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  1. Article ; Online: Complement activation is a crucial pathogenic factor in catastrophic antiphospholipid syndrome.

    Barratt-Due, Andreas / Fløisand, Yngvar / Orrem, Hilde L / Kvam, Ann K / Holme, Pål A / Bergseth, Grethe / Tjønnfjord, Geir E / Mollnes, Tom E

    Rheumatology (Oxford, England)

    2016  Volume 55, Issue 7, Page(s) 1337–1339

    Language English
    Publishing date 2016-07
    Publishing country England
    Document type Letter
    ZDB-ID 1464822-2
    ISSN 1462-0332 ; 1462-0324
    ISSN (online) 1462-0332
    ISSN 1462-0324
    DOI 10.1093/rheumatology/kew040
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  2. Article ; Online: Soluble IL-1 receptor 2 is associated with left ventricular remodelling in patients with ST-elevation myocardial infarction.

    Orrem, Hilde L / Shetelig, Christian / Ueland, Thor / Limalanathan, Shanmuganathan / Nilsson, Per H / Husebye, Trygve / Aukrust, Pål / Seljeflot, Ingebjørg / Hoffmann, Pavel / Eritsland, Jan / Mollnes, Tom E / Andersen, Geir Øystein / Yndestad, Arne

    International journal of cardiology

    2018  Volume 268, Page(s) 187–192

    Abstract: Background: The inflammatory response following myocardial infarction (MI) is prerequisite for proper healing of infarcted tissue, but can also have detrimental effects on cardiac function. Interleukin (IL)-1α and IL-1β are potent inflammatory mediators ...

    Abstract Background: The inflammatory response following myocardial infarction (MI) is prerequisite for proper healing of infarcted tissue, but can also have detrimental effects on cardiac function. Interleukin (IL)-1α and IL-1β are potent inflammatory mediators and their bioactivity is tightly regulated by IL-1 receptor antagonist (IL-1ra) and soluble (s) IL-1 receptors (R). We aimed to examine whether levels of soluble regulators of IL-1 signalling are changed during ST-elevation MI (STEMI) and their associations with parameters of cardiac injury and ventricular remodelling.
    Methods: Plasma levels of IL-1Ra, sIL-1R1, sIL-1R2 and sIL-1R accessory protein (sIL-1RAcP) were measured by immunoassays in repeated samples from patients with STEMI (n = 255) and compared to healthy controls (n = 65).
    Results: IL-1Ra, sIL-1R1 and sIL-1R2 levels were all significantly elevated after STEMI, while levels of sIL-1RAcP were lower compared to controls. sIL-1R2 levels (at different time points) correlated positively with C-reactive protein, myocardial infarct size and change in indexed left ventricular end-diastolic and end-systolic volume (LVEDVi and LVESVi) measured by cardiac MR acutely and after 4 months, and negatively with LV ejection fraction. Patients with >median levels of sIL-1R2 in the acute phase were more likely to have increased change in LVEDVi and LVESVi. Importantly, sIL-1R2 remained significantly associated with change in LVEDVi and LVESVi also after adjustment for clinical covariates.
    Conclusion: Levels of sIL-1R2 are independently associated with parameters of LV adverse remodelling following STEMI.
    MeSH term(s) Aged ; Biomarkers/blood ; Female ; Humans ; Male ; Middle Aged ; Percutaneous Coronary Intervention/trends ; Receptors, Interleukin-1 Type II/blood ; ST Elevation Myocardial Infarction/blood ; ST Elevation Myocardial Infarction/diagnostic imaging ; ST Elevation Myocardial Infarction/surgery ; Stroke Volume/physiology ; Ventricular Remodeling/physiology
    Chemical Substances Biomarkers ; IL1R2 protein, human ; Receptors, Interleukin-1 Type II
    Language English
    Publishing date 2018-05-28
    Publishing country Netherlands
    Document type Clinical Trial ; Journal Article
    ZDB-ID 779519-1
    ISSN 1874-1754 ; 0167-5273
    ISSN (online) 1874-1754
    ISSN 0167-5273
    DOI 10.1016/j.ijcard.2018.05.032
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  3. Article: Combined inhibition of C5 and CD14 efficiently attenuated the inflammatory response in a porcine model of meningococcal sepsis.

    Hellerud, Bernt C / Orrem, Hilde L / Dybwik, Knut / Pischke, Søren E / Baratt-Due, Andreas / Castellheim, Albert / Fure, Hilde / Bergseth, Grethe / Christiansen, Dorte / Nunn, Miles A / Espevik, Terje / Lau, Corinna / Brandtzæg, Petter / Nielsen, Erik W / Mollnes, Tom E

    Journal of intensive care

    2017  Volume 5, Page(s) 21

    Abstract: Background: Fulminant meningococcal sepsis, characterized by overwhelming innate immune activation, mostly affects young people and causes high mortality. This study aimed to investigate the effect of targeting two key molecules of innate immunity, ... ...

