Minna Kaikkonen-Määttä is a Professor of Cardiovascular Genomics, and Director of the Single Cell Genomics Core at the University of Eastern Finland. She obtained her Bachelor’s degree in Cellular Biology and Physiology from Claude Bernard University Lyon 1, France, in 2002, and a Master’s degree in Molecular Biology from the University of Jyväskylä, Finland, in 2005. She obtained her PhD in Molecular Medicine in 2008. She did her postdoctoral studies at the University of California San Diego investigating transcriptional gene regulation and enhancer RNAs (2009–2012) before moving to the University of Eastern Finland to establish her own research group. She is the Vice Director of Research, at the A.I. Virtanen Institute, President of the Finnish Society of Atherosclerosis, and a board member of the European Society of Cardiology (ESC) Council on Cardiovascular Genomics and of the Nucleus of the ESC working group on Atherosclerosis and Vascular Biology
Yes, I did. Although at the time I actually had two career options in mind—I either wanted to become a French interpreter or a scientist. I ended up missing the entrance exam for the French interpreter program, but I did take the biology entrance exam. So I often say that fate decided for me that I would choose biology. Fortunately, I was still able to keep French as a hobby, and later I even lived in France for a couple of years.
Over time, research has really become a passion for me, so most of the time it doesn’t even feel like work. What I value a lot is the academic freedom to explore new ideas and directions, and the chance to discover or learn something new almost every day. I also really enjoy the creative side of research—designing studies, asking new questions, and trying to solve complex problems. Another very rewarding part is collaborating with inspiring colleagues from around the world and mentoring younger scientists as they develop their own ideas and careers.
In many ways, it’s a unique career because you essentially get to be curious for a living and contribute, even in a small way, to new knowledge that might eventually benefit society. I think this is something we as scientists should talk about more, especially with younger generations, to show how exciting and rewarding this path can be. Too often the conversation about science focuses on budget cuts, temporary contracts, and stress, whereas we should also highlight the many inspiring and fulfilling aspects of an academic career.
Our work studies the genetic basis of atherosclerosis and coronary artery disease. We’re interested in interpreting the signals from genome-wide association studies to understand what the causal elements in the genome are, what the causal cell types are through which the variants act, which genes they regulate, and ultimately how this predisposes to disease. Our efforts particularly focus on looking at the vascular cell contribution to the risk, not just the traditional cholesterol- or liver-specific view of coronary artery disease but now looking at the vasculature itself and how the cells there can be really important for the disease.
I think the coolest cell types at the moment are smooth muscle cells, fibroblast-like cells, and endothelial cells. They seem to carry a large part of the genetic risk for atherosclerosis. But it’s probably also important to remember that different cell types may play key roles at different stages of the disease. In the very early stages for prevention, we should focus on preventing endothelial dysfunction which often is one of the disease initiating events. But when the disease has progressed already to subclinical atherosclerosis or even further, then we should shift the focus to smooth muscle cells. Here then the progression of the disease and development of plaque could be inhibited if we somehow are able to inhibit the disease associated changes that happen in these cells. So I think there is a lot of potential there.
That’s a difficult question. I think now that there are a lot of really cool new technologies like spatial transcriptomics, we can actually look at interactions between cells. What we believe, for example, is that endothelial cells and smooth muscle cells are the ones that mediate a large part of the genetic risk. But it doesn’t mean that immune cells like macrophages, T cells, or B cells are less important. It’s more like these vascular stromal cells load the gun, and then you need the immune cells, which interact with them, to trigger the gun. The immune cells being the effectors.
So what changes in the interactions between the stromal cells and immune cells that promotes disease progression? I think that’s a really key question to answer in the future, which we can only now tackle because we can really look at the cellular interactions in the actual lesions themselves.
Single-cell RNA sequencing, for sure, has really revolutionized the field. I think it was 2018 when it was selected as the Breakthrough of the Year by Science, and now it’s considered a fairly standard methodology. Previously, we did bulk RNA sequencing on tissues, and now it’s totally standard to do everything with single-cell RNA sequencing. If you based your key manuscript findings on bulk RNA sequencing, you are likely to get reviewer comments saying that you should prove your findings are also seen at single cell level, not confounded by measurement of a mixture of cells. So these technologies have really become a mainstay.
