Overvåking av Ytre Oslofjord - Bentosundersøkelser 2009. Fagrapport

Det ble i 2009 gjennomført undersøkelser på bløtbunn med SPI kamera og rammeundersøkelser i fjæra i Ytre Oslofjord. Generelt var bunnforholdene i de åpne delene av fjorden meget gode eller gode (tilstandsklasse I og II) og det er liten variasjon mellom årene 2007 til 2009 på de fleste stasjoner. Større problemområder er Drammensfjorden, Horten havn, Tønsberg, Frierfjorden og Iddefjorden. Til sammen ble det registrert 50 taksa av alger og 39 taksa av dyr på de 10 fjærestasjonene som ble undersøkt i 2009. I Larviksfjorden var det fattig med både alger og dyr, og det var her de største grønnalgeforekomstene ble registrert. Stasjonene i ytre Drammensfjord, i Larviksfjorden og i Løperen har lav saltholdighet i overflaten og det er sannsynligvis derfor de har få dyretaksa i det øvre nivåe

Overvåking av Ytre Oslofjord - Bentosundersøkelser 2009. Fagrapport

Det ble i 2009 gjennomført undersøkelser på bløtbunn med SPI kamera og rammeundersøkelser i fjæra i Ytre Oslofjord. Generelt var bunnforholdene i de åpne delene av fjorden meget gode eller gode (tilstandsklasse I og II) og det er liten variasjon mellom årene 2007 til 2009 på de fleste stasjoner. Større problemområder er Drammensfjorden, Horten havn, Tønsberg, Frierfjorden og Iddefjorden. Til sammen ble det registrert 50 taksa av alger og 39 taksa av dyr på de 10 fjærestasjonene som ble undersøkt i 2009. I Larviksfjorden var det fattig med både alger og dyr, og det var her de største grønnalgeforekomstene ble registrert. Stasjonene i ytre Drammensfjord, i Larviksfjorden og i Løperen har lav saltholdighet i overflaten og det er sannsynligvis derfor de har få dyretaksa i det øvre nivåetFagrådet for Ytre Oslofjord, Klima -og forurensningsdirektoratet. Bjørn Svendsen er Fagrådets kontaktperso

Proresolving and cartilage-protective actions of resolvin D1 in inflammatory arthritis

Rheumatoid arthritis (RA) is a debilitating disease characterized by persistent accumulation of leukocytes within the articular cavity and synovial tissue. Metabololipidomic profiling of arthritic joints from omega-3 supplemented mice identified elevated levels of specialized proresolving lipid mediators (SPM) including resolvin D1 (RvD1). Profiling of human RA synovial fluid revealed physiological levels of RvD1, which - once applied to human neutrophils - attenuated chemotaxis. These results prompted analyses of the antiarthritic properties of RvD1 in a model of murine inflammatory arthritis. The stable epimer 17R-RvD1 (100 ng/day) significantly attenuated arthritis severity, cachexia, hind-paw edema, and paw leukocyte infiltration and shortened the remission interval. Metabololipidomic profiling in arthritic joints revealed 17R-RvD1 significantly reduced PGE2 biosynthesis, while increasing levels of protective SPM. Molecular analyses indicated that 17R-RvD1 enhanced expression of genes associated with cartilage matrix synthesis, and direct intraarticular treatment induced chondroprotection. Joint protective actions of 17R-RvD1 were abolished in RvD1 receptor-deficient mice termed ALX/fpr2/3-/- . These investigations open new therapeutic avenues for inflammatory joint diseases, providing mechanistic substance for the benefits of omega-3 supplementation in RA

Annexin A1 attenuates cardiac diastolic dysfunction in mice with inflammatory arthritis.

Rheumatoid arthritis (RA) carries a twofold increased incidence of heart failure with preserved ejection fraction, accompanied by diastolic dysfunction, which can lead to death. The causes of diastolic dysfunction are unknown, and there are currently no well-characterized animal models for studying these mechanisms. Current medications for RA do not have marked beneficial cardio-protective effects. K/BxN F1 progeny and KRN control mice were analyzed over time for arthritis development, monitoring left ventricular diastolic and systolic function using echocardiography. Excised hearts were analyzed by flow cytometry, qPCR, and histology. In pharmacological experiments, K/BxN F1 mice were treated with human recombinant AnxA1 (hrAnxA1, 1 μg/mouse) or vehicle daily. K/BxN F1 mice exhibited fully developed arthritis with normal cardiac function at 4 wk; however, by week 8, all mice displayed left ventricular diastolic dysfunction with preserved ejection fraction. This dysfunction was associated with cardiac hypertrophy, myocardial inflammation and fibrosis, and inflammatory markers. Daily treatment of K/BxN F1 mice with hrAnxA1 from weeks 4 to 8 halted progression of the diastolic dysfunction. The treatment reduced cardiac transcripts of proinflammatory cytokines and profibrotic markers. At the cellular level, hrAnxA1 decreased activated T cells and increased MHC IIlow macrophage infiltration in K/BxN F1 hearts. Similar effects were obtained when hrAnxA1 was administered from week 8 to week 15. We describe an animal model of inflammatory arthritis that recapitulates the cardiomyopathy of RA. Treatment with hrAnxA1 after disease onset corrected the diastolic dysfunction through modulation of both fibroblast and inflammatory cell phenotype within the heart

Targeting Extracellular Vesicles to the Arthritic Joint using a Damaged Cartilage Specific Antibody

The targeted delivery of therapies to diseased tissues offers a safe opportunity to achieve optimal efficacy whilst limiting systemic exposure. These considerations apply to many disease indications, but are especially relevant for rheumatoid arthritis (RA), as RA is a systemic autoimmune disease which affects multiple joints. We have identified an antibody that is specific to damaged arthritic cartilage (anti-ROS-CII) that can be used to deliver treatments specifically to arthritic joints, yielding augmented efficacy in experimental arthritis. In the current study, we demonstrate that scaffold enriched with bioactive payloads can be delivered precisely to an inflamed joint and achieve superior efficacy outcomes consistent with the pharmacological properties of these payloads. As a scaffold, we have used extracellular vesicles (EV) prepared from human neutrophils (PMN), which possess intrinsic anti-inflammatory properties and the ability to penetrate inflamed arthritic cartilage. EV fortified with anti-ROS-CII (EV/anti-ROS-CII) retained anti-ROS-CII specificity and bound exclusively to the damaged cartilage. Following systemic administration EV/anti-ROS-CII: a) exhibited the ability to localise specifically in the arthritic joint in vivo and b) was able to specifically target single (viral IL-10 or anti-TNF) or combined (viral IL-10 and anti-TNF) anti-inflammatory treatments to the arthritic joint, which accelerated attenuation of clinical and synovial inflammation. Overall, this study demonstrates the attainability of targeting a pro-resolving biological scaffold to the arthritic joint. The potential of targeting scaffolds such as EV, nanoparticles or combination thereof alongside combined therapeutics is paramount for designing systemically administered broad-spectrum of anti-inflammatory treatments