    Abstract Background: Fulminant meningococcal sepsis, characterized by overwhelming innate immune activation, mostly affects young people and causes high mortality. This study aimed to investigate the effect of targeting two key molecules of innate immunity, complement component C5, and co-receptor CD14 in the Toll-like receptor system, on the inflammatory response in meningococcal sepsis.
    Methods: Meningococcal sepsis was simulated by continuous intravenous infusion of an escalating dose of heat-inactivated
    Results: A substantial increase in plasma complement activation in the untreated group was completely abolished in the treatment group (
    Conclusion: Inhibition of C5 and CD14 may be beneficial in attenuating the detrimental effects of complement activation and modulating the cytokine storm in patients with fulminant meningococcal sepsis.
    Language English
    Publishing date 2017-02-27
    Publishing country England
    Document type Journal Article
    ZDB-ID 2739853-5
    ISSN 2052-0492
    ISSN 2052-0492
    DOI 10.1186/s40560-017-0217-0
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  4. Article ; Online: Acute heart failure following myocardial infarction: complement activation correlates with the severity of heart failure in patients developing cardiogenic shock.

    Orrem, Hilde L / Nilsson, Per H / Pischke, Søren E / Grindheim, Guro / Garred, Peter / Seljeflot, Ingebjørg / Husebye, Trygve / Aukrust, Pål / Yndestad, Arne / Andersen, Geir Ø / Barratt-Due, Andreas / Mollnes, Tom E

    ESC heart failure

    2018  Volume 5, Issue 3, Page(s) 292–301

    Abstract: Aims: Heart failure (HF) is an impending complication to myocardial infarction. We hypothesized that the degree of complement activation reflects severity of HF following acute myocardial infarction.: Methods and results: The LEAF trial (LEvosimendan ...

    Abstract Aims: Heart failure (HF) is an impending complication to myocardial infarction. We hypothesized that the degree of complement activation reflects severity of HF following acute myocardial infarction.
    Methods and results: The LEAF trial (LEvosimendan in Acute heart Failure following myocardial infarction) evaluating 61 patients developing HF within 48 h after percutaneous coronary intervention-treated ST-elevation myocardial infarction herein underwent a post hoc analysis. Blood samples were drawn from inclusion to Day 5 and at 42 day follow-up, and biomarkers were measured with enzyme immunoassays. Regional myocardial contractility was measured by echocardiography as wall motion score index (WMSI). The cardiogenic shock group (n = 9) was compared with the non-shock group (n = 52). Controls (n = 44) were age-matched and sex-matched healthy individuals. C4bc, C3bc, C3bBbP, and sC5b-9 were elevated in patients at inclusion compared with controls (P < 0.01). The shock group had higher levels compared with the non-shock group for all activation products except C3bBbP (P < 0.05). At Day 42, all products were higher in the shock group (P < 0.05). In the shock group, sC5b-9 correlated significantly with WMSI at baseline (r = 0.68; P = 0.045) and at Day 42 (r = 0.84; P = 0.036). Peak sC5b-9 level correlated strongly with WMSI at Day 42 (r = 0.98; P = 0.005). Circulating endothelial cell activation markers sICAM-1 and sVCAM-1 were higher in the shock group during the acute phase (P < 0.01), and their peak levels correlated with sC5b-9 peak level in the whole HF population (r = 0.32; P = 0.014 and r = 0.30; P = 0.022, respectively).
    Conclusions: Complement activation discriminated cardiogenic shock from non-shock in acute ST-elevation myocardial infarction complicated by HF and correlated with regional contractility and endothelial cell activation, suggesting a pathogenic role of complement in this condition.
    MeSH term(s) Acute Disease ; Aged ; Anterior Wall Myocardial Infarction/complications ; Anterior Wall Myocardial Infarction/diagnosis ; Anterior Wall Myocardial Infarction/surgery ; Complement Activation/physiology ; Echocardiography ; Female ; Heart Failure/blood ; Heart Failure/diagnosis ; Heart Failure/etiology ; Humans ; Male ; Middle Aged ; Percutaneous Coronary Intervention ; Severity of Illness Index ; Shock, Cardiogenic/complications ; Shock, Cardiogenic/diagnosis ; Shock, Cardiogenic/physiopathology
    Language English
    Publishing date 2018-02-09
    Publishing country England
    Document type Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
    ZDB-ID 2814355-3
    ISSN 2055-5822 ; 2055-5822
    ISSN (online) 2055-5822
    ISSN 2055-5822
    DOI 10.1002/ehf2.12266
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  5. Article ; Online: Cholesterol crystals use complement to increase NLRP3 signaling pathways in coronary and carotid atherosclerosis.

