When an earthquake strikes, the most visible damage is the cracks left in the ground. Yet what buildings actually feel are the aftershocks that ripple through the rock long after the initial rupture. A similar picture may apply to certain catalysts, according to new research that suggests it is not the directly visible defects in a material that matter most, but the less tangible electronic disturbances that propagate through the entire system.
A team led by Dr. Lulu Li and Prof. Núria López at the Institute of Chemical Research of Catalonia (ICIQ) has reported in the Journal of the American Chemical Society (JACS) a detailed study of how platinum clusters behave when supported on cerium oxide. The article has been selected as a Front Cover by the journal. Combining quantum mechanical calculations with machine learning, the researchers show that highly mobile electronic states known as polarons, rather than oxygen vacancies alone, govern how the metal clusters adapt under reaction conditions.
The study revisits a long-standing puzzle in catalysis known as strong metal support interaction, first reported in the early 1980s, where metal particles on oxide materials were observed to change shape under certain conditions. The effect was evident, but its microscopic origin remained unclear. Platinum on cerium oxide is a widely used catalytic system known for driving CO oxidation below 150 ℃. Under operation, cerium oxide can lose oxygen atoms, leaving behind vacancies and extra electrons in the material.
These electrons do not remain static. They localise on cerium atoms and form polarons, which can move rapidly across the material. Dr. Lulu Li, first author of the study and Marie Skłodowska Curie Fellow, explains: “We found that the real actors in this story are not the oxygen vacancies you can see and count, they are the polarons, these quantum particles that form around the vacancies and travel dynamically through the ceria lattice. It is their collective behavior, their swarm dynamics, that ultimately determines how a platinum cluster reshapes itself under reducing conditions.”
Using advanced computer simulations supported by machine learning at the Barcelona Supercomputer Center, the team analysed many possible atomic arrangements of platinum clusters on cerium oxide. Rather than finding a simple link between the number of oxygen vacancies and the cluster shape, they observed that the distribution and movement of polarons played the central role. In this picture, the oxide support is not just a background material. It actively reshapes the electronic environment at the interface, and the metal cluster adjusts in response.
As Dr. Lulu Li notes: “This gives us an actionable design principle: if we want to tune a metal cluster catalyst, do not just count oxygen vacancies, think about how to control polaron distribution. That is a subtler lever, but a much more powerful one. And because this framework is general, it can be extended to other metal-oxide systems beyond platinum and ceria.”
The Front Cover selected by JACS reflects this conceptual shift. Rather than depicting a static surface dotted with defects, the image portrays glowing currents moving across the oxide support. These currents represent migrating polarons that continually reshape the electronic barrier at the metal–oxide interface. The platinum cluster above responds by adjusting both its structure and its electronic distribution. The visual aims to convey a system in constant motion, where adaptability arises not from fixed defects but from the dynamic flow of charge.
Reference publication
Dynamic Polaronic Control of Metal Cluster Adaptability on Reducible Oxides
Li, L.; Geiger, J.; Sanz Berman, P.; López, N.
J. Am. Chem. Soc. 2026
DOI: 10.1021/jacs.5c13140
La entrada Aftershocks at the atomic scale reshape platinum catalysts se publicó primero en ICIQ.
PHARO and BioSeal, led by Dr Maria Soler and Dr Salvio Suárez respectively, have been awarded funding in this call and will advance innovative nanotechnology-based solutions for medical applications through close collaboration with leading clinical institutions.
Europe is taking a step forward in improving the cardiovascular health of cancer patients with the launch of COMPASS (Cardio-Oncology Multidisciplinary Patient Assistance Solution), an ambitious European project that leverages artificial intelligence and digital technologies to prevent and treat cardiotoxicity associated with cancer treatments.
The initiative, funded by the European Union under the Innovative Health Initiative (IHI), has a budget of over €50 million and involves more than 60 organisations from 25 countries, including hospitals, research centres, universities, technology companies and patient organisations.
The Carlos III National Centre for Cardiovascular Research (CNIC) is taking part in this ambitious project, which aims to transform care in the field of cardio-oncology through the use of artificial intelligence, advanced biomarkers and digital technologies.
The project, which began on 1 March 2026, will run for five years and aims to improve the early detection of cardiac damage, optimise clinical decision-making and advance towards more personalised medicine in cardio-oncology.
