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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

En av de vanligste, men minst studerte, utfordringene med å bli eldre er problemer med å kommunisere. Mange eldre sliter spesielt med pragmatiske ferdigheter, som å forstå undertekst, eller tilpasse det de sier til personen de snakker med. 

La oss si at en lege må gi en alvorlig beskjed til en pasient. For å gjøre det litt lettere å takle, bruker legen vagere språk, som "kanskje" i stedet for "sannsynligvis". Mens yngre voksne ofte tar hensyn til høflighetsstrategier i måten de tolker det som blir sagt på, har eldre ofte vanskelig for å forstå når noen snakker indirekte. Mange eldre voksne har vanskelig for å forstå ikke-bokstavelig språk og kan misforstå alvorlighetsgraden av diagnosen. Dette kan påvirke beslutningen deres om behandling, noe som kan føre til utilsiktede konsekvenser. 

Siden god kommunikasjon er viktig både i viktige medisinske samtaler og i hverdagen, er det viktig at vi finner ut hva som gjør at eldre kan ha vansker med å forstå og bli forstått. RESILIENCE skal hjelpe til med denne utfordringen ved å samle data om praktiske, kognitive og språklige ferdigheter hos voksne i alderen 18-90 år over tid. Dette vil gi oss en stor mengde data om pragmatiske, kognitive og språk ferdigheter og gjøre det tilgjengelig for forskning. Med denne dataen som grunnlag har vi følgende mål: 

• Forstå hvordan praktiske evner endrer seg generelt gjennom voksenlivet. 
• Finne ut hvilke mekanismer som påvirker pragmatiske evner på forskjellige tidspunkter i livet.
 • Utvikle en teoretisk modell som forklarer hvordan pragmatiske ferdigheter endrer seg med alderen.
 • Lage algoritmer som kan forutsi hvordan pragmatiske evner vil utvikle seg for enkeltpersoner i årene som kommer. 
• Utvikle og teste et verktøy som kan måle pragmatisk helse (både pragmatiske ferdigheter og deres underliggende mekanismer), noe som kan åpne  for å iverksette tiltak. 

Dette vil gi oss muligheten til å forstå bedre hvordan folk kan utvikle pragmatisk resiliens gjennom livsløpet.

A cornerstone of human communication is our reliance on pragmatic skills to guide linguistic interactions (e.g., reasoning about others' mental states to bridge the gap between what is said and intended in conversation). However these skills are highly sensitive to age-related decline, leading to miscommunication and uninformed decision making in the older adult population. This raises an important question, one which has puzzled linguistics and psychologists for decades: if pragmatic competence is fundamental to communication, why do individuals vary so much in this capacity? 

Traditionally, psychologists have approached pragmatic competence from a cognitive angle, reasoning that individual differences in executive functions (i.e., the cognitive skills associated with goal-directed actions) are what underlie effective pragmatic behavior. In a similar vein, language scientists have taken a linguistic approach, reasoning that one’s language background (e.g., the frequency with which individuals shift between languages) shapes pragmatic skills by enhancing sensitivity to the communicative context. This focus on either cognitive or linguistic influences has resulted in two expansive yet disparate areas of research.

RESILIENCE will unite these disciplines to pursue a longstanding debate on what underlies pragmatic resilience and decline using a large-scale, interdisciplinary and longitudinal approach. By gathering data on adults' (ages 18-90) pragmatic, cognitive and language skills over multiple time points, we will develop a comprehensive theoretical model that explains how cognitive and linguistic systems interact to shape pragmatic competence as we age, and create algorithms that predict the trajectory of an individual’s pragmatic abilities in upcoming years. Based on these results we will design a multidimensional tool that detects the earliest signs of pragmatic deficits, leading to future interventions, allowing us to uncover the paths to pragmatic resilience.