    Niyonzima, Nathalie / Bakke, Siril S / Gregersen, Ida / Holm, Sverre / Sandanger, Øystein / Orrem, Hilde L / Sporsheim, Bjørnar / Ryan, Liv / Kong, Xiang Yi / Dahl, Tuva Børresdatter / Skjelland, Mona / Sørensen, Kirsten Krohg / Rokstad, Anne Mari / Yndestad, Arne / Latz, Eicke / Gullestad, Lars / Andersen, Geir Ø / Damås, Jan Kristian / Aukrust, Pål /
    Mollnes, Tom E / Halvorsen, Bente / Espevik, Terje

    EBioMedicine

    2020  Volume 60, Page(s) 102985

    Abstract: Background: During atherogenesis, cholesterol precipitates into cholesterol crystals (CC) in the vessel wall, which trigger plaque inflammation by activating the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome. We investigated the ... ...

    Abstract Background: During atherogenesis, cholesterol precipitates into cholesterol crystals (CC) in the vessel wall, which trigger plaque inflammation by activating the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome. We investigated the relationship between CC, complement and NLRP3 in patients with cardiovascular disease.
    Methods: We analysed plasma, peripheral blood mononuclear cells (PBMC) and carotid plaques from patients with advanced atherosclerosis applying ELISAs, multiplex cytokine assay, qPCR, immunohistochemistry, and gene profiling.
    Findings: Transcripts of interleukin (IL)-1beta(β) and NLRP3 were increased and correlated in PBMC from patients with acute coronary syndrome (ACS). Priming of these cells with complement factor 5a (C5a) and tumour necrosis factor (TNF) before incubation with CC resulted in increased IL-1β protein when compared to healthy controls. As opposed to healthy controls, systemic complement was significantly increased in patients with stable angina pectoris or ACS. In carotid plaques, complement C1q and C5b-9 complex accumulated around CC-clefts, and complement receptors C5aR1, C5aR2 and C3aR1 were higher in carotid plaques compared to control arteries. Priming human carotid plaques with C5a followed by CC incubation resulted in pronounced release of IL-1β, IL-18 and IL-1α. Additionally, mRNA profiling demonstrated that C5a and TNF priming followed by CC incubation upregulated plaque expression of NLRP3 inflammasome components.
    Interpretation: We demonstrate that CC are important local- and systemic complement activators, and we reveal that the interaction between CC and complement could exert its effect by activating the NLRP3 inflammasome, thus promoting the progression of atherosclerosis.
    MeSH term(s) Carotid Artery Diseases/etiology ; Carotid Artery Diseases/metabolism ; Carotid Artery Diseases/pathology ; Cholesterol/metabolism ; Complement C5a/immunology ; Complement System Proteins/immunology ; Computational Biology/methods ; Coronary Artery Disease/etiology ; Coronary Artery Disease/metabolism ; Coronary Artery Disease/pathology ; Cytokines/metabolism ; Disease Susceptibility ; Gene Expression Profiling ; Humans ; Inflammasomes/metabolism ; Inflammation Mediators/metabolism ; Leukocytes, Mononuclear/immunology ; Leukocytes, Mononuclear/metabolism ; Leukocytes, Mononuclear/pathology ; Liquid Crystals ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Plaque, Atherosclerotic ; Signal Transduction
    Chemical Substances Cytokines ; Inflammasomes ; Inflammation Mediators ; NLR Family, Pyrin Domain-Containing 3 Protein ; Complement C5a (80295-54-1) ; Complement System Proteins (9007-36-7) ; Cholesterol (97C5T2UQ7J)
    Language English
    Publishing date 2020-09-11
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2020.102985
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  6. Article ; Online: IL-6 Receptor Inhibition by Tocilizumab Attenuated Expression of C5a Receptor 1 and 2 in Non-ST-Elevation Myocardial Infarction.

    Orrem, Hilde L / Nilsson, Per H / Pischke, Søren E / Kleveland, Ola / Yndestad, Arne / Ekholt, Karin / Damås, Jan K / Espevik, Terje / Bendz, Bjørn / Halvorsen, Bente / Gregersen, Ida / Wiseth, Rune / Andersen, Geir Ø / Ueland, Thor / Gullestad, Lars / Aukrust, Pål / Barratt-Due, Andreas / Mollnes, Tom E

    Frontiers in immunology

    2018  Volume 9, Page(s) 2035

    Abstract: Background: ...

