Building better landscapes for wildlife

Autumn brings shorter days and colder weather here to the UK, with many of us thinking back on the past summer spent hiking, barbequing, and enjoying the elusive British summer sun. Regardless of the outdoor activities you enjoy the most, you’re probably not the only who looks forward to those long summer days. In addition to your neighbours, friends, and fellow hikers, you’ll also find singing birds, pollinating bees, and burrowing rabbits. But as urban areas continue to increase in size while farms continue to use large areas to grow food for growing populations, wildlife are finding it more difficult to have a place to call home. Thanks to conservation biologist Dr. Jenny Hodgson from our Adaptation to Environmental Change theme, IIB is involved with collaborative research with conservation groups for restoring landscapes and building better habitat networks for wildlife populations.

meJenny recently became a lecturer here at IIB and joined the institute as a tenure-track fellow in late 2012. She is currently working on methods to scientifically prioritise where to create new habitats and where to improve degraded ones. But why is this necessary at all, can’t you just restore a habitat anywhere and it will be better than before? “We need to choose carefully because we don’t just want to boost wildlife within the boundaries of our restoration projects. If we choose smartly, we could see benefits cascading away from our projects and long into the future, because we will affect the populations at many sites which are linked together into a network” Jenny commented while describing the key concept at the centre of her research: the theory of metapopulations.

A metapopulation is a group of several wild populations that are linked together by individuals who occasionally disperse between smaller subgroups. Each population inhabits its own ‘island’ of habitat, and separation can be driven between groups by barriers such as roads, buildings, or geographical distance. A well-connected network of habitats can lead to more stable populations than island populations trying to persist in isolation. Conservation groups want to make sure that existing populations are mutually supportive rather than isolated, and they also want to know how to prepare habitat restoration plans for climate change. Increasing temperatures will likely drive animals from their current habitats and into new areas where there may not be adequate habitats for them to move into.

This is where Jenny’s research comes in: her group is using new modelling approaches that can make habitats better connected using the theory of metapopulations. Jenny is currently involved in a research project with conservation groups including the North Pennines Area of Outstanding Natural Beauty and the North York Moors National Park on restoration planning. This project involves developing user-friendly software ( which conservation groups can use to find the most efficient locations. Efficient locations are where a small amount of habitat increase leads to a large improvement in the conductance, or speed of movement, for the predicted amount of time that a species will spread through the landscape.


The set-up for the Condatis software is simple: you first input a GIS map of known habitats in your area of interest. From there, you select your source, the habitat that the population will start in, and the target, where you want the population to end up. You also define a typical dispersal distance, or how far a species normally moves around, as well as the reproduction rate of the species you are interested in. No additional scientific knowledge is needed to use the software and the results appear as colour-coded maps and bar charts showing conservationists where the best places for new habitats are.

Within the software, Condatis uses mathematical models which incorporate the principles of metapopulation dynamics to determine how habitat patches connect and how subsequent generations of dispersal and reproduction can lead to the species reaching the target. The software can also identify potential bottlenecks, which are gaps in the habitat network that constrain a population’s ability to reach the target. Focusing restoration efforts on these areas can increase the ability and the speed that wildlife can move around. This also enables wildlife to become better able to respond to environmental or climate changes.

Developing the software was no easy task, and Condatis took a full-time software programmer one year to complete. The project has so far been well-received by conservation groups and people working on habitat restoration efforts. When asked if conservationists are hesitant to use a tool founded completely on mathematical models for restoration decision-making efforts, Jenny replied “The groups we work with do want to know what the limitations of the software are, but in general the conservation groups that come to us think the software is useful. The more the model is demonstrated to work with practical applications, the more people will be convinced it’s worth the time to understand it.”

Jenny is now working to bridge these uncertainties by maintaining regular contact with conservation groups and stakeholders as well as by organizing training events on the use and application of the software. The majority of Jenny’s work keeps her at the office, but she still finds occasional opportunities for getting out into the field. Jenny’s students actively collect environmental data, which allows her group to maintain the connections between the real-world context of conservation planning and to test ecological theories against actual data.

Jenny began her career in conservation biology after earning her undergraduate degree in Natural Sciences from the University of Cambridge. From there she worked at the World Conservation Monitoring Centre in Cambridge, an agency of the UN Environment Programme, as a species program assistant. After working at the Monitoring Centre for 9 months, Jenny found that she craved more of an intellectual challenge and found a PhD on a topic which had inspired her as an undergraduate. Her PhD at the University of York focussed on butterfly metapopulations and involved a combination of field work and population modelling.

