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Limb wounds in horses are common, however healing is exceedingly slow and fraught with complications. Contrary to body wounds, limb wounds demonstrate only a small amount of wound contraction. The specialist procedure of applying split-thickness skin grafts to limb wounds stimulates wound contraction by unknown mechanisms. The objective of this project is to identify those mechanisms to develop a treatment strategy for equine limb wounds for use in general  practice. Limb wounds are severely impacting animal welfare due to an extended healing/treatment duration, and the risk of euthanasia due to a poor functional outcome. By stimulating wound contraction, healing time will be reduced, and the functional outcome improved, directly benefitting the welfare of wounded horse and reducing treatment cost for the owner. Aim: To identify dermal components stimulating wound contraction, and to develop this knowledge into future state-of-the-art treatment of equine limb wounds for use in general practice. Hypotheses: i) Application of dermal fractions to collagen gels seeded with equine fibroblasts will increase gel contraction in vitro; ii) Application of dermal fractions to experimental limb wounds in vivo, will increase wound contraction resulting in a faster healing time versus wounds treated by conventional methods. Methods: i) The contractile effect of different dermal components will be assessed in a collagen gel/ fibroblast model; ii) Identified dermal components will be tested in a standardized experimental limb wound model in vivo (n=5). Ultimately, results from this project are expected to improve wound treatment in horses, directly impacting animal welfare by reducing healing time and improving the functional outcome of wounded horses. This will also directly benefit horse owners and caretakers and making veterinarians able to offer better treatment solutions.

HESTEFORSK - Raskere og bedre sårheling hos hest med autologe hudkomponenter

Prosjektet «Wheelchair Activity Monitoring» (WHAM) sikter både på å øke fysisk aktivitet blant rullestolbrukere, og på å bidra til bredere mål om mangfold og inkludering av personer med nedsatt mobilitet, ved å fremme større tilgjengelighet og deltakelse gjennom innovativ teknologi og forskning.

Rullestolbrukere er tre til fem ganger mindre aktive enn den generelle befolkningen, noe som øker risikoen for å utvikle forebyggbare sykdommer. Selv om det finnes retningslinjer for fysisk aktivitet som er tilpasset rullestolbrukere, trenger vi fortsatt effektive måter å implementere disse på samt nøyaktig teknologi for å spore mulige endringer i fysisk aktivitet. WHAM har som mål å bidra til økt fysisk aktivitet blant rullestolbrukere ved å lage digitale verktøy for å monitorere og gi tilbakemelding på rullestolbrukerens aktivitet. WHAM består av tre faser: to år ved University of British Columbia (UBC), som inkluderer et samarbeid med eksperter innen atferdsendrings-intervensjoner for rullestolbrukere; ett år ved Norges teknisk-naturvitenskapelige universitet (NTNU) og et halvt år ved Maastricht Instruments - de to siste fasene er viet til å utvikle de digitale teknologiene. 

WHAMs mål er:
1)	Å teste effekten av et treningsprogram på fysisk aktivitetsnivå og fitness blant rullestolbrukere,
2)	Å utvikle nøyaktige algoritmer for monitorering av fysisk aktivitet blant rullestolbrukere,
3)	Å lage et system som både monitorerer og gir tilbakemelding på fysisk aktivitet blant rullestolbrukere.

Wheelchair users (WCU) are three to five times more inactive than the general population, leading to a high risk of developing preventable secondary conditions. Although physical activity (PA) guidelines have been specifically developed for WCU, we lack systematic approaches to implement them in practice, as well as valid algorithms to monitor PA change in WCU through sensor-based solutions. Accordingly, the overall scientific aim of the WHeelchair Activity Monitoring project (WHAM) is to advance PA research and practice in WCU by developing valid digital markers for monitoring of and providing feedback on PA, paving the way for implementation and intervention. I will accomplish this through combining the complementary research fields of 1) behavioral intervention studies focusing on increasing PA in WCU (core competence University of British Columbia, UBC; outgoing phase) and 2) sensor-based PA monitoring (core competence Norwegian University of Science and Technology, NTNU; returning phase – consolidated by non-academic placement at Maastricht Instruments, which develop research prototypes including PA monitors). WHAM’s scientific aim is achieved through three objectives: 1) Measure the effect of a pragmatic exercise intervention trial on self-reported physical activity levels and cardio-respiratory fitness, 2) Develop valid algorithms for tracking PA markers in WCU, and 3) Co-create
a framework that outlines how PA can be conjointly monitored and provided feedback on in WCU. This fellowship will enable me to become established as an internationally recognized researcher in the field of “physical activity and disability”, while bringing together ongoing national disjointed research activities in this field. Altogether, my overall ambition is to contribute to reducing inequalities in daily-life participation among WCU compared to the rest of the population.

