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Sökning: L773:1476 9255 > (2015-2019)

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2.
  • Alehagen, Urban, et al. (författare)
  • Decrease in inflammatory biomarker concentration by intervention with selenium and coenzyme Q10 : a subanalysis of osteopontin, osteoprotergerin, TNFr1, TNFr2 and TWEAK
  • 2019
  • Ingår i: Journal of Inflammation. - : Springer Science and Business Media LLC. - 1476-9255. ; 16
  • Tidskriftsartikel (refereegranskat)abstract
    • Background:Inflammation is central to the pathogenesis of many diseases. Supplementation with selenium and coenzyme Q10 has been shown to reduce cardiovascular mortality, and increase cardiac function in elderly persons with a low intake of selenium. There are indications that one of the mechanisms of this positive effect is a decrease in inflammation.Methods:Osteopontin, osteoprotegerin, sTNF receptor 1, sTNF receptor 2 and the tumor necrosis factor-like weak inducer of apoptosis called TWEAK, were determined in plasma after 6 months and 42months in 219 community-living elderly persons, of whom 119 received supplements of selenium (200g/day) and coenzyme Q10 (200mg/day), and 101 received a placebo. Repeated measures of variance were used to evaluate the levels, and the results were validated through ANCOVA analyses with adjustments for important covariates.Results:Significantly lower concentrations of four of the five biomarkers for inflammation were observed as a result of the intervention with the supplements. Only TWEAK did not show significant differences.Conclusion:In this sub-analysis of the intervention with selenium and coenzyme Q10 or placebo in an elderly community-living population, biomarkers for inflammation were evaluated. A significantly lower concentration in four of the five biomarkers tested could be demonstrated as a result of the supplementation, indicating a robust effect on the inflammatory system. The decrease in inflammation could be one of the mechanisms behind the positive clinical results on reduced cardiovascular morbidity and mortality reported earlier as a result of the intervention. The study is small and should be regarded as hypothesis-generating, but nonetheless adds important data about mechanisms presently known to increase the risk of clinical effects such as reduced cardiovascular mortality, increased cardiac function and better health-related quality of life scoring, as previously demonstrated in the active treatment group.
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3.
  • Hansson, Elisabeth, 1955, et al. (författare)
  • Coupled cell networks are target cells of inflammation, which can spread between different body organs and develop into systemic chronic inflammation
  • 2015
  • Ingår i: Journal of Inflammation-London. - : Springer Science and Business Media LLC. - 1476-9255. ; 12
  • Forskningsöversikt (refereegranskat)abstract
    • Several organs in the body comprise cells coupled into networks. These cells have in common that they are excitable but do not express action potentials. Furthermore, they are equipped with Ca2+ signaling systems, which can be intercellular and/or extracellular. The transport of small molecules between the cells occurs through gap junctions comprising connexin 43. Examples of cells coupled into networks include astrocytes, keratinocytes, chondrocytes, synovial fibroblasts, osteoblasts, connective tissue cells, cardiac and corneal fibroblasts, myofibroblasts, hepatocytes, and different types of glandular cells. These cells are targets for inflammation, which can be initiated after injury or in disease. If the inflammation reaches the CNS, it develops into neuroinflammation and can be of importance in the development of systemic chronic inflammation, which can manifest as pain and result in changes in the expression and structure of cellular components. Biochemical parameters of importance for cellular functions are described in this review.
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4.
  • Jacobsson, Sofie, et al. (författare)
  • Leptin independently predicts development of sepsis and its outcome
  • 2017
  • Ingår i: Journal of Inflammation. - London : BioMed Central (BMC). - 1476-9255. ; 14
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Sepsis is a life-threatening condition and obesity is related to the clinical outcome. The underlying reasons are incompletely understood, but the adipocyte derived hormones leptin and adiponectin may be involved.Methods: Patients aged 18 years or more with documented first time sepsis events were included in a nested case-referent study if they had participated in previous health surveys. Two matched referents free of known sepsis were identified. Circulating levels of leptin and adiponectin were determined in stored plasma, and their impact on a future sepsis event and its outcome was evaluated.Results: We identified 152 patients (62% women) with a sepsis event and a previous participation in a health survey. Eighty-three % had also blood samples from the acute event. Hyperleptinemia at health survey associated with a future sepsis event (OR 1.77, 95% CI 1.04-3.00) and with hospital death. After adjustment for BMI leptin remained associated with sepsis in men, but not in women. High levels in the acute phase associated with increased risk for in hospital death in women (OR 4.18, 95% CI 1.17-15.00), while being protective in men (OR 0.05, 95% CI 0.01-0.48). Furthermore, leptin increased more from baseline to the acute phase in men than in women. Adiponectin did not predict sepsis and did not relate to outcome.Conclusions: Hyperleptinemia independently predicted the development of sepsis and an unfavourable outcome in men, and inertia in the acute response related to worse outcome.
