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  1. Artikel ; Online: NG2 glia protect against prion neurotoxicity by inhibiting microglia-to-neuron prostaglandin E2 signaling.

    Liu, Yingjun / Guo, Jingjing / Matoga, Maja / Korotkova, Marina / Jakobsson, Per-Johan / Aguzzi, Adriano

    Nature neuroscience

    2024  

    Abstract: Oligodendrocyte-lineage cells, including NG2 glia, undergo prominent changes in various neurodegenerative disorders. Here, we identify a neuroprotective role for NG2 glia against prion toxicity. NG2 glia were activated after prion infection in cerebellar ...

    Abstract Oligodendrocyte-lineage cells, including NG2 glia, undergo prominent changes in various neurodegenerative disorders. Here, we identify a neuroprotective role for NG2 glia against prion toxicity. NG2 glia were activated after prion infection in cerebellar organotypic cultured slices (COCS) and in brains of prion-inoculated mice. In both model systems, depletion of NG2 glia exacerbated prion-induced neurodegeneration and accelerated prion pathology. Loss of NG2 glia enhanced the biosynthesis of prostaglandin E2 (PGE2) by microglia, which augmented prion neurotoxicity through binding to the EP4 receptor. Pharmacological or genetic inhibition of PGE2 biosynthesis attenuated prion-induced neurodegeneration in COCS and mice, reduced the enhanced neurodegeneration in NG2-glia-depleted COCS after prion infection, and dampened the acceleration of prion disease in NG2-glia-depleted mice. These data unveil a non-cell-autonomous interaction between NG2 glia and microglia in prion disease and suggest that PGE2 signaling may represent an actionable target against prion diseases.
    Sprache Englisch
    Erscheinungsdatum 2024-05-27
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 1420596-8
    ISSN 1546-1726 ; 1097-6256
    ISSN (online) 1546-1726
    ISSN 1097-6256
    DOI 10.1038/s41593-024-01663-x
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Microsomal prostaglandin E synthase-1 inhibition promotes shunting in arachidonic acid metabolism during inflammatory responses in vitro.

    Liu, Jianyang / Peng, Bing / Steinmetz-Späh, Julia / Idborg, Helena / Korotkova, Marina / Jakobsson, Per-Johan

    Prostaglandins & other lipid mediators

    2023  Band 167, Seite(n) 106738

    Abstract: Microsomal Prostaglandin E Synthase 1 (mPGES-1) is the key enzyme for the generation of the pro-inflammatory lipid mediator prostaglandin ... ...

    Abstract Microsomal Prostaglandin E Synthase 1 (mPGES-1) is the key enzyme for the generation of the pro-inflammatory lipid mediator prostaglandin E
    Mesh-Begriff(e) Mice ; Animals ; Prostaglandin-E Synthases/metabolism ; Cyclooxygenase 2/metabolism ; Arachidonic Acid ; Prostaglandins ; Inflammation/drug therapy ; Inflammation/metabolism ; Dinoprostone/metabolism ; Eicosanoids
    Chemische Substanzen Prostaglandin-E Synthases (EC 5.3.99.3) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Arachidonic Acid (27YG812J1I) ; Prostaglandins ; Dinoprostone (K7Q1JQR04M) ; Eicosanoids
    Sprache Englisch
    Erscheinungsdatum 2023-04-23
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 1426962-4
    ISSN 2212-196X ; 1098-8823 ; 0090-6980
    ISSN (online) 2212-196X
    ISSN 1098-8823 ; 0090-6980
    DOI 10.1016/j.prostaglandins.2023.106738
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Urinary prostanoids are elevated by anti-TNF and anti-IL6 receptor disease-modifying antirheumatic drugs but are not predictive of response to treatment in early rheumatoid arthritis.

    Liu, Jianyang / Idborg, Helena / Korotkova, Marina / Lend, Kristina / van Vollenhoven, Ronald / Lampa, Jon / Rudin, Anna / Nordström, Dan / Gudbjornsson, Bjorn / Gröndal, Gerdur / Uhlig, Till / Hørslev-Petersen, Kim / Lund Hetland, Merete / Østergaard, Mikkel / Nurmohamed, Michael / Jakobsson, Per-Johan

    Arthritis research & therapy

    2024  Band 26, Heft 1, Seite(n) 61

    Abstract: Background: Disease-modifying antirheumatic drugs (DMARDs) are widely used for treating rheumatoid arthritis (RA). However, there are no established biomarkers to predict a patient's response to these therapies. Prostanoids, encompassing prostaglandins, ...