Now I guess the new wave is spatial transcriptomics technologies, which are getting better and better. We can now investigate almost all the genes in cells in the spatial context. So basically doing single-cell RNA sequencing but retaining the spatial context of the tissue. I think that’s super exciting.
What will come next, I guess, is multimodal technologies where you can measure from the same sample RNA, epigenetics, proteins, and metabolites. Building different layers of information can give even further insight. You could also look at metabolic fluxes within the tissue context. That would be exciting, but there is still some way to go. I hope that future developments will also help bring down the cost of these still fairly expensive technologies.
One thing close to my heart is using genetic information, because genetics is the same from birth. For younger people, many of the classic risk factors have not appeared yet, while genetic predisposition is already fixed. That’s why genetic risk scores may be especially informative when evaluating risk in this group.
In Finland, we would like to initiate population-based trials where individuals at 40 years old would have their polygenic risk scores measured and combined with traditional risk scores like SCORE2. Combining these layers could help identify high-risk individuals earlier and enable earlier initiation of preventive treatment.
Current standard methods—such as cholesterol and other laboratory measures—are insufficient, as a large proportion of patients who experience myocardial infarction are classified as low risk by traditional risk scores. There is a significant fraction of patients who, based on genetic information, should be assigned preventive medication, such as statins, earlier. There are also imaging-based methods, like those being developed in the PESA cohort, as well as metabolomics and proteomic markers that are emerging.
Ideally, these layers should be combined to achieve the most accurate identification of individuals at risk. However, clinical trials are needed to demonstrate the cost-effectiveness of integrating such measures into standard care and to show that improved risk prediction translates into better therapeutic outcomes.
Currently, one strategy for individuals at higher risk is earlier treatment of risk factors, for example by initiating statin therapy at a younger age (e.g. around 40) before symptoms occur. Increasing awareness of individual risk may also help motivate lifestyle changes. In the future, we hope that we will have other drugs besides lipid-lowering therapies. We are probably going to see more anti-inflammatory drugs, and maybe new drugs that target vascular wall changes, emerging as alternatives for preventing disease.
Yes, so I guess if statins don’t work for some people, they might need more aggressive lipid-lowering treatments or other therapies. Blood pressure medication also affects the cells of the vascular wall. Anti-inflammatory drugs are definitely going to be important; they are already in clinical trials, and we’re going to see more and more of them being used, particularly in secondary prevention, but also in primary prevention.
And then there are future drugs. It’s hard to predict what those will be. Ideally, if we want to move fast, we hope that some drugs already on the market could be repurposed and tailored for these indications. But it might also require the design of entirely new drugs that target vascular changes.
Oh, absolutely, yes. About half of the risk for coronary disease is mediated through genetics and the other half through lifestyle. So definitely, the best prevention at the population level would be for everyone to exercise more and eat healthily.
Exactly, it’s easy to say. Unfortunately, it seems just easier to take drugs. That is probably the problem. But we are facing a massive epidemic of obesity, for example, and finding ways to control that and improve people’s lifestyles would have a tremendous effect on health and also on the economy.
What is also needed are studies that look at the interaction between genetics and environment. They clearly interact, but we are not yet able to fully understand how lifestyle and genes work together in health and disease.
I don’t necessarily have a definite answer to that, but I think these drugs are definitely going to make a big change, and we’re going to see a major decrease in obesity because of them. But does that mean people will use these drugs long-term? Currently, that seems likely, because it’s easier to take a drug than to change lifestyle. Of course, that’s not an ideal solution, and it really shows that we still need strong public health efforts to support healthier lifestyles and prevent obesity in the first place.
I don’t personally work with these obesity drugs, but I do see that they are transforming the field. These drugs also decrease cardiovascular disease risk at large, so there is huge potential for health benefits worldwide.
We don’t have it yet. People at high risk of coronary artery disease or stroke are treated with blood pressure medication and lipid-lowering therapy, but it’s not really personalized. Most patients receive similar treatments.
Personalized prevention would mean including polygenic risk scores, other omics layers and/or imaging data in risk evaluation. You would gather as much information as possible about a person and use that to guide treatment decisions. For example, someone with a high combined risk might benefit from starting statin therapy earlier—this is how personalization is currently envisioned.
