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  1. Book ; Conference proceedings: Tight junctions

    Burkhardt, Harald

    6. Rheumatologisches Ddermatologisches Forschungssymposium Frankfurt a. M., 5./6.12.2014

    (Thieme drug report ; 9,11)

    2015  

    Event/congress Rheumatologisches Dermatologisches Forschungssymposium (6., 2014, FrankfurtamMain)
    Author's details [Hrsg.: Harald Burkhardt ...]
    Series title Thieme drug report ; 9,11
    Collection
    Language German
    Size 15 S. : Ill., graph. Darst.
    Publisher Thieme
    Publishing place Stuttgart u.a.
    Publishing country Germany
    Document type Book ; Conference proceedings
    HBZ-ID HT018617879
    Database Catalogue ZB MED Medicine, Health

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  2. Book ; Online ; Thesis: Routineeinsatz von Leflunomid bei Rheumatoider Arthritis

    Weigt, Gundula / Aringer, Martin / Burkhardt, Harald

    Wirksamkeit und unerwünschte Arzneimittelwirkungen in Monotherapie und Kombinationstherapie

    2023  

    Author's details Gundula Weigt ; Gutachter: Martin Aringer, Harald Burkhardt
    Subject code 610 ; 616.994
    Language German
    Size 1 Online-Ressource
    Publisher Technische Universität Dresden
    Publishing place Dresden
    Publishing country Germany
    Document type Book ; Online ; Thesis
    Thesis / German Habilitation thesis Dissertation, Dresden, Technische Universität Dresden, 2023
    HBZ-ID HT030339398
    Database Catalogue ZB MED Medicine, Health

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    2023 E 1223 order for loan Magazin

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  3. Article ; Online: Mechanismen immunologischer Toleranz und ihrer Dysregulation bei rheumatischen Erkrankungen.

    Meier, Florian / Burkhardt, Harald

    Zeitschrift fur Rheumatologie

    2023  Volume 82, Issue 4, Page(s) 269–277

    Abstract: The major tasks of the immune system are protection against infectious agents, maintaining homeostasis by recognizing and neutralizing noxious substances from the environment, and monitoring pathological, e.g. neoplastic tissue changes. It accomplishes ... ...

    Title translation Mechanisms of immunological tolerance and their dysregulation in rheumatic diseases.
    Abstract The major tasks of the immune system are protection against infectious agents, maintaining homeostasis by recognizing and neutralizing noxious substances from the environment, and monitoring pathological, e.g. neoplastic tissue changes. It accomplishes these tasks through complex interactions of cellular and humoral components of the innate and adaptive immune system. This review article focuses on a central problem of self versus non-self discrimination in the development of B and T lymphocytes as carriers of adaptive immunity. During maturation of the lymphocytes in the bone marrow, large repertoires of lymphocyte receptors are randomly generated by somatic recombination, which as a whole have the capability of recognizing any foreign antigen. In order to reduce the implicit risk of autoaggressive immunity that might arise from evolutionary conserved structural motifs in self and foreign antigens, the adaptive immune system must provide redundant mechanisms (clonal deletion, anergy, quiescence and suppression) to eliminate or inactivate lymphocytes expressing highly avid receptors for autoantigens. Thus, the provision of costimulatory signals resulting in a reduced activation threshold of potentially autoreactive anergic T cells through infection, molecular mimicry, disrupted apoptosis regulation, altered "self" by post-translational modification, genetic changes in transcription factors with critical importance for thymic tolerance induction or signaling components of apoptosis can lead to a disruption of self-tolerance and the induction of pathogenic autoimmunity.
    MeSH term(s) Humans ; Autoimmune Diseases ; Immune Tolerance ; T-Lymphocytes ; Self Tolerance ; Autoimmunity ; Autoantigens ; Rheumatic Diseases
    Chemical Substances Autoantigens
    Language German
    Publishing date 2023-04-26
    Publishing country Germany
    Document type English Abstract ; Journal Article ; Review
    ZDB-ID 124985-x
    ISSN 1435-1250 ; 0340-1855 ; 0301-6382
    ISSN (online) 1435-1250
    ISSN 0340-1855 ; 0301-6382
    DOI 10.1007/s00393-023-01352-3
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  4. Book ; Online: Mechanismen immunologischer Toleranz und ihrer Dysregulation bei rheumatischen Erkrankungen ; Mechanisms of immunological tolerance and their dysregulation in rheumatic diseases

    Meier, Florian / Burkhardt, Harald

    2023  

    Abstract: 269 ... 277 ... The major tasks of the immune system are protection against infectious agents, maintaining homeostasis by recognizing and neutralizing noxious substances from the environment, and monitoring pathological, e.g. neoplastic tissue changes. It ... ...