    Abstract Background:
    MeSH term(s) Aged ; Antibodies, Monoclonal, Humanized/administration & dosage ; Female ; Gene Expression Regulation/drug effects ; Humans ; Male ; Middle Aged ; Non-ST Elevated Myocardial Infarction/blood ; Non-ST Elevated Myocardial Infarction/drug therapy ; Receptor, Anaphylatoxin C5a/blood ; Receptors, Chemokine/blood ; Receptors, Interleukin-6/antagonists & inhibitors ; Receptors, Interleukin-6/metabolism
    Chemical Substances Antibodies, Monoclonal, Humanized ; C5AR1 protein, human ; C5aR2 protein, human ; IL6R protein, human ; Receptor, Anaphylatoxin C5a ; Receptors, Chemokine ; Receptors, Interleukin-6 ; tocilizumab (I031V2H011)
    Language English
    Publishing date 2018-09-12
    Publishing country Switzerland
    Document type Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2018.02035
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  7. Article ; Online: Cholesterol crystals use complement to increase NLRP3 signaling pathways in coronary and carotid atherosclerosis

    Nathalie Niyonzima / Siril S. Bakke / Ida Gregersen / Sverre Holm / Øystein Sandanger / Hilde L. Orrem / Bjørnar Sporsheim / Liv Ryan / Xiang Yi Kong / Tuva Børresdatter Dahl / Mona Skjelland / Kirsten Krohg Sørensen / Anne Mari Rokstad / Arne Yndestad / Eicke Latz / Lars Gullestad / Geir Ø. Andersen / Jan Kristian Damås / Pål Aukrust /
    Tom E. Mollnes / Bente Halvorsen / Terje Espevik

    EBioMedicine, Vol 60, Iss , Pp 102985- (2020)

    2020  

    Abstract: Background: During atherogenesis, cholesterol precipitates into cholesterol crystals (CC) in the vessel wall, which trigger plaque inflammation by activating the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome. We investigated the ... ...

    Abstract Background: During atherogenesis, cholesterol precipitates into cholesterol crystals (CC) in the vessel wall, which trigger plaque inflammation by activating the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome. We investigated the relationship between CC, complement and NLRP3 in patients with cardiovascular disease. Methods: We analysed plasma, peripheral blood mononuclear cells (PBMC) and carotid plaques from patients with advanced atherosclerosis applying ELISAs, multiplex cytokine assay, qPCR, immunohistochemistry, and gene profiling. Findings: Transcripts of interleukin (IL)-1beta(β) and NLRP3 were increased and correlated in PBMC from patients with acute coronary syndrome (ACS). Priming of these cells with complement factor 5a (C5a) and tumour necrosis factor (TNF) before incubation with CC resulted in increased IL-1β protein when compared to healthy controls. As opposed to healthy controls, systemic complement was significantly increased in patients with stable angina pectoris or ACS. In carotid plaques, complement C1q and C5b-9 complex accumulated around CC-clefts, and complement receptors C5aR1, C5aR2 and C3aR1 were higher in carotid plaques compared to control arteries. Priming human carotid plaques with C5a followed by CC incubation resulted in pronounced release of IL-1β, IL-18 and IL-1α. Additionally, mRNA profiling demonstrated that C5a and TNF priming followed by CC incubation upregulated plaque expression of NLRP3 inflammasome components. Interpretation: We demonstrate that CC are important local- and systemic complement activators, and we reveal that the interaction between CC and complement could exert its effect by activating the NLRP3 inflammasome, thus promoting the progression of atherosclerosis.
    Keywords Cholesterol crystals ; Complement system ; NLRP3 inflammasome ; Coronary artery disease ; Carotid atherosclerosis ; Atherosclerosis ; Medicine ; R ; Medicine (General) ; R5-920
    Subject code 610
    Language English
    Publishing date 2020-10-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
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  8. Article: Hemophagocytic lymphohistiocytosis in leprosy.

    Høyvoll, Liv R / Fløisand, Yngvar / Orrem, Hilde Lang / Gunnarsson, Ragnar / Landrø, Linn / Brevig, Trine / Gaustad, Peter / Nordøy, Ingvild

    Leprosy review

    2015  Volume 86, Issue 4, Page(s) 403–406

    Abstract: A patient from Southeast Asia was diagnosed with systemic lupus erythematosus. One year later, she experienced exacerbation of skin lesions and was diagnosed with erythema nodosum leprosum. Upon treatment, the patient developed hemophagocytic ... ...

    Abstract A patient from Southeast Asia was diagnosed with systemic lupus erythematosus. One year later, she experienced exacerbation of skin lesions and was diagnosed with erythema nodosum leprosum. Upon treatment, the patient developed hemophagocytic lymphohistiocytosis with multi-organ failure and died from invasive fungal infection. Hemophagocytic lymphohistiocytosis has to our knowledge, not previously been reported in leprosy.
    MeSH term(s) Adult ; Female ; Humans ; Leprosy/complications ; Lymphohistiocytosis, Hemophagocytic/etiology
    Language English
    Publishing date 2015-12
    Publishing country England
    Document type Case Reports ; Journal Article
    ZDB-ID 415137-9
    ISSN 0305-7518 ; 0024-1032
    ISSN 0305-7518 ; 0024-1032
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