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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

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

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

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

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.

Bilingual Experiences, Cognitive Ageing and underlying Mechanisms

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.

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

Rundt 7% av norske 4-åringer har så store psykiske vansker at de kvalifiserer for en diagnose, men det tar ofte lang tid fra vanskene oppstår, til de blir oppdaget og barna får rett hjelp. Myndighetene har derfor lagt tydelige føringer for at de som jobber med barn, må vite hva de skal se etter og hvordan de skal gå frem for at barna skal få den hjelpen de trenger. I Norge går over 95% av barna i barnehage hvor pedagogene blir godt kjent med barna over tid i deres naturlige miljø og har utviklingssamtaler med de foresatte 1-2 ganger i året. Barnehagen skulle derfor være en ideell arena for tidlig oppdagelse av psykiske vansker. Det har imidlertid ikke vært tilgjengelig noen tilpasset metode for de arbeidsformene og terminologi som er vanlig i barnehagene. Vi har derfor utviklet metoden Dialogbasert tidlig oppdagelse (DBTO) i nært samarbeid med pedagoger og foreldre i 8 ulike barnehager. Metoden går ut på å bruke utviklingssamtalen mer systematisk ved at både foreldre og barnehagelærer på forhånd fyller ut et spørreskjema om mulige bekymringer de har hatt for barnets utvikling og trivsel de siste månedene. I samtalen kan de så utforske og forsøke å enes om forståelsen av barnet og om det er behov for ytterligere vurdering eller andre tiltak. Tilbakemeldingene under utviklingen og tidlig utprøving tyder på at metoden fungerer godt og oppleves som et nyttig verktøy i foreldresamarbeidet. For å få tydeligere dokumentert kunnskap om hvordan DBTO fungerer i barnehagene, har vi utviklet forskningsprosjektet PRO-DIALOG. Vi ønsker med det å få kunnskap om (1) hvordan DBTO fungerer som et screening-instrument, (2) hvor brukervennlig den er, (3) hvordan den påvirker tidspunkt for igangsetting av tiltak og (4) hvordan den påvirker utviklingen av den psykiske helsen til barna over tid. 12 barnehager er plukket tilfeldig ut til å gjennomføre metoden, mens 11 skal fungere som kontroller. Foresatte til rundt 300 barn som har tre år igjen av barnehagen, vil bli spurt om å delta.

There is an unambiguous call for early interventions at the municipal level for children at risk of developing mental health problems. However, there is a surprisingly absence of socially valid methods for detecting children in need of early support.
        The aim of the project is to establish the properties of such a novel method; Dialogue Based Early Detection (DBED). We will study its properties as a mental health screener, how well it is adapted in an ordinary kindergarten context, and whether it affects activation of interventions for mental health concerns and children’s future mental health.
        The novel aspect of DBED is the systematic assessment of the child’s development and well-being by the kindergarten teacher and his/her parents, and the subsequent dialogue that aims to explore and converge their understanding of the child and conclude whether there is a need for further assessment or supportive actions.
        Parents of approximately 300 children in 23 different kindergartens aged 2-3 years will be invited to participate for the three last years before school start and follow-up the next two years. The kindergartens will be randomized to an implementation group or a control group. Parents’ socio-demographic characteristics and data from parent-teacher meetings, initiated interventions, user satisfaction, parental stress, and child mental health will be collected biannually, as well as tape recordings from interviews about user experiences of parents and teachers.
        The most critical challenges of the project will be participation rate of the invited parents in addition to attrition due to the time pressures in a busy workday in the kindergartens, and willingness of the control parents to complete the repeated questionnaires. Appropriate measures are made to take those risks into account.

Promoting mental health in young children – a sustainable dialogue based approach in kindergartens (PRO-DIALOG)

Midlene fra BIO-1.02.Food, Agriculture and Fisheries, and Biotechnology fordelt på år

Midlene fra BIO-1.02.Food, Agriculture and Fisheries, and Biotechnology fordelt på fylker

Midlene fra BIO-1.02.Food, Agriculture and Fisheries, and Biotechnology fordelt på fagområde

Ecosystem-based Responsive Fisheries Management in Europe

We apply for a grant from the DAAD and the Norwegian Research council (NRC) for travel and accommodation to discuss and develop common projects in the field of pain and treatment of pain between the Central Institute of Mental Health, Mannheim, Germany, a nd the University of Tromsø, Norway. 
Pain is the most common symptom in patients seeking treatment from health care personnel. Almost all treatment induces an expectation of relief, and expectations alone, in the absence of active treatment, have been sh own to reduce pain. This is termed placebo analgesia, and is an example of how the brain controls bodily function. 
At present, the group in Norway of Magne Flaten is developing models to test the effects of psychological processes (learning, expectations , emotions) in samples of patients with chronic pain, and this is the background for the present proposal. 
The group of Herta Flor at the CIMH in Germany is currently involved in a research group funded by the German Research Foundation which focuses mai nly on the placebo effect. The underlying mechanisms of the placebo effects are still unclear. Two explanatory psychological mechanisms have been discussed with respect to placebo and nocebo effects: expectancy theory  and classical conditioning. 
The pro jects conducted at both locations (Mannheim & Tromsø) aim to describe the psychobiological mechanisms underlying the modulation of pain, and try to implement this knowledge in treatment programmes for chronic pain. 
The aim of the mutual visits is to deve lop experimental designs that examine the specific influence on learning on the placebo response and to test these effects in patient populations and thus combine the two research paths into one common project that aims to translate the basic research que stions about placebo analgesia with clinical applications.