    Abstract Background: Disease-modifying antirheumatic drugs (DMARDs) are widely used for treating rheumatoid arthritis (RA). However, there are no established biomarkers to predict a patient's response to these therapies. Prostanoids, encompassing prostaglandins, prostacyclins, and thromboxanes, are potent lipid mediators implicated in RA progression. Nevertheless, the influence of DMARDs on prostanoid biosynthesis in RA patients remains poorly understood. This study aims to assess the impact of various DMARDs on urinary prostanoids levels and to explore whether urinary prostanoid profiles correlate with disease activity or response to therapy.
    Methods: This study included 152 Swedish female patients with early RA, all rheumatoid factor (RF) positive, enrolled in the NORD-STAR trial (registration number: NCT01491815). Participants were randomized into four therapeutic regimes: methotrexate (MTX) combined with (i) prednisolone (arm ACT), (ii) TNF-α blocker certolizumab pegol (arm CZP), (iii) CTLA-4Ig abatacept (arm ABA), or (iv) IL-6R blocker tocilizumab (arm TCZ). Urine samples, collected before start of treatment and at 24 weeks post-treatment, were analyzed for tetranor-prostaglandin E metabolite (tPGEM), tetranor-prostaglandin D metabolite (tPGDM), 2,3-dinor thromboxane B
    Results: Patients receiving MTX combined with CZP or TCZ exhibited significant elevations in urinary tPGEM and TXBM levels after 24 weeks of treatment. Other eicosanoids did not show significant alterations in response to any treatment. Baseline urinary eicosanoid levels did not correlate with baseline clinical disease activity index (CDAI) levels, nor with changes in CDAI from baseline to week 24. Their levels were also similar between patients who achieved CDAI remission and those with active disease at week 24.
    Conclusions: Treatment with anti-TNF or anti-IL6R agents in early RA patients leads to an increased systemic production of proinflammatory and prothrombotic prostanoids. However, urinary eicosanoid levels do not appear to be predictive of the response to DMARDs therapy.
    Mesh-Begriff(e) Humans ; Female ; Prostaglandins ; Antirheumatic Agents/therapeutic use ; Tumor Necrosis Factor Inhibitors ; Arthritis, Rheumatoid/drug therapy ; Methotrexate ; Certolizumab Pegol ; Dimaprit/analogs & derivatives
    Chemische Substanzen Prostaglandins ; Antirheumatic Agents ; Tumor Necrosis Factor Inhibitors ; S-(2-(N,N-diisopropylamino)ethyl)isothiourea (142620-95-9) ; Methotrexate (YL5FZ2Y5U1) ; Certolizumab Pegol (UMD07X179E) ; Dimaprit (ZZQ699148P)
    Sprache Englisch
    Erscheinungsdatum 2024-03-05
    Erscheinungsland England
    Dokumenttyp Randomized Controlled Trial ; Journal Article
    ZDB-ID 2107602-9
    ISSN 1478-6362 ; 1478-6354
    ISSN (online) 1478-6362
    ISSN 1478-6354
    DOI 10.1186/s13075-024-03295-9
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: High-mannose glycans from

    Almeida, Luís / van Roey, Ruthger / Patente, Thiago Andrade / Otto, Frank / Veldhuizen, Tom / Ghorasaini, Mohan / van Diepen, Angela / Schramm, Gabriele / Liu, Jianyang / Idborg, Helena / Korotkova, Marina / Jakobsson, Per-Johan / Giera, Martin / Hokke, Cornelis Hendrik / Everts, Bart

    Frontiers in immunology

    2024  Band 15, Seite(n) 1372927

    Abstract: The parasitic ... ...

    Abstract The parasitic helminth
    Mesh-Begriff(e) Animals ; Schistosoma mansoni/immunology ; Dinoprostone/metabolism ; Th2 Cells/immunology ; Th2 Cells/metabolism ; Lectins, C-Type/metabolism ; Lectins, C-Type/immunology ; Mannose/metabolism ; Mannose/immunology ; Mice ; Polysaccharides/immunology ; Polysaccharides/metabolism ; Antigens, Helminth/immunology ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Schistosomiasis mansoni/immunology ; Schistosomiasis mansoni/metabolism ; Schistosomiasis mansoni/parasitology ; Ovum/immunology ; Ovum/metabolism ; Mice, Inbred C57BL ; OX40 Ligand/metabolism
    Sprache Englisch
    Erscheinungsdatum 2024-04-29
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2024.1372927
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  5. Artikel ; Online: The skeletal muscle arachidonic acid cascade in health and inflammatory disease.