In the future, we hope to have a broader range of drugs that act through different mechanisms. Then, based on a person’s genetic and clinical profile, we could assign the therapy from which they would benefit most — for example, an anti-inflammatory drug or a combination therapy. But we’re not there yet unfortunately. Also, because atherosclerosis arises from many interacting factors and partly unpredictable processes, risk prediction will likely never be perfectly precise.
Laura Lerena, a PhD student under Prof. Antonio M. Echavarren’s supervision, has successfully defended her thesis today entitled Navigating the Synthesis of Complex Molecular Architectures: From Acenes to Gold(I) Cavitand Carbenoids.
The members of the evaluation committee have been Prof. Juan Manuel Cuerva from Universidad de Granada (Spain), Prof. Paz Muñoz from Lancaster University (United Kingdom), Prof. Arjan W. Kleij from ICIQ (Spain).
First, we will know more about yourself: where are you from, where and what you studied, your hobbies, and any other information you would like to include.
I was born in Jerez de la Frontera, (Cádiz). I earned my bachelor’s degree in Chemistry at the University of Cádiz, and then I moved to Salamanca, where I completed my master’s degree in Evaluation and Development of Drugs. Although my favourite sport is swimming, I enjoy all kinds of sports and try to practice them whenever I have the opportunity, such as weightlifting, climbing, running, playing padel, beach volleyball and skiing.
Why did you become a scientist?
Because I have always been very curious about the origin of things and why they are the way they are. I’ve also always wanted to know how things are formed. In short, I wanted to understand the world around us.
What do you want to achieve as a scientist?
I aspire to contribute to making the world a better place.
What is your thesis about?
My thesis focuses on the synthesis of complex molecular architectures involving gold, either as a catalyst in certain transformations or as the metal center in carbenoids species.
What triggered your interest for the subject of your thesis?
The complexity of the molecules obtained in my thesis made the work more challenging.
What applications can your thesis have in the future?
It contributes to expanding the understanding and applicability of gold(I) transformations.
The thing that I like most about my thesis is….
The progress I made through the different projects.
From the lessons learnt at ICIQ, which one do you value the most?
The feeling of community at ICIQ is something I truly value. When I started at ICIQ, I thought this would be individual work, but it turned out to be the opposite. No matter if you are having a bad day or going through a blocked period in your thesis, your lab mates are always there to support you.
What ICIQ moment you’ll never forget?
Luch breaks with my colleagues.
What will you miss the most from ICIQ?
My lab mates when I started in the Echavarren group.
What do you wish you had known at the beginning of your PhD?
Time runs too fast, so make the most of your time here and live each experience as if it were unique.
What advice do you have for someone who’s starting their PhD now?
Enjoy your time here and try to take advantage of every opportunity your PhD gives you.
From your experience at ICIQ, what do you think we can improve?
I don’t think it is a big deal, but bureaucracy can be annoying sometimes, and in some cases the procedures are not very clear. However, administrative staff is always available to answer our questions.
Who has been your biggest influence?
The former members of my group have been my biggest influence, as I was able to witness their development and their growth into excellent professionals.
Where are you going next? What will you do there?
I will be joining Innovalab in the KTT Unit at ICIQ as a Project Researcher. I will continue working in the lab, with the main objective of optimizing and scaling up the synthesis of different targets.
Chemistry is fun because…
Each scientific project presents a new challenge. Every step along the way is an opportunity to learn, regardless of whether the results are positive or negative.
What is your favourite molecule?
Water (H2O) is my favourite molecule because it has played a crucial role throughout my life.
If you were a piece of lab equipment, what would you be?
I would be a glass adapter, because it allows different pieces to fit together when they seem incompatible.
Tell us something about you that people might not know…
I’m actually more introverted than I appear.
La entrada ¡Felicidades, Dra. Lerena! se publicó primero en ICIQ.
Tiene nombre de dios nórdico y es la máquina molecular que permite comer y crecer a muchísimas especies distintas: hongos, plantas, ballenas, humanos, moscas… Es la gran proteína TOR. Una expedición a la Isla de Pascua hace medio siglo llevó a su descubrimiento, y hoy sigue siendo objeto de intenso estudio. Lucas Tafur, investigador del Centro Nacional de Investigaciones Oncológicas (CNIO), acaba de resolver la estructura de uno de los interruptores moleculares que la regulan.
Es un avance que ayudará a entender por qué cuando esta gran proteína no funciona aparecen el cáncer y otras enfermedades. Se publica en la revista Nature Structural & Molecular Biology.