Uncovering the paths to pragmatic resilience

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

Noen av oss tåler stressende livshendelser godt. Andre derimot utvikler vedvarende fysiske og psykiske plager som følger av stress. Hvor godt vi håndterer stress avhenger av et komplekst samspill mellom miljøfaktorer, sosiale forhold, biologisk sårbarhet og indre motstandskraft. Forskning på stressreaksjonene til dyr og pasientgrupper som til vanlig lever under mye stress viser at en gruppe signalstoffer i kroppen som aktiverer det samme hjernesystemet som cannabis – endocannabinoidene – kan begrense styrken på stressreaksjoner og bidra til at man raskere kommer seg til hektene. I dette prosjektet skal vi undersøke hvordan mestring av stress på kort og lang sikt henger sammen med nivåer av endocannabinoider i kroppen for å forstå hvorfor noen personer er mer motstandsdyktige mot stress enn andre. I den ene studien følger vi pasienter som skal gjennomgå en stressende, men veldig vanlig, situasjon: kirurgi. Her måler vi pasientenes opplevelse av stress, samt mentale og fysiske helse, fra tiden før til to år etter operasjonen og undersøker hvordan dette henger sammen med nivåene deres av endocannabinoider og andre stresshormoner. I den andre studien bruker vi data fra et eksperiment hvor deltakerne har blitt utsatt for psykososialt stress til å undersøke om endocannabinoidnivået deres påvirker hvordan de reagerer på stress, og om stresset i seg selv kan påvirke kroppens produksjon av endocannabinoider. Til syvende og sist er målet med studien å vurdere hvorvidt målinger av endocannabinoidnivåer kan brukes til å forebygge helseplager og til å evaluere behovet for økt oppfølging etter alvorlig stressende påkjenninger i livet.

In the face of major life stressors, some individuals cope well whereas others develop ill health and long-term adverse outcomes. Predicting who needs additional support in response to major life stressors is essential for targeted prevention and more efficient allocation of resources. The endocannabinoid system is emerging as a promising target for understanding vulnerability and resilience to stress. This system appears to buffer stress in two ways: by limiting the magnitude of the stress response, and by facilitating recovery after a stressful event. While the early findings are intriguing, they mainly stem from studies in rodents and small clinical groups with high stress burden. What role endocannabinoids have more globally for human resilience, health and well-being remains elusive. 

In this project we address this gap by leveraging comprehensive experimental and clinical data on two potent stress models: psychosocial stress and surgery. Drawing on these unique datasets, which combine experimental control with ecological validity, we will decipher how endocannabinoid levels influence people’s stress response and recovery across minutes, days, weeks and years. The project represents a novel directional shift for endocannabinoid research and will (i) determine the value of endocannabinoid levels as a biomarker to predict outcomes after surgery, (ii) quantify sex differences, (iii) assess endocannabinoid interplay with opioid analgesics, sex hormones and other stress markers (iv) spearhead open and reproducible science practices in endocannabinoid research, and (v) make this fine-grained and novel data available through an interactive web application. 

This project represents an ambitious effort to understand endocannabinoids’ role in stress resilience and will determine the value of endocannabinoids as a predictive biomarker and potential target for individualized treatment.

Deciphering endocannabinoid stress buffering in humans: 
Mechanistic and clinical investigations

Borderline Personality Disorder: Memory and Identity in Adolescence

BOLD MINDS aspires to enhance the understanding of vulnerability factors underlying the emergence of borderline personality disorder (BPD), with an ultimate aim of increasing the potential for young individuals to receive early, evidence-based help when their mental health is at risk. BOLD MINDS will achieve this by investigating whether disruptions in two aspects of autobiographical memory (AM), narrative identity (NI) and involuntary AM (IAM), are associated with BPD features and problem behaviours in adolescents concurrently and over time. In doing so, BOLD MINDS will strengthen the understanding of mechanisms underlying the emergence of BPD in adolescence and lay a groundwork for developing evidence-based early interventions for BPD. While currently limited, the study of AM in this field is essential for two reasons. Firstly, because the aspects of AM under investigation, NI and IAM, are known to be involved in identity formation and emotion regulation which represent two key psychological processes that are disrupted in adults with BPD and are linked to problem behaviours such as self-harm and suicidality. Secondly, because promising research is emerging on the use of AM targets in the treatment of emotional disorder in adults, and provides a strong model for future treatment development with vulnerable adolescents. In addition, this timely research program aligns with calls from international organizations to prioritize early interventions to promote adolescent mental health. BOLD MINDS will adopt and adapt state-of-the-art ecological momentary assessment and analytical techniques and work at the crossroads of clinical and cognitive psychological perspectives, allowing for a multidimensional approach to understanding BPD vulnerability. Training-through-research and formalized training of the experienced researcher will prepare her for a permanent academic position and the founding of her own research lab specializing in AM and early interventions for BPD.

