Students from across the country get a taste of studying at Cambridge at the Cambridge Festival
We were delighted to welcome pupils from Warrington’s Lymm High School, Ipswich High School, The Charter School in North Dulwich, Rickmansworth School, Sutton Valance School in Maidstone as well as schools closer to home such as St Peter’s Huntingdon, Fenstanton Primary School, Barton Primary School, Impington Village College and St Andrews School in Soham.
Running over two days (25/26 March 2025) and held in the Cambridge Sports Centre, students went on a great alien hunt with Dr Matt Bothwell from the Institute of Astronomy, stepped back in time to explore Must Farm with Department of Archaeology and the Cambridge Archaeological Unit as well as learning to disagree well with Dr Elizabeth Phillips from The Woolf Institute.
Schools had a choice of workshops from a range of departments including, how to think like an engineer and making sustainable food with biotechnology with researchers from the Department of Chemical Engineering and Biotechnology, as well as the chance to get hands-on experience in the world of materials science and explore how properties of materials can be influenced by temperature at the Department of Materials Science and Metallurgy.
The Department of Veterinary Medicine offered students the opportunity to find out what a career in veterinary medicine may look like with workshops on animal x-rays, how different professionals work together to treat animals in a veterinary hospital as well as meeting the departments horses and cows and learn how veterinarians diagnose and treat these large animals.
Students also had the opportunity to learn about antibodies and our immune system with the MRC Toxicology Unit. The students learnt about the incredible job antibodies do defending our bodies against harmful invaders like bacteria and viruses.
Alongside this, a maths trail, developed by Cambridgeshire County Council, guided students around the West Cambridge site whilst testing their maths skills with a number of problems to solve.
Now in their third year, the Cambridge Festival schools days are offering students the opportunity to experience studying at Cambridge with a series of curriculum linked talks and hands on workshops.
The Cambridge Festival runs from 19 March – 4 April and is a mixture of online, on-demand and in-person events covering all aspects of the world-leading research happening at Cambridge. The public have the chance to meet some of the researchers and thought-leaders working in some of the pioneering fields that will impact us all.
Over 500 KS2 and KS3 students from as far away as Warrington got the chance to experience studying at the University of Cambridge with a selection of lectures and workshops held as part of the Cambridge Festival.
Students make antibody keychains during a workshop with the MRC Toxicology Unit
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When inflammation goes too far
Clare Bryant, Professor of Innate Immunity, is a molecular detective. Clare allows us to see how inflammation functions across species, and when our defence systems go too far.
Scientists identify genes that make humans and Labradors more likely to become obese
Researchers studying British Labrador retrievers have identified multiple genes associated with canine obesity and shown that these genes are also associated with obesity in humans.
The dog gene found to be most strongly associated with obesity in Labradors is called DENND1B. Humans also carry the DENND1B gene, and the researchers found that this gene is also linked with obesity in people.
DENND1B was found to directly affect a brain pathway responsible for regulating the energy balance in the body, called the leptin melanocortin pathway.
An additional four genes associated with canine obesity, but which exert a smaller effect than DENND1B, were also mapped directly onto human genes.
“These genes are not immediately obvious targets for weight-loss drugs, because they control other key biological processes in the body that should not be interfered with.
But the results emphasise the importance of fundamental brain pathways in controlling appetite and body weight,” said Alyce McClellan in the University of Cambridge’s Department of Physiology, Development and Neuroscience, and joint first author of the report.
“We found that dogs at high genetic risk of obesity were more interested in food,” said Natalie Wallis in the University of Cambridge’s Department of Physiology, Development and Neuroscience, and joint first author of the report.
She added: “We measured how much dogs pestered their owners for food and whether they were fussy eaters. Dogs at high genetic risk of obesity showed signs of having higher appetite, as has also been shown for people at high genetic risk of obesity.”
The study found that owners who strictly controlled their dogs’ diet and exercise managed to prevent even those with high genetic risk from becoming obese - but much more attention and effort was required.