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5.
  • Karlsson, Torbjörn (författare)
  • Evaluation of a competitive hepcidin ELISA assay in the differential diagnosis of iron deficiency anaemia with concurrent inflammation and anaemia of inflammation in elderly patients
  • 2017
  • Ingår i: Journal of Inflammation. - : BIOMED CENTRAL LTD. - 1476-9255. ; 14
  • Tidskriftsartikel (refereegranskat)abstract
    • In this study, a competitive hepcidin ELISA assay was evaluated for its ability to differentiate between iron deficiency anaemia with concurrent inflammation and anaemia of inflammation in elderly patients, using the absence of stainable bone marrow iron as the diagnostic criterion for iron deficiency. In addition, correlation coefficients for hepcidin versus C-reactive protein, ferritin and interleukin-6 were determined. The optimal cut-off for hepcidin was 21 mu g/L, corresponding to sensitivity and specificity of 100% and 67%, respectively, for iron deficiency. For ferritin, a sensitivity and specificity of 91% and 83%, respectively, correspond to an optimal cut-off of 87 mu g/L. Receiver operating characteristics curve analysis revealed that ELISA analysis of hepcidin is not superior to ferritin in the diagnosis of iron deficiency in elderly anaemic patients with concurrent inflammation. Hepcidin shows a strong positive correlation with ferritin, and also correlates positively with C-reactive protein in this patient population.
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6.
  • Nilsen, Tom, et al. (författare)
  • A new turbidimetric immunoassay for serum calprotectin for fully automatized clinical analysers
  • 2015
  • Ingår i: Journal of Inflammation. - : Springer Science and Business Media LLC. - 1476-9255. ; 12
  • Tidskriftsartikel (refereegranskat)abstract
    • Serum and plasma calprotectin concentration is shown to be elevated when neutrophils are activated, and may therefore be used as a marker for inflammatory diseases. A serum calprotectin immunoassay was developed based on calprotectin values observed in samples from the intensive care unit. The polyclonal avian antibodies were raised and affinity purified with calprotectin antigens. The performance was tested and it was observed that the assay was linear in the range 0.3-24.7 mg/L, the limit of quantitation was observed to be lower than 0.3 mg/L, no antigen excess was observed up to 54 mg/L, all CVs were lower than 1.8 % in the precision study, the calibration curve stability was longer than 6 weeks, and there was no significant interference detected for haemoglobin, intralipid or bilirubin. The serum calprotectin immunoassay presented in this paper performs well within the criteria carefully set from the limited clinical experience obtained in both serum and plasma. In addition it is commutable with Bühlmann MRP8/14 ELISA.
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7.
  • Perez-Baos, Sandra, et al. (författare)
  • Inhibition of pSTAT1 by tofacitinib accounts for the early improvement of experimental chronic synovitis
  • 2019
  • Ingår i: Journal of Inflammation. - : BioMed Central (BMC). - 1476-9255. ; 16
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: In order to gain insight into the early effects drawn by JAK inhibitors on intra-joint JAK/STAT-dependent signaling, we sought synovial activation of STATs and their end-products, along with their modification with tofacitinib (TOFA), at flare-up in antigen induced arthritis (AIA). New Zealand rabbits were randomly assigned to four groups –healthy controls, AIA, TOFA-treated AIA, or TOFA-treated controls–. AIA was induced with 4 weekly intra-articular ovalbumin injections in sensitized animals. TOFA (10 mg·kg− 1·day− 1) was administered for the last 2 weeks. Animals were euthanized 24 h after the last injection.Results: AIA animals showed high-grade synovitis, which was partially improved by TOFA. No effects of the treatment were found on serum C-reactive protein or on the synovial macrophage infiltration at this stage. Synovial MMP-1,-3 and -13 expression levels in treated AIA rabbits were found to drop to those of controls, while a downregulation of IL6, IFNγ and TNF was evident in treated versus untreated AIA rabbits. Concurrently, a reduction in pSTAT1 and SOCS1, but not in pSTAT3, SOCS3 or active NFκB-p65, was noted with TOFA.Conclusions: Studying the mechanism of action of immunomodulatory drugs represents a major challenge in vivo, since drug-dependent decreases in inflammation very likely mask direct effects on disease mechanisms. This study design allowed us to prevent any confounding effect resulting from reductions in the overall inflammatory status, hence assessing the true pharmacological actions of TOFA in a very severe synovitis. Our findings point to pSTAT1 and MMPs as early molecular readouts of response to this JAK inhibitor.
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