Kunnskapskartlegging-produksjon av stor laksesmolt

Basert på forskning og erfaringer kan det gis noen anbefalinger for produksjon av storsmolt med tanke på sentrale produksjonsparametere i den landbaserte fasen av produksjonen. En temperatur på 10-12 °C anbefales for å sikre god vekst i sjøfase og redusere tidlig kjønnsmodning hos hannfisk. Det anbefales ikke å gå bort fra lysstyring for å indusere smoltifisering før det foreligger mer dokumentasjon på effekten av dette på prestasjon i sjø. En salinitet mellom 12-15 ppt er i mange studier oppgitt å gi optimal vekst, og ble av oppdrettere ansett for å gi færre problem med skinnhelse og sårdannelse, noe som også støttes av vitenskapelige funn. Men det er usikkert om 12-15 ppt er tilstrekkelig for å opprettholde sjøvannstoleranse i en storsmolt. Det anbefales at fisken akklimatiseres til temperaturen den skal settes ut på slik at endringen i temperatur blir maks 3-5 °C. Det er ikke anbefalt å sette ut storsmolt på kalde vintertemperaturer. Flere oppdrettere erfarer utfordringer med fiskevelferd hvis tettheten overstiger 65-70 kg/m3 og majoriteten mener at 65 kg/m3 er en god grenseverdi som ivaretar vannkvalitet og fiskehelse. En vannhastighet på om lag 1.0 kroppslengder per sekund, synes optimalt basert på vitenskapelige studier på postsmolt fra 60 og opp til 480 g. Vitenskapelige studier indikerer at verdier under 15 mg/L CO2 i brakkvann ikke gir en stor reduksjon i vekst, og er også anbefalt som grenseverdi av Mattilsynet

Na-K-ATPase regulates intercellular communication in the vascular wall via cSrc kinase-dependent connexin43 phosphorylation

Communication between vascular smooth muscle cells (VSMCs) is dependent on gap junctions and is regulated by the Na-K-ATPase. The Na-K-ATPase is therefore important for synchronized VSMC oscillatory activity, i.e., vasomotion. The signaling between the Na-K-ATPase and gap junctions is unknown. We tested here the hypothesis that this signaling involves cSrc kinase. Intercellular communication was assessed by membrane capacitance measurements of electrically coupled VSMCs. Vasomotion in isometric myograph, input resistance, and synchronized [Ca2+]i transients were used as readout for intercellular coupling in rat mesenteric small arteries in vitro. Phosphorylation of cSrc kinase and connexin43 (Cx43) were semiquantified by Western blotting. Micromole concentration of ouabain reduced the amplitude of norepinephrine-induced vasomotion and desynchronized Ca2+ transients in VSMC in the arterial wall. Ouabain also increased input resistance in the arterial wall. These effects of ouabain were antagonized by inhibition of tyrosine phosphorylation with genistein, PP2, and by an inhibitor of the Na-K-ATPase-dependent cSrc activation, pNaKtide. Moreover, inhibition of cSrc phosphorylation increased vasomotion amplitude and decreased the resistance between cells in the vascular wall. Ouabain inhibited the electrical coupling between A7r5 cells, but pNaKtide restored the electrical coupling. Ouabain increased cSrc autophosphorylation of tyrosine 418 (Y418) required for full catalytic activity whereas pNaKtide antagonized it. This cSrc activation was associated with Cx43 phosphorylation of tyrosine 265 (Y265). Our findings demonstrate that Na-K-ATPase regulates intercellular communication in the vascular wall via cSrc-dependent Cx43 tyrosine phosphorylation

Emotional faces processing in major depressive disorder and prediction of antidepressant treatment response: A NeuroPharm study

Background: Major depressive disorder (MDD) is a prevalent neuropsychiatric illness for which it is important to resolve underlying brain mechanisms. Current treatments are often unsuccessful, precipitating a need to identify predictive markers. Aim: We evaluated (1) alterations in brain responses to an emotional faces functional magnetic resonance imaging (fMRI) paradigm in individuals with MDD, compared to controls, (2) whether pretreatment brain responses predicted antidepressant treatment response, and (3) pre–post change in brain responses following treatment. Methods: Eighty-nine medication-free, depressed individuals and 115 healthy controls completed the fMRI paradigm. Depressed individuals completed a nonrandomized, open-label, 8-week treatment with escitalopram, including the option to switch to duloxetine after 4 weeks. We examined patient–control group differences in regional fMRI responses at baseline, whether baseline fMRI responses predicted treatment response at 8 weeks, including early life stress moderating effects, and change in fMRI responses in 36 depressed individuals rescanned following 8 weeks of treatment. Results: Task reaction time was 5% slower in patients. Multiple brain regions showed significant task-related responses, but we observed no statistically significant patient–control group differences (Cohen’s d < 0.35). Patient pretreatment brain responses did not predict antidepressant treatment response (area under the curve of the receiver operator characteristic (AUC-ROC) < 0.6) and brain responses were not statistically significantly changed after treatment (Cohen’s d < 0.33). Conclusion: This represents the largest prediction study to date examining emotional faces fMRI features as predictors of antidepressant treatment response. Brain response to this fMRI emotional faces paradigm did not distinguish depressed individuals from healthy controls, nor was it predictive of antidepressant treatment response. Clinical Trial Registration: Site: https://clinicaltrials.gov, Trial Number: NCT02869035, Trial Title: Treatment Outcome in Major Depressive Disorder