fewer FTE GPs per 10,000 patients in the most deprived areas compared to the least deprived areas.

The same was the case for total direct patient care staff (all patient-facing general practice staff excluding GPs and nurses), with 1.5 fewer FTE staff per 10,000 patients in the most deprived areas compared to the least deprived areas.

The lower GP numbers in deprived areas, was compensated, in part, by more nurses.

The analysis used data captured between September 2015 and December 2020 from the NHS Digital General Practice Workforce collection. They compared this workforce data against practice population sizes and levels of deprivation across England.

In addition to their report, the team have today launched an interactive dashboard that maps local-level primary care workforce inequalities to accompany the national-level analysis done in the paper. Clear local-level inequalities in GP distribution can be seen within West, North and East Cumbria, Humber, Coast and Vale, and Coventry and Warwickshire STP (Sustainability and Transformation Plan) areas, among others. 

Workforce shortages, especially in primary care, have been a problem for health care systems for some time now, and the gap between the growing demand for services and sufficient staff has been widening. Although the number of consultations in general practice has been increasing, staff numbers have not kept up with demand. The number of GPs relative to the size of population has been decreasing since 2009, and the GP workforce is ageing. Doctors are increasingly working part-time, which suggests that shortages will grow steadily worse.

In 2015, then-Secretary of State for Health Jeremy Hunt promised an additional 5,000 GPs for the NHS by 2020, but this was not achieved. Instead, it is predicted that there will be a shortage of 7,000 GPs by 2024.

Dr John Ford from the Department of Public Health and Primary Care at the University of Cambridge, the study’s senior author, said: “People who live in disadvantaged regions of England are not only more likely to have long-term health problems, but are likely to find it even more difficult to see a GP and experience worse care when they see a GP. This is just one aspect of how disadvantage accumulates for some people leading to poor health and early death.

“There may be some compensation due to increasing number of other health professionals, which may partially alleviate the undersupply of GPs in more socioeconomically disadvantaged areas. But this is not a like-for-like replacement and it is unlikely to be enough.”

The researchers say there are a number of reasons that may account for why GP workforce shortages disproportionately affect practices in areas of higher deprivation. Previous studies have suggested that the primary driver of GP inequality was the opening and closing of practices in more disadvantaged areas, with practice closures increasing in recent years.

Claire Nussbaum, the study’s first author, added: “The government has made reducing health inequalities a core commitment, but this will be challenging with the increasing shortage of GPs in areas of high socioeconomic disadvantage, where health needs are greatest. The primary care staffing inequalities we observed are especially concerning, as they suggest that access to care is becoming increasingly limited where health needs are greatest.

“Addressing barriers to health care access is even more urgent in the context of COVID-19, which has widened pre-existing health and social inequities.”

The researchers say that the imbalance in recruitment of staff within primary care must be addressed by policymakers, who will need to consider why practices and networks in disadvantaged areas are relatively under-staffed, and how this can be reversed. Potential options include increased recruitment to medical school from disadvantaged areas, incentivisation of direct patient care posts in under-staffed areas, enhanced training offers for these roles, and offering practices and networks in under-staffed areas additional recruitment support.

Expanded use of additional roles under the Additional Roles Reimbursement Scheme, designed to provide financial reimbursement for Primary Care Networks to build workforce capacity, may partially alleviate GP workload in overstretched practices, but the report’s authors argue that there is a risk that additional workforce will gravitate to more affluent areas, further perpetuating inequity in primary care staffing.

Dr James Matheson, a GP at Hill Top Surgery in Oldham, said: "People living in socioeconomically disadvantaged areas shoulder a much higher burden of physical and mental health problems but have less access to the GPs who could support them towards better health. For the primary care teams looking after them this means a greater workload with fewer resources - a burnout risk which can further exacerbate the problem.

“General Practice in disadvantaged areas is challenging but also enjoyable and professionally rewarding but now, more than ever, we need to see a more equitable distribution of workforce and resources to ensure it is sustainable."

Reference
Nussbaum, C et al. Inequalities in the distribution of the general practice workforce in England. BJGP Open; 18 Aug 2021; DOI: 10.3399/BJGPO.2021.0066

Areas of high socioeconomic disadvantaged are being worst hit by shortages of GPs, a trend that is only worsening with time and is likely to widen pre-existing health inequalities, say researchers at the University of Cambridge.

health servicesinequalityJohn FordClaire NussbaumSchool of Clinical MedicineDepartment of Public Health and Primary CareThe government has made reducing health inequalities a core commitment, but this will be challenging with the increasing shortage of GPs in areas of high socioeconomic disadvantage, where health needs are greatestClaire NussbaumpunggolzenithGP


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Ageing cuttlefish can remember the details of last week’s dinner

Wed, 18/08/2021 - 08:04

The results, published today in the journal Proceedings of the Royal Society B, are the first evidence of an animal whose memory of specific events does not deteriorate with age.

Researchers from the University of Cambridge, the Marine Biological Laboratory in Woods Hole, Massachusetts, and the University of Caen, conducted memory tests on twenty-four common cuttlefish, Sepia officinalis. Half of these were 10-12 months old - not-quite adult, and the other half were in old age at 22-24 months - equivalent to humans in their 90s.

“Cuttlefish can remember what they ate, where and when, and use this to guide their feeding decisions in the future. What’s surprising is that they don’t lose this ability with age, despite showing other signs of ageing like loss of muscle function and appetite,” said Dr Alexandra Schnell in the University of Cambridge’s Department of Psychology, first author of the paper.

As humans age, we gradually lose the ability to remember experiences that happened at particular times and places – for example, what we had for dinner last Tuesday. This is termed ‘episodic memory’, and its decline is thought to be due to deterioration of a part of the brain called the hippocampus.

Cuttlefish do not have a hippocampus, and their brain structure is dramatically different to ours. The ‘vertical lobe’ of the cuttlefish brain is associated with learning and memory. This does not deteriorate until the last two to three days of the animal’s life, which the researchers say could explain why episodic-like memory is not affected by age in cuttlefish.

To conduct the experiment, the cuttlefish were first trained to approach a specific location in their tank marked with a black and white flag. Then they were trained to learn that two foods they commonly eat were available at specific flag-marked locations and after specific delays. At one spot, the flag was waved and a piece of king prawn, their less preferred food, was provided. Live grass shrimp, which they like more, was provided at a different spot where another flag was also waved - but only every three hours. This was repeated for four weeks.

Then the cuttlefishes’ recall of which food would be available, where, and when was tested. To make sure they hadn’t just learned a pattern, the two feeding locations were unique each day. All the cuttlefish - regardless of age - watched which food first appeared at each flag and used that to work out which feeding spot was best at each subsequent flag-waving. This suggests that episodic-like memory does not decline with age in cuttlefish, unlike in humans.

“The old cuttlefish were just as good as the younger ones in the memory task – in fact, many of the older ones did better in the test phase. We think this ability might help cuttlefish in the wild to remember who they mated with, so they don’t go back to the same partner,” said Schnell.

Cuttlefish only breed at the end of their life. By remembering who they mated with, where, and how long ago, the researchers think this helps the cuttlefish to spread their genes widely by mating with as many partners as possible.  

Cuttlefish have short lifespans – most live until around two years old – making them a good subject to test whether memory declines with age. Since it is impossible to test whether animals are consciously remembering things, the authors used the term ‘episodic-like memory’ to refer to the ability of cuttlefish to remember what, where and when specific things happened.

This research was funded by the Royal Society and the Grass Foundation. 

Reference
Schnell, A.K. et al: ‘Episodic-like memory is preserved with age in cuttlefish.’ Proceedings of the Royal Society B, August 2021. DOI: 10.1098/rspb.2021.1052

Cuttlefish can remember what, where, and when specific things happened - right up to their last few days of life, researchers have found.

animal behaviourZoologyAlex SchnellNicola ClaytonMarine Biological LaboratoryUniversity of CaenDepartment of PsychologySchool of the Biological SciencesThe old cuttlefish were just as good as the younger ones in the memory task Alexandra Schnell Ageing cuttlefish can remember the details of last week’s dinner


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Discovery of origin of oesophageal cancer cells highlights importance of screening for pre-cancerous Barrett’s oesophagus

Thu, 12/08/2021 - 19:00

The study, published today in Science, found that a particular subtype of oesophageal cancer known as oesophageal adenocarcinoma is always preceded by Barrett’s oesophagus – abnormal cells of the oesophagus – even if these cells are no longer visible at the time of cancer diagnosis. This confirms that screening for Barrett’s is an important approach to oesophageal cancer control.

Cancer of the oesophagus is the sixth most deadly cancer, and oesophageal adenocarcinoma is on the rise in western countries. Scientists and doctors have known for some time that the development of this cancer is linked with Barrett’s oesophagus, which shows up in endoscopy as a pink ‘patch’ in the surface of oesophagus and affects around one out of every 100 to 200 people in the United Kingdom – and between 3 and 13 people out of 100 with this condition will go on to develop oesophageal adenocarcinoma in their lifetime. However, the question of where these abnormal cells come from has been a mystery that has baffled scientists for decades.