Bilingual Experiences, Cognitive Ageing and underlying Mechanisms

The goal of the Bilingual Experiences, Cognitive Ageing and underlying Mechanisms (BECAME) project is to examine the functional neuroplastic mechanisms underlying mitigatory effects of bilingual experience on age-related cognitive decline. While evidence is available for structural brain changes supporting bilingualism-induced effects on cognitive aging (CA), functional mechanisms underlying such effects are not yet well understood. BECAME aims to fill this gap by investigating the trajectory of bilingualism-induced functional neuroplasticity across the adult lifespan (ages 18-85), crucially adopting an individual differences approach related to measurable degree of bilingual engagement. Importantly, although such benefits are thought to be rooted early in the lifespan, evidence for the timeframe and conditions of their early emergence is scarce. The choice of including the whole adult lifespan allows us to investigate these mechanisms and their emergence more directly from a lifespan perspective. I combine behavioral testing with brain recordings via electroencephalography (EEG). EEG is widely used in cognitive neuroscience to assess brain activity and the degree of communication between brain regions (functional connectivity) in response to stimuli and at rest. Combining behavioral and EEG modalities will allow me to test bilingualism’s effect on functional connectivity, as well as its consequences for functional efficiency, the minimum required neural activation to successfully perform a task. This will enable a detailed, evidence-based account of the protective effects observed in older-aged bilinguals, and how they are built from earlier life stages. By illuminating the relationship between multilingualism and resulting neurocognitive adaptations, BECAME will enable to capitalize on it as a health initiative, with manifold societal implications and the potential to be translated into actionable policies exploiting multilingualism to ameliorate effects of CA.

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.

Despites dental pulp capping materials should meet the certain requirements, the available materials have one or more shortcomings—poor biocompatibility and rheological properties, fail to maintain pulp vitality and to simulate reparative dentine formation and expensive etc. Mineral trioxide aggregate (MTA) is widely used material because of its beneficial properties. However, its composition bismuth oxide, which is suspectable to toxicity, has an impact on rheological properties. This emphasizes the necessity of looking for inexpensive alternatives to materials that meet the specifications. This project's goal and novelty are to investigate the potential processing of the dental pulp capping cement, which is made of strontium silicate (SrSiO3), strontium fluoride (SrF2), piezoelectric material (PZM) and tricalcium silicate (Ca3O5Si) and its rheological properties and hemocompatibility. Because SrSiO3, SrF2, PZM and Ca3O5Si have the promising properties. This project's work packages are split into four categories based on the interdisciplinary approach since it involves the synthesis and characterization of PZM, the processing and characterization of cement, the identification of rheological parameters utilizing ISO standardizations, and hemocompatibility, and acquiring new transferrable skills. Additionally, the interactions among the selected compounds will be determined. The scientific impact of this project is comprehending the physical properties and the immune system's response to evaluate the cement's suitability as a replacement for existing materials, as well as resulting in further uses in dentistry and medicine. The societal impact is providing millions of patients in Europe with predictable and outstanding treatment outcomes each year to maintain pulp vitality and health. Eventually, it will ease the financial load on millions of patients who need dental care, will be avoiding inflated medical expenses and misuse of the patent (economic impact).

SrSiO3-based Dental Pulp Capping Cement

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

Effekter av polyploidisering ved adaptiv evolusjon hos gjær (PloidYeast)

Midlene fra BIONÆR-Bionæringsprogram fordelt på år

Midlene fra BIONÆR-Bionæringsprogram fordelt på fylker

Midlene fra BIONÆR-Bionæringsprogram fordelt på fagområde

Climate change, habitat destruction and other human activities are threating the sustainability of food security. UN has launched four aims within the sustainable development plan to maintain and ensure food security. 
In PloidYeast, we aim to apply a new collection of yeasts to offer new biotechnological approaches that will address the UN challenges and bring the food chain in a more sustainable direction, including more circular processes. 
To accomplish this objective, we will make use of a recurrent evolutionary phenomenon observed in several industrial yeasts and other organisms. This phenomenon is called polyploidization, which leads to an increase in the number of copies of the genome. Polyploidization facilitates the adaptation of the organism to new environmental conditions, such as the harsh conditions found in the food industry. Through several evolutionary steps, we aim to generate yeasts with desired industrial traits, accommodated to reach the sustainability of the food security. We will apply a multidisciplinary approach combining microbiology, molecular and genetic engineering methods, bioinformatics and mathematical modelling to select and generate a new yeast collection. At the end of the project, we expect to learn how polyploidization improves adaptation to industrial conditions, which will help to solve some of the UN challenges.
Not so far, but we already know that by increasing the number of copies in the yeast genome through hybridization will combine traits from the parental yeasts and in this way introduce  desired industrial traits.