Similarly, people at high genetic risk of developing obesity will not necessarily become obese, if they follow a strict diet and exercise regime - but they are more prone to weight gain.
As with human obesity, no single gene determined whether the dogs were prone to obesity; the net effect of multiple genetic variants determined whether dogs were at high or low risk.
The results are published today in the journal 'Science'.
“Studying the dogs showed us something really powerful: owners of slim dogs are not morally superior. The same is true of slim people. If you have a high genetic risk of obesity, then when there’s lots of food available you’re prone to overeating and gaining weight unless you put a huge effort into not doing so,” said Dr Eleanor Raffan, a researcher in the University of Cambridge’s Department of Physiology, Development and Neuroscience who led the study.
She added: “By studying dogs we could measure their desire for food separately to the control owners exerted over their dog’s diet and exercise. In human studies, it’s harder to study how genetically driven appetite requires greater willpower to remain slim, as both are affecting the one person.”
The current human obesity epidemic is mirrored by an obesity epidemic in dogs. About 40-60% of pet dogs are overweight or obese, which can lead to a range of health problems.
Dogs are a good model for studying human obesity: they develop obesity through similar environmental influences as humans, and because dogs within any given breed have a high degree of genetic similarity, their genes can be more easily linked to disease.
To get their results, the researchers recruited owners with pet dogs in which they measured body fat, scored ‘greediness’, and took a saliva sample for DNA. Then they analysed the genetics of each dog. By comparing the obesity status of the dog to its DNA, they could identify the genes linked to canine obesity.
Dogs carrying the genetic variant most associated with obesity, DENND1B, had around 8% more body fat than those without it.
The researchers then examined whether the genes they identified were relevant to human obesity. They looked at both large population-based studies, and at cohorts of patients with severe, early onset obesity where single genetic changes are suspected to cause the weight gain.
The researchers say owners can keep their dogs distracted from constant hunger by spreading out each daily food ration, for example by using puzzle feeders or scattering the food around the garden so it takes longer to eat, or by choosing a more satisfying nutrient composition for their pets.
Raffan said: “This work shows how similar dogs are to humans genetically. Studying the dogs meant we had reason to focus on this particular gene, which has led to a big advance in understanding how our own brain controls our eating behaviour and energy use.”
The research was funded by Wellcome, the BBSRC, Dogs Trust, Morris Animal Foundation, MRC, France Genomique consortium, European Genomic Institute for Diabetes, French National Center for Precision Diabetic Medicine, Royal Society, NIHR, Botnar Foundation, Bernard Wolfe Health Neuroscience Endowment, Leducq Fondation, Kennel Club Charitable Trust.
Reference
Wallis, N.J. et al: ‘Canine genome-wide association study identifies DENND1B as an obesity gene in dogs and humans.’ Science, March 2025. DOI: 10.1126/science.ads2145
Researchers at the University of Cambridge have discovered genes linked to obesity in both Labradors and humans. They say the effects can be over-ridden with a strict diet and exercise regime.
Dogs at high genetic risk of obesity showed signs of having higher appetite, as has also been shown for people at high genetic risk of obesity.Natalie WallisJames Barker on UnsplashLabrador licking nose
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Feeding your good gut bacteria through fibre in diet may boost body against infections
The group of bacteria called Enterobacteriaceae, including Klebsiella pneumoniae, Shigella, E.coli and others, is present at low levels as part of a healthy human gut microbiome. But at high levels - caused for example by increased inflammation in the body, or by eating contaminated food - these bugs can cause illness and disease. In extreme cases, too much Enterobacteriaceae in the gut can be life-threatening.
Researchers have used computational approaches including AI to analyse the gut microbiome composition of over 12,000 people across 45 countries from their stool samples. They found that a person’s microbiome ‘signature’ can predict whether a person’s gut is likely to be colonised by Enterobacteriaceae. The results are consistent across different states of health and geographic locations.