As cancer survival rates rise, so do cardiovascular side effects. It is estimated that one in four cancer treatments requires warnings about potential cardiac or vascular complications, posing new challenges for patients and healthcare systems.
COMPASS involves leading research centres, hospitals, technology companies and patient organisations
COMPASS will tackle this challenge by developing predictive models based on artificial intelligence, using blood biomarkers, advanced medical imaging techniques and continuous monitoring systems. These tools will enable the identification of risk before symptoms appear and facilitate safer, more personalised care.
Coordinated by King’s College London, COMPASS involves leading research centres, hospitals, technology companies and patient organisations from across Europe.
As explained by Dr Borja Ibáñez, scientific director of the CNIC, cardiologist at the Hospital Universitario Jiménez Díaz and group leader at CIBERCV, the CNIC is involved in a number of projects. “We use experimental models of anthracycline-induced cardiotoxicity, in which we test different imaging probes to assess whether it is possible to develop new imaging modalities that enable the early detection of cardiotoxicity.”
In the clinical arm of the project, led by the CNIC within the consortium, the aim is to develop new risk scales to identify the likelihood of cardiovascular events in long-term cancer survivors. “We will bring together international databases comprising around 100,000 patients to develop models capable of predicting cardiovascular risk. In addition, we will analyse the impact of immunotherapy on silent atherosclerosis as part of a complementary sub-project,” explains Dr Ibáñez.
Furthermore, COMPASS will promote integrated care models that strengthen collaboration between cardiologists, oncologists and other healthcare professionals, as well as long-term follow-up strategies for the growing number of cancer survivors.
In the fields of artificial intelligence, data analysis and predictive modelling, projects such as GRACE and RESILIENCE stand out
The initiative also takes the patients’ perspective into account, through the development of educational materials, digital tools and awareness-raising activities designed to improve understanding of the cardiovascular risks associated with cancer and its treatments.
COMPASS builds on a strong track record in research and the collective experience of its partners in previous European initiatives. In the fields of artificial intelligence, data analysis and predictive modelling, projects such as GRACE and RESILIENCE are particularly noteworthy.
The expected outcomes include validated new biomarkers, AI-based predictive models, digital monitoring platforms, clinical decision support systems, and new care pathways for cancer patients at cardiovascular risk.
With this multidisciplinary and innovative approach, COMPASS aims to mark a turning point in the prevention and management of cardiotoxicity, moving towards a more precise, integrated and patient-centred form of medicine.
Abstract: We utilize the universality of pion–pion (ππ) final-state interactions at small invariant masses to understand their enhanced localized CP violation in B±→K±π+π−, using a dispersive approach. From a fit to the integrated CP-asymmetry data, we successfully predict the Dalitz-plot kinematic distribution of the asymmetry in the low-energy ππ region, including the large localized CP violation recently observed by LHCb. An essential role is played by the contributions of isospin 2. This formalism, whose parameters have a physical meaning, can be adapted straightforwardly to other systems with CP violation enhanced by final-state interactions.
Abstract: We compute the Form Factors of both neutral and charged pion using a non-perturbative running of the strong coupling constant αs obtained using a double-dilaton Holographic QCD model. These form factors remain poorly understood in the intermediate-energy region, which marks the transition between low- and high-energy physics. In particular, experimental data for the neutral pion Form Factor exhibits a deviation from the expected asymptotic behavior, and the charged pion form factor remains comparatively less explored. To address these issues, we employ the pion distribution amplitude formalism to investigate the Form Factor behavior in this intermediate regime. Our results suggests that non-perturbative physics of the strong interaction is relevant even at energy scales traditionally considered perturbative, implying that the perturbative regime could occur at higher energies than previously thought. Finally, our approach allows us to study isospin-breaking effects through the quadratic pion mass difference.
Abstract: The study of two-neutrino double-beta decay ($2nubetabeta$), an allowed process within the Standard Model in which two neutrons convert into two protons with the emission of two electrons and two antineutrinos, provides a unique window into nuclear structure and plays a crucial role in constraining theoretical descriptions of double-beta decay [1]. In particular, it offers valuable benchmarks for the nuclear matrix elements (NMEs) that also govern neutrinoless double-beta decay ($0nubetabeta$), a hypothetical process beyond the Standard Model of particle physics (BSM) in which no antineutrinos are emitted. The observation of $0nubetabeta$ would have important implications for particle physics, shedding light on open questions such as the origin of neutrino masses and the matter–antimatter asymmetry of the Universe [2].