Polyploidization is a recurrent evolutionary phenomenon that generates diversity and facilitates adaptation. The food production chain requires new industrial strains, more efficient or with innovative solutions to particular problems. Synthetic biology tools can introduce biological parts for improving industrial strains. However, some of those parts are still unknown. Industrially relevant yeasts are polyploids suggesting polyploidization as a mechanism to generate new industrial strains. Allopolyploids can combine multiple parental traits. But, the effects of polyploidization are not well understood. In PloidYeast, we will apply a multidisciplinary approach combining microbiology, molecular and genetic engineering methods, bioinformatics and mathematical modelling to generate a new generation of industrial strains with application in the food production chain and advance in our understanding of adaptation by polyploidization. First, we will ask whether polyploidization mechanism is a suitable mechanism to improve bioprocesses (Q1). We selected wild yeast species (WP1) to generate auto- and allopolyploids (WP2). We will test whether multi-species allopolyploids show multiple traits (Hypothesis: H1). Then, we will evolve the new polyploids on environments mimicking three industrial conditions (WP3) expecting adaptation to them (H2). After 500 generations of evolution, we will ask whether the effects of polyploidization are repeated (Q2) by sequencing the genomes, transcriptomes and quantifying their proteome, metabolome and other phenotypic traits (WP4). If Q2 is true, we will isolate genomic regions relevant to solve a biotechnological challenge (H3). We envision to use this new multiomic dataset to build the bases of a new generation of mathematical models applied to yeast polyploids to select wild strains (H4) and isolate biological parts contributing to solutions for sustainability of food systems and promotion of circular bioeconomy.

Effects of polyploidization during adaptive evolution in yeasts (PloidYeast)

Kreft er den nest ledende dødsårsaken på verdensbasis, og representerer en økende global helsekrise og en av de mest utfordrene sykdommene menneskeheten noen gang har møtt. For de fleste kreftformer er det bare en liten brøkdel av pasientene som får effektive resultater av dagens behandlinger, noe som betyr at de fleste kreftrelaterte helsekostnader «kastes bort» på ineffektive behandlinger. Eggstokkreft (EK) forblir i hovedsak en uhelbredelig sykdom hvor overlevelsesstatistikken bare har blitt moderat forbedret, noe som understreker det pressende behovet for å identifisere innovative strategier for dets behandling. Hemispherian har identifisert et nytt medikament – GLIX5 – som retter seg mot en tidligere ukjent genregulerings-metode og har en enestående svulst-minskende effekt. Dette legemiddelet har potensiale til å bli utviklet sammen med en sensitivitetsprediktiv biomarkør (SPB), som gir en unik pasientsentrert tilnærming for å utvikle effektive og personlige behandlingstiltak. Enda viktigere er at preliminære resultater har vist foreløpig god effekt mot et bredt spekter av forskjellige kreftformer, og viser potensiale for utbredt bruk i andre indikasjoner som også har et udekket behov for effektive terapier. I dette prosjektet tar vi sikte på å fremme den prekliniske utviklingen av GLIX5, samtidig som vi screener for andre foretrukne indikasjoner for denne behandlingen, gjennom en SPB-drevet tilnærming. Vår løsning svarer på det pressende behovet for smartere inngrep som gir bedre dekning, mer målrettet behandling og lavere utgifter knyttet til sykehusinnleggelse eller unødvendige behandlinger. Denne løsningen gir et vesentlig nytt terapeutisk alternativ som følger visjonen for presisjonsmedisin i klinisk praksis og gir EK-pasienter sjansen til flere viktige stunder sammen med familie og venner.