A multidisciplinary group of scientists led by Professor Rebecca Fitzgerald at the Medical Research Council Cancer Unit, University of Cambridge, today provides the most comprehensive explanation to date.

Dr Lizhe Zhuang, joint first author of the study, said: “It’s intriguing that, although Barrett’s oesophagus predominately occurs in the lower part of oesophagus close to stomach, it has so-called ‘goblet cells’ resembling a much more distant organ, the small intestine. Over the past twenty years there have been at least six different hypotheses about the origin of Barrett’s oesophagus. Using the latest techniques, we believe we have arrived at an answer to this mystery.”

The research team analysed tissue samples from patients with Barrett’s oesophagus and from organ donors who have never had the condition. The samples were collected as part of the Cambridge Biorepository for Translational Medicine at Addenbrooke’s Hospital, part of Cambridge University Hospitals NHS Foundation Trust.

Lead authors Dr Karol Nowicki-Osuch and Dr Lizhe Zhuang established a detailed ‘atlas’ of human cells and tissues from all possible origins of Barrett’s oesophagus, including oesophageal submucosal glands, an elusive tissue structure that acts in a similar way to saliva glands and has never before been isolated from fresh human tissue.

The researchers then compared the maps of cells from healthy tissues, Barrett’s oesophagus and oesophageal adenocarcinoma using a number of state-of-the-art molecular technologies. These included single cell RNA sequencing, a powerful technology that enables researchers to investigate the functions of a large number of individual cells. They also looked at methylation profiles –chemical modifications to the DNA of cells in the tissue – and at genetic linage to trace back where a particular cell type originated.

The results showed a striking similarity between stomach cells and Barrett’s oesophagus, suggesting that the cells at the very top of the stomach can be reprogrammed to adopt a new tissue identity, becoming more like intestine cells, and replace the oesophageal cells. Furthermore, in this new study the team showed that two genes, MYC and HNF4A, are the keys that switch the tissue identity from stomach to intestinal cells.

Dr Karol Nowicki-Osuch, joint first author of the study, said: “The techniques we used have shown us the internal processes that happen in the stomach cells when they become Barrett’s. The big question now is: what triggers these genes? It’s likely to be a complex combination of factors that include bile acid reflux (often felt as heartburn) and other risk factors, such as obesity, age, male sex and Caucasian ethnicity.”

Importantly, the researchers found that all oesophageal adenocarcinoma cells begin as stomach cells before transforming into Barrett’s cells and then into cancer cells.

Professor Fitzgerald added: “Even if the pre-cancerous Barrett’s is not visible at the time of cancer diagnosis, our data suggests the cancer cells will have been through this stage. This has been debated for some time, but our conclusion is important as it means that screening for Barrett’s is an important approach to controlling oesophageal cancer.”

Michelle Mitchell, Chief Executive of Cancer Research UK, said, “Today’s insights into the origin of oesophageal adenocarcinoma could help inform future research efforts into how to diagnose this type of cancer early – which is key for improving patient outcomes.

“This research goes hand in hand with other recent successes in early detection such as Cytosponge, the sponge-on a-string test, which we funded to detect Barrett’s in patients with heartburn symptoms.”

Detecting cancer earlier will be a key focus of the Cambridge Cancer Research Hospital, a partnership between Cambridge University Hospitals NHS Foundation Trust and the University of Cambridge to build a new specialist cancer hospital. The hospital will combine modern NHS clinical space with two new research institutes, including the National Institute for the Early Detection of Cancer, which will lead the way in helping advance early cancer detection techniques.

The research was largely funded by the Medical Research Council, Wellcome and Cancer Research UK.

Further information on oesophageal cancer and Barrett’s oesophagus is available via Cancer Research UK.

Reference
Nowicki-Osuch, K & Zhuang, L et al. Molecular phenotyping reveals the identity of Barrett’s esophagus and its malignant transition. Science; 13 Aug 2021; DOI: 10.1126/science.abd1449

Abnormal cells that go on develop into oesophageal cancer – cancer that affects the tube connecting the mouth and stomach – start life as cells of the stomach, according to scientists at the University of Cambridge.

Canceroesophageal cancerRebecca FitzgeraldKarol Nowicki-OsuchLizhe ZhuangMedical Research CouncilWellcomeCancer Research UK (CRUK)School of Clinical MedicineCancer Research UK Cambridge InstituteCambridge Cancer CentreMedical Research Council (MRC) Cancer UnitThe techniques we used have shown us the internal processes that happen in the stomach cells when they become Barrett’s. The big question now is: what triggers these genes?Karol Nowicki-OsuchAdobe StockMan experiencing heartburn


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AI could detect dementia years before symptoms appear

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Dandelion clock (Credit: Ýlona María Rybka)

Dandelion clock (Credit: Ýlona María Rybka)

Artificial intelligence could spot the early signs of dementia from a simple brain scan long before major symptoms appear – and in some cases before any symptoms appear – say Cambridge researchers.

Dementias are characterised by the build-up of different types of protein in the brain, which damages brain tissue and leads to cognitive decline. In the case of Alzheimer’s disease, these proteins include beta-amyloid, which forms ‘plaques’, clumping together between neurons and affecting their function, and tau, which accumulates inside neurons.

Molecular and cellular changes to the brain usually begin many years before any symptoms occur. Diagnosing dementia can take many months or even years. It typically requires two or three hospital visits and can involve a range of CT, PET and MRI scans as well as invasive lumber punctures.

A team led by Professor Zoe Kourtzi at the University of Cambridge and Alan Turing Institute has developed machine learning tools that can detect dementia in patients at a very early stage. Using brain scans from patients who went on to develop Alzheimer’s, their machine learning algorithm learnt to spot structural changes in the brain. When combined with the results from standard memory tests, the algorithm was able to provide a prognostic score – that is, the likelihood of the individual having Alzheimer’s disease.

For those patients presenting with mild cognitive impairment – signs of memory loss or problems with language or visual/spatial perception – the algorithm was higher than 80% accurate in predicting those individuals who went on to develop Alzheimer’s disease. It was also able to predict how fast their cognition will decline over time.

MRI brain scan of healthy volunteer (Credit: Timothy Rittman)

MRI brain scan of healthy volunteer (Credit: Timothy Rittman)

MRI brain scan of Alzheimer's patient (Credit: TImothy Rittman)

MRI brain scan of Alzheimer's patient (Credit: TImothy Rittman)

Professor Kourtzi, from Cambridge's Department of Psychology, said: “We have trained machine learning algorithms to spot very early signs of dementia just by looking for patterns of grey matter loss – essentially, wearing away – in the brain. When we combine this with standard memory tests, we can predict whether an individual will show slower or faster decline in their cognition.

“We’ve even been able to identify some patients who were not yet showing any symptoms, but went on to develop Alzheimer’s."

"In time, we hope to be able to identify patients as early as five to ten years before they show symptoms as part of a health check.”Professor Zoe Kourtzi, Department of Psychology

Although the algorithm has been optimised to look for signs of Alzheimer’s disease, Professor Kourtzi and colleagues are now training it to recognise different forms of dementia, each of which has its own characteristic pattern of volume loss.

Dr Timothy Rittman from the Department of Clinical Neurosciences and a consultant at Addenbrooke’s Hospital, part of Cambridge University Hospitals (CUH) NHS Foundation Trust, is now leading a trial to look at whether this approach is useful in a clinical setting.

“We’ve shown that this approach works in a research setting – we now need to test it in a ‘real world’ setting,” explained Dr Rittman.

To date around 80 patients have taken part in the trial, which was run by CUH, Cambridgeshire and Peterborough NHS Foundation Trust and two NHS trusts in Brighton.

Catching dementia early is important for several reasons, explained Dr Rittman. “When patients begin to experience memory and cognitive problems, this can understandably be a very difficult time. Being able to provide an accurate diagnosis gives them clarity and, depending on the diagnosis, can either ease their minds or help them and their loved ones put preparations in place for the longer term."

“If we catch the disease early enough, there are lifestyle changes we can recommend – blood pressure medication, improved diet and exercise, stopping smoking, for example – that may help slow the progression of the disease.”Dr Timothy Rittman

There are currently very few drugs available to help treat dementia. One of the reasons that clinical trials often fail is thought to be because once a patient has developed symptoms, it may be too late to make a major difference. Having the ability to identify individuals at a very early stage could therefore help researchers develop new medicines.

If the trial is successful, the algorithm could be rolled out to thousands more patients across the country.

Living with Alzheimer’s disease

Addenbrooke’s patient Dennis Clark was one of the first people in the country to take part in the new trial. Before lockdown, the 75-year-old retired sales director had been enjoying his retirement with wife Penny, going on holiday and walking his two dogs. But Penny soon noticed he was starting to forget things.