Topfinancing - WHeelchair Activity Monitoring project (WHAM)

The project will mainly host the IEEE flagship conference IEEE SmartGridComm 2024 in Oslo, Norway. The support from RCN is very important for the success of the event. The cost in organizing conferences in Norway is normally very high and Norwegian kroner is weak in recent years. With such reason, we have been declined few times before by IEEE when we applied to host conferences in Oslo, Norway.
The RCN’s support will be mainly used to cover the conference venue and the keynote speakers’ travel cost. The conference venue in Oslo city center has high cost. We have received an offer from a conference hotel and the renting cost is quite high. It is very challenging to only use conference registration fee to cover the cost.

The 15th IEEE International Conference on Smart Grid Communications (IEEE SmartGridComm 2024)

Hovedmålet med kreftbehandling er å eliminere kreftceller og dette er tradisjonelt oppnådd ved kirurgi, bruk av giftige medikamenter (cellegift) og stråling. En ny og betydningsfull tilnærming til kreftbehandling kalt immunterapi, har derimot fått mye oppmerksomhet det siste tiåret; Her forsøker leger og forskere å utnytte immunsystemet vårt for å målrettet  ødelegge kreftceller. En nøkkelaktør i denne banebrytende tilnærmingen er en gruppe «drapsmenn» i immunsystemet kjent som cytotoxiske T-lymfocytter (CTL-er). Disse cellene har en bemerkelsesverdig evne til å oppdage kreftceller ved å gjenkjenne unormale molekyler på overflaten av kreftcellene - molekyler som friske celler ikke har. Når CTL-er gjenkjenner kreftcellene ødelegger de dem ved å frigjøre giftige molekyler som initierer kreftcellenes selvdestruksjon. 
 
Selv om betydelige innsats har blitt dedikert til å forstå hvordan CTL-er aktiveres og hvordan de gjenkjenner kreftceller, vet vi mindre om de påfølgende hendelsene inne i kreftcellene som fører til deres død. Fra før vet vi at CTL-er kan initiere to forskjellige typer celledød i kreft: den første, kalt apoptose, er en stille og ordnet prosess der kreftcellene krymper og brytes opp uten å varsle immunsystemet; den andre, kalt pyroptose, er en mer dramatisk prosess som involverer dannelse av åpninger i cellemembranen, noe som fører til at cellene svulmer opp og sprekker. Under denne cellebristen blir innholdet inne i cellene frigitt i omgivelsene, og dette kan fungere som 'faretegn' som kan stimulere en sterkere immunrespons mot kreftcellene. Betydningen av denne cellebristen for å forsterke anti-tumorresponsene vil bli undersøkt i dette prosjektet. 
 
Videre er vi fascinert av muligheten for å avdekke ytterligere, ennå ukjente, former for celledød indusert av CTL-er. Utforsking av disse dødsrelaterte prosessene i kreftcellene kan potensielt øke effektiviteten av immunterapi og bidra betydelig i den pågående kampen mot kreft.

The primary goal of most cancer therapies is to induce cancer cell death. Immunotherapy relies on the cytotoxic activity of lymphocytes such as natural killer cells (NKs) and cytotoxic T lymphocytes (CTLs) to achieve this. While a significant amount of research in immunotherapy focuses on the events within cytotoxic lymphocytes or at the interface between cytotoxic lymphocytes and cancer cells, less is known about the molecular mechanisms that orchestrate cancer cell death, particularly in the case of CTL-mediated death.
CTLs are known to induce two types of cell death in cancer: non-inflammatory apoptosis and proinflammatory pyroptosis. Pyroptotic cancer cells release proinflammatory signals that attract immune cells to the tumor site, thereby enhancing the anti-tumor response. Cell lysis is a common outcome of pyroptotic cell death. It is unclear whether lysis can be decoupled from pyroptosis in cancer cells and whether the proinflammatory properties of pyroptotic cancer cell death depend on lysis. Moreover, it remains unknown whether CTLs can induce other forms of cell death in cancer, apart from apoptosis and pyroptosis.
Studying the mechanisms of CTL-mediated cancer cell death is challenging because CTLs selectively target cells expressing specific antigens. However, given the critical role of CTLs in immunotherapy, it is essential to deepen our understanding of CTL-induced cancer cell death.
This project aims to develop novel methodologies to investigate the death mechanisms that are initiated by CTLs. In addition, we will identify new pathways and mediators involved in CTL-induced cancer cell death. Furthermore, we will assess the contribution of proinflammatory cell death and lysis in promoting anti-tumor responses in vivo. Overall, this research will improve our knowledge of the molecular mechanisms of CTL-mediated cancer cell death and potentially reveal novel targets to enhance the efficacy of cancer immunotherapy.