    Korotkova, Marina / Lundberg, Ingrid E

    Nature reviews. Rheumatology

    2014  Band 10, Heft 5, Seite(n) 295–303

    Abstract: Muscle atrophy and weakness are often observed in patients with chronic inflammatory diseases, and are the major clinical features of the autoimmune myopathies, polymyositis and dermatomyositis. A general understanding of the pathogenesis of muscle ... ...

    Abstract Muscle atrophy and weakness are often observed in patients with chronic inflammatory diseases, and are the major clinical features of the autoimmune myopathies, polymyositis and dermatomyositis. A general understanding of the pathogenesis of muscle atrophy and the impaired muscle function associated with chronic inflammatory diseases has not been clarified. In this context, arachidonic acid metabolites, such as the prostaglandin and leukotriene subfamilies, are of interest because they contribute to immune and nonimmune processes. Accumulating evidence suggests that prostaglandins and leukotrienes are involved in causing muscular pain and inflammation, and also in myogenesis and the repair of muscles. In this Review, we summarize novel findings that implicate prostaglandins and leukotrienes in the muscle atrophy and weakness that occur in inflammatory diseases of the muscles, with a focus on inflammatory myopathies. We discuss the role of the arachidonic acid cascade in skeletal muscle growth and function, and individual metabolites as potential therapeutic targets for the treatment of inflammatory muscle diseases.
    Mesh-Begriff(e) Arachidonic Acid/metabolism ; Humans ; Leukotrienes/metabolism ; Leukotrienes/physiology ; Muscle, Skeletal/metabolism ; Myositis/metabolism ; Prostaglandins/metabolism ; Prostaglandins/physiology
    Chemische Substanzen Leukotrienes ; Prostaglandins ; Arachidonic Acid (27YG812J1I)
    Sprache Englisch
    Erscheinungsdatum 2014-01-28
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2491532-4
    ISSN 1759-4804 ; 1759-4790
    ISSN (online) 1759-4804
    ISSN 1759-4790
    DOI 10.1038/nrrheum.2014.2
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Persisting eicosanoid pathways in rheumatic diseases.

    Korotkova, Marina / Jakobsson, Per-Johan

    Nature reviews. Rheumatology

    2014  Band 10, Heft 4, Seite(n) 229–241

    Abstract: An unmet clinical need exists for early treatment of rheumatic diseases and improved treatment strategies that can better maintain remission with reduced ongoing subclinical inflammation and bone destruction. Eicosanoids form one of the most complex ... ...

    Abstract An unmet clinical need exists for early treatment of rheumatic diseases and improved treatment strategies that can better maintain remission with reduced ongoing subclinical inflammation and bone destruction. Eicosanoids form one of the most complex networks in the body controlling many physiological and pathophysiological processes, including inflammation, autoimmunity and cancer. Persisting eicosanoid pathways are thought to be involved in the development of rheumatic diseases, and targeting this pathway might enable improved treatment strategies. Several enzymes of the arachidonic acid cascade as well as eicosanoid receptors (all part of the eicosanoid pathway) are today well-recognized targets for anti-inflammatory drugs that can reduce symptoms of inflammation in rheumatic diseases. In this Review, we outline the evidence supporting pivotal roles of eicosanoid signalling in the pathogenesis of rheumatic diseases and discuss findings from studies in animals and humans. We focus first on rheumatoid arthritis and discuss the upregulation of the cyclooxygenase and lipoxygenase pathways as most data are available in this condition. Research into the roles of eicosanoids in other rheumatic diseases (osteoarthritis, idiopathic inflammatory myopathies, systemic lupus erythematosus and gout) is also progressing rapidly and is discussed. Finally, we summarize the prospects of targeting eicosanoid pathways as anti-inflammatory treatment strategies for patients with rheumatic diseases.
    Mesh-Begriff(e) Animals ; Arthritis, Rheumatoid/enzymology ; Arthritis, Rheumatoid/etiology ; Arthritis, Rheumatoid/physiopathology ; Eicosanoids/metabolism ; Humans ; Lipoxygenase/metabolism ; Prostaglandin-Endoperoxide Synthases/metabolism ; Rheumatic Diseases/drug therapy ; Rheumatic Diseases/enzymology ; Rheumatic Diseases/physiopathology
    Chemische Substanzen Eicosanoids ; Lipoxygenase (EC 1.13.11.12) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1)
    Sprache Englisch
    Erscheinungsdatum 2014-02-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2491532-4
    ISSN 1759-4804 ; 1759-4790
    ISSN (online) 1759-4804
    ISSN 1759-4790
    DOI 10.1038/nrrheum.2014.1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Characterization of microsomal prostaglandin E synthase 1 inhibitors.