“If I asked him to do something, he would do the opposite. Then when we went out for a meal – which we didn’t do for a long time because of lockdown – he couldn’t remember how to pay for anything.”

Penny decided to call the GP for help when Dennis, who had always taken pride in his appearance, started to wear the same clothes over and over again.

“The GP did a quick test over the phone and said Dennis needed to be referred. I had heard Addenbrooke’s had a very comprehensive memory unit, so I was really pleased that we were able to be referred there.

“We had an initial consultation and we were asked if we wanted to go down the research route, which I was really keen for Dennis to do because it doesn’t just help him, it helps others as well.”

Dennis underwent an MRI scan and later that same day he and Penny received the news that his results were consistent with early onset of Alzheimer’s disease. Dennis will begin taking medication to help treat the symptoms of Alzheimer’s disease.

“We are very grateful to Addenbrooke’s and would recommend other people take up trials as well. Quicker diagnosis means Dennis will be able to start medication that will hopefully delay his disease. It also means we can plan for the future and start to accept what is happening.”

Case study courtesy of Cambridge University Hospitals NHS Foundation Trust.

Reference

Giorgio, J et al. Modelling prognostic trajectories of cognitive decline due to Alzheimer's disease. NeuroImage: Clinical; 26 Jan 2020; DOI: 10.1016/j.nicl.2020.102199

Giorgio, J et al. Predicting future regional tau accumulation in asymptomatic and early Alzheimer’s disease. BioRXiv (pre-print)

Article posted 12 August 2021

TopBuilt with Shorthand Summary: 

Artificial intelligence could spot the early signs of dementia from a simple brain scan long before major symptoms appear – and in some cases before any symptoms appear – say Cambridge researchers.Artificial intelligence (AI) could spot the early signs of dementia from a simple brain scan long before major symptoms appear – and in some cases before any symptoms appear – say Cambridge researchers.

Image: Affiliation (schools and institutions): School of Clinical MedicineSchool of the Biological SciencesDepartment of Clinical NeurosciencesDepartment of PsychologyAddenbrooke's HospitalCambridge University Hospitals NHS Foundation TrustExternal Affiliations: The Alan Turing InstitutePeople (our academics and staff): Zoe KourtziTimothy RittmanSubject (including Spotlight on ... where applicable): Spotlight on neuroscienceNeurosciencehealthdementiaAlzheimer's diseaseArtificial intelligenceSection: ResearchNews type: Features

Lab-grown beating heart cells identify potential drug to prevent COVID-19-related heart damage

Thu, 05/08/2021 - 09:35

The heart is one the major organs damaged by infection with SARS-CoV-2, particularly the heart cells, or ‘cardiomyocytes’, which contract and circulate blood. It is also thought that damage to heart cells may contribute to the symptoms of long COVID.

Patients with underlying heart problems are more than four times as likely to die from COVID-19, the disease caused by SARS-CoV-2 infection. The case fatality rate in patients with COVID-19 rises from 2.3% to 10.5% in these individuals.

To gain entry into our cells, SARS-CoV-2 hijacks a protein on the surface of the cells, a receptor known as ACE2.  Spike proteins on the surface of SARS-CoV-2 – which give it its characteristic ‘corona’-like appearance – bind to ACE2. Both the spike protein and ACE2 are then cleaved, allowing genetic material from the virus to enter the host cell. The virus manipulates the host cell’s machinery to allow itself to replicate and spread.

A team of scientists at the University of Cambridge has used human embryonic stem cells to grow clusters of heart cells in the lab and shown that these cells mimic the behaviour of the cells in the body, beating as if to pump blood. Crucially, these model heart cells also contained the key components necessary for SARS-CoV-2 infection – in particular, the ACE2 receptor.

Working in special biosafety laboratories and using a safer, modified synthetic (‘pseudotyped’) virus decorated with the SARS-CoV-2 spike protein, the team mimicked how the virus infects the heart cells. They then used this model to screen for potential drugs to block infection.

Dr Sanjay Sinha from the Wellcome-MRC Cambridge Stem Cell Institute said: “Using stem cells, we’ve managed to create a model which, in many ways, behaves just like a heart does, beating in rhythm. This has allowed us to look at how the coronavirus infects cells and, importantly, helps us screen possible drugs that might prevent damage to the heart.”

The team showed that some drugs that targeted the proteins involved in SARS-CoV-2 viral entry significantly reduced levels of infection. These included an ACE2 antibody that has been shown previously to neutralise pseudotyped SARS-CoV-2 virus, and DX600, an experimental drug.

DX600 is an ACE2 peptide antagonist – that is, a molecule that specifically targets ACE2 and inhibits the activity of peptides that play a role in allowing the virus to break into the cell.

DX600 was around seven times more effective at preventing infection compared to the antibody, though the researchers say this may be because it was used in higher concentrations. The drug did not affect the number of heart cells, implying that it would be unlikely to be toxic.

Professor Anthony Davenport from the Department of Medicine and a fellow at St Catharine’s College, Cambridge said: “The spike protein is like a key that fits into the ‘lock’ on the surface of the cells – the ACE2 receptor – allowing it entry. DX600 acts like gum, jamming the lock’s mechanism, making it much more difficult for the key to turn and unlock the cell door.

“We need to do further research on this drug, but it could provide us with a new treatment to help reduce harm to the heart in patients recently infected with the virus, particularly those who already have underlying heart conditions or who have not been vaccinated. We believe it may also help reduce the symptoms of long COVID.”

The research was largely supported by Wellcome, Addenbrooke’s Charitable Trust, Rosetrees Trust Charity and British Heart Foundation.

Reference
Williams, TL et al. Human embryonic stem cell-derived cardiomyocyte platform screens inhibitors of SARS-CoV-2 infection. Communications Biology; 29 Jul 2017; DOI: 10.1038/s42003-021-02453-y

Cambridge scientists have grown beating heart cells in the lab and shown how they are vulnerable to SARS-CoV-2 infection. In a study published in Communications Biology, they used this system to show that an experimental peptide drug called DX600 can prevent the virus entering the heart cells.

Stem cellsCOVID-19Coronavirusheartcardiovascular disease (CVD)Anthony DavenportSanjay SinhaWellcomeAddenbrooke’s Charitable TrustRosetrees TrustBritish Heart FoundationSchool of Clinical MedicineDepartment of MedicineWellcome-MRC Cambridge Stem Cell InstituteDepartment of Experimental Medicine and ImmunotherapeuticsSt Catharine's CollegeUsing stem cells, we’ve managed to create a model which, in many ways, behaves just like a heart does, beating in rhythm. This has allowed us to look at how the coronavirus infects cells and, importantly, helps us screen possible drugs that might prevent damage to the heartSanjay Sinha Beating heart cells infected with virus sbtlneetHeart


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Artificial pancreas trialled for outpatients with type 2 diabetes for first time

Wed, 04/08/2021 - 15:00

Diabetes is the most common cause of kidney failure, accounting for just under a third (30%) of cases. As the number of people living with type 2 diabetes increases, so too does the number of people requiring dialysis or a kidney transplant. Kidney failure increases the risk of hypoglycaemia and hyperglycaemia – abnormally low or high levels of blood sugar respectively – which in turn can cause complications from dizziness to falls and even to coma.

Managing diabetes in patients with kidney failure is challenging for both patients and healthcare professionals. Many aspects of their care are poorly understood, including targets for blood sugar levels and treatments. Most oral diabetes medications are not recommended for these patients, so insulin injections are the most commonly used diabetes therapy – though optimal insulin dosing regimens are difficult to establish.

A team at the University of Cambridge and Cambridge University Hospitals NHS Foundation Trust has previously developed an artificial pancreas with the aim of replacing insulin injections for patients living with type 1 diabetes. In research published today in Nature Medicine, the team – working with researchers at Bern University Hospital and University of Bern, Switzerland – has shown that the device can be used to support patients living with both type 2 diabetes and kidney failure.

Unlike the artificial pancreas being used for type 1 diabetes, this version is a fully closed loop system – whereas patients with type 1 diabetes need to tell their artificial pancreas that they are about to eat to allow adjustment of insulin, for example, with this new version they can leave the device to function entirely automatically.

Dr Charlotte Boughton from the Wellcome-MRC Institute of Metabolic Science at the University of Cambridge, who led the study, said: “Patients living with type 2 diabetes and kidney failure are a particularly vulnerable group and managing their condition – trying to prevent potentially dangerous highs or lows of blood sugar levels – can be a challenge. There’s a real unmet need for new approaches to help them manage their condition safely and effectively.”

The artificial pancreas is a small, portable medical device designed to carry out the function of a healthy pancreas in controlling blood glucose levels, using digital technology to automate insulin delivery. The system is worn externally on the body, and is made up of three functional components: a glucose sensor, a computer algorithm to calculate the insulin dose, and an insulin pump. Software in the user’s smartphone sends a signal to an insulin pump to adjust the level of insulin the patient receives. The glucose sensor measures the patient’s blood sugar levels and sends these back to the smartphone to enable it to make further adjustments.