T-cell-mediated proinflammatory cell death and lysis in cancer

Sink er et essensielt mikronæringsstoff som kreves for funksjonen til hundrevis av proteiner involvert i et bredt spekter av biologiske prosesser. Etter inntak av sink fra kosten reguleres nivåene i kroppen nøye gjennom absorpsjon, sekresjon og ekskresjon via spesialiserte proteiner, såkalte sinktransportører, i tarmen. Enhver ubalanse er skadelig for menneskers helse, spesielt er tarmen følsom for sinkfluktuasjoner, hvilket påvirker tarmbarrieren og kan føre til inflammatoriske sykdommer og kreft i tarmen. 
På molekylært nivå er de presise mekanismene som styrer funksjonen til de ulike sinktransportørene fortsatt uklare. Hos mennesker finnes det over tjue slike proteiner, og de fleste inneholder områder rike på aminosyren histidin. Disse histidinene mistenkes å spille en avgjørende rolle i å binde sink. Nylig oppdaget vi et enzym som modifiserer disse områdene ved å sette metylgrupper på histidin, og viste at metylerte histidiner har en lavere affinitet for sink. Dette prosjektet har som mål å identifisere nye mekanismer som regulerer sinknivåer gjennom histidinmetylering av sinktransportører, å utvikle forskningsverktøy for effektiv studie av histidinmetylering, og å legge grunnlaget for nye behandlinger av tarmsykdommer.

The delicate balance of zinc levels in the body is essential for human health. Zinc is absorbed and excreted via intestinal zinc transporter proteins, and perturbations of this process are associated with pathologies, including inflammatory diseases and cancers of the bowel. The precise molecular mechanisms regulating zinc transport, however, remain a major knowledge gap. Based on the recent discovery of an enzyme methylating histidine residues in zinc transporters, and drawing on preliminary findings which demonstrate reduced affinity of methylated histidines to zinc, this project aims to identify novel mechanisms regulating zinc homeostasis through histidine methylation. We will examine the regulation and effect of histidine methylation on zinc transport in intestinal cell culture and organoids, and examine how knockout of the methylhistidine-generating enzyme affects the integrity and pathology of the intestinal tract in mouse models. In addition, we will identify reader proteins specifically recognizing methylhistidines and develop anti-methylhistidine antibodies and inhibitors to use as tools for detection, enrichment, and inhibition of histidine methylation. Such tools are urgently needed by the international research community, as none are currently available commercially. Overall, this project will lead to great advances in the field of protein regulation, and may uncover novel mechanisms in intestinal zinc transport and pathology.

Zinc transport regulation through histidine methylation

The RealSim project proposal aims to connect machine simulation to reality in the framework of heavy machinery, which is an interdisciplinary application. The results of this project are expected to optimize machine performance, accurately and reliably predict machine failure, and reduce overall development and operation costs, thus, serving the Europe’s priority of green transformation and the United Nation’s sustainable development goal 9. The RealSim project will close the gaps of: (1) Onboard estimations of force and pressure components of heavy machinery; (2) Estimating deformability, cylinder friction, leakage, and valve dynamics of heavy machinery using independent nonlinear Kalman filters; (3) Employing dependent nonlinear Kalman filters in state estimators of heavy machinery; (4) Tuning algorithms for the covariance matrix of plant noise in the state estimation of heavy machinery.   I will consolidate and leverage my research career and position as a leading researcher in the field through integration in Assoc. Prof. Mohammad Poursina’s group at the Department of Engineering Sciences of the University of Agder (UiA), Norway. Here, I will acquire hands-on experience of working with actual mechatronic systems and develop efficient control algorithms. I will improve my knowledge of fluid power designing, control theory, instrumentation, and develop efficient coding skills. I will also develop entrepreneurial skills. The skills, knowledge, and international network that I will develop during this fellowship will put me in an excellent position to achieve my long-term goal of becoming a professor with my own independent research group at an esteemed university in EU. This fellowship will help me to prepare a strong ERC Starting Grant application in the future. It will also cater my additional goal of setting-up a research-related start-up in the future.

Reality-Connected Machine Simulation of Heavy Machinery

Information theory is a discipline at the intersection of statistics, engineering and computer science. As the study of information quantities, such as compression or communication capacities, information content or measures of statistical dependency, it is one of the theoretical underpinnings of data science.  Computational problems in information theory are highly non-linear. The goal of this project is to transfer state-of-the-art methods of computational non-linear algebra to information theory, to study the inherent algebraic complexity of information-theoretical problems and to provide tools for solving them in practice. The algebraic point of view has proven to be fruitful in seemingly unrelated areas, as witnessed by a surge of recent work in algebraic statistics, in particular on likelihood geometry. However, maximizing the likelihood function is the same as minimizing relative entropy — a specific information quantity. Hence, this project also aims at generalizing the techniques developed in likelihood geometry.  One focus is on the practical computation of information quantities using numerical and differential algebraic geometry. Such quantities are defined via non-linear optimization problems and we aim to pinpoint the algebraic complexity of these problems in instances of general interest, such as common information measures. The final objective is finding fundamental laws and limits of data science imposed by non-linear inequalities constraining the entropic region. These inequalities provide, by duality, universal bounds for many of the optimization problems studied in information theory.