    Korotkova, Marina / Jakobsson, Per-Johan

    Basic & clinical pharmacology & toxicology

    2014  Band 114, Heft 1, Seite(n) 64–69

    Abstract: Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible terminal synthase in PGE2 biosynthesis by inflammatory and cancer cells. Clinical and experimental data emphasize that mPGES-1 might be a valuable target, with improved selectivity and ... ...

    Abstract Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible terminal synthase in PGE2 biosynthesis by inflammatory and cancer cells. Clinical and experimental data emphasize that mPGES-1 might be a valuable target, with improved selectivity and safety compared to traditional NSAIDs or selective COX-2 inhibitors, in the treatment of inflammatory diseases, different types of cancer as well as central symptoms elicited by peripheral inflammation. Since the first characterization of mPGES-1, the numbers of publications on mPGES-1 structure, pathogenic role and inhibitor development have increased exponentially; however, there are currently no selective mPGES-1 inhibitors available for clinical use. In this MiniReview, we focus on recent advances in the development of selective inhibitors of mPGES-1 activity, with the aim to discuss the effects of targeting mPGES-1 in different inflammatory models in vitro and in vivo.
    Mesh-Begriff(e) Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Cyclooxygenase 2 Inhibitors/pharmacology ; Disease Models, Animal ; Down-Regulation ; Humans ; Inflammation/drug therapy ; Intramolecular Oxidoreductases/antagonists & inhibitors ; Intramolecular Oxidoreductases/metabolism ; Microsomes/drug effects ; Neoplasms/drug therapy ; Prostaglandin-E Synthases
    Chemische Substanzen Anti-Inflammatory Agents, Non-Steroidal ; Cyclooxygenase 2 Inhibitors ; Intramolecular Oxidoreductases (EC 5.3.-) ; PTGES protein, human (EC 5.3.99.3) ; Prostaglandin-E Synthases (EC 5.3.99.3)
    Sprache Englisch
    Erscheinungsdatum 2014-01
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2134679-3
    ISSN 1742-7843 ; 1742-7835
    ISSN (online) 1742-7843
    ISSN 1742-7835
    DOI 10.1111/bcpt.12162
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: High-content screening of drug combinations of an mPGES-1 inhibitor in multicellular tumor spheroids leads to mechanistic insights into neuroblastoma chemoresistance.

    Zaghmi, Ahlem / Aybay, Erdem / Jiang, Long / Shang, Mingmei / Steinmetz-Späh, Julia / Wermeling, Fredrik / Kogner, Per / Korotkova, Marina / Östling, Päivi / Jakobsson, Per-Johan / Seashore-Ludlow, Brinton / Larsson, Karin

    Molecular oncology

    2023  Band 18, Heft 2, Seite(n) 317–335

    Abstract: High-throughput drug screening enables the discovery of new anticancer drugs. Although monolayer cell cultures are commonly used for screening, their limited complexity and translational efficiency require alternative models. Three-dimensional cell ... ...

    Abstract High-throughput drug screening enables the discovery of new anticancer drugs. Although monolayer cell cultures are commonly used for screening, their limited complexity and translational efficiency require alternative models. Three-dimensional cell cultures, such as multicellular tumor spheroids (MCTS), mimic tumor architecture and offer promising opportunities for drug discovery. In this study, we developed a neuroblastoma MCTS model for high-content drug screening. We also aimed to decipher the mechanisms underlying synergistic drug combinations in this disease model. Several agents from different therapeutic categories and with different mechanisms of action were tested alone or in combination with selective inhibition of prostaglandin E
    Mesh-Begriff(e) Humans ; Prostaglandin-E Synthases ; Drug Resistance, Neoplasm ; Spheroids, Cellular ; Neuroblastoma/drug therapy ; Drug Discovery/methods
    Chemische Substanzen Prostaglandin-E Synthases (EC 5.3.99.3)
    Sprache Englisch
    Erscheinungsdatum 2023-08-21
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2415106-3
    ISSN 1878-0261 ; 1574-7891
    ISSN (online) 1878-0261
    ISSN 1574-7891
    DOI 10.1002/1878-0261.13502
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Microsomal prostaglandin E synthase-1 inhibition prevents adverse cardiac remodelling after myocardial infarction in mice.