The team recruited 26 patients requiring dialysis between October 2019 and November 2020. Thirteen participants were randomised to receive the artificial pancreas first and 13 to receive standard insulin therapy first. The researchers compared how long patients spent in the target blood sugar range (5.6 to 10.0mmol/L) over a 20-day period as outpatients.

Patients using the artificial pancreas spent on average 53% of their time in the target range, compared to 38% when they used the control treatment. This equated to around 3.5 additional hours every day spent in the target range compared with the control therapy.

Mean blood sugar levels were lower with the artificial pancreas (10.1 vs. 11.6 mmol/L). The artificial pancreas reduced the amount of time patients spent with potentially dangerously low blood sugar levels, or ‘hypos’.

The efficacy of the artificial pancreas improved considerably over the study period as the algorithm adapted, and the time spent in the target blood sugar range increased from 36% on day one to over 60% by the twentieth day. This finding highlights the importance of using an adaptive algorithm, which can adjust in response to an individual’s changing insulin requirements over time.

When asked about their experiences of using the artificial pancreas, everyone who responded said they would recommend it to others. Nine out of ten (92%) reported that they spent less time managing their diabetes with the artificial pancreas than during the control period, and similar numbers (87%) were less worried about their blood sugar levels when using it.

Other benefits of the artificial pancreas reported by study participants included less need for finger-prick blood sugar checks, less time required to manage their diabetes resulting in more personal time and freedom, and improved peace of mind and reassurance. Downsides included discomfort wearing the insulin pump and carrying the smartphone.

Senior author Professor Roman Hovorka, also from the Wellcome-MRC Institute of Metabolic Science, said: “Not only did the artificial pancreas increase the amount of time patients spent within the target range for the blood sugar levels, it also gave the users peace of mind. They were able to spend less time having to focus on managing their condition and worrying about their blood sugar levels, and more time getting on with their lives.”

Dr Boughton added: “Now that we’ve shown the artificial pancreas works in one of the more difficult-to-treat groups of patients, we believe it could prove useful in the wider population of people living with type 2 diabetes.”

The team is currently trialling the artificial pancreas for outpatient use in people living with type 2 diabetes who do not need dialysis and exploring the system in complex medical situations such as perioperative care.

Dr Lia Bally, who co-led the study in Bern, said: “The artificial pancreas has the potential to become a key feature of integrated personalised care for people with complex medical needs.”

The research was supported by the NIHR Cambridge Biomedical Research Centre, The Novo Nordisk UK Research Foundation, Swiss Society for Endocrinology and Diabetes, and Swiss Diabetes Foundation and Swiss Kidney Foundation.

Reference
Boughton, CK et al.  Fully automated closed-loop glucose control compared with standard insulin therapy in adults with type 2 diabetes requiring dialysis: an open-label, randomised crossover trial. Nat Med; 4 Aug 2021; DOI: 10.1038/s41591-021-01453-z

An artificial pancreas could soon help those people living with type 2 diabetes who also require kidney dialysis. Tests led by the University of Cambridge and Inselspital, University Hospital of Bern, Switzerland, show that the device can help patients safely and effectively manage their blood sugar levels and reduce the risk of low blood sugar levels.

type 2 diabetesCharlotte BoughtonRoman HovorkaNIHR Cambridge Biomedical Research CentreNovo Nordisk UK Research FoundationSwiss Society for Endocrinology and DiabetesSwiss Diabetes FoundationSwiss Kidney FoundationSchool of Clinical MedicineWellcome-MRC Institute of Metabolic ScienceCambridge University Hospitals NHS Foundation TrustPatients living with type 2 diabetes and kidney failure are a particularly vulnerable group and managing their condition can be a challenge. There’s a real unmet need for new approaches to help them manage their condition safely and effectivelyCharlotte BoughtonUniversity of CambridgePatient using the artificial pancreas


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Scientists can detect brain tumours using a simple urine or blood plasma test

Fri, 23/07/2021 - 16:05

The team say that a test for detecting glioma using urine is the first of its kind in the world.

Although the research, published in EMBO Molecular Medicine, is in its early stages and only a small number of patients were analysed, the team say their results are promising.

The researchers suggest that in the future, these tests could be used by GPs to monitor patients at high risk of brain tumours, which may be more convenient than having an MRI every three months, which is the standard method.

When people have a brain tumour removed, the likelihood of it returning can be high, so they are monitored with an MRI scan every three months, which is followed by biopsy.

Blood tests for detecting different cancer types are a major focus of research for teams across the world, and there are some in use in the clinic. These tests are mainly based on finding mutated DNA, shed by tumour cells when they die, known as cell-free DNA (cfDNA).

However, detecting brain tumour cfDNA in the blood has historically been difficult because of the blood-brain-barrier, which separates blood from the cerebrospinal fluid (CSF) that surrounds the brain and spinal cord, preventing the passage of cells and other particles, such as cfDNA.

Researchers have previously looked at detecting cfDNA in CSF, but the spinal taps needed to obtain it can be dangerous for people with brain tumours so are not appropriate for patient monitoring.

Scientists have known that cfDNA with similar mutations to the original tumour can be found in blood and other bodily fluids such as urine in very low levels, but the challenge has been developing a test sensitive enough to detect these specific mutations.

The researchers, led by Dr Florent Mouliere who is based at the Rosenfeld Lab of the Cancer Research UK Cambridge Institute and at the Amsterdam UMC, and Dr Richard Mair, who is based at Cancer Research UK Cambridge Institute and the University of Cambridge developed two approaches in parallel to overcome the challenge of detecting brain tumour cfDNA.

The first approach works for patients who have previously had glioma removed and biopsied. The team designed a tumour-guided sequencing test that was able to look for the mutations found in the tumour tissue within the cfDNA in the patient’s urine, CSF, and blood plasma.

A total of eight patients who had suspected brain tumours based on MRIs were included in this part of the study. Samples were taken at their initial brain tumour biopsies, alongside CSF, blood and urine samples.

By knowing where in the DNA strand to look, the researchers found that it was possible to find mutations even in the tiny amounts of cfDNA found in the blood plasma and urine.

The test was able to detect cfDNA in 7 out of 8 CSF samples, 10 out of the 12 plasma blood samples and 10 out of the 16 urine samples.

For the second approach the researchers looked for other patterns in the cfDNA that could also indicate the presence of a tumour, without having to identify the mutations.

They analysed 35 samples from glioma patients, 27 people with non-malignant brain disorders, and 26 healthy people. They used whole genome sequencing, where all the cfDNA of the tumour is analysed, not just the mutations.

They found in the blood plasma and urine samples that fragments of cfDNA, which came from patients with brain tumours were different sizes than those from patients with no tumours in CSF. They then fed this data into a machine learning algorithm which was able to successfully differentiate between the urine samples of people with and without glioma.

The researchers say that while the machine learning test is cheaper and easier, and a tissue biopsy from the tumour is not needed, it is not as sensitive and is less specific than the first tumour-guided sequencing approach.

MRIs are not invasive or expensive, but they do require a trip to the hospital, and the three-month gap between checks can be a regular source of anxiety for patients.

The researchers suggest that their tests could be used between MRI scans, and could ultimately be able to detect a returning brain tumour earlier.

The next stage of this research will see the team comparing both tests against MRI scans in a trial with patients with brain tumours who are in remission to see if it can detect if their tumours are coming back at the same time or earlier than the MRI. If the tests prove that they can detect brain tumours earlier than an MRI, then the researchers will look at how they can adapt the tests so they could be offered in the clinic, which could be within the next ten years.

“We believe the tests we’ve developed could in the future be able to detect a returning glioma earlier and improve patient outcomes,” said Mair. “Talking to my patients, I know the three-month scan becomes a focal point for worry. If we could offer a regular blood or urine test, not only will you be picking up recurrence earlier, you can also be doing something positive for the patient’s mental health.”

Michelle Mitchell, Chief Executive of Cancer Research UK said, “While this is early research, it’s opened up the possibility that within the next decade we could be able to detect the presence of a brain tumour with a simple urine or blood test. Liquid biopsies are a huge area of research interest right now because of the opportunities they create for improved patient care and early diagnosis. It’s great to see Cancer Research UK researchers making strides in this important field.”

Sue Humphreys, from Wallsall, a brain tumour patient, said: "If these tests are found to be as accurate as the standard MRI for monitoring brain tumours, it could be life changing.

If patients can be given a regular and simple test by their GP, it may help not only detect a returning brain tumour in its earliest stages, it can also provide the quick reassurance that nothing is going on which is the main problem we all suffer from, the dreaded Scanxiety.

The problem with three-monthly scans is that these procedures can get disrupted by other things going on, such as what we have seen with the Covid pandemic. As a patient, this causes worry as there is a risk that things may be missed, or delayed, and early intervention is the key to any successful treatment.”