Algebraic Theory of Information Quantities

WHeelchair Activity Monitoring project (WHAM)

Wheelchair users (WCU) are three to five times more inactive than the general population, leading to a high risk of developing preventable secondary conditions. Although physical activity (PA) guidelines have been specifically developed for WCU, we lack systematic approaches to implement them in practice, as well as valid algorithms to monitor PA change in WCU through sensor-based solutions. Accordingly, the overall scientific aim of the WHeelchair Activity Monitoring project (WHAM) is to advance PA research and practice in WCU by developing valid digital markers for monitoring of and providing feedback on PA, paving the way for implementation and intervention. I will accomplish this through combining the complementary research fields of 1) behavioural intervention studies focusing on increasing PA in WCU (core competence University of British Columbia, UBC; outgoing phase) and 2) sensor-based PA monitoring (core competence Norwegian University of Science and Technology, NTNU; returning phase – consolidated by non-academic placement at Maastricht Instruments, which develop research prototypes including PA monitors). WHAM’s scientific aim is achieved through three objectives: 1) Measure the effect of a pragmatic exercise intervention trial on self-reported physical activity levels and cardio-respiratory fitness, 2) Develop valid algorithms for tracking PA markers in WCU, and 3) Co-create a framework that outlines how PA can be conjointly monitored and provided feedback on in WCU. This fellowship will enable me to become established as an internationally recognized researcher in the field of “physical activity and disability”, while bringing together ongoing national disjointed research activities in this field. Altogether, my overall ambition is to contribute to reducing inequalities in daily-life participation among WCU compared to the rest of the population.

Per- og polyfluorerte stoffer (PFAS) er en stor gruppe menneskeskapte kjemikalier med høyt fluorinnhold som antas å ha negative helseeffekter. Kilder til PFAS kan være produksjon av vann-, varme- og flekkbestandige produkter og disse kjemikaliene er en del av hverdagen vår. PFAS påvirkning av biologiske systemer er ikke fullstendig forstått. Noen PFAS er antatt å øke risikoen for å utvikling av ikke-alkoholisk fettleversykdom (NAFLD) og øke risikoen for diabetes. 

For å forstå hvordan PFAS påvirker organene våre ønsker vi å bruke små laboratoriedyrkede organmodeller, kalt organoider. Disse miniatyrorganene kan dyrkes fra menneskelige stamceller og tilbyr et kontrollert miljø for å studere hvordan PFAS påvirker f.eks lever og bukspyttkjertelen vår, uten bruk av dyreforsøk.

For å studere helseeffekter må vi kunne måle nivået av biomolekyler som fettstoffer i leveren og hormoner i bukspyttkjertelen. Til dette trenger vi å utvikle analytiske verktøy for å måle effektene. Først vil vi bekrefte at når leverorganoidene eksponeres for enkelte PFAS-forbindelser utvikles det NAFLD-lignende sykdom ved å sammenligne den biokjemiske profilen (proteiner og metabolitter) til organoider av lever med PFAS-eksponerte organoider. Deretter vil vi utvide den analytiske verktøykassen for å undersøke hvilke metabolske veier som påvirkes, og om effekten er den samme i NAFLD-induserte og PFAS-eksponerte organoider. Vi vil også eksponere insulinproduserende bukspyttkjertelorganoider for PFAS for å undersøke effekten av PFAS på hormonproduksjon. Når effektene av PFAS-eksponering på lever- og bukspyttkjertel-organoider er etablert, vil organoidene bli samkultivert i en chip, og effektene av PFAS-eksponering vil bli undersøkt og sammenlignet med individuelle organoider.

Persistent organic pollutants (POPs) are believed to contribute to metabolic diseases, such as non-alcoholic fatty liver disease (NAFLD) and type 1 diabetes. HE-POP aims to investigate the effects of per- and polyfluoroalkyl compounds (PFAS), a type of POPs), on organ function in a controlled environment.

Organoids are multicellular laboratory-grown miniature organs, that are grown from stem cells. HE-POP will use organoids to examine how PFAS affects our organs and develop cutting-edge bioanalytical tools and methodology to measure these effects using liquid chromatography-mass spectrometry. HE-POP hypothesizes that PFAS negatively affects organ function, as evidenced by changes in hormone and lipid levels characteristic of NAFLD and type 1 diabetes. 

Organoids offer a controlled environment to study the effects of PFAS on the liver and pancreas, without the use of animal models. HE-POP aims to gain evidence of the negative effects of PFAS on organ function through controlled experiments on organoids and aid in understanding the biological mechanisms underlying NAFLD and type 1 diabetes.

HE-POP has fundaments in UN sustainable development goals, specifically #3, #12, and #14/15, seeking an understanding of diseases with worldwide prevalence, and understanding how POPs affect our life and surroundings and help enable the right regulatory actions and replacement chemicals.