Before coming to IIB, Jenny found herself doing a patchwork of jobs, which she used as a time to think about her career and to look for potential long-term leads. “I was lucky I could survive being unemployed for short periods, and I used the time to focus on writing papers. It was a productive but stressful time, and in the end I was able to publish the work from my PhD and a variety of collaborative projects and to show that my ideas were useful for the field.” said Jenny.

Jenny greatly enjoys her time as a researcher here at IIB. “The best part of my job is doing the science, seeing the results first-hand, and connecting with others. The people that I collaborate with in conservation groups are always clever, interesting, and dedicated people with great ideas, and I really enjoy working with people who are involved in both science and policy.” said Jenny. Jenny finds scientific research stimulating, interesting, and challenging, and considers these all to be her motivating factors even amidst the uncertainty and stresses of grant writing and time management in an academic research post. In the next few years, Jenny will be following up with other projects related to the use of the Condatis software, including how to improve movement within marginal habitats, which are areas that can only support a population in the short-term.

While there is still a lot of work to be done in the field of conservation biology and bracing the world for climate change, Jenny is optimistic about the impact of her work. “There is a solution to these problems within wildlife conservation and habitat restoration, and you can see parts of it coming together already. People really do want to see wildlife where they live, but we know that their habitats are eroded and that certain species can’t easily cope with change. While we still don’t know the most effective trade-offs between our needs and the needs of wildlife, we are starting to build smarter ways of better integrating wildlife into landscapes that are full of people.” commented Jenny.

If you want to see the Condatis software first-hand, be sure to check out the tutorial made by Jenny and her PhD student here:


A Tale of Two Salmonellas

Thoughts of Salmonella are more likely to get your stomach churning than stimulate your interest. But Salmonella is more than a bacterium that causes a bad stomach ache: certain types of the bacteria can cause serious damage. Professor Jay Hinton, a professor in IIB’s Dynamics and Management of Host Microbe Interactions theme, is finding out how different types of Salmonella cause such a wide range of symptom severity. His group uses gene expression to find out what factors differ between Salmonella subtypes in order to identify new treatments for the nastier types of Salmonella.

Jay has been working on microbial diseases for the past 30 years. In that timehinton, he’s kept a sharp focus on studying Salmonella ever since he finished his PhD. “Salmonella bacteria are great to work with since you can do just about any experiment you want with them. There are also a lot of scientific resources available, including 50 years of research on their genetics and biochemistry. Anytime you work with Salmonella, you’re really standing on the shoulders of giants.” Jay commented.

For over 20 years, Jay has researched the type of Salmonella which is found all over the world, the one you’d likely run into if you happen to eat a bit of undercooked chicken (we’ll refer to it here as ‘Global Salmonella’). He first focused on the role of global gene expression in the ability of Salmonella to make people ill. Jay’s work demonstrates that the more potent types Salmonella express higher levels of certain genes in order to make more of the proteins required to infect their host.

Global Salmonella is a rather innocent subtype. It’s tough enough to survive on dry surfaces and is responsible for severe gastroenteritis in healthy individuals—but there are other far more potent strains. One strain now in focus at Jay’s lab belongs to the ST313 sequence type—the numbering system simply means that it’s the 313th Salmonella type to be discovered. ST313 was first discovered in 2002 in sub-Saharan Africa. Global Salmonella is usually responsible for stomach upsets while ST313 causes a much nastier infection. ST313 kills 20% of the people it infects and the disease is also resistant to 9 antibiotics. ST313 also causes an especially dangerous disease if the patient is immunocompromised by malaria, HIV, or malnutrition. When these patients are infected with ST313, the Salmonella can spread to the liver and spleen and cause severe fever and diarrhoea.hmi-jh-figure“To find ways to cure the disease, we must understand how the infection works. There have been very few new antibiotics made against Salmonella in recent years, so our group is using tools to learn why some Salmonella strains are much more dangerous than others.” said Jay. His group’s approach is to look for differences in virulence factors by comparing Salmonella strains at both the genomic and the gene expression levels. “Looking at the genome alone isn’t enough. The gene content of an organism does suggest potential phenotypes, but if a gene’s not expressed then it can’t cause a change in virulence. The approach we use is to consider both what genes are available and what genes are actually being expressed.” Jay commented.