 

Reference:
Florent Mouliere et al. ‘Fragmentation patterns and personalized sequencing of cell-free DNA in urine and plasma of glioma patients.’ EMBO Molecular Medicine (2021). DOI: 10.15252/emmm.202012881

Adapted from a Cancer Research UK press release.

Researchers from the Cancer Research UK Cambridge Institute have developed two tests that can detect the presence of glioma, a type of brain tumour, in patient urine or blood plasma.

Cancerdiagnosticbrainbrain tumourstumoursFlorent MouliereRichard MairCancer Research UK (CRUK)Cancer Research UK Cambridge InstituteSchool of Clinical Medicine


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Blushing plants reveal when fungi are growing in their roots

Fri, 23/07/2021 - 08:06

This is the first time this vital, 400 million year old process has been visualised in real time in full root systems of living plants. Understanding the dynamics of plant colonisation by fungi could help to make food production more sustainable in the future.

Almost all crop plants form associations with a particular type of fungi – called arbuscular mycorrhiza fungi – in the soil, which greatly expand their root surface area. This mutually beneficial interaction boosts the plant’s ability to take up nutrients that are vital for growth. 

The more nutrients plants obtain naturally, the less artificial fertilisers are needed. Understanding this natural process, as the first step towards potentially enhancing it, is an ongoing research challenge. Progress is likely to pay huge dividends for agricultural productivity.

In a study published in the journal PLOS Biology, researchers used the bright red pigments of beetroot – called betalains – to visually track soil fungi as they colonised plant roots in a living plant. 

“We can now follow how the relationship between the fungi and plant root develops, in real-time, from the moment they come into contact. We previously had no idea about what happened because there was no way to visualise it in a living plant without the use of elaborate microscopy,” said Dr Sebastian Schornack, a researcher at the University of Cambridge’s Sainsbury Laboratory and joint senior author of the paper. 

To achieve their results, the researchers engineered two model plant species – a legume and a tobacco plant – so that they would produce the highly visible betalain pigments when arbuscular mycorrhiza fungi were present in their roots. This involved combining the control regions of two genes activated by mycorrhizal fungi with genes that synthesise red-coloured betalain pigments.

The plants were then grown in a transparent structure so that the root system was visible, and images of the roots could be taken with a flatbed scanner without disturbing the plants.

Using their technique, the researchers could select red pigmented parts of the root system to observe the fungus more closely as it entered individual plant cells and formed elaborate tree-like structures – called arbuscules – which grow inside the plant’s roots. Arbuscules take up nutrients from the soil that would otherwise be beyond the reach of the plant. 

Other methods exist to visualise this process, but these involve digging up and killing the plant and the use of chemicals or expensive microscopy. This work makes it possible for the first time to watch by eye and with simple imaging how symbiotic fungi start colonising living plant roots, and inhabit parts of the plant root system over time.

“This is an exciting new tool to visualise this, and other, important plant processes. Beetroot pigments are a distinctive colour, so they’re very easy to see. They also have the advantage of being natural plant pigments, so they are well tolerated by plants,” said Dr Sam Brockington, a researcher in the University of Cambridge’s Department of Plant Sciences, and joint senior author of the paper.

Mycorrhiza fungi are attracting growing interest in agriculture. This new technique provides the ability to ‘track and trace’ the presence of symbiotic fungi in soils from different sources and locations. The researchers say this will enable the selection of fungi that colonise plants fastest and provide the biggest benefits in agricultural scenarios.

Understanding and exploiting the dynamics of plant root system colonisation by fungi has potential to enhance future crop production in an environmentally sustainable way. If plants can take up more nutrients naturally, this will reduce the need for artificial fertilisers – saving money and reducing associated water pollution. 

This research was funded by the Biotechnology and Biological Sciences Research Council, Gatsby Charitable Foundation, Royal Society, and Natural Environment Research Council. 

Reference
Timoneda, A. & Yunusov, T. et al: ‘MycoRed: Betalain pigments enable in vivo real-time visualisation of arbuscular mycorrhizal colonisation.’ PLOS Biology, July 2021. DOI: 10.1371/journal.pbio.3001326

Scientists have created plants whose cells and tissues ‘blush’ with beetroot pigments when they are colonised by fungi that help them take up nutrients from the soil.

plant sciencesGlobal food securitySustainable agricultureSustainable EarthSam BrockingtonSebastian SchornackCambridge University Botanic GardenDepartment of Plant SciencesSainsbury LaboratorySchool of the Biological SciencesWe can now follow how the relationship between the fungi and plant root develops, in real-time, from the moment they come into contact.Sebastian SchornackTemur Yunusov and Alfonso TimonedaCells of roots colonised by fungi turn red


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Scientists reverse age-related memory loss in mice

Thu, 22/07/2021 - 15:18

In a study published in Molecular Psychiatry, the team show that changes in the extracellular matrix of the brain – ‘scaffolding’ around nerve cells – lead to loss of memory with ageing, but that it is possible to reverse these using genetic treatments.

Recent evidence has emerged of the role of perineuronal nets (PNNs) in neuroplasticity – the ability of the brain to learn and adapt – and to make memories. PNNs are cartilage-like structures that mostly surround inhibitory neurons in the brain. Their main function is to control the level of plasticity in the brain. They appear at around five years old in humans, and turn off the period of enhanced plasticity during which the connections in the brain are optimised. Then, plasticity is partially turned off, making the brain more efficient but less plastic.

PNNs contain compounds known as chondroitin sulphates. Some of these, such as chondroitin 4-sulphate, inhibit the action of the networks, inhibiting neuroplasticity; others, such as chondroitin 6-sulphate, promote neuroplasticity. As we age, the balance of these compounds changes, and as levels of chondroitin 6-sulphate decrease, so our ability to learn and form new memories changes, leading to age-related memory decline.

Researchers at the University of Cambridge and University of Leeds investigated whether manipulating the chondroitin sulphate composition of the PNNs might restore neuroplasticity and alleviate age-related memory deficits.

To do this, the team looked at 20-month old mice – considered very old – and using a suite of tests showed that the mice exhibited deficits in their memory compared to six-month old mice.

For example, one test involved seeing whether mice recognised an object. The mouse was placed at the start of a Y-shaped maze and left to explore two identical objects at the end of the two arms. After a short while, the mouse was once again placed in the maze, but this time one arm contained a new object, while the other contained a copy of the repeated object. The researchers measured the amount of time the mouse spent exploring each object to see whether it had remembered the object from the previous task. The older mice were much less likely to remember the object.

The team treated the ageing mice using a ‘viral vector’, a virus capable of reconstituting the amount of 6-sulphate chondroitin sulphates to the PNNs and found that this completely restored memory in the older mice, to a level similar to that seen in the younger mice.

Dr Jessica Kwok from the School of Biomedical Sciences at the University of Leeds said: “We saw remarkable results when we treated the ageing mice with this treatment. The memory and ability to learn were restored to levels they would not have seen since they were much younger.”

To explore the role of chondroitin 6-sulphate in memory loss, the researchers bred mice that had been genetically-manipulated such that they were only able to produce low levels of the compound to mimic the changes of ageing. Even at 11 weeks, these mice showed signs of premature memory loss. However, increasing levels of chondroitin 6-sulphate using the viral vector restored their memory and plasticity to levels similar to healthy mice.

Professor James Fawcett from the John van Geest Centre for Brain Repair at the University of Cambridge said: “What is exciting about this is that although our study was only in mice, the same mechanism should operate in humans – the molecules and structures in the human brain are the same as those in rodents. This suggests that it may be possible to prevent humans from developing memory loss in old age.”

The team have already identified a potential drug, licensed for human use, that can be taken by mouth and inhibits the formation of PNNs. When this compound is given to mice and rats it can restore memory in ageing and also improves recovery in spinal cord injury. The researchers are investigating whether it might help alleviate memory loss in animal models of Alzheimer's disease.

The approach taken by Professor Fawcett’s team – using viral vectors to deliver the treatment – is increasingly being used to treat human neurological conditions. A second team at the Centre recently published research showing their use for repairing damage caused by glaucoma and dementia.

The study was funded by Alzheimer’s Research UK, the Medical Research Council, European Research Council and the Czech Science Foundation.

