Poor feeding opportunities and reduced condition factor for salmon post-smolts in the Northeast Atlantic Ocean

During the last few decades, many wild Atlantic salmon populations have declined dramatically. One possible contributing factor for the decline is reduced prey availability at sea. Here, we examine post-smolt diet and investigate if post-smolts show signs of selective feeding based on 2546 post-smolts sampled from west of Ireland to the northern Norwegian Sea over a 25-year period. We also test for changes over time in stomach fullness, diet, condition factor and body length. There was a clear reduction in condition factor for post-smolts sampled in the Norwegian Sea in the period 2003–2012. The post-smolt stomach fullness was also reduced in the same period. The reduction in condition factor is partly explained by reduced stomach fullness, including a reduction of highly energetic fish larvae and Amphipoda in the diet. Feeding on other prey, such as meso-zooplankton and insects, cannot substitute the high-quality fish larvae and Amphipoda in the post-smolt diet. This is the first study to document how salmon post-smolts feeding in the Norwegian Sea are affected by reduced feeding conditions. Possible causes for the observed changes in post-smolt feeding are ocean warming, decreased primary productivity, and reduced recruitment of important fish larvae.publishedVersio

Stoler vi mer på menneskers intuisjon dersom de beskriver seg selv som intuitive?

Hensikten med oppgaven er å undersøke om vi stoler på andre menneskers intuisjon dersom de beskriver seg selv som intuitive. Gjennom en historisk tidslinje, tar eksisterende teori om intuisjon for seg både intuisjon som et fenomen, ledelsesforskning på intuisjon og hvordan det fungerer i praksis. Teorien belyser også hvordan kjønn og intuisjon henger sammen, og om det er finnes noen forklarende forskjeller her. Basert på teorien ble det utviklet to hypoteser, der mellomgruppeforskjeller ble testet i resultatet. Oppgaven er forankret i kvantitativ metode, og det har blitt utført et eksperiment med 133 voksne deltakere i arbeid. I eksperimentet ble det undersøkt hvilket medikament deltakerne ville valgt sett ut ifra to uavhengige variabler som var randomisert i en vignett. Deltakernes holdninger rundt egne intuitive og rasjonelle evner og preferanser ble målt for å teste sammenhengen mellom tillit og intuisjon, samt om kjønn ville ha en påvirkning. Resultatet viste at legens beskrivelse av seg selv som intuitiv ikke har en påvirkning på respondentenes valg av medikament. Betingelsen kjønn har i henhold til resultatet heller ingen effekt på valget. Det foreligger derimot en sterk korrelasjon mellom intuitive evner og intuitiv preferanse, samt rasjonelle evner og rasjonell preferanse. Dette funnet støttes av eksisterende teori om emnet. Konklusjonen belyser viktigheten av lederes bruk av intuisjon i kombinasjon med rasjonalitet i beslutningstaking og hvordan dette kan påvirke organisatoriske faktorer som effektivitet og resultat. Et viktig poeng er at ledere må anerkjenne hvordan andre ser på hans eller hennes intuisjon for at intuisjon skal være et nyttig verktøy. Det er også sentralt at fokuset flyttes fra individ og kjønn over på oppgaven som foreligger

Sosial inkludering for elever som mottar spesialundervisning. "Det er ikke barna som er spesielle, de har ikke spesielle behov, men de har noen behov som er spesielle"

Temaet for oppgaven vår, er å se på hvordan skolehverdagen ser ut for de elevene som mottar spesialundervisning. Hovedfokuset ligger på klassetilhørighet, og vår problemstilling er som følger: Hvordan ivaretar Fjæra skole sosial inkludering for elever som mottar spesialundervisning? For å svare på problemstillingen har vi samlet empiri ved Fjæra skole, vi ønsket å få reell tilgang til feltet, og var bevisste på å ha både formell og uformell kontakt med våre informanter. Vi anvendte metodene intervju og observasjon innenfor de kvalitative forskningsdesignene, fenomenologi og casedesign. Fjæra skole hadde utviklet en egen modell for spesialundervisning, der det sentrale innholdet var få ansatte med ansvar for spesialundervisning, samt segregerte tilbud i form av intensive kurs. Modellen var fleksibel, der elevenes behov for deltakelse i klassefellesskapet var fremtredende. Det sosiale innholdet var viktig, og de arbeidet kontinuerlig med åpenhet og holdninger. Vi har drøftet empirien opp mot intensjoner og realiteter, der blant annet styringsdokumenter og rapporter har dannet vårt teorigrunnlag. Våre resultater viser at klassefellesskapet danner grunnlaget for sosial inkludering. Fjæra skole fremmer deltakelse på sosiale arenaer, gjennom sin organisering av spesialundervisning. Undervisningen tar utgangspunkt i elevenes behov, og de intensive kursene fremstår som inkluderende segregerte tilbud

The STARTEC decision support tool for better tradeoffs between food safety, quality, nutrition, and costs in production of advanced ready-to-eat foods