HE-POP: Studying the Health Effects of Persistent Organic Pollutants, Using Mass Spectrometry, Organoids, and Organ-On-A-Chip

Norge har under Parisavtalen påtatt seg en forpliktelse til å redusere klimautslippene sine med minst 55 prosent innen 2030 sammenlignet med nivået i 1990. Hittil har vi kun oppnådd 5 prosent av dette målet; vi har følgelig kun syv år på å redusere de resterende 50 prosent for å imøtekomme målene. For 2050 har vi satt oss enda større mål: å redusere klimautslippene med hele 90 prosent. Bakgrunnen for målene er at vi prøver å unngå de verste scenarioene FNs klimautvalg skisserer opp i sine rapporter. I tillegg har energiforbruket økt, og prognosene fra Statnett for ulike scenarier viser at energiforbruket skal fortsette å øke. Vi trenger følgelig mer energi. Dette har bidrat til at diskusjoner rundt kjernekraft i Norge er høyaktuelle og pågående. Norsk Kjernekraft AS har blitt opprettet med formål om å bygge Norges første kjernekraftverk. I tillegg ble det i fjor også bevilget 200 millioner kroner fra Regjeringen til et nytt senter som skal drive med nukleær forskning. Målet er å styrke den norske kunnskapsberedskapen på det nukleære området. Dette betyr at vi beveger oss i en retning hvor kjernekraft en dag kan bli aktuelt i Norge, og noen mener at dette er den eneste veien å gå hvis vi skal nå målene våre for 2050. Men i dag sitter vi med flere spørsmål enn svar, blant annet: Hvilken teknologi og leverandør burde vi velge? Er regelverket for snevert og strengt? Hvordan kan dette gjøres og samtidig ivareta sikkerhet? Hvordan tjener et kjernekraftverk penger?

Dette prosjektet skal svare på samtlige av disse spørsmålene i en detaljert og omfattende analyse. Her bruker vi grunnlagsdata til å vurdere dagens forskning opp mot hvordan industrien i andre land opererer, og ut ifra dette forsøke estimere hva risikoen knyttet til å bygge kjernekraft som industri i Norge er. Prosjektet sikter på å gi et så helhetlig bilde som mulig slik at vi kan gjøre oss opp en mening basert på fakta; om kjernekraft passer inn i miksen av det som utgjør norsk energi.

Denne prosjektbeskrivelsen skisserer forskningen Vala Maria Valsdottir (omtales herunder som stipendiaten) skal utføre innenfor sin doktorgradsavhandling. Prosjektet skal være en del av Senter for nukleær forskning (SNF) som fikk midler vinteren 2023.
Ph.d.-prosjektet er initiert av Inmeta Consulting AS, som igjennom denne ph.d.-stillingen vil bli en del av SNF. Inmeta planlegger en prosjektperiode på fire år, hvor stipendiaten arbeider 75 % med ph.d.-prosjektet og 25 % med vanlig virksomhet hos Inmeta. 
Prosjektet skal undersøke muligheten for kjernekraft som industri i Norge. Dette er både en samfunnsaktuell problemstilling samt en som medlemmene i SNF er interessert i å utforske. Stipendiaten kommer derfor til å samarbeide med alle aktørene som er involvert i senteret og benytte forskningsdata fra dem. Dette gjelder da spesielt Institutt for energiteknikk (IFE) som har mest grunnlagsdata som er relevant for dette prosjektet.
Kandidaten ferdigstilte en masteroppgave høsten 2020 i kjernefysikk på Universitetet i Oslo (UiO) og har derfor gode og relevante grunnkunnskaper for å ta på seg et slikt prosjekt. I tillegg har kandidaten tre års erfaring innenfor energibransjen, og er derfor oppdatert på industrien og forstår deres problemstillinger godt.

Er kjernekraft aktuelt for Norge?

Midlene fra SSF-Svalbard Science Forum fordelt på år

Midlene fra SSF-Svalbard Science Forum fordelt på fylker

Midlene fra SSF-Svalbard Science Forum fordelt på fagområde

PhD Student

Hydroacoustic surveys may be underestimating or overestimating biomass due to species avoidance of vessel light. Therefore we propose a controlled environment experiment to quantify the effect of light on fish behaviour. A small change in the orientation of fish can cause large changes in biomass estimates from acoustic surveys. What are the changes in the orientation of fish due to light from vessels? Are research vessel based hydroacoustic surveys underestimating fish biomass?
AZKABAN (Arrested Zooplankton Kept Alive for Broadband Acoustic Net) experiment is a 12000 L microcosm that will be mounted off the side of a research vessel for acoustic measurements of a known population of zooplankton and fish. The behaviour of the species in the microcosm due to different light regimes will be studied with an optical camera. The effect on the change in behaviour will be evaluated to quantify the impact of artificial light on hydroacoustic biomass estimates. In addition, I will compare the results to a method, inverse informed method. that can account for behaviour change from orientation changes (evasion or attraction) within the biomass calculation.

AZKABAN experiment for light reaction, RiS ID 11578

Development of innovative proton and neutron therapies with high cancer specificity by 'hijacking' the intracellular chemistry of haem biosynthesis.