    Zhang, Yuze / Steinmetz-Späh, Julia / Idborg, Helena / Zhu, Liyuan / Li, Huihui / Rao, Haojie / Chen, Zengrong / Guo, Ziyi / Hu, Lejia / Xu, Chuansheng / Chen, Hong / Korotkova, Marina / Jakobsson, Per-Johan / Wang, Miao

    British journal of pharmacology

    2023  Band 180, Heft 15, Seite(n) 1981–1998

    Abstract: Background and purpose: Heart failure with reduced ejection fraction (HFrEF) is a major consequence of myocardial infarction (MI). The microsomal prostaglandin E synthase-1 (mPGES-1)/PGE: Experimental approach: Mice were subjected to left anterior ... ...

    Abstract Background and purpose: Heart failure with reduced ejection fraction (HFrEF) is a major consequence of myocardial infarction (MI). The microsomal prostaglandin E synthase-1 (mPGES-1)/PGE
    Experimental approach: Mice were subjected to left anterior descending coronary artery ligation, followed by intraperitoneal treatment with the mPGES-1 inhibitor compound III (CIII) or 118, celecoxib (cyclooxygenase-2 inhibitor) or vehicle, once daily for 28 days. Urinary prostanoid metabolites were measured by liquid chromatography-tandem mass spectrometry.
    Key results: Chronic administration of CIII improved cardiac function in mice after MI compared with vehicle or celecoxib. CIII did not affect thrombogenesis or blood pressure. In addition, CIII reduced infarct area, augmented scar thickness, decreased collagen I/III ratio, decreased the expression of fibrosis-related genes and increased capillary density in the ischaemic area. Shunting to urinary metabolites of PGI
    Conclusion and implications: Inhibition of mPGES-1 prevented chronic adverse cardiac remodelling via an augmented PGI
    Mesh-Begriff(e) Animals ; Mice ; Prostaglandin-E Synthases/metabolism ; Celecoxib/pharmacology ; Heart Failure ; Cicatrix ; Ventricular Remodeling ; Stroke Volume ; Myocardial Infarction/genetics ; Cyclooxygenase 2 Inhibitors
    Chemische Substanzen Prostaglandin-E Synthases (EC 5.3.99.3) ; Celecoxib (JCX84Q7J1L) ; Cyclooxygenase 2 Inhibitors
    Sprache Englisch
    Erscheinungsdatum 2023-03-10
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.16061
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Exploring inflammatory signatures in arthritic joint biopsies with Spatial Transcriptomics.

    Carlberg, Konstantin / Korotkova, Marina / Larsson, Ludvig / Catrina, Anca I / Ståhl, Patrik L / Malmström, Vivianne

    Scientific reports

    2019  Band 9, Heft 1, Seite(n) 18975

    Abstract: Lately it has become possible to analyze transcriptomic profiles in tissue sections with retained cellular context. We aimed to explore synovial biopsies from rheumatoid arthritis (RA) and spondyloarthritis (SpA) patients, using Spatial Transcriptomics ( ... ...

    Abstract Lately it has become possible to analyze transcriptomic profiles in tissue sections with retained cellular context. We aimed to explore synovial biopsies from rheumatoid arthritis (RA) and spondyloarthritis (SpA) patients, using Spatial Transcriptomics (ST) as a proof of principle approach for unbiased mRNA studies at the site of inflammation in these chronic inflammatory diseases. Synovial tissue biopsies from affected joints were studied with ST. The transcriptome data was subjected to differential gene expression analysis (DEA), pathway analysis, immune cell type identification using Xcell analysis and validation with immunohistochemistry (IHC). The ST technology allows selective analyses on areas of interest, thus we analyzed morphologically distinct areas of mononuclear cell infiltrates. The top differentially expressed genes revealed an adaptive immune response profile and T-B cell interactions in RA, while in SpA, the profiles implicate functions associated with tissue repair. With spatially resolved gene expression data, overlaid on high-resolution histological images, we digitally portrayed pre-selected cell types in silico. The RA displayed an overrepresentation of central memory T cells, while in SpA effector memory T cells were most prominent. Consequently, ST allows for deeper understanding of cellular mechanisms and diversity in tissues from chronic inflammatory diseases.
    Mesh-Begriff(e) Adult ; Arthritis, Rheumatoid/immunology ; Arthritis, Rheumatoid/pathology ; Biopsy ; Female ; Gene Expression Profiling ; Humans ; Inflammation/immunology ; Inflammation/pathology ; Male ; Middle Aged ; Oligonucleotide Array Sequence Analysis ; Spondylarthritis/immunology ; Spondylarthritis/pathology ; Synovial Membrane/immunology ; Synovial Membrane/pathology ; Transcriptome/immunology
    Sprache Englisch
    Erscheinungsdatum 2019-12-12
    Erscheinungsland England
    Dokumenttyp Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-55441-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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