PAIN: PSYCHOBIOLOGICAL MECHANISMS AND THEIR RELEVANCE FOR TREATMENT

It is applied for a conference on imaging in neuroscience research in Tromsø 14-15/5 2009. The aim of the conference is to establish contacts between researchers, firstly at a national, but also at an international level. The conference will target areas that are relevant for ongoing research in Norway. The intention is to strengthen the neuroscience milieus working in Tromsø and at the other universities and hospitals, and to introduce imaging methods in research that at present is not using these method s. The conference is a follow-up to the first International Conference on Imaging in Neuroscience in Tromsø in April 2007. 

The conference will target four themes. The program and proposed speakers are described in more detail in the application
1. Affec tive and cognitive neuroscience

2. Brain imaging in psychiatric research

3. Signal processing methods

4. Brain imaging of pain and pain modulation

All speakers will be asked to reply within November 1st 2008. 

The organizing committee: Magne Arve Fla ten (chair), Svein Dahl, Trond Bratlid, Torbjørn Eltoft, Torgil Vangberg, Niels Chr. Stenklev, Ingebrigt Sylte, Wenche Heia (adm.), Turid Klokkervoll (adm.), and Bente Brunvold (conference secretary).

Programme committee: Svein Dahl (chair), Trond Bratli d, Torbjørn Eltoft, Niels Christian Stenklev,Lars Folkow, Magne Arve Flaten, Svein Ivar Mellgren, Ingebrigt Sylte, Kenneth Hugdahl, Joel Glover, Annemie van der Linden and Olav Haraldset

Second International Conference on Imaging in Neuroscience

The relationship between the pain stimulus (wounds, lesions, external stimuli) and experienced pain can be modified by the context in which pain occurs: Some patients can have intolerable pain but without any physiological sign of damage. On the other han d, severe wounds may not cause pain under certain conditions, e.g. under high stress. Pain seems to be modulated by the context in which it is experienced. One especially intriguing form of pain modulation is placebo analgesia, the reduction of pain after  information that a painkiller has been administrated, even if placebo is administrated. This is thought to be due to expectations that pain will be reduced. It is unclear, however, how a cognitive process like expectancy can mediate reduced pain. We prop ose that expectancies mediate reduced pain via affective mechanisms: Expectancies of reduced pain should reduce stress, which is associated with reduced pain. Four experiments that test this hypothesis is presented: Participants are chronic pain patients and healthy volunteers. Pain is either clinical or experimentally induced by thermal stimulation. Emotions are induced experimentally by use of emotional pictures and video. Pain and subjective stress are registered by visual analogue scales and questionn aires. Physiological indices of stress and emotions are startle reflex modification, skin conductance, cortisol, catecholamines, and beta-endorphin levels.

Emotional factors and individual differences in placebo analgesia. Psychophysiological experiments.

This is a research project on how environmental contingencies can modify drug responses, through the mechanism of drug expectancy. 
	Drug expectancy refers to the belief or expectation that symptoms should decrease or disappear after a specific treatment.  Thus, a person experiencing, e.g., a toothache, expects the pain to subside after ingestion of a painkiller. Such beliefs are part of almost all treatments, and were the reason for the introduction of the double-blind method, the current gold standard, i n drug trials. There is an ambivalence in this: by excluding the role of expectations in the study of drug effects, one treats expectations as a source of error that needs to be controlled or removed. On the other hand, this implies that expectations may affect the results after drug treatment. 
	Drug expectations may have two consequences in addition to the placebo effect: 1. They may modify the drug response. Thus, expectations of drug effects may increase the drug effect, or may even decrease the drug effect under other conditions. This latter phenomenon is known as associative drug tolerance and has been widely studied in animals. 2. Drug expectations may interact with the drug effect. This is known as active placebo and there are virtually no publish ed studies on this theme. This is not an instance where expectations increase the drug response, but rather the other way around. The drug response is thought to potentiate the placebo effect.

NA - DRUG EFFECTS AND DRUG EXPECTANCY

It is applied for a conference on imaging in neuroscience research in Tromsø 26-27/4 2007. The aim of the conference is to establish contacts between researchers, firstly at a national, but also at an international level. The conference will target areas that are relevant for ongoing research in Norway. The intention is to strengthen the neuroscience milieus working in Tromsø and at the other universities and hospitals, and to introduce imaging methods in research that at present is not using these method s. 

The conference will target four themes: EEG/ERP, fMRI, PET, and cellular and molecular imaging. 