The researchers identified 135 gut microbe species that are commonly found in the absence of Enterobacteriaceae, likely protecting against infection.
Notable amongst the protective gut species are a group of bacteria called Faecalibacterium, which produce beneficial compounds called short-chain fatty acids by breaking down fibre in the foods we eat. This seems to protect against infection by a range of disease-causing Enterobacteriaceae bugs.
The researchers suggest that eating more fibre in our diet will support the growth of good bacteria - and crowd out the bad ones to significantly reduce the risk of illness.
In contrast, taking probiotics - which don’t directly change the environment in the gut - is less likely to affect the likelihood of Enterobacteriaceae infection.
The results are published today in the journal Nature Microbiology.
“Our results suggest that what we eat is potentially very important in controlling the likelihood of infection with a range of bacteria, including E.coli and Klebsiella pneumoniae, because this changes our gut environment to make it more hostile to invaders,” said Dr Alexandre Almeida, a researcher at the University of Cambridge’s Department of Veterinary Medicine and senior author of the paper.
He added: “By eating fibre in foods like vegetables, beans and whole grains, we can provide the raw material for our gut bacteria to produce short chain fatty acids - compounds that can protect us from these pathogenic bugs.”
Klebsiella pneumonia can cause pneumonia, meningitis and other infections. The alarming global rise in antibiotic resistance to this bacterial pathogen has led scientists to look for new ways of keeping it, and other similar infectious bacteria, under control.
“With higher rates of antibiotic resistance there are fewer treatment options available to us. The best approach now is to prevent infections occurring in the first place, and we can do this by reducing the opportunities for these disease-causing bacteria to thrive in our gut,” said Almeida.
A new understanding of gut microbe interactions
Earlier research to understand interactions between the different bacteria in our gut has used mouse models. But some of these new results are at odds with previous findings.
The new study revealed that 172 species of gut microbe can coexist with disease-causing Enterobacteriaceae bugs. Many of these species are functionally similar to the bugs: they need the same nutrients to survive. Previously it was thought that competition for resources would stop the disease-causing bacteria from getting established in the gut.
This has important implications for treatment: taking probiotics that compete for the same nutrients with the bad bacteria to try and starve them out isn’t going to work. The researchers say that it will be more beneficial to change the environment in the gut, for instance through diet, to reduce the risk of infection with Enterobacteriaceae.
“This study highlights the importance of studying pathogens not as isolated entities, but in the context of their surrounding gut microbiome,” said Dr Qi Yin, a visiting researcher at the University of Cambridge’s Department of Veterinary Medicine and first author of the report.
The research was funded by the Medical Research Council.
Reference: Yin, Q. et al: 'Ecological dynamics of Enterobacteriaceae in the human gut microbiome across global populations.’ Jan 2025, Nature Microbiology. DOI: 10.1038/s41564-024-01912-6.
A new study has found that the composition of your gut microbiome helps predict how likely you are to succumb to potentially life-threatening infection with Klebsiella pneumoniae, E.coli and other bugs - and it may be altered by changing your diet.
Our results suggest that what we eat is potentially very important in controlling the likelihood of infection with a range of bacteria.Alexandre AlmeidaCredit Oleksandra Troian GettyIntestine with microbiome
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System to auto-detect new variants will inform better response to future infectious disease outbreaks
The new approach uses samples from infected humans to allow real-time monitoring of pathogens circulating in human populations, and enable vaccine-evading bugs to be quickly and automatically identified. This could inform the development of vaccines that are more effective in preventing disease.
The approach can also quickly detect emerging variants with resistance to antibiotics. This could inform the choice of treatment for people who become infected - and try to limit the spread of the disease.
It uses genetic sequencing data to provide information on the genetic changes underlying the emergence of new variants. This is important to help understand why different variants spread differently in human populations.