 

Reference
Yang, S et al. Chondroitin 6-sulphate is required for neuroplasticity and memory in ageing. Molecular Psychiatry; 16 July 2021; DOI: doi.org/10.1038/s41380-021-01208-9

Scientists at Cambridge and Leeds have successfully reversed age-related memory loss in mice and say their discovery could lead to the development of treatments to prevent memory loss in people as they age.

brainNeuroscienceageingneurodegenerationanimal researchJames FawcettUniversity of LeedsAlzheimer's Research UKEuropean Research CouncilMedical Research CouncilCzech Science FoundationJohn van Geest Centre for Brain RepairSchool of Clinical MedicineAlthough our study was only in mice, the same mechanism should operate in humans – the molecules and structures in the human brain are the same as those in rodents. This suggests that it may be possible to prevent humans from developing memory loss in old ageJames FawcettMichael Shribak, Marine Biological Laboratory, Woods Hole, MASpatially oriented neurons (mouse brain)


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Llama ‘nanobodies’ could hold key to preventing deadly post-transplant infection

Thu, 22/07/2021 - 10:07

Around four out of five people in the UK are thought to be infected with HCMV, and in developing countries this can be as high as 95%. For the majority of people, the virus remains dormant, hidden away inside white blood cells, where it can remain undisturbed and undetected for decades. If the virus reactivates in a healthy individual, it does not usually cause symptoms. However, for people who are immunocompromised – for example, transplant recipients who need to take immunosuppressant drugs to prevent organ rejection – HCMV reactivation can be devastating.

At present, there is no effective vaccine against HCMV, and anti-viral drugs often prove ineffective or have very serious side-effects.

Now, in a study published in Nature Communications, researchers at Vrije Universiteit Amsterdam in the Netherlands and at the University of Cambridge have found a way to chase the virus from its hiding place using a special type of antibody known as a nanobody.

Nanobodies were first identified in camels and exist in all camelids – a family of animals that also includes dromedary, llamas and alpacas. Human antibodies consist of two heavy and two light chains of molecules, which together recognise and bind to markers on the surface of a cell or virus known as antigens. For this special class of camelid antibodies, however, only a single fragment of the antibody – often referred to as single domain antibody or nanobody – is sufficient to properly recognize antigens.

Dr Timo De Groof from Vrije Universiteit Amsterdam, the study’s joint first author, said: “As the name suggests, nanobodies are much smaller than regular antibodies, which make them perfectly suited for particular types of antigens and relatively easy to manufacture and adjust. That’s why they’re being hailed as having the potential to revolutionise antibody therapies.”

The first nanobody has been approved and introduced onto the market by biopharmaceutical company Ablynx, while other nanobodies are already in clinical trials for diseases like rheumatoid arthritis and certain cancers. Now, the team in The Netherlands and the UK have developed nanobodies that target a specific virus protein (US28), one of the few elements detectable on the surface of a HCMV latently infected cell and a main driver of this latent state.

Dr Ian Groves from the Department of Medicine at the University of Cambridge said: “Our team has shown that nanobodies derived from llamas have the potential to outwit human cytomegalovirus. This could be very important as the virus can cause life-threatening complications in people whose immune systems are not functioning properly.”

In laboratory experiments using blood infected with the virus, the team showed that the nanobody binds to the US28 protein and interrupts the signals established through the protein that help keep the virus in its dormant state. Once this control is broken, the local immune cells are able to 'see' that the cell is infected, enabling the host’s immune cells to hunt down and kill the virus, purging the latent reservoir and clearing the blood of the virus.

Dr Elizabeth Elder, joint first author, who carried out her work while at the University of Cambridge, said: “The beauty of this approach is that it reactivates the virus just enough to make it visible to the immune system, but not enough for it to do what a virus normally does – replicating and spreading. The virus is forced to put its head above the parapet where it can then be killed by the immune system.”

Professor Martine Smit, also from from the Vrije Universiteit Amsterdam, added: “We believe our approach could lead to a much-needed new type of treatment for reducing – and potentially even preventing – CMV infectious in patients eligible for organ and stem cell transplants.”

The research was funded by the Dutch Research Council (NWO), Wellcome and the Medical Research Council, with support from the NIHR Cambridge Biomedical Research Centre.

 

Reference
De Groof TWM, Elder E, et al. Targeting the latent human cytomegalovirus reservoir for T-cell mediated killing with virus specific nanobodies. Nature Communications (2021). DOI: 10.1038/s41467-021-24608-5

Scientists have developed a ‘nanobody’ – a small fragment of a llama antibody – that is capable of chasing out human cytomegalovirus (HCMV) as it hides away from the immune system. This then enables immune cells to seek out and destroy this potentially deadly virus.

medicinevirologytransplantationInfectious diseasesElizabeth ElderIan GrovesVrije Universiteit AmsterdamDutch Research Council (NWO)WellcomeMedical Research CouncilDepartment of MedicineSchool of Clinical MedicineNIHR Cambridge Biomedical Research CentreOur team has shown that nanobodies derived from llamas have the potential to outwit human cytomegalovirusIan GrovesJessica Knowlden on UnsplashLlamas


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Biological ‘fingerprints’ of long COVID in blood could lead to diagnostic test, say Cambridge scientists

Mon, 19/07/2021 - 08:39

The team has received funding from the National Institute for Health Research to develop a test that could complement existing antibody tests. They also aim to use similar biological signatures to develop a test and monitor for long COVID.

While most people recover from COVID-19 in a matter of days or weeks, around one in ten people go on to develop symptoms that can last for several months. This can be the case irrespective of the severity of their COVID-19 – even individuals who were asymptomatic can experience so-called ‘long COVID’.

Diagnosing long COVID can be a challenge, however. A patient with asymptomatic or mild disease may not have taken a PCR test at the time of infection – the gold standard for diagnosing COVID-19 –  and so has never had a confirmed diagnosis.  Even antibody tests – which look for immune cells produced in response to infection – are estimated to miss around 30% of cases, particularly among those who have had only mild disease and or beyond six months post-initial illness.

A team at the University of Cambridge and Cambridge University Hospital NHS Foundation Trust has received £370,000 from the National Institute for Health Research to develop a COVID-19 diagnostic test that would complement existing antibody tests and a test that could objectively diagnose and monitor long COVID.

The research builds on a pilot project supported by the Addenbrooke’s Charitable Trust. The team has been recruiting patients from the Long COVID Clinic established in May 2020 at Addenbrooke’s Hospital, part of Cambridge University Hospital NHS Foundation Trust.

During the pilot, the team recruited 85 patients to the Cambridge NIHR COVID BioResource, which collects blood samples from patients when they are first diagnosed and then at follow-up intervals over several months. They now hope to expand their cohort to 500 patients, recruited from Cambridgeshire and Peterborough.

In their initial findings, the team identified a biomarker – a biological fingerprint – in the blood of patients who had previously had COVID-19. This biomarker is a molecule known as a cytokine produced by T cells in response to infection. As with antibodies, this biomarker persists in the blood for a long time after infection. The team plans to publish their results shortly.

Dr Mark Wills from the Department of Medicine at the University of Cambridge, who co-leads the team, said: “We need a reliable and objective way of saying whether someone has had COVID-19. Antibodies are one sign we look for, but not everyone makes a very strong response and this can wane over time and become undetectable.

“We’ve identified a cytokine that is also produced in response to infection by T cells and is likely to be detectable for several months – and potentially years – following infection. We believe this will help us develop a much more reliable diagnostic for those individuals who did not get a diagnosis at the time of infection.”

By following patients for up to 18 months post-infection, the team hopes to address several questions, including whether immunity wanes over time. This will be an important part of helping understand whether people who have been vaccinated will need to receive boosters to keep them protected.

As part of their pilot study, the team also identified a particular biomarker found in patients with long COVID. Their work suggests these patients produce a second type of cytokine, which persists in patients with long COVID compared to those that recover quickly and might be one of the drivers behind the many symptoms that patients experience. This might therefore prove to be useful for diagnosing long COVID.

Dr Nyarie Sithole, also from the Department of Medicine at the University of Cambridge, who co-leads the team and helps to manage long COVID patients, said:  “Because we currently have no reliable way of diagnosing long COVID, the uncertainty can cause added stress to people who are experiencing potential symptoms. If we can say to them ‘yes, you have a biomarker and so you have long COVID’, we believe this will help allay some of their fears and anxieties.

“There is anecdotal evidence that patients see an improvement in symptoms of long COVID once they have been vaccinated – something that we have seen in a small number of patients in our clinic. Our study will allow us to see how this biomarker changes over a longer period of time in response to vaccination.”

At the moment, the team is using the tests for research purposes, but by increasing the size of their study cohort and carrying out further work, they hope to adapt and optimise the tests that can be scaled up and speeded up, able to be used by clinical diagnostic labs.

As well as developing a reliable test, the researchers hope their work will help provide an in-depth understanding of how the immune system responds to coronavirus infection – and why it triggers long COVID in some people.

Dr Sithole added: “One of the theories of what’s driving long COVID is that it’s a hyperactive immune response – in other words, the immune system switches on at the initial infection and for some reason never switches off or never goes back to the baseline. As we’ll be following our patients for many months post-infection, we hope to better understand whether this is indeed the case.”

In addition, having a reliable biomarker could help in the development of new treatments against COVID. Clinical trials require an objective measure of whether a drug is effective. Changes in – or the disappearance of – long-COVID-related cytokine biomarkers with corresponding symptom improvement in response to drug treatment would suggest that a treatment intervention is working.