A prototype decision support IT-tool for the food industry was developed in the STARTEC project. Typical processes and decision steps were mapped using real life production scenarios of participating food companies manufacturing complex ready-to-eat foods. Companies looked for a more integrated approach when making food safety decisions that would align with existing HACCP systems. The tool was designed with shelf life assessments and data on safety, quality, and costs, using a pasta salad meal as a case product. The process flow chart was used as starting point, with simulation options at each process step. Key parameters like pH, water activity, costs of ingredients and salaries, and default models for calculations of Listeria monocytogenes, quality scores, and vitamin C, were placed in an interactive database. Customization of the models and settings was possible on the user-interface. The simulation module outputs were provided as detailed curves or categorized as "good"; "sufficient"; or "corrective action needed" based on threshold limit values set by the user. Possible corrective actions were suggested by the system. The tool was tested and approved by end-users based on selected ready-to-eat food products. Compared to other decision support tools, the STARTEC-tool is product-specific and multidisciplinary and includes interpretation and targeted recommendations for end-users

Mutations in MAPKBP1 cause late onset cilia-independent nephronophthisis

Nephronophthisis (NPH), an autosomal recessive tubulointerstitial nephritis, is the most common cause of heriditary end-stage renal disease in the first three decades of life. Since most NPH gene products (NPHP) function at the primary cilium, NPH is classified as ciliopathy. We identified mutations in a novel candidate gene in 10 individuals from 6 families presenting late onset NPH with massive renal fibrosis. This gene encodes MAPKBP1, a poorly characterized scaffolding protein for JNK signaling. Immunofluorescence analyses showed that MAPKBP1 is not present at the primary cilium and that fibroblasts from affected individuals did not display ciliogenesis defects indicating that MAPKBP1 may represent a new family of NPHP not involved in cilia-associated functions. Instead, MAPKBP1 is recruited to mitotic spindle poles (MSPs) during the early phases of mitosis where it colocalizes with its paralog WDR62, which plays a key role at MSP. Detected mutations compromise recruitment of MAPKBP1 to the MSP and/or its interaction with JNK2 or WDR62. Additionally, we show increased DNA damage response signaling in patients fibroblasts and upon knockdown of Mapkbp1 in murine cell lines, a phenotype previously associated with NPH. In conclusion, we identified mutations in MAPKBP1 as a genetic cause of late onset and cilia-independent NPH and propose “NPHP21” as an alias for MAPKBP1

Mutations in MAPKBP1 Cause Juvenile or Late-Onset Cilia-Independent Nephronophthisis

Nephronophthisis (NPH), an autosomal-recessive tubulointerstitial nephritis, is the most common cause of hereditary end-stage renal disease in the first three decades of life. Since most NPH gene products (NPHP) function at the primary cilium, NPH is classified as a ciliopathy. We identified mutations in a candidate gene in eight individuals from five families presenting late-onset NPH with massive renal fibrosis. This gene encodes MAPKBP1, a poorly characterized scaffolding protein for JNK signaling. Immunofluorescence analyses showed that MAPKBP1 is not present at the primary cilium and that fibroblasts from affected individuals did not display ciliogenesis defects, indicating that MAPKBP1 may represent a new family of NPHP not involved in cilia-associated functions. Instead, MAPKBP1 is recruited to mitotic spindle poles (MSPs) during the early phases of mitosis where it colocalizes with its paralog WDR62, which plays a key role at MSP. Detected mutations compromise recruitment of MAPKBP1 to the MSP and/or its interaction with JNK2 or WDR62. Additionally, we show increased DNA damage response signaling in fibroblasts from affected individuals and upon knockdown of Mapkbpl in murine cell lines, a phenotype previously associated with NPH. In conclusion, we identified mutations in MAPKBP1 as a genetic cause of juvenile or late-onset and cilia-independent NPH

Mutations in MAPKBP1 Cause Juvenile or Late-Onset Cilia-Independent Nephronophthisis

Nephronophthisis (NPH), an autosomal-recessive tubulointerstitial nephritis, is the most common cause of hereditary end-stage renal disease in the first three decades of life. Since most NPH gene products (NPHP) function at the primary cilium, NPH is classified as a ciliopathy. We identified mutations in a candidate gene in eight individuals from five families presenting late-onset NPH with massive renal fibrosis. This gene encodes MAPKBP1, a poorly characterized scaffolding protein for JNK signaling. Immunofluorescence analyses showed that MAPKBP1 is not present at the primary cilium and that fibroblasts from affected individuals did not display ciliogenesis defects, indicating that MAPKBP1 may represent a new family of NPHP not involved in cilia-associated functions. Instead, MAPKBP1 is recruited to mitotic spindle poles (MSPs) during the early phases of mitosis where it colocalizes with its paralog WDR62, which plays a key role at MSP. Detected mutations compromise recruitment of MAPKBP1 to the MSP and/or its interaction with JNK2 or WDR62. Additionally, we show increased DNA damage response signaling in fibroblasts from affected individuals and upon knockdown of Mapkbp1 in murine cell lines, a phenotype previously associated with NPH. In conclusion, we identified mutations in MAPKBP1 as a genetic cause of juvenile or late-onset and cilia-independent NPH