When looking at the genome itself, researchers focus on natural genetic differences known as single nucleotide polymorphisms (SNPs). A SNP occurs when a single letter in a gene’s code is different between two individuals. Even in organisms of the same species, there are many SNPs that exist between individuals. Because of all this diversity, it’s not always easy to interpret the biological role of particular SNPs. For example, when comparing Global Salmonella and the ST313, there are 1000 different SNPs and over 300 genes which distinguish the two types. “It’s difficult to get information that helps us understand the actual biological differences when just looking at SNPs and genes. So we are using gene expression patterns to map functional information onto these two genomes.” says Jay.

When comparing gene expression between Global Salmonella and the African ST313 types, Jay’s group came across a protein which was much more highly expressed in ST313. Because this protein helps bacteria to survive in human serum, Jay believes that an increase in the amount of this protein allows ST313 to grow and live in the bloodstream. Jay’s group then wanted to understand the mechanism of the increased expression of this key protein, and focused on the nucleotide sequence differences between the two types of Salmonella. They were able to find a key SNP difference in the regulatory region of the gene that actually controls the level of expression.

This work is the culmination of a 4 year project by Jay and his group which was recently been completed, and his group is now getting ready to submit a manuscript for publication. The paper will include experimental work done by several post-docs and PhD students and will include data from infection models that show the role of this protein in causing disease. Jay hopes that the approach of using both genomics and gene expression will be applied by other researchers to identify and validate how other types of bacteria cause disease. “You need to study more strains to gain a broader understanding of how the extremely dangerous Salmonella infections happen.” said Jay.

Jay greatly enjoys sharing his work outside of his scientific community. He finds it easy to connect to others since most people he meets will have some form of a ‘Salmonella’ story. He also thinks that scientists as a whole need to be more proactive at communicating research. “Scientists don’t do enough to talk about the good we are doing. I’m lucky because my field is one that’s easy for people to understand, since everyone agrees that this research on Salmonella is worthwhile. As scientists, it is good to be outward facing with our research. The way we interact with people influences the way they see our work.” said Jay. Jay always strives to be collaborative and open to new ideas, whether it’s working with clinicians in Malawi or sharing techniques with colleagues. “The key for scientists is not to compete with one another but to work together.” Jay emphasized.

Jay started his career by earning his bachelor’s degree in microbiology. “I love microbiology because your experiments will yield results quite quickly—I’m not patient enough for really long experiments!” said Jay. He completed his PhD in plant pathogenesis by identifying virulence genes of Erwinia, the bacterium that causes potato rot. Jay then became more interested in gene regulation and identified Salmonella as the best available model system to study microbe-host interactions. This combination of a great model system and its impact on human health gives Jay his “get out of bed in the morning” factor.

Jay’s day-to-day job involves research, grant writing, and mentoring a group of 6 post-docs, 3 PhD students, and 1 MSc student. He also lectures first-year biology students on topics including “Infections in the 21st century.” When asked about a normal day at work, Jay motioned to his desk piled with papers and books and replied casually “A bit messy!” While Jay did make it a summer goal to clean his desk (which, by the autumn, was halfway finished), he admitted that it was hard to find the time within his endless to-do list. “There’s always more papers to read, another grant to write, or just rushing around from office to office between meetings.” said Jay. Jay also strives to leave time to step back from his to-do list and make time to reflect on ideas, concepts, and to gain new perspectives.

Jay’s group will be kept busy in the coming months with a new research project just funded by the Global Challenges Research Fund. This “10,000 Salmonella Genome Project” involves sequencing Salmonella isolates from thousands of patients in Africa and South America. “By discovering the types of Salmonella that are causing disease across the developing world, we hope our research will lead to new interventions that will improve the lives of people affected by these diseases.” said Jay about the impact of this newly-funded research.hmi_group-photoJay’s group is itself a reflection of the global nature of his work, with researchers from Chile, Spain, Wales, Switzerland, Malawi, Colombia, and the UK. Jay’s research and his group truly embody what it means to be an ‘outward facing’ scientist, including the stuffed microbes that greet you with a friendly smile as you enter his office.