Cancer is the second-leading cause of death worldwide, representing a growing global health crisis and one of the most intractable diseases humanity has ever faced. For most cancers, only a small fraction of patients gets a meaningful benefit from current therapies, which means that most cancer-associated healthcare costs are “wasted” on ineffective treatments. Ovarian cancer (OC) remains essentially an incurable disease for which survival rates have only modestly improved, highlighting the urgent need to identify innovative strategies for its targeting. Hemispherian has identified a novel drug – GLIX5 – which targets a previously unknown DNA regulatory pathway with unprecedented anti-tumour efficacy. This drug has the potential to be co-developed with a sensitivity predictive biomarker (SPB), providing a one-of-a-kind patient-centric approach to devise effective and personalized treatment interventions. Importantly, GLIX5 has demonstrated preliminary strong efficacy against a broad range of different cancers, revealing its potential for widespread application in other indications with unmet need for effective therapies. In this project, we aim at advancing the preclinical development of GLIX5, while screening for other preferred indications for this treatment, through a SPB-driven approach. In addition, we will develop a new, scalable, and cost-efficient CMC process for GLIX5 synthesis and GMP production, which will precede pharmacological preclinical safety studies. Our solution answers the urgent need for smarter interventions that translate into better coverage, more targeted healthcare, and lower spending on hospitalization or unnecessary treatments. Crucially, this solution brings a new therapeutic option that follows the vision for precision medicine in clinical practice and offers OC patients the chance for more moments that matter, with family and friends.

GLIXOV: GLIX5 for Ovarian Cancer

Glioblastoma multiforme er det høyeste globale udekkede behovet innen onkologi. Glioblastoma multiforme (GBM) er den 17. største årsaken til kreft og den nest viktigste årsaken til kreft hos barn. På grunn av sin aggressive natur resulterer en diagnose med GBM i alvorlig reduksjon i livskvalitet, og sykdommen forårsaker raskt død. GBM er en ledende dødsårsak hos barn, nest etter trafikkskader i Vest-Europa og den tredje viktigste årsaken til barnedød i USA.

Gjennom et tiår med vitenskapelig forskning på DNA-basemodifikasjoner ved Oslo universitetssykehus, identifiserte vår sjefforsker og hans forskningsgruppe en tidligere ukjent reguleringsmekanisme for cellesyklus som pekte mot en ny DNA-replikasjonsreguleringsvei. Teamet utnyttet denne veien for å identifisere svært spesifikke antitumormedisiner og identifiserte noen få molekyler. En av disse molekylene viste seg å være spesielt god til å drepe GBM-svulster - GLIX1. Forskningsgruppen ledet det grunnleggende arbeidet som førte til innlevering av patentbeskyttelse for denne familien av forbindelser.

Gitt den meget positive og nylige utviklingen av GLIX1, tar Hemispherian nå sikte på å fremme dette legemidlet ved hjelp av en medisin-diagnostisk medutviklingsstrategi. Vi vil søke etter nye biomarkører som kan veilede kliniske utviklingsfaser. Etter fullføring av de prekliniske studiene vil GLIX1 gå inn i kliniske studier for behandling av GBM. Hemispherians langsiktige visjon er å kommersialisere en pasientsentrert tilnærming, ved å kombinere terapibeslutninger med molekylær innsikt -- et første i sitt slag medisin kombinert med det respektive diagnostiske verktøyet. Dette prosjektet er av strategisk betydning for Hemispherian. FoU-utfallet av dette prosjektet vil være en preklinisk validert ny legemiddelkandidat for GBM (medikamentell og følgesvenn diagnostisk analyse), klar for kliniske studier på mennesker (kliniske fase I-studier).