“Todas las células tienen mecanismos para percibir cuántos nutrientes hay, y para transmitir esa información a otras proteínas que regulan el crecimiento celular”, explica Tafur. “Cuando faltan nutrientes TOR se inhibe y la célula frena el crecimiento, y cuando hay muchos recursos, como aminoácidos o glucosa, pasa al contrario: TOR se activa y promueve el crecimiento celular y la proliferación”.
Así funciona TOR a grandes rasgos, pero es importante entender esa maquinaria con mucho más detalle. Conocer bien cómo se regula la actividad de TOR, por ejemplo, abriría vías al diseño de nuevos fármacos.
Hoy se sabe que los nutrientes no regulan TOR directamente, sino mediante otros complejos de proteínas. Y es que TOR, también llamado mTOR en mamíferos, en realidad actúa como parte de dos grandes complejos de varias proteínas ensambladas, TORC1 y TORC2.
“Un fármaco que interfiera con la actividad total de TOR tiene muchos efectos secundarios”, explica Tafur, jefe del Grupo de Mecanismos Estructurales del Crecimiento Celular del CNIO. “Pero si entendemos en detalle la maquinaria que regula a TOR, podemos encontrar la manera de intervenir más selectivamente”.
Un ‘kit molecular’ para que los seres vivos coman y crezcan
Si las proteínas son las máquinas moleculares que hacen funcionar las células, TOR es uno de los engranajes centrales del sistema. Y está en muchos organismos distintos porque resuelve un problema común a todos ellos: detectar nutrientes disponibles para decidir si hay recursos para crecer o no. TOR es el equivalente a un kit molecular estándar que hace muy bien esa tarea y, como resultado, la evolución lo ha conservado a lo largo de miles de millones de años.
En primates y en hongos; en aves e insectos; en rosales y en merluzas, TOR es el sistema que decide si hay comida al alcance y por tanto se puede crecer, o si en cambio no la hay, y toca ahorrar energía.
Tafur investiga TOR en levaduras. Es de hecho el único científico en el CNIO que trabaja con este microorganismo, Saccharomyces cerevisiae, convenientemente alojado en recipientes en su laboratorio. La similitud de los componentes de TOR entre humanos y levadura hacen que hallazgos en un sistema sirvan para entender cómo funciona TOR en otro.
Montar un puzzle 3D sin tener las piezas
TOR es el acrónimo de Target of Rapamycin, que se refiere a la molécula a la que se une la rapamicina, un compuesto descubierto en 1975 en muestras recogidas en una expedición a la Isla de Pascua. La rapamicina tiene propiedades inmunosupresoras y anticancerígenas y ya se usaba en varios fármacos –por ejemplo, para evitar el rechazo de trasplantes– antes de que en los años 90 se descubriera, usando levadura, que TOR es su diana.
El reto de tratar de explicar cómo funciona TOR es equiparable a montar un dificilísimo rompecabezas tridimensional microscópico, con la dificultad añadida de que ni siquiera se conoce la forma de todas las piezas. Ese es precisamente el primer desafío: determinar la estructura de cada diminuto engranaje.
En los últimos años grupos de investigación en todo el mundo han ido avanzando en este reto. Todos usan la crio-microscopía electrónica, una técnica que congela las muestras a temperaturas próximas a la temperatura del nitrógeno líquido, −196 °C, y obtiene imágenes 3D a resolución cuasi atómica de los complejos moleculares. Con esta técnica Tafur ha resuelto la estructura de un regulador clave de TOR: el complejo SEA (también llamado GATOR).
SEA, el gran regulador de TOR
“SEA es un complejo enorme que integra muchas señales al mismo tiempo”, dice Tafur. “En la célula, todo lo que tiene que ver con nutrientes pasa a través de ese complejo: aminoácidos, colesterol, glucosa… Y lo cierto es que no sabemos bien cómo se integran todas las señales”.
El nuevo resultado publicado en Nature Structural & Molecular Biology desvela dos aspectos nuevos sobre el funcionamiento de SEA. El primero es que la regulación del complejo TOR por SEA no es como se creía.
El complejo está formado por dos partes, y se suponía que la actividad de una de ellas regulaba la actividad de la otra mediante un sistema que el estudio de Tafur rechaza. “Vemos que ese concepto no es completamente cierto, no hay una subdivisión dentro del complejo de forma que una parte bloquea a la otra, sino que funciona como un todo”.