Want to see the Salmonella group in action? Check out their video:

Providing new hope to patients with difficult-to-treat Rheumatoid Arthritis

Our hands do a lot of work for us on a daily basis, from tying our shoe laces to typing emails. We may take the work done by our hands for granted, but imagine if moving your hands and fingers was so painful that even the simplest task, such as getting dressed or making a cup of tea, felt impossible. This is what every day feels like for people living with rheumatoid arthritis. While there are medications available to treat some forms of the disease, occasionally patients won’t respond well to these treatments and find themselves unable to do even the easiest tasks. Dr. Helen Wright, a research fellow here at IIB as part of our Molecular Basis of Therapeutic Targeting research theme, is focused on learning more about this disease and developing new ways to screen patients. This research will better enable doctors to work with individual patients in order to find their best treatment options available.mbtt_group-photo-2

Helen has been here at the University of Liverpool since earning her PhD in 2009. Her research focuses on the role of neutrophils in autoimmune diseases, including rheumatoid arthritis. Neutrophils are the most abundant type of white blood cells, with billions of these cells circulating in our blood stream. They are the blood cells that provide us with fast, ‘first-line’ protection against infection. When these cells are working normally, neutrophils patrol the blood stream and when they come across any bacteria, fungus, or other ‘foreign’ invader, they secrete toxic chemicals that can break down and kill the infecting agent. This attack causes the inflammation and red colouring that you’ll see on your own skin when you get a small cut or scrape.

But neutrophils sometimes don’t attack just foreign invaders: in autoimmune diseases, there is a widespread activation of neutrophils, and they’ll attack your own cells with these toxic chemicals in the same way that they attack an infection. Rheumatoid arthritis happens when these hyper-active neutrophils get into joints and cause inflammation and a break-down of cartilage. “Patients with arthritis have many joints – including hands, feet and knees – that are in a lot of pain, and even basic things like brushing their hair become very painful and difficult. Many people with manual jobs, or any sort of work that involves using their hands or having to stand for long periods of time, will have to quit their jobs”, Helen commented. Over 500,000 adults in the UK live with the disease, and in general many people do well with standard drug treatments, with only occasional disease flare-ups. But a small yet significant number of patients have extreme forms of the disease and don’t respond at all to standard treatments. These patients find it difficult to complete simple tasks such as cooking or getting dressed without significant help.

mbtt-wright-figureHelen’s research group is studying how autoimmune diseases manifest and how diseases like arthritis can be better treated for the patients that don’t respond well to a typical drug regimen. One of their approaches is to focus on how arthritis drugs target neutrophils. “We know that these drugs work in reducing inflammation and arthritic symptoms, but we don’t know exactly how a lot of these drugs work, or how these drugs specifically alter neutrophil activation”, Helen said. Having a better understanding of how these drugs work and what properties allow them to target neutrophils can allow for the design of better and more effective drugs in the future.

While Helen’s group is very active and focused on a diverse set of topics, one of her most exciting projects is in finding out ways to tell if a person will respond well to a typical arthritis drug regimen or not. Helen’s approach – an example of personalised medicine – is to use gene expression differences between patients who responded well to drugs and those who didn’t. This data is then used to see what biomarkers could be developed as a way to screen patients before therapeutic treatments begin.

By looking at differences in gene expression, Helen has been able to find out what genes are more prevalent in patients that respond well to drugs and those that don’t. Using a method called RNA-seq, Helen’s group has taken RNA (the form that expressed genes take after they are copied from the genomic DNA) from patients who respond well to treatment and those who don’t. Her group has identified which genes are expressed at higher or lower levels in patients who do or don’t respond to therapy. This allowed Helen’s group to identify two separate groups of genes that are only expressed in responders (10 genes) or non-responders (13 genes) to treatment and these genes are able to distinguish the two groups of patients.


The next step of Helen’s work is to develop these biomarkers as a tool that can be used by clinicians to predict if a patient will or won’t respond to a drug therapy. “By doing these predictive screens, you can save time and money by not giving a standard drug to someone it won’t work for, and you can focus that time and energy on getting them on a treatment that will work better for them.” says Helen about the importance of being able to use these screening tools in the clinic.

The next step is also one that will require a new set of collaborations and experiences: setting up a full clinical trial. Helen is currently working on grant proposals to get the trial off the ground, one that will involve over 200 patients, at least six collaborating research centres and medical clinics, and patient follow-throughs of up to 12 months after the trial. The clinical study in its entirety will take almost 3 years from start to finish.