    Abstract 269

    277

    The major tasks of the immune system are protection against infectious agents, maintaining homeostasis by recognizing and neutralizing noxious substances from the environment, and monitoring pathological, e.g. neoplastic tissue changes. It accomplishes these tasks through complex interactions of cellular and humoral components of the innate and adaptive immune system. This review article focuses on a central problem of self versus non-self discrimination in the development of B and T lymphocytes as carriers of adaptive immunity. During maturation of the lymphocytes in the bone marrow, large repertoires of lymphocyte receptors are randomly generated by somatic recombination, which as a whole have the capability of recognizing any foreign antigen. In order to reduce the implicit risk of autoaggressive immunity that might arise from evolutionary conserved structural motifs in self and foreign antigens, the adaptive immune system must provide redundant mechanisms (clonal deletion, anergy, quiescence and suppression) to eliminate or inactivate lymphocytes expressing highly avid receptors for autoantigens. Thus, the provision of costimulatory signals resulting in a reduced activation threshold of potentially autoreactive anergic T cells through infection, molecular mimicry, disrupted apoptosis regulation, altered “self” by post-translational modification, genetic changes in transcription factors with critical importance for thymic tolerance induction or signaling components of apoptosis can lead to a disruption of self-tolerance and the induction of pathogenic autoimmunity.

    82

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    Keywords Adaptive immunity ; Autoimmunity ; B and T lymphocytes ; Immune system ; Inflammatory rheumatic diseases
    Subject code 570
    Language German
    Publishing country de
    Document type Book ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Book ; Online ; Thesis: Routineeinsatz von Leflunomid bei Rheumatoider Arthritis

    Weigt, Gundula [Verfasser] / Aringer, Martin [Gutachter] / Burkhardt, Harald [Gutachter]

    Wirksamkeit und unerwünschte Arzneimittelwirkungen in Monotherapie und Kombinationstherapie

    2023  

    Author's details Gundula Weigt ; Gutachter: Martin Aringer, Harald Burkhardt
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Technische Universität Dresden
    Publishing place Dresden
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  6. Book: Rituximab

    Burkhardt, Harald / Müller-Ladner, Ulf

    aktueller Stand der B-Zell-Therapie mit Rituximab bei Patienten mit rheumatoider Arthritis

    (Thieme drug report ; 5,7)

    2011  

    Author's details [Harals Burkhardt ; Ulf Müller-Ladner]
    Series title Thieme drug report ; 5,7
    Collection
    Language German
    Size 11 S. : Ill., graph. Darst.
    Publisher Thieme
    Publishing place Stuttgart u.a.
    Publishing country Germany
    Document type Book
    HBZ-ID HT017018263
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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    Zs A 6601 -5,7- verfügbar in Königswinter Königswinter

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  7. Article ; Online: Therapiestrategien der Psoriasisarthritis.

    Köhm, Michaela / Burkhardt, Harald / Behrens, Frank

    Deutsche medizinische Wochenschrift (1946)

    2020  Volume 145, Issue 11, Page(s) 773–780

    Abstract: Psoriatic arthritis is a heterogeneous immune-mediated disease that usually involves skin and joints but can also affect entheses and extraarticular structures in the disease course. In addition, associated diseases must be considered when choosing the ... ...

    Title translation Treatment strategies in psoriatic arthritis.
    Abstract Psoriatic arthritis is a heterogeneous immune-mediated disease that usually involves skin and joints but can also affect entheses and extraarticular structures in the disease course. In addition, associated diseases must be considered when choosing the appropriate therapeutic strategy. Different recommendations for treatment of psoriatic arthritis are available for clinical use. The recommendations of the European League Against Rheumatism (EULAR) and the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) are the two internationally accepted guidelines frequently used to assist therapeutic decisions in clinical practice. New targeted treatment options developed based on a better knowledge of critical pathogenic pathways, will enlarge our armamentarium for optimized pharmacotherapy of psoriatic arthritis and improve personalized patient care.
    MeSH term(s) Arthritis, Psoriatic/drug therapy ; Europe ; Humans ; Practice Guidelines as Topic
    Language German
    Publishing date 2020-06-03
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 200446-x
    ISSN 1439-4413 ; 0012-0472
    ISSN (online) 1439-4413
    ISSN 0012-0472
    DOI 10.1055/a-0964-0231
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ua VI Zs.60: Show issues Location:
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  8. Article ; Online: The role of YAP1 target gene CTGF in the anoikis resistance of rheumatoid arthritis synovial fibroblasts.