In this talk, we present new predictions for $2nubetabeta$ decay half-lives to the first excited $0_2^+$ states in nuclei of experimental interest, including $^{76}$Ge, $^{82}$Se, $^{130}$Te, and $^{136}$Xe. A major source of theoretical uncertainty in these calculations arises from the NMEs, on which the decay half-lives depend quadratically. We compute the NMEs within the nuclear shell-model framework, including contributions up to next-to-leading order in chiral effective field theory [3] and incorporating important corrections from the lepton energy expansion [4]. Finally, we discuss how uncertainties in the NMEs are connected to key features of nuclear structure, such as nuclear deformation [5]. We show that larger deformation differences between the initial and final states yield to smaller NMEs.
References:
[1] J. Engel, J. Menéndez, Rep. Prog. Phys. 80 (2017) 046301.
[2] M. Agostini, G. Benato, J. A. Detwiler, J. Menéndez, F. Vissani, Rev. Mod. Phys. 95 (2023) 025002.
[3] S. el Morabit, R. Bouabid, V. Cirigliano, J. de Vries, L. Gráf, E. Mereghetti, J. High Ener. Phys. 06 (2025).
[4] F. Simkovic, R. Dvornický, D. Stefánik, A. Faessler, Phys. Rev. C 97 (2018) 034315.
[5] T. R. Rodríguez, G. Martínez-Pinedo, Phys. Rev. Lett. 105 (2010) 252503.
Researcher Danielle Medina Hernández, from Wake Forest University School of Medicine, who was part of the group led by Dr Borja Ibáñez at the Carlos III National Centre for Cardiovascular Research (CNIC), has been awarded the JACC: CardioOncology 2025 Young Author Award by the American College of Cardiology (ACC). This award recognises the scientific excellence of young authors whose contributions have had a significant impact in the field of cardiovascular research.
This award recognises her outstanding contribution to the field of cardiovascular medicine through the article entitled “SGLT2i Therapy Prevents Anthracycline-Induced Cardiotoxicity in a Large Animal Model by Preserving Myocardial Energetics”, published in JACC: Cardio-Oncology in February 2025.
The JACC: CardioOncology Young Author Award recognises the exceptional scientific rigour, originality and clinical relevance of the selected papers. The award reflects not only the quality of the published research, but also the author’s emerging leadership and her impact on the cardiovascular community.
This award highlights the quality and relevance of the research carried out by Dr Medina Hernández during her time at the CNIC, as well as her contribution to the advancement of knowledge in cardiology. Furthermore, this recognition underscores the CNIC’s strong research and mentoring environment, which fosters the development of high-calibre work and the advancement of cardiovascular science.
Dr Medina Hernández received the award during a special ceremony held as part of the ACC Annual Meeting 2026 in New Orleans.
Un equipo de investigación del Centro de Biología Molecular Severo Ochoa (CBM-CSIC-UAM) ha descubierto un mecanismo hasta ahora desconocido que promueve los procesos de inflamación en enfermedades como la psoriasis. El trabajo, publicado en la revista Journal of Allergy and Clinical Immunology, muestra además que un medicamento ya aprobado para tratar ciertos tipos de leucemia (dasatinib) bloquea un vía concreta del sistema inmunitario y logra reducir la inflamación asociada a la psoriasis en un modelo experimental de esta enfermedad.
La psoriasis, una enfermedad inflamatoria crónica que provoca enrojecimiento, descamación y engrosamiento de la piel, afecta a millones de personas en todo el mundo. Se origina cuando el sistema inmunitario se activa en exceso y produce sustancias que irritan la piel. Y este estudio muestra que dasatinib actúa como un interruptor que interrumpe ese proceso, en el que intervienen distintas moléculas que utilizan las células inmunitarias para comunicarse entre sí.
Entre estas moléculas destacan las citoquinas, pequeñas proteínas que actúan como señales químicas. Una de estas señales, llamada interleucina 23 (IL-23), activa a determinadas células inmunitarias y las empuja a producir otra molécula inflamatoria llamada IL-17, que contribuye a desencadenar la inflamación en la piel. Este “diálogo” entre las dos interleucinas (IL‑23 y IL‑17) es uno de los motores principales de la psoriasis, y cuando se frena la inflamación, disminuye.