PRELIMINARY PROGRAM
Thursday 26th April
Introduction Svein Dahl and Magne Arve Flaten, UiTø
Cognitive function assessed by fMRI, K. Hughdal, UiB (confir med)
fMRI applications, O. Haraldseth, NTNU (confirmed)

PET applications	F. Willoch (confirmed)
Cognitive function and PET	Lars Nyberg, Umeå University
Title will be announced	Lars Farde, Karolinska Institutionen

Friday 27th April

Cognitive function an d ERP, Risto Näätänen, Helsinki University
EEG and ERP in the study of pain, Lars Arendt Nielsen, Aalborg University
ERP in the study of regeneration of sensory cells, Niels Christian Stenklev, UNN (confirmed)

Mats Ulfendahl, Karolinska Institutionen (co nfirmed)
Ingebrigt Sylte, UiTø (confirmed)
Joel Glover, UiO (confirmed)
Claus Müller, Max Plank, Berlin (confirmed)
May-Britt or Edvard Moser, NTNU
Sigurd Lindal, UiTø


All speakers have been invited and asked to reply within November 1st 2006. 

The org anizing committee: Magne Arve Flaten (chair), Svein Dahl, Trond Bratlid, Torbjørn Eltoft, Wenche Heia (adm.), Turid Klokkervoll (adm.), and Bente Brunvold (conference secretary).

Programme committee: Svein Dahl (chair), Trond Bratlid, Torbjørn Eltoft, Ni els Christian Stenklev,Lars Folkow, Magne Arve Flaten, Svein Ivar Mellgren, Ingebrigt Sylte, Robert Jenssen, Kenneth Hugdahl, Joel Glover, and Olav Haraldseth

Tromsø Conference on Imaging in Neuroscience

The dynamics of fear

Informasjon om virkninga til eit legemiddel kan indusere psykologiske og fysiologiske endringar i organismen, sjølv om "legemiddelet" er ein inaktiv substans eller placebo. For eksempel kan informasjon om at ein kapsel eller injeksjon virkar smertedempand e produsere smertelindring, og informasjon om at eit preparat virkar avslappande kan redusere psykologisk og fysiologisk aktivering sjølv om placebo administrerast. Dette er placebo responsen. Prosjektet undersøker mekanismene i placebo responsen ved å un dersøke følgande problemstillingar: 
<h>1. Kan placebo responsen forklarast ved at informasjon om legemiddelet sin effekt endrar aktiveringsnivå, f.eks. endrar fysiologisk aktivering, og dermed endrar absorpsjon av legemiddelet til blod? Korleis interager er placebo responsen med legemiddelet? Vil sterkare placebo reaksjonar observerast hos personar som får aktivt legemiddel? 
<h>2. Vil stimuli som er assosiert med inntak av eit legemiddel, f.eks. smak eller lukt av legemiddelet, produsere dei samme effekt ene som legemiddelet? Kan slike betinga stimuli også produsere effekter som er motsette til legemiddelet, såkalte nocebo responsar, og bevirke toleranse? 
<h>3. Kroppen sitt eige morfin, endorfinene, har sannsynligvis ei viktig rolle i placebo smertelindr ing, og vi er dei første som har undersøkt dette direkte. Ein ønsker å undersøke under kva for betingelsar endorfiner utskillast og bidrar til smertelindring.

0 projects

IS-DAAD-Forskerutveksl. Norge-Tyskland

PAIN: PSYCHOBIOLOGICAL MECHANISMS AND THEIR RELEVANCE FOR TREATMENT

Awarded: NOK 60,000

Project Period: 2011-2013

Location: Troms - Romsa - Tromssa

NEVRONOR-Nasjonal satsing på nevrovitenskap f

Second International Conference on Imaging in Neuroscience

Awarded: NOK 0.40 mill.

Project Period: 2009-2009

Location: Troms - Romsa - Tromssa

FRIMED-Klinisk medisin og folkehelse

Emotional factors and individual differences in placebo analgesia. Psychophysiological experiments.

Awarded: NOK 2.5 mill.

Project Period: 2006-2010

Location: Troms - Romsa - Tromssa

INT-BILAT-BILAT-ordningen

NA - DRUG EFFECTS AND DRUG EXPECTANCY

Awarded: NOK 95,109

Project Period: 2006-2008

Location: Troms - Romsa - Tromssa

NEVRONOR-Nasjonal satsing på nevrovitenskap f

Tromsø Conference on Imaging in Neuroscience

Awarded: NOK 0.40 mill.

Project Period: 2006-2007

Location: Troms - Romsa - Tromssa

FRIMED-Klinisk medisin og folkehelse

The dynamics of fear

Awarded: NOK 2.0 mill.

Project Period: 2004-2008

Location: Troms - Romsa - Tromssa

MENTAL-Mental helse

Mekanismer bak placeboresponsen

Awarded: NOK 1.2 mill.

Project Period: 2001-2004

Location: Troms - Romsa - Tromssa