Un interruptor que activa rápidamente a TOR
Otro resultado importante es que basta una mutación específica en un aminoácido para que el sistema deje de funcionar. “Esta actividad es como un interruptor, que no solamente se necesita –como siempre se ha pensado–, para inhibir a TOR, sino que también se necesita para activarlo rápidamente”, dice Tafur.
Es un hallazgo que ayudará a entender por qué cuando esta gran proteína no funciona aparecen el cáncer y otras enfermedades, y quizás también llegue a abrir vías para modular su acción de manera selectiva. Y nos recuerda, además, lo mucho que compartimos con los demás seres vivos.
Sobre el Centro Nacional de Investigaciones Oncológicas (CNIO)
El Centro Nacional de Investigaciones Oncológicas (CNIO) es un centro público de investigación dependiente del Ministerio de Ciencia, Innovación y Universidades. Es el mayor centro de investigación en cáncer en España y uno de los más importantes en Europa. Integra a medio millar de científicos y científicas, más el personal de apoyo, que trabajan para mejorar la prevención, el diagnóstico y el tratamiento del cáncer.
La entrada Más cerca de descifrar TOR, la máquina molecular que nos hace crecer a humanos y levaduras se publicó primero en CNIO.
Sant Joan d’Alacant hosted more than 140 experts at the Systems-IN-Action Meeting, an international conference focused on the latest advances in systems neuroscience and on studying the brain in action during behavior. Held from March 16 to 18, the meeting was promoted by the Institute for Neurosciences (IN), a joint center of the Spanish National Research Council (CSIC) and the Miguel Hernández University of Elche (UMH), within the framework of the Severo Ochoa Centres of Excellence Programme.
Group photo of the organizers and participants of the first Systems-IN-Action Meeting, held from March 16 to 18 in Sant Joan d’Alacant. Source: IN CSIC-UMH.
At a time of profound transformation in neuroscience, this conference brought together leading researchers from around the world who use state-of-the-art tools to study the brain in action. The integration of new experimental technologies with computational methods is enabling advances in understanding how neural circuits process sensory information, generate perceptions, and give rise to actions and behavior. “This meeting aims to bring together experts working at different levels of brain analysis to jointly address how neural activity is translated into behavior”, explain the conference organizers: Isabel Pérez-Otaño, who leads the Plasticity and remodeling of neural circuits laboratory and the scientific programme Synaptic modulation of neural circuits and behavior; Ramón Reig, who leads the Sensory-motor processing by subcortical areas laboratory; and Andreas Kardamakis, who leads the Neural circuits in vision for action laboratory.
Over three days, the scientific programme was structured into five thematic sessions covering different levels of organization of the nervous system, from the activity of neural circuits to their impact on behavior. This integrative approach helped bridge experimental and theoretical perspectives, fostering the exchange of ideas between established researchers and early-career scientists, and promoting new ways of understanding how the brain generates behavior.
The meeting featured leading international figures such as Matteo Carandini, from University College London (UK); Megan Carey, from the Champalimaud Foundation (Portugal); Tony Zador, from Cold Spring Harbor Laboratory (USA); and Marie Carlén, from the Karolinska Institutet (Sweden), among others. They addressed key topics, including how neural networks in the brain are organized and function, the development of predictive brain models using artificial intelligence, and new theoretical approaches to understanding neural systems.
As a highlight, the conference included a panel discussion on the impact and future of artificial intelligence in neuroscience. In this session, experts discussed how these tools are transforming data analysis, neuronal modelling, and the understanding of complex cognitive processes. The programme was further enriched by a strong poster session and short talk sessions, in which Institute for Neurosciences researchers John Wesseling, Andreas Kardamakis, Ramón Reig, Félix Leroy, and Isabel del Pino presented the latest advances in their research lines. These contributions reflected the diversity of research at the institute and provided a valuable platform for the direct exchange of results, fostering interaction between established and early-career researchers.
Researchers Andreas Kardamakis, Matteo Carandini, Marie Carlén, John Wesseling, Tony Zador, Megan Carey, and Michael Hausser during the panel discussion on whether artificial intelligence (AI) and deep learning models can help to understand brain function. Source: IN CSIC-UMH.