Deep-lying cancers, such as glioblastoma multiforme (GBM) brain cancer, are very difficult to access and incurable by the current standards of care. The fluorescence of photosensitive molecules (PSs) can precisely guide surgical resection of GBM. Nevertheless, photomedical treatments like photodynamic therapy (PDT) show limited efficacies due to the low penetration of light into tissue. Proton radiotherapy can reach deep-lying disease through therapeutic energy deposition in a spatially confined region called Bragg peak. Current neutron-based therapies, like Boron Neutron Capture Therapy (BNCT), have sufficient penetration depth but lack cancer specificity. In NuCapCure, we propose to 'hijack' intracellular biosynthetic pathways and use them to produce custom-made drugs that will facilitate two genuinely new cancer treatments: i) "NuCapCure Proton", combining proton radiotherapy, protondynamic therapy through PS proton activation, and proton capture therapy (BPCT) through three produced alpha particles; and ii) "NuCapCure neutron", combining GBM specific BNCT and PS neutron activation as demonstrated in our FET-open project FRINGE. The main scientific breakthroughs of NuCapCure will be to demonstrate the custom production of novel compounds through native intracellular biosynthesis but also to establish experimental proof-of-principle, both in vitro and in vivo, of the proposed two novel therapies. Our highly interdisciplinary project team comprises world-renowned experts from a unique combination of disciplines: proton and neutron physics, synthetic chemistry, photochemistry, photobiology, radiobiology, medical physics, nuclear reactor and particle accelerator technology and radio-oncology to lay the foundations for novel, targeted and curative therapies against currently fatal cancer indications like GBM.

When an organism experiences physiological stresses, such as nutrient starvation, it activates several mechanisms to promote its survival. One of these mechanisms is autophagy, which is a catabolic pathway conserved from yeast to man that functions as a recycling system during normal physiology, and which helps provide nutrients to sustain essential cellular processes during starvation. Although autophagy is an intensively studied process that plays a major role both in normal development and in a wide variety of diseases, several important aspects of autophagy remain to be elucidated. For instance, whereas the vast majority of studies have focused on how cells regulate the activation of autophagy, it remains largely unknown how cells and organisms shut off autophagy in response to returning nutrient availability. The limited knowledge of autophagy termination is partly due to a lack of available tools and appropriate methods. Addressing these challenges will not only provide important insight in this fundamental aspect of the autophagic process, but may potentially also identify new targets for development of drugs to manipulate this phase of autophagy. In FINALphagy I will develop new genetic and computational tools to quantify and manipulate the temporal dynamics of autophagy in an entire organism. I will unravel key mechanism of autophagy termination in individual cells within a tissue and dissect how this connects to systemic signaling and behavioral changes. This will generate a comprehensive toolbox for time- and space-resolved manipulation and quantification of autophagy levels, produce a whole-organism map of autophagy responses at the tissue-level, and conceptualize our understanding of the dynamics of autophagy regulation in an entire organism during changing nutrient levels.

Final act of the autophagy symphony: Whole-organism orchestration of autophagy termination

Mental disorders represent one of the largest burdens for the European Health Care system, due to large number of patients and a lack of efficient treatment options. Today, drug treatment of mental disorders is characterized by severe adverse effects and suboptimal response in more than a third of the patients. Optimizing treatment is based on a trial-and-error approach, which combined with frequent multi-morbidities, often leads to polypharmacy and poor outcome. Due to limited understanding of the disease mechanisms that underlie mental disorders, new drugs with novel therapeutic targets are lacking, and existing treatments are ineffective for many people. It is therefore urgent that cutting-edge research approaches are deployed to develop innovative tools to individualize treatments using available psychiatric medication, and thus improve clinical outcomes and reduce costs for health care systems. The main goal of the multidisciplinary REALMENT project is to optimize treatment of mental disorders through novel precision medicine strategies based on current pharmaceutical options. REALMENT includes world leading research institutes and pharmaceutical industry at the very forefront of mental disorder research. REALMENT will achieve its objectives by exploiting population-scale Real-World Data (RWD) in combination with Randomized Clinical Trial (RCT) data available to the partners. Big data from populations (Nordic registries), cohorts (European biobanks), and eHealth samples (medical records), including whole genome genotypes (n=1.9 million), will be analysed in an EU-wide sustainable infrastructure using artificial intelligence and machine learning to develop prediction and stratification tools (precision psychiatry). These algorithms will be validated in large RCT data (n=10k) and re-phenotyping projects, and implemented in a clinical management platform (4MENT), which will be made available to provide decision support to clinicians to optimize therapeutic effects.

Using real-world big data from eHealth, biobanks and national registries, integrated with clinical trial data to improve outcome of severe mental disorders