Aunque en los últimos años se han desarrollado tratamientos que bloquean estas señales y han mejorado mucho el control de la enfermedad, todavía se conoce poco cómo se transmite la señal de interleucina 23 dentro de las células, algo muy importante para encontrar nuevas dianas terapéuticas. Y este estudio se centra precisamente en ese mecanismo interno.
Para estudiar este proceso, los investigadores utilizaron células del sistema inmunitario capaces de responder a la señal IL-23. Para ello evaluaron medicamentos que ya están aprobados para otras enfermedades con el fin de identificar nuevos usos terapéuticos, una estrategia que se denomina reposicionamiento de fármacos. Esta aproximación permite estudiar compuestos cuya seguridad y funcionamiento básico ya se conocen, lo que facilita avanzar más rápido hacia aplicaciones clínicas en nuevos contextos.
En este caso, los investigadores analizaron una colección de fármacos autorizados por las agencias reguladoras y observaron que algunos de ellos interferían en la vía inflamatoria activada por la molécula IL‑23. Y entre todos ellos, dasatinib, utilizado actualmente en ciertos tipos de leucemia, destacó por su capacidad para bloquear la producción de IL‑17 en las células del sistema inmunitario.
Los experimentos mostraron que Dasatinib bloquea de forma eficaz la producción de IL-17 inducida por IL-23 en células inmunitarias. Es decir, Dasatinib actúa como un “interruptor” que apaga la señal inflamatoria.
A continuación, los investigadores comprobaron si este efecto inhibidor también podía observarse en un modelo experimental de inflamación cutánea similar a la psoriasis. Y los resultados mostraron que el tratamiento con Dasatinib reducía varios signos característicos de esta enfermedad, como el engrosamiento de la piel, la acumulación de células inmunitarias en la zona inflamada y la presencia de células productoras de IL-17. Además, estos efectos se observaron cuando el fármaco se administraba de forma sistémica (llega a todo el organismo a través de la sangre) y también cuando se aplicaba directamente sobre la piel, lo que sugiere la posibilidad de poder aplicarlo de forma localizada en forma de cremas, evitando la exposición del resto del organismo al fármaco.
El estudio también permitió identificar cómo se transmite la señal inflamatoria dentro de las células. Los investigadores descubrieron que IL-23 activa una cadena de proteínas que funcionan como interruptores moleculares y que terminan activando complejos celulares llamados mTOR, que regulan la actividad y el metabolismo de las células, y son importantes en el proceso de inflamación.
En este proceso participa una proteína concreta llamada Blk, que actúa como intermediaria entre la señal de IL-23 y la activación de la respuesta inflamatoria. Hasta ahora no se sabía que Blk actuaba como mediadora en la cascada inflamatoria de la psoriasis, por lo que este hallazgo abre una nueva diana terapéutica para futuros tratamientos.
En conjunto, los resultados de esta investigación describen una nueva vía molecular que ayuda a explicar cómo se activan las respuestas inflamatorias asociadas a la psoriasis. Además, sugieren que medicamentos ya existentes como Dasatinib podrían explorarse en el futuro como posibles tratamientos para enfermedades inflamatorias relacionadas con esta vía.
Aunque serán necesarios más estudios para evaluar su seguridad y eficacia en este contexto, el trabajo abre nuevas vías para el desarrollo de terapias contra enfermedades inflamatorias crónicas.
Valle-Pastor MJ, Cayuela I, Yebra JS, Senach-Rasilla L, Pastor-Fernández G, Oliva A, Traba J, Navarro MN. “Drug screening identifies the Src/Abl inhibitor Dasatinib as suppressor of IL-23 signalling in skin inflammation”. J Allergy Clin Immunol. 2026 Mar 9:S0091-6749(26)00174-0. 10.1016/j.jaci.2026.02.036
La entrada Un fármaco ya aprobado para otro uso reduce la inflamación asociada a la psoriasis en un modelo experimental se publicó primero en Centro de Biología Molecular Severo Ochoa.
Held within the Severo Ochoa excellence programme, the event brought together leading experts to discuss advances in electrocatalysis for sustainable energy solutions.