Today, patients diagnosed with glioblastoma (GBM) have limited treatment options. The current standard of care for GBM treatment is a combination of surgical resection, radiation, and one or more courses of generally ineffective chemotherapy. With the currently available treatment, the median overall survival of GBM patients is 13.9 months with 2-year survival of 22.5% and 5-year survival of 5.3%. Compounding the poor patient survival rates, currently available treatments often cause debilitating side-effects, resulting in poor quality of life. This poor patient survival rate and horrendous end-of-life quality highlights an urgent need to identify novel strategies to target GBM.
Through a decade of scientific research Hemispherian AS (HEMI) identified a molecule (GLIX1) that targets DNA replication and has been shown to kill GBM tumours. Furthermore, this molecule showed no side-effects and indicate a striking reduction in tumour mass or even total remission.
Building on very positive results and milestones reached until today, HEMI aims now to further advance the GLIX1 development by using a drug-diagnostic co-development model strategy, searching for new biomarkers that can guide clinical development phases, while also conducting preclinical studies, to determine if GLIX1 is safe for initial use in humans. To enable this work HEMI will lead a consortium of world-class partners (OUH, NTNU, UIO). 
HEMI’s long term vision is to commercialize a patient-centric approach, by combining therapy decisions with molecular insights, a first-of-a-kind drug combined with the respective diagnostic tool. 
Funding from IPN programme would allow the participating SME to strengthen its current market position, expanding its vision of bringing a new and effective drug to the oncology market.

GLIX1 - A new drug to treat glioblastoma multiforme (GBM)

Gliomas constitute 60% of all brain tumors and 50% of these are considered aggressive malignant tumors. Among aggressive gliomas, Glioblastoma multiforme (GBM) is the deadliest. Patients with GBM, which is the most frequent and malignant form of glioma, present a median overall survival of approximately 15 months after diagnosis. This is mainly due to the poor and unpredictable response to the standard-of-care therapy that includes radio- and chemotherapy, after surgical resection. Importantly, in children, GBM is the most frequent solid neoplastic disorder and the primary cancer-related cause of death.
Despite devastating prognosis, there are only 3 FDA approved drugs to treat GBM, all providing only marginal improvements of <5 months to patient survival, and there are no drugs approved for malignant pediatric brain tumors. The lack of therapies is primarily due to the inability of drugs to penetrate the blood-brain barrier (BBB), the greatest challenge in GBM drug development and the limiting factor to changing standard of care (SoC). In detail, primary treatment for newly diagnosed GBM consists of surgical resection and radiotherapy (RT) and one or more courses of generally ineffective chemotherapy; however, this intense treatment is limited to patients with high Karnofsky scores (low impairment). Even if there is complete tumor removal, GBM recurs in 80% of cases. Therefore, the goal of primary treatment is to alleviate symptoms associated with intracranial pressure and increase survival time.
In order to tackle this problem, Hemispherian has developed two promising lead compounds – called GLIX1 and GLIX5 respectively – that showed to be highly efficient in targeting GBM malignant cells. Unlike competitors (immunotherapies that can target, at best, 20-30% of the GBM population), GLIX1 – which is a nucleotide analogue – may target a novel mechanism that acts as a barrier to replication, enabling us to target most GBM patients, and other cancers in the future.

Travel to Find International Private Capital to finance development of Hemispherian's lead glioblastoma multiforme therapeutic

Hemispherian AS is developing a novel group of compounds to combat glioblastoma multiforme (GBM). These compounds have shown promising pre-clinical results and our lead compound GLIX1 will enter pre-IND studies by 2021.
The current process of synthesis for these compounds is expensive and not easily scalable, thus a new synthesis process needs to be developed and optimised. The SME Innovation Associate programme project is necessary for Hemispherian to initiate internal chemistry, manufacturing and control (CMC) activities to ensure the optimal synthesis method, and downstream purification and manufacturing processes, are developed at an early stage. 

Currently, we do not possess in-house expertise in production and process development of pharmaceuticals that are essential for this project and therefore looking to recruit an Innovation Associate with the required skill-set in CMC. Acquiring these skills is fundamental for Hemispherian to maintain a streamlined drug development process internally and maximise our chances for successful regulatory approval of our drug.

Hemispherian have identified a promising synthesis method which requires further development. The project will address this goal, with the overall objectives including:
- Optimise the chemical synthesis process along with purification scheme
- Small scale synthesis ramping up to larger scale synthesis in preparation for large quantities for clinical studies
- Overseeing use of drug in first pre-IND studies and establishing a regulatory pathway along with appropriate documentation
The most critical R&D challenges in this project include: developing a chemical synthesis method with high enough yield and any regulatory hurdles. These will be minimised by onboarding the skilled Innovation Associate to the team, and appropriate use of external experts in chemical manufacturing and regulatory affairs.