Outsourcing cancer immunity to healthy donors

Despite recent advances in cancer immunotherapy, most patients with metastatic cancer are not cured. Major reasons are lack of homogeneously and highly expressed molecules that can be safely targeted and evoke efficient T-cell responses. I propose that the strong T-cell responses leading to rejection of transplanted organs can be exploited to “reject” cancer by specific recognition of tissue-restricted targets. To this end, I recently demonstrated that healthy donor blood provides a rich source of T cells expressing TCRs that specifically and strongly react to peptides from tissue-restricted self-proteins, when presented on mismatched, foreign Human Leukocyte Antigens (HLA). I propose that patient T cells genetically equipped with such donor TCRs (dTCR T cell therapy) may “reject” cancer-affected organs, including metastases. A high and homogeneous expression of tissue-specific antigens is often maintained on both primary tumor and metastatic cancer cells. Here, I will identify peptides from tissue-restricted proteins as novel candidate TCR targets. Next, I will identify donor T cells that recognize such self-peptides in complex with foreign HLA by use of my patented method, and sequence reactive TCRs. Finally, I will establish a preclinical pipeline to characterize safety and efficacy of TCRs in vitro and in vivo in innovative mouse models. Outsourcing cancer immunity to dTCR T cells may bypass major limitations in current immunotherapies, including checkpoint inhibition and T cells gene-modified with chimeric antigen receptors (CARs). Thus, dTCRs can recognize i) intracellular targets and thus manifold more targets than CARs, ii) tumor-associated self-antigens with high affinity in contrast to patient-derived TCRs, and iii) self-antigens, which are more homogeneously expressed than mutations. dTCR T cell therapy could treat malignancies in organs that are non-essential for survival, such as prostate, or that can be replaced by a transplant, such as bone marrow.

Predicting comorbid cardiovascular disease in individuals with mental disorder by decoding disease mechanisms

Comorbid cardiovascular disease in people with severe mental disorders is a major public health concern and poses a considerable financial burden on European Health Care. The CoMorMent project will uncover mechanisms underlying the higher incidence of cardiovascular disease in people with mental disorders. This project builds on our recent findings that genetic variation that affects genes expressed in the brain and which increase the risk of mental disorders also impact lifestyle and behaviour (e.g. diet, exercise, and smoking) that increase cardiovascular risk. The project will identify molecular mechanisms common to mental disorders and unhealthy lifestyles that increase the risk of cardiovascular disease. We will take advantage of our genotyped biobank samples united with large national registries with information about disease trajectories and comorbidity in over 1.8 million people. The “big data” available to CoMorMent means that we can apply new statistical tools to discover novel sequence variants conferring risk of both mental disorders and cardiovascular diseases and determine how these may be mediated by lifestyle or behaviour. We will characterize the underlying mechanisms by identifying accompanying structural brain changes and body fat composition from MRI data in combination with gene expression and functional studies. The CoMorMent multidisciplinary expert team in clinical science (cardiology, psychiatry), genetic epidemiology, molecular genetics, and neuroscience combined with experts in machine learning and computation will generate findings that will form the basis of novel stratification and prediction tools, which will be tested and validated in clinical samples. Thus, CoMorMent will form the basis for a new approach in clinical studies by providing precision medicine tools for clinical implementation to remediate a major public health issue.

Brains and minds in transition: The dark side of neuroplasticity during sensitive life phases

The potential and boundaries of the human mind is determined by dynamic interactions between the environment and the individual genetic architecture. However, despite several breakthroughs, the genetic revolution has not provided a coherent account of the development of the mind and its disorders, and the missing heritability is large across human traits. One explanation of this impasse is the complexity of the gene-environment interactions. Current knowledge about the determinants of a healthy mind is largely based on studies whose modus operandi is to treat the environment as a static entity, neglecting to consider the crucial fact that environmental inputs and their genetic interactions vary dramatically between life phases.   The objective of BRAINMINT is to provide this missing link by zeroing in on two major life transitions, namely adolescence and pregnancy. These phases are characterized by temporarily increased brain plasticity, offering windows for adaptation and growth, but also host the emergence of common mental disorders. I propose that a multi-level investigation with this dark side of brain plasticity as the axis mundi will add a mechanistic understanding of this link between growth and vulnerability. I will test the main hypothesis that mechanisms that boost neuroplasticity promote adaptation to a dynamic environment, but at the cost of increased risk of psychopathology if exposed to a combination of genetic and environmental triggers. To this end I will utilize cutting-edge longitudinal brain imaging, electrophysiology, rich cognitive and clinical data, immune markers, gene expression and genetics. I will leverage on massive imaging data (n>40,000) and novel tools to increase power and generalizability and improve brain- and gene-based predictions of complex traits. Aiming to help resolving one of the modern day enigmas, BRAINMINT is a pioneering and high risk/high gain effort to find mechanisms of brain plasticity that support and harm the brain. 