Markers in our blood – ‘fingerprints’ of infection – could help identify individuals who have been infected by SARS-CoV-2, the coronavirus that causes COVID-19, several months after infection even if the individual had only mild symptoms or showed no symptoms at all, say Cambridge researchers.

COVID-19CoronavirusdiagnosticInfectious diseasesimmunologyNyarie SitholeMark WillsNational Institute for Health Research (NIHR)School of Clinical MedicineDepartment of MedicineCambridge University Hospitals NHS Foundation TrustAddenbrooke's HospitalCambridge Infectious DiseasesBecause we currently have no reliable way of diagnosing long COVID, the uncertainty can cause added stress to people who are experiencing potential symptoms. If we can say to them ‘yes, you have a biomarker and so you have long COVID’, we believe this will help allay some of their fears and anxietiesNyarie SitholeAnnie SprattTired looking woman


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University of Cambridge launches roadmap to support future growth of life sciences cluster

Fri, 16/07/2021 - 10:49

The roadmap sets out a clear plan to create a bridge between two of Cambridge’s historical strengths — biomedical research and cutting-edge technology — and bring these specialisms together to develop new treatments and health tech with real world applications. The solutions in the roadmap are scalable beyond Cambridge and also applicable to other disciplines and sectors.

Professor Andy Neely, Pro-Vice-Chancellor for Enterprise and Business Relations at the University of Cambridge, said: “Cambridge has a deep and rich history of discovery and collaboration, and its interdisciplinary environment is the perfect testbed for new models of innovation in the life sciences. Our roadmap sets out a plan to do just that and will ensure that Cambridge remains a global leader in health technology into the next generation.

“This will require us to pioneer new ways of working and creating connections between different institutions across disciplines, be they academic or private enterprise. Such a model has been proven to work at a small scale – our proposal in the roadmap is to scale this up and apply it across the cluster and beyond.”

The University sits at the heart of the so-called ‘Cambridge cluster’, in which more than 5,300 knowledge-intensive firms employ more than 67,000 people and generate £18 billion in turnover. Cambridge has the highest number of patent applications per 100,000 residents in the UK.

The mission of the University is to contribute to society through the pursuit of education, learning and research at the highest international levels of excellence. This includes cultivating and delivering excellent research and world-leading innovation and training of the next generation of highly skilled researchers and entrepreneurs, thereby underpinning the UK's economic growth and competitiveness.

Professor Tony Kouzarides, Director of the Milner Therapeutics Institute at the University of Cambridge, said: “The pandemic has clearly shown the importance of rapid innovation in healthcare. We are determined to harness the power of innovation, creativity and collaboration in Cambridge, and apply this towards solving some of the biggest medical challenges facing the country, and the world.”

The Connect: Health Tech roadmap is a result of consultation with major stakeholders and a series of road-mapping workshops with the Cambridge community. It aims to shape the future success of the Cambridge cluster in health tech through a supportive and dynamic ecosystem that aligns with the needs of the community.

The roadmap includes ambitious steps to build strong foundations for the Cambridge cluster for the next 20 years and will support the region's economic recovery post-pandemic and bring cutting-edge research, businesses and innovators together to be better prepared and connected for the future. Connect: Health Tech will also increase access to the Cambridge ecosystem extending reach and helping to level up growth and investment across the East of England and the Oxford-Cambridge Arc.

One of the major recommendations in the report is to create and foster connectivity at the interface between medicine and technology and across sectors. This recommendation has been piloted by expanding the Cambridge cluster from a physical community to a digital one.

The COVID19 pandemic has required the creation of an innovative model of access and navigation to Cambridge. The digital platform simplifies navigation of the Cambridge research community and enables new companies based all over the world to access expertise and knowledge across the University with the aim of increasing inward investment in the life sciences. It also pilots an approach to navigation and connectivity that can be scaled up across the Arc and the UK. This new way of working will speed up the development of new healthcare innovations and technologies that the NHS will use in years to come.

Connect: Health Tech is a Cambridge University initiative funded by Research England. Connect: Health Tech UEZ has been created to build a highly effective interdisciplinary bridge between two Cambridge research hubs and beyond: the West science and technology hub anchored at the Maxwell Centre and South biomedical hub anchored at the Milner Therapeutics Institute. The bridge will bring together and integrate a community from across the University, research institutes, NHS, industry, investors, local and national Government, with a focus on medtech, digital health and therapeutics, to create opportunities that will transform ideas at the interface between medicine and technology into reality.

Read Creating a University Enterprise Zone for Cambridge across the life and physical sciences

Connect: Health Tech, the University of Cambridge Enterprise Zone, has today launched a roadmap, ‘Creating a University Enterprise Zone for Cambridge across the life and physical sciences’, that examines the challenges faced in futureproofing and sustaining the growth of the life sciences cluster to maintain Cambridge as a global centre of excellence for health tech.

Innovationspotlight on innovationenterpriseAndy NeelyTony KouzaridesCambridge Biomedical CampusSchool of Clinical MedicineMilner Therapeutics InstituteCambridge has a deep and rich history of discovery and collaboration, and its interdisciplinary environment is the perfect testbed for new models of innovation in the life sciencesAndy NeelyAstraZenecaCambridge Biomedical Campus


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Top UK organisations release annual statistics for use of animals in research

Thu, 15/07/2021 - 10:07

This is to coincide with the Home Office’s publication of Great Britain’s statistics for animals used in research in 2020.

These ten organisations carried out 1,343,893 procedures, 47% or nearly half of the 2,883,310 procedures carried out in Great Britain in 2020. More than 99% of these 1,343,893 procedures were carried out in rodents or fish.

The statistics are freely available on the organisations’ websites as part of their ongoing commitment to transparency and openness around the use of animals in research.

The ten organisations are listed below alongside the total number of procedures that they carried out in 2020. This is the sixth consecutive year organisations have come together to publicise their collective statistics and examples of their research.

Organisation Number of Procedures The Francis Crick Institute 183,811 University of Cambridge 177,219 Medical Research Council 173,637 University of Oxford 169,511 University of Edinburgh 151,669 UCL 142,988 University of Glasgow 102,526 University of Manchester 93,448 King's College London 85,414 Imperial College London 63,670 TOTAL 1,343,893

A further breakdown of Cambridge’s numbers, including the number of procedures by species and detail of the levels of severity, can be found on our animal research pages.

Animal research has been essential for developing lifesaving vaccines and treatments for Covid-19. Ferrets and macaque monkeys were used to test the safety and efficacy of Covid-19 vaccines, including the successful Oxford / AstraZeneca vaccine. Hamsters are being used to develop Covid-19 treatment strategies as they display a more severe form of the disease than ferrets and monkeys. Guinea pigs have also been used in regulatory research to batch test vaccine potency.

Despite all this research to develop vaccines and treatments for Covid-19, the majority of UK research facilities carried out significantly less research than usual due to the various national lockdowns. Therefore, the 2020 figures cannot be reasonably compared with previous statistics.

All organisations are committed to the ‘3Rs’ of replacement, reduction and refinement. This means avoiding or replacing the use of animals where possible; minimising the number of animals used per experiment and optimising the experience of the animals to improve animal welfare. However, as institutions expand and conduct more research, the total number of animals used can rise even if fewer animals are used per study.

All organisations listed are signatories to the Concordat on Openness on Animal Research in the UK, a commitment to be more open about the use of animals in scientific, medical and veterinary research in the UK. More than 120 organisations have signed the Concordat including UK universities, medical research charities, research funders, learned societies and commercial research organisations.

Wendy Jarrett, Chief Executive of Understanding Animal Research, which developed the Concordat on Openness, said:

"Animal research has been essential to the development and safety testing of lifesaving COVID-19 vaccines and treatments. Macaque monkeys and ferrets have been used to develop vaccines, including the Oxford / AstraZeneca vaccine, hamsters are being used to develop treatments, and guinea pigs are used to quality-check each batch of vaccines.

"Animal testing provided scientists with initial data that the vaccines were effective and safe enough to move into human clinical trials. During these trials, thousands more humans than animals were used to test how effective and safe the vaccines were in people. The pandemic has led to increased public interest in the way vaccines and medicines are developed and UAR has worked with research institutions and funding bodies throughout the UK to develop resources that explain to the public how animals have been used in this critical research."

University of Cambridge Establishment Licence Holder Dr Martin Vinnell said:

“Animal research currently plays an essential role in our understanding of health and disease and in the development of modern medicines and surgical techniques. Without the use of animals, we would not have many of the modern medicines, antibiotics, vaccines and surgical techniques we take for granted in both human and veterinary medicine.

“We always aim to use as few animals as possible, refining our research and actively looking for ways of replacing their use, for example in the development of ‘mini-organs’ grown from human cells, which can be used to model disease.”

Adapted from a press release by Understanding Animal Research.

  Find out more

A team in the University of Cambridge’s Department of Engineering is developing implantable devices to bypass nerve damage and restore movement to paralysed limbs.