Chemical synthesis of a new drug family to treat glioblastoma multiforme (GBM), the highest global unmet need in oncology

Glioblastoma multiforme, et høyverdig gliom, er den mest utbredte og aggressive ondartede
svulst i sentralnervesystemet. Glioblastom multiforme er den ledende dødsårsaken av
sykdom hos barn. Med den nåværende tilgjengelige behandlingen, er den mediane samlede overlevelse av
Glioblastompasienter er 13,9 måneder med 2 års overlevelse på 22,5% og 5 års overlevelse på 5,3%.
Sammenligning av de fattige pasientoverlevelsesratene, forårsaker ofte tilgjengelige behandlinger ofte
svekkende bivirkninger, noe som resulterer i dårlig livskvalitet. Denne dårlige pasientens overlevelsesrate og
fryktelig utelatt kvalitet fremhever et presserende behov for å identifisere nye strategier for å målrette
glioblastom multiforme. Som nylig rapporterte og viktige opinionsledere antyder, er glioblastom multiforme a
lidelse med et av de høyest mulige behovene i onkologi. I samarbeid med verdensklasse
eurosurgeons og medisinske kjemikere vi tar sikte på å utvikle legemidler som
Vi har oppdaget å behandle glioblastom multiforme pasienter. Hemispherian
forskere har identifisert og fremmer to forbindelser som er svært effektive i
behandle disse dødelige hjernetumorene.

Treatment for the Glioblastoma Multiforme: the greatest unmet need in oncology - drug synthesis

Hemispherian Oncology (a subsidiary of Hemispherian AS) is an R&D-centric SME developing novel treatments for glioblastoma multiforme (GBM). GBM is the most common and aggressive malignant tumour of the central nervous system. Devastatingly, GBM is also the leading cause of death by disease in children.

We have made significant advances in developing a side-effect free treatment for GBM. We have two candidate compounds; both compounds are well tolerated in mice and are highly effective at reducing GBM tumour size in mouse models. Our primary aim of this project is to move these newly discovered anti-cancer molecules from the laboratory to the clinic in an effort to more effectively treat GBM patients. Our objectives can be summarized as follows:

1) Safety trials in animal models
2) Improved chemical synthesis process for cost-effective production of the molecules 
3) Preparing for clinical trials in humans

Funding from the Eurostars programme for this project is essential for Hemispherian to undertake these next costly, but vital steps in treatment development. To do this we require a collaborative effort from partnerships strategically placed in chemical manufacturing and drug development. Our objectives for this project to conduct safety trials in animal models, improve the chemical synthesis process of our molecules and preparations for human clinical trials represent significant R&D challenges in the establishment of this project. However, with our impressive track record in successful collaborations and partnerships we are confident that these challenges will not be barriers. We already have in place a partnership for chemical synthesis and have collaborations with multiple research institutions, both in Europe and further afield.

0 antall prosjekter

BIA-Brukerstyrt innovasjonsarena

GLIXOV: GLIX5 for Ovarian Cancer

Tildelt: kr 16,0 mill.

Prosjektperiode: 2024-2025

Sted: Oslo

BIA-Brukerstyrt innovasjonsarena

GLIX1 - A new drug to treat glioblastoma multiforme (GBM)

Tildelt: kr 14,6 mill.

Prosjektperiode: 2021-2023

Sted: Oslo

PES2020-Prosj.etabl.støtte H2020

Travel to Find International Private Capital to finance development of Hemispherian's lead glioblastoma multiforme therapeutic

Tildelt: kr 39 999

Prosjektperiode: 2020-2020

Sted: Oslo

PES2020-Prosj.etabl.støtte H2020

Chemical synthesis of a new drug family to treat glioblastoma multiforme (GBM), the highest global unmet need in oncology

Tildelt: kr 0,20 mill.

Prosjektperiode: 2019-2020

Sted: Oslo

FORNY20-FORNY2020

Treatment for the Glioblastoma Multiforme: the greatest unmet need in oncology - drug synthesis

Tildelt: kr 0,50 mill.

Prosjektperiode: 2019-2020

Sted: Oslo

PES2020-Prosj.etabl.støtte H2020

Killing a Killer: Bringing New Therapeutics for Glioblastoma Multiforme to Clinical Trials

Tildelt: kr 99 999

Prosjektperiode: 2018-2019

Sted: Oslo