There are very few systems in place to keep watch for emerging variants of infectious diseases, apart from the established COVID and influenza surveillance programmes. The technique is a major advance on the existing approach to these diseases, which has relied on groups of experts to decide when a circulating bacteria or virus has changed enough to be designated a new variant.
By creating ‘family trees’, the new approach identifies new variants automatically based on how much a pathogen has changed genetically, and how easily it spreads in the human population – removing the need to convene experts to do this.
It can be used for a broad range of viruses and bacteria and only a small number of samples, taken from infected people, are needed to reveal the variants circulating in a population. This makes it particularly valuable for resource-poor settings.
The report is published today in the journal Nature.
“Our new method provides a way to show, surprisingly quickly, whether there are new transmissible variants of pathogens circulating in populations - and it can be used for a huge range of bacteria and viruses,” said Dr Noémie Lefrancq, first author of the report, who carried out the work at the University of Cambridge’s Department of Genetics.
Lefrancq, who is now based at ETH Zurich, added: “We can even use it to start predicting how new variants are going to take over, which means decisions can quickly be made about how to respond.”
“Our method provides a completely objective way of spotting new strains of disease-causing bugs, by analysing their genetics and how they’re spreading in the population. This means we can rapidly and effectively spot the emergence of new highly transmissible strains,” said Professor Julian Parkhill, a researcher in the University of Cambridge’s Department of Veterinary Medicine who was involved in the study.
Testing the technique
The researchers used their new technique to analyse samples of Bordetella pertussis, the bacteria that causes whooping cough. Many countries are currently experiencing their worst whooping cough outbreaks of the last 25 years. It immediately identified three new variants circulating in the population that had been previously undetected.
“The novel method proves very timely for the agent of whooping cough, which warrants reinforced surveillance given its current comeback in many countries and the worrying emergence of antimicrobial resistant lineages,” said Professor Sylvain Brisse, Head of the National Reference Center for whooping cough at Institut Pasteur, who provided bioresources and expertise on Bordetella pertussis genomic analyses and epidemiology.
In a second test, they analysed samples of Mycobacterium tuberculosis, the bacteria that causes Tuberculosis. It showed that two variants with resistance to antibiotics are spreading.
“The approach will quickly show which variants of a pathogen are most worrying in terms of the potential to make people ill. This means a vaccine can be specifically targeted against these variants, to make it as effective as possible,” said Professor Henrik Salje in the University of Cambridge’s Department of Genetics, senior author of the report.
He added: “If we see a rapid expansion of an antibiotic-resistant variant, then we could change the antibiotic that’s being prescribed to people infected by it, to try and limit the spread of that variant.”
The researchers say this work is an important piece in the larger jigsaw of any public health response to infectious disease.
A constant threat
Bacteria and viruses that cause disease are constantly evolving to be better and faster at spreading between us. During the COVID pandemic, this led to the emergence of new strains: the original Wuhan strain spread rapidly but was later overtaken by other variants, including Omicron, which evolved from the original and were better at spreading. Underlying this evolution are changes in the genetic make-up of the pathogens.
Pathogens evolve through genetic changes that make them better at spreading. Scientists are particularly worried about genetic changes that allow pathogens to evade our immune system and cause disease despite us being vaccinated against them.
“This work has the potential to become an integral part of infectious disease surveillance systems around the world, and the insights it provides could completely change the way governments respond,” said Salje.
The research was primarily funded by the European Research Council.
Reference: Lefrancq, N. et al: ‘Learning the fitness dynamics of pathogens from phylogenies.’ January 2025, DOI: 10.1038/s41586-024-08309-9
Researchers have come up with a new way to identify more infectious variants of viruses or bacteria that start spreading in humans - including those causing flu, COVID, whooping cough and tuberculosis.
The approach will quickly show which variants of a pathogen are most worrying in terms of the potential to make people ill. This means a vaccine can be specifically targeted against these variants, to make it as effective as possible.Henrik SaljeMilan Krasula on Getty
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