“Our aim is to make muscles wireless by intercepting electrical signals from the brain before they enter the damaged nerve and sending them directly to the target muscles via radio waves,” says Sam Hilton, a Research Assistant in the team.

The procedure has been tested and refined in computer simulations, and on cells grown in the lab. But before it can be tested in humans there is another important step: testing its safety in living rats. To avoid testing in animals entirely would place untenable risk on the first human recipients of this new device. All the experiments are carefully designed to ensure that just enough animals are used to produce convincing data, without resulting in unnecessary excess.

By working out how complex microelectronics can interface with living tissue in a very precise and controlled way, this work has potential to improve or restore movement in patients suffering severe nerve damage - improving their quality of life and easing the burden on our healthcare services.

The ten organisations in Great Britain that carry out the highest number of animal procedures – those used in medical, veterinary and scientific research - have today released their annual statistics.

animal researchUnderstanding Animal ResearchSchool of Clinical MedicineSchool of Biological SciencesWe always aim to use as few animals as possible, refining our research and actively looking for ways of replacing their use. Martin Vinnell


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Climate changed the size of our bodies and, to some extent, our brains

Thu, 08/07/2021 - 10:21

An interdisciplinary team of researchers, led by the Universities of Cambridge and Tübingen, has gathered measurements of body and brain size for over 300 fossils from the genus Homo found across the globe. By combining this data with a reconstruction of the world’s regional climates over the last million years, they have pinpointed the specific climate experienced by each fossil when it was a living human.

The study reveals that the average body size of humans has fluctuated significantly over the last million years, with larger bodies evolving in colder regions. Larger size is thought to act as a buffer against colder temperatures: less heat is lost from a body when its mass is large relative to its surface area. The results are published today in the journal Nature Communications.

Our species, Homo sapiens, emerged around 300,000 years ago in Africa. The genus Homo has existed for much longer, and includes the Neanderthals and other extinct, related species such as Homo habilis and Homo erectus.

A defining trait of the evolution of our genus is a trend of increasing body and brain size; compared to earlier species such as Homo habilis, we are 50% heavier and our brains are three times larger. But the drivers behind such changes remain highly debated.

“Our study indicates that climate - particularly temperature - has been the main driver of changes in body size for the past million years,” said Professor Andrea Manica, a researcher in the University of Cambridge’s Department of Zoology who led the study.

He added: “We can see from people living today that those in warmer climates tend to be smaller, and those living in colder climates tend to be bigger. We now know that the same climatic influences have been at work for the last million years.”

The researchers also looked at the effect of environmental factors on brain size in the genus Homo, but correlations were generally weak. Brain size tended to be larger when Homo was living in habitats with less vegetation, like open steppes and grasslands, but also in ecologically more stable areas. In combination with archaeological data, the results suggest that people living in these habitats hunted large animals as food - a complex task that might have driven the evolution of larger brains.

“We found that different factors determine brain size and body size – they’re not under the same evolutionary pressures. The environment has a much greater influence on our body size than our brain size,” said Dr Manuel Will at the University of Tubingen, Germany, first author of the study.

He added: “There is an indirect environmental influence on brain size in more stable and open areas: the amount of nutrients gained from the environment had to be sufficient to allow for the maintenance and growth of our large and particularly energy-demanding brains.”

This research also suggests that non-environmental factors were more important for driving larger brains than climate, prime candidates being the added cognitive challenges of increasingly complex social lives, more diverse diets, and more sophisticated technology.

The researchers say there is good evidence that human body and brain size continue to evolve. The human physique is still adapting to different temperatures, with on average larger-bodied people living in colder climates today. Brain size in our species appears to have been shrinking since the beginning of the Holocene (around 11,650 years ago). The increasing dependence on technology, such as an outsourcing of complex tasks to computers, may cause brains to shrink even more over the next few thousand years.

“It’s fun to speculate about what will happen to body and brain sizes in the future, but we should be careful not to extrapolate too much based on the last million years because so many factors can change,” said Manica.

This research was funded by the European Research Council and the Antarctic Science Platform.

Reference

Will, M. et al: ‘Different environmental variables predict body and brain size evolution in Homo.’ Nature Communications, July 2021. DOI: 10.1038/s41467-021-24290-7

The average body size of humans has fluctuated significantly over the last million years and is strongly linked to temperature. Colder, harsher climates drove the evolution of larger body sizes, while warmer climates led to smaller bodies. Brain size also changed dramatically but did not evolve in tandem with body size.

evolutionClimate changeAndrea ManicaUniversity of TübingenDepartment of ZoologyClare CollegeSchool of the Biological SciencesOur study indicates that climate - particularly temperature - has been the main driver of changes in body size for the past million years.Andrea ManicaHuman fossils illustrating the variation in brain (skulls) and body size (thigh bones) during the Pleistocene.


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Rare genetic variants confer largest increase in type 2 diabetes risk seen to date

Wed, 07/07/2021 - 12:10

Type 2 diabetes is thought to be driven in part by inherited genetic factors, but many of these genes are yet unknown. Previous large-scale studies have depended on efficient ‘array genotyping’ methods to measure genetic variations across the whole genome. This approach typically does a good job at capturing the common genetic differences between people, though individually these each confer only small increases in diabetes risk.

Recent technical advances have allowed more comprehensive genetic measurement by reading the complete DNA sequences of over 20,000 genes that code for proteins in humans. Proteins are essential molecules that enable our bodies to function. In particular, this new approach has allowed for the first time a large-scale approach to study the impact of rare genetic variants on several diseases, including type 2 diabetes.

By looking at data from more than 200,000 adults in the UK Biobank study, researchers from the Medical Research Council (MRC) Epidemiology Unit at the University of Cambridge used this approach to identify genetic variants associated with the loss of the Y chromosome. This is a known biomarker of biological ageing that occurs in a small proportion of circulating white blood cells in men and indicates a weakening in the body’s cellular repair systems. This biomarker has been previously linked to age-related diseases such as type 2 diabetes and cancer.

In results published today in Nature Communications, the researchers identified rare variants in the gene GIGYF1 that substantially increase susceptibility to loss of the Y chromosome, and also increase an individual’s risk of developing type 2 diabetes six-fold. In contrast, common variants associated with type 2 diabetes confer much more modest increases in risk, typically much lower than two-fold.

Around 1 in 3,000 individuals carries such a GIGYF1 genetic variant. Their risk of developing type 2 diabetes is around 30%, compared to around 5% in the wider population. In addition, people who carried these variants had other signs of more widespread ageing, including weaker muscle strength and more body fat.

GIGYF1 is thought to control insulin and cell growth factor signalling. The researchers say their findings identify this as a potential target for future studies to understand the common links between metabolic and cellular ageing, and to inform future treatments.

Dr John Perry, from the MRC Epidemiology Unit and a senior author on the paper, said: “Reading an individual’s DNA is a powerful way of identifying genetic variants that increase our risk of developing certain diseases. For complex diseases such as type 2 diabetes, many variants play a role, but often only increasing our risk by a tiny amount. This particular variant, while rare, has a big impact on an individual’s risk.”

Professor Nick Wareham, Director of the MRC Epidemiology Unit, added: “Our findings highlight the exciting scientific potential of sequencing the genomes of very large numbers of people. We are confident that this approach will bring a rich new era of informative genetic discoveries that will help us better understand common diseases such as type 2 diabetes. By doing this, we can potentially offer better ways to treat – or even to prevent – the condition.”

Ongoing research will aim to understand how the loss of function variants in GIGYF1 lead to such a substantial increase in the risk of developing type 2 diabetes. Their future research will also examine other links between biomarkers of biological ageing in adults and metabolic disorders.

The research was funded by the Medical Research Council. UK Biobank is supported Wellcome, the Medical Research Council, British Heart Foundation, Cancer Research UK, Department of Health, Northwest Regional Development Agency and the Scottish Government.

Reference
Zhao, Y. et al. GIGYF1 loss of function is associated with clonal mosaicism and adverse metabolic health. Nature Communications 2021; 07 Jul 2021; DOI: 10.1038/s41467-021-24504-y

Scientists at the University of Cambridge have identified rare genetic variants – carried by one in 3,000 people – that have a larger impact on the risk of developing type 2 diabetes than any previously identified genetic effect.

Spotlight on public healthPublic healthtype 2 diabetesdiabetesgeneticsGenomicsJohn PerryNick WarehamMedical Research CouncilUK BiobankWellcomeCancer Research UK (CRUK)British Heart FoundationDepartment of HealthNorthwest Regional Development AgencyScottish GovernmentSchool of Clinical MedicineMedical Research Council (MRC) Epidemiology UnitFor complex diseases such as type 2 diabetes, many variants play a role [in disease risk], but often only increasing our risk by a tiny amount. This particular variant, while rare, has a big impact on an individual’s riskJohn PerryqimonoDNA jigsaw


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