“This is my first time being involved with a project as big as this, and I’ve realised that scaling up this project into a national study will take a lot of time and energy. In this field, you go from the science to the clinical aspects and then into the legal and business side of things, and I’m completely new to the legal and business aspects of this work.” said Helen.

When Helen isn’t busy analysing data or writing grants for the clinical trial, she can be found either in the lab or in the hospital working with patients, doctors, and researchers. She and her group members are all trained to take blood on healthy individuals and can be found regularly recruiting fellow staff at IIB for blood donations. “We need to have fresh neutrophils for our experiments in the lab,” Helen said, and admitted that she and other members of the group have had their fair share of blood drawn from themselves to get enough samples to work with.

In the hospital, Helen and her team visit arthritis clinics to collect blood from patients, with all collections done on a volunteer basis. They work with clinical specialists to identify patients with rheumatoid arthritis who have varying responses to drugs and then Helen and her research team will talk with each patient about the work they are doing and what its impact will be. Since blood is already taken as part of a normal screen, it usually takes very little additional time to provide a research sample by filling an extra couple of collection tubes with blood.

Helen has found that most patients are generally interested in what her group is doing and are happy to help. “You have to say that the work you’re doing won’t directly impact the patient themselves but could instead help a future patient. So when you talk to patients, you have to have an altruistic angle in how you talk about the work.” Helen said. “The only reason we have so many drugs to treat rheumatoid arthritis now is because some patients in the past donated their blood for research, to benefit the patients of today”, she added. “Someone diagnosed with rheumatoid arthritis today has a much better chance of being treated in a way that prevents serious damage to their joints than someone diagnosed, say, 30 years ago. But we still have a lot of work to do, particularly for those patients with very severe, hard-to-treat, rheumatoid arthritis.” commented Helen.

While Helen’s career is driven by her degree and background in molecular biology and biochemistry, her passion comes from having a connection to people and patients in her work. “I spent a lot of time studying signalling pathways in university but I was always more of a people-person, and I wanted my work to focus on treating human diseases. I like my job because it feels satisfying to have this balance between science and connecting with people,” Helen said. Helen received her undergraduate degree from the University of Central Lancashire as a mature student and was 35 years old when she completed her PhD at the University of Liverpool. She transitioned into research with more direct clinical applications by collaborating with doctors in the rheumatology clinics at the Royal Liverpool and Broadgreen Hospital and University Hospital Aintree. She is very passionate about her research and at the end of her PhD was awarded an Arthritis Research UK Foundation Fellowship to support her work.

Helen enjoys that each day is very different, with time spent analysing data, working with students and postdocs, and visiting hospitals and clinics to talk to patients. “By far the best part of my job is talking to patients, explaining the science of what we do, and convincing patients and clinicians to help us out. I’m really driven by the human side of research. There are so many patients with rheumatoid arthritis that are so hard to treat, but if we can find a better way to find out who these patients are, it can help doctors find better treatments for them so they can get back to living their lives freed from the pain of arthritis.” said Helen.

If you want to see Helen’s group in action, check out their video:

From Genomes to Biological Systems: Understanding molecular machinery

Our lives are surrounded by man-made structures, from the simple self-assembled furniture in our homes to the massive bridges and motorways that connect cities and countries. Regardless of how complex a piece of furniture or a bridge may be, there needs to be a blueprint in order to make the pieces fit together and function as a whole.

But what about the structures that aren’t man-made, like the proteins and cells in our body? How are these complex biological structures put together, and can we learluning-liu-1-2n how to use these biological blueprints to build cells of our own? Dr. Luning Liu, a research fellow and tenured lecturer at IIB, is working with his interdisciplinary group to better understand the blueprints that describe how living organisms are put together.

Luning came to the University of Liverpool in December 2012 and has been a tenured lecturer since July 2015. The Liu lab is focused on learning how nano-scaled biological machinery are assembled, and one of their interests is in how the parts of algae cells that control photosynthesis are put together. “During photosynthesis, the specialised cell membrane converts solar light into the chemical energy that supports the life on Earth, and we’re using cyanobacteria to understand how these cells build devices that can capture and convert light energy. We can then use that information to learn how we can build our own devices that we can use to enhance the movement of energy within a cell” said Luning.