How distress alters opioid drug effects and abuse liability

As the opioid epidemic escalates, we must ask: why are opioids so addictive? Non-human animal research links addiction with the powerful relief opioids can offer to animals in distress. In humans, epidemiological and clinical studies converge upon social stressors and a poor social support network as key risk factors for addiction. Despite this, it is currently unknown how pre-drug distress might alter opioid drug effects. Tremendous resources are dedicated to charting how people feel after taking a drug, sidestepping the potentially profound influence of how people feel before they take the drug. Here, I will turn the current approach on its head. Using acute social distress induction before morphine administration in healthy humans, I will create a human model to determine the psychological, physiological and brain underpinnings of how social stressors increase opioids’ abuse liability.  First, I will test the hypothesis that pre-drug distress enhances drug wanting (self-administration) but not drug liking (self-report) compared to drug effects in a control condition. Second, I will use opioid blockade to confirm or falsify the hypothesis that opioid drugs ‘hijack’ brain mechanisms underpinning social support. Third, I will determine to what extent opioid drug effects are dopamine-dependent by blocking dopamine before morphine administration. I will also apply computational modelling and functional imaging to elucidate the underlying brain mechanisms. Thus, the proposal offers a powerful new methodology for resolving hotly debated questions on the independent contributions of opioids and dopamine for reward and abuse liability.  In sum, the project aims to achieve a breakthrough in our understanding of how a pre-drug social distress state can alter opioid drug mechanisms. The mechanistic understanding arising from this project could have profound implications for science, as well as for clinical care and new policies designed to contain the opioid epidemic. 

Coincidence detection of proteins and lipids in regulation of cellular membrane dynamics

Specific recruitment of different proteins to distinct intracellular membranes is fundamental in the biology of eukaryotic cells, but the molecular basis for specificity is incompletely understood. This proposal investigates the hypothesis that coincidence detection of proteins and lipids constitutes a major mechanism for specific recruitment of proteins to intracellular membranes in order to control cellular membrane dynamics.  CODE will establish and validate mathematical models for coincidence detection, identify and functionally characterise novel coincidence detectors, and engineer artificial coincidence detectors as novel tools in cell biology and biotechnology.

Set to change: early life factors restricting and promoting neurocognitive plasticity through life

Cognitive function in old age can be predicted from how you functioned when you were young. This is remarkable, as there are substantial cognitive age changes. Are we neurodevelopmentally set to change through life in certain ways? The objective of Set-to-change is to test whether and how early life environmental factors and genetic makeup interact to regulate neurocognitive plasticity through the lifespan. Neurocognitive plasticity; i.e. changes in brain and cognition in response to environmental demands over time, shows huge individual variability, for unknown reasons. Neurodevelopmental origins of functional variation through the lifespan are acknowledged, but the pathways need to be identified. As individual constitution and environment are intrinsically correlated, to make progress beyond state of the art, this can only be tested in an experimental setting.  The novelty and ground-breaking nature of the project lies in the synthesis of a targeted experimental approach testing differences in neurocognitive plasticity by training of younger and older adult mono- (MZ) and dizygotic twins (total n = 400 individuals), with varying degrees of prenatal environmental variance, as indexed by their extent of discordance in birth weight (BW). BW discordance in MZ twins enables me to disentangle early environmental and genetic influences on neurocognitive plasticity. I will employ a novel ecologically valid memory intervention utilizing navigation with true locomotion and prospective memory in virtual reality. Twins will be assessed with brain MRI, cognitive, health and epigenetic measures at multiple time points spread across 2.5 years pre- and post- 3 months intervention in a AB/BA crossover design, to investigate neurocognitive plasticity and age change longitudinally, as well as possible lifestyle and epigenetic mediators. I hypothesize that early life environmental influences will interact with genetic makeup in determining neurocognitive plasticity in adulthood.

0 projects

EIC-The European Innovation Council (EIC)

Development of innovative proton and neutron therapies with high cancer specificity by 'hijacking' the intracellular chemistry of haem biosynthesis.

Awarded: NOK 25.2 mill.

Project Period: 2024-2028

Location: Oslo

ERC-European Research Council (ERC)

Final act of the autophagy symphony: Whole-organism orchestration of autophagy termination

Awarded: NOK 15.2 mill.

Project Period: 2023-2027

Location: Oslo

H20-HEALTH-Health, demographic change and wellbeing

Using real-world big data from eHealth, biobanks and national registries, integrated with clinical trial data to improve outcome of severe mental disorders

Awarded: NOK 17.9 mill.

Project Period: 2021-2025

Location: Oslo og 2 andre

H20-ERC-European Research Council

Outsourcing cancer immunity to healthy donors

Awarded: NOK 19.7 mill.

Project Period: 2020-2025

Location: Oslo

H20-HEALTH-Health, demographic change and wellbeing

Predicting comorbid cardiovascular disease in individuals with mental disorder by decoding disease mechanisms

Awarded: NOK 15.0 mill.

Project Period: 2020-2024

Location: Oslo

H20-ERC-European Research Council

Brains and minds in transition: The dark side of neuroplasticity during sensitive life phases

Awarded: NOK 13.9 mill.

Project Period: 2019-2024

Location: Oslo

H20-ERC-European Research Council

How distress alters opioid drug effects and abuse liability

Awarded: NOK 14.4 mill.

Project Period: 2019-2024

Location: Oslo

H20-ERC-European Research Council

Coincidence detection of proteins and lipids in regulation of cellular membrane dynamics

Awarded: NOK 23.3 mill.

Project Period: 2019-2023

Location: Oslo

H20-ERC-European Research Council

Set to change: early life factors restricting and promoting neurocognitive plasticity through life

Awarded: NOK 18.7 mill.

Project Period: 2018-2023

Location: Oslo