With this initiative, the Institute for Neurosciences CSIC-UMH reinforces its commitment to research excellence and to promoting international scientific forums that contribute to advancing knowledge of the brain. The Systems-IN-Action Meeting was supported by the Severo Ochoa Centres of Excellence Programme at the Institute for Neurosciences, the Generalitat Valenciana, the Federation of European Neuroscience Societies (FENS), the Spanish Society for Neuroscience (SENC), as well as the companies BIOGEN Científica and RWD Life Science.
For more information: see the programme in the attached document (PDF file)
Source: Institute for Neurosciences CSIC-UMH (in.comunicacion@umh.es)
La entrada Alicante brings together leading international experts in neuroscience at the first Systems-IN-Action Meeting, a conference on the brain in action se publicó primero en Instituto de Neurociencias de Alicante.
On March 18th, 2026, the 5 Talks in Combinatorics thematic day took place in the Joan Maragall Room at the Faculty of Philology and Communication of the University of Barcelona, in the historic building. The event focused on modern combinatorics and its connections with algebra, geometry, information theory, and discrete mathematics. Five international researchers participated in an intensive one-day programme.
The first talk was delivered by Carolina Benedetti Velásquez, Associate Professor at the Department of Mathematics of the Universidad de los Andes (Bogotá, Colombia) and Lluís Santaló Fellow 2026—a visiting position created in memory of Lluís Santaló to host Latin American researchers during research stays in Catalonia.
Benedetti is a Colombian mathematician whose work focuses on combinatorics, algebraic structures, and geometry. She studied at the Universidad Nacional de Colombia, completed her MSc at the Universidad de los Andes, and obtained her PhD in 2013 from York University (Toronto, Canada), with the dissertation Combinatorial Hopf algebras and supercharacters. She has been a visiting professor at Michigan State University and is currently co–Executive Director of Mathematical Circles Colombia, as well as a member of the Comunidad Colombiana de Combinatoria and the Gender and Equity Commission.
Combinatorics of some products of (quantum) Schubert polynomials
In her talk, Benedetti introduced Schubert polynomials, a fundamental basis of the polynomial ring over the integers, deeply connected to algebraic geometry through Schubert varieties. She showed how many of their properties can be expressed through permutation combinatorics and presented combinatorial rules for products of both classical and quantum versions.
The work presented is joint with N. Bergeron, L. Colmenarejo, F. Saliola, and F. Sottile.
Next, Amanda Montejano (Universidad Nacional Autónoma de México) offered an overview of the various discrete formulations of the classical Brunn–Minkowski inequality, a cornerstone of convex geometry. She discussed the historical development of the problem and highlighted the use of heavy sets as a tool to derive meaningful inequalities in arbitrary dimensions.
The third talk was given by Oriol Farràs Ventura (Universitat Rovira i Virgili), who explored the connection between matroid theory and secret sharing schemes—cryptographic methods in which a secret can be recovered only from certain authorised subsets of information. As shown by Brickell and Davenport, the access structure of ideal schemes determines a matroid.
Farràs presented polynomial secret sharing schemes and proved that, over sufficiently large fields, the access structures of ideal polynomial schemes are determined by algebraic matroids.
After the lunch break, Yannic Vargas (CUNEF Universidad Madrid) introduced the concept of nested pre-Lie operads, a non-associative generalisation of classical operads in which horizontal associativity is replaced by a pre-Lie law. He showed how this structure arises naturally in graphs, trees, and set partitions, and discussed potential extensions to the braid arrangement.
To close the day, Eleni Tzanaki (University of Crete) presented interval hypergraphic polytopes, a special class of hypergraphic polytopes whose hyperedges are intervals. These polytopes can be interpreted as deformations of the associahedron, and Tzanaki showed that their vertex posets correspond exactly to intervals in the Tamari lattice. She also characterised the interval hypergraphs that yield simple polytopes and described a new family of directed trees called weeping willows.
The event highlighted the diversity of perspectives that coexist in modern combinatorics—from deep algebraic structures to applications in information theory, as well as discrete geometry and polytope theory. It offered a vivid snapshot of a field that continues to expand in scope and connections.
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CRM CommNatalia Vallina
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The post 5 Talks, 1 Topic: A Day of Combinatorics first appeared on Centre de Recerca Matemàtica.