Cyanobacteria are known as ‘blue-green algae’ and are a type of bacteria that get their energy from the sun. During photosynthesis, the energy from light hits the external membranes of the cell, which break down water into oxygen molecules and generate protons (in the form of hydrogen atoms) and free electrons. The protons are then used to produce energy molecules that the cell can use to generate sugars, amino acids, and starches through the Calvin-Benson cycle. These bacteria have also developed specialised carbon fixation mechanisms, using biological structures known as carboxysomes. Carboxysomes are used to help bacteria get enough carbon so they can complete photosynthesis. g2s-ll-figure

Luning and his group are working on how the photosynthetic machinery in cyanobacteria is organised and how the cells optimise these biochemical reactions to efficiently harvest solar energy and accumulate carbon. In a recent publication from the Liu lab, his group were able to add fluorescent tags to the carboxysomes. These tagged proteins allowed them to track the location and amount of the carbon-trapping carboxysomes while the bacteria were growing. The Liu lab were able to see first-hand how carboxysome movement could be linked to the energy state of the bacterial cell and how they allow the cyanobacteria to optimise how carbon is uptaken depending on the amount of light present.

One of the big picture goals of Luning’s research isn’t just to better understand photosynthesis and carbon fixation, but to work towards design systems that are more efficient, especially in terms of food and biofuel security. “Our goal is to improve the process of photosynthesis so we can improve yields of a wide range of food crops” Luning said.

One challenge faced by the Liu lab is the role of their work in the realm of genetically modified organisms. While his group works primarily on fundamental research, he has encouraged members of his group to be ready for questions on the topic when doing public engagement work and when applying for grants about their research.“Our research has potentially a lot of promise to make a difference but we have to be solid on understanding technology and the mechanism before we can apply them in the real world” added Luning.

Luning and his group work with plant scientists, biophysicists, chemists, synthetic biologists, and microbiologists: a truly interdisciplinary approach towards a better understanding of these complex biological structures. Luning commented: “Nowadays all work in science is multidisciplinary, and you can’t use one technique to solve everything.  The advantage in our group is that there are advanced technologies that we can use to bring our ideas to life. We can ask questions about how natural structures are built in the cells and then work with plant scientists who are looking for a fundamental understanding of the system to see what approaches and techniques they use.”

Luning regularly sends students to technical workshops so they can gain more knowledge and training in the latest technologies and techniques. However he also makes sure that he and his group stick to the basic principles of the scientific method. “I focus on the question more than just the technique by itself. You can use lots of different techniques and technologies to do science, but having a clear question is the most important starting point. The biggest challenge is that there is no one who can tell you what will work, so you really have to explore lots of ideas and try a lot of things before you get something that works” said Luning.

Luning received his undergraduate degree in Biochemistry before earning a joint PhD in microbiology from Shandong University (China) and Leiden University (Netherlands). After spending 2 years carrying out research on biological membranes at the Institute Curie in Paris, he started working on cyanobacteria as a researcher at Queen Mary University of London before joining IIB in 2012. Luning describes himself as driven by curiosity: “Every day is exciting; there are new technologies and papers to keep up with, working with my students on their projects, and reaching out to new collaborators. I enjoy discussing and exploring new ideas by working with colleagues in such an open-minded work environment at IIB.” g2s-group-photo

The Liu lab currently consists of seven PhD students, one post-doc and one technician. Luning works to recruit a multidisciplinary team in his lab, including researchers specialising in molecular biology, biochemistry, biophysics, and plant science. This diverse approach allows group members to learn from one another and enables them to approach problems with different types of perspectives. “Sometimes the biology students have a hard time with the physics, so having a diverse team with diverse sets of skills and knowledge is crucial to making these complex experiments work.” Luning commented.

Luning can regularly be found working in the lab alongside his students and post-doc while encouraging his students to enjoy this time in their research careers as much as possible. Luning replied when asked what his students thought about having their boss pipetting alongside them: “Being a PhD student is the most exciting time in a scientist’s career, because it’s a time when you get to focus on the research and not have to deal with the stressors of applying for grants and funding. I try to help them enjoy this time as much as possible and to help them out.”

Luning is also focused on achieving his own life-work balance, spending the hours from 9am to 5pm in the lab and office before heading home to spend time with his two young children. He then finishes off the evening hours with grant applications, papers, and emails. “The job can be very stressful, especially since this is a very new area, and I try to work hard to stay on top of things. It’s also tough since my kids need my time too, so I don’t go to as many big conferences now so I can spend more time with my family. It’s important to make time for family and do things apart from work”.