    Janczi, Tomasz / Fehrl, Yuliya / Kinne, Raimund W / Böhm, Beate / Burkhardt, Harald

    Rheumatology (Oxford, England)

    2022  Volume 62, Issue 2, Page(s) 850–860

    Abstract: Objective: To analyse pro-survival mechanisms elicited in RA synovial fibroblasts (RASFs) upon detachment from their extracellular matrix dependent on the disintegrin metalloproteinase ADAM15 and Yes-associated protein kinase 1 (YAP1).: Methods: ... ...

    Abstract Objective: To analyse pro-survival mechanisms elicited in RA synovial fibroblasts (RASFs) upon detachment from their extracellular matrix dependent on the disintegrin metalloproteinase ADAM15 and Yes-associated protein kinase 1 (YAP1).
    Methods: Detachment-induced apoptosis was determined by caspase 3/7 assays. Immunofluorescent stainings, cell surface biotinylation and immunoblotting were applied to analyse phosphorylated kinases and subcellular localization of YAP1 and connective tissue growth factor (CTGF). Caspase and transwell transmigration assays served to study CTGF function.
    Results: Silencing of ADAM15 or YAP1 in RASFs leads to significantly increased levels of detachment-induced caspase activity. In non-silenced RASFs detachment causes simultaneous ADAM15-enhanced phosphorylation of YAP1 at S127, known for promoting its cytoplasmic localization, and Src-dependent phosphorylation at tyrosine Y357. The majority of nuclear YAP1 leaves the nucleus shortly after cell detachment, but prolonged detachment causes a marked nuclear re-entry of YAP1, resulting in significantly increased synthesis of CTGF. The newly synthesized CTGF, however, is not detectable in the supernatant, but is bound to the outside of the plasma membrane. In vitro studies demonstrated autocrine binding of CTGF to the EGF receptor and β1 integrin, with concomitant triggering of survival kinases, AKT1, ERK1/2, Src and focal adhesion kinase. Functional studies revealed anti-apoptotic effects of CTGF on detached RASFs and an enhancement of their potential for endothelial transmigration using HUVEC-coated transwells.
    Conclusion: The elucidation of a new molecular mechanism that protects RASFs in the highly pro-apoptotic environment of inflamed RA joints by promoting anoikis-resistance and transendothelial migration via ADAM15/YAP1-mediated CTGF upregulation uncovers potentially new targets for future therapeutic intervention.
    MeSH term(s) Humans ; Connective Tissue Growth Factor/genetics ; Connective Tissue Growth Factor/metabolism ; Anoikis ; Signal Transduction ; Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/metabolism ; Adaptor Proteins, Signal Transducing/metabolism ; Fibroblasts/metabolism ; Synovial Membrane/metabolism ; Cells, Cultured ; Membrane Proteins/metabolism ; ADAM Proteins/metabolism ; ADAM Proteins/pharmacology
    Chemical Substances Connective Tissue Growth Factor (139568-91-5) ; Adaptor Proteins, Signal Transducing ; ADAM15 protein, human (EC 3.4.24.-) ; Membrane Proteins ; ADAM Proteins (EC 3.4.24.-)
    Language English
    Publishing date 2022-06-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1464822-2
    ISSN 1462-0332 ; 1462-0324
    ISSN (online) 1462-0332
    ISSN 1462-0324
    DOI 10.1093/rheumatology/keac354
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  9. Article ; Online: The role of antidrug antibodies in ustekinumab therapy and the impact of methotrexate.

    Mojtahed Poor, Sorwe / Henke, Marina / Ulshöfer, Thomas / Köhm, Michaela / Behrens, Frank / Burkhardt, Harald / Schiffmann, Susanne

    Rheumatology (Oxford, England)

    2023  Volume 62, Issue 12, Page(s) 3993–3999

    Abstract: Objective: We investigated the impact of concomitant MTX on ustekinumab (UST) levels and antidrug antibody (ADA) formation in PsA and evaluated consequences in pharmacodynamics and pharmacokinetics.: Methods: We conducted a post-hoc analysis on 112 ... ...

    Abstract Objective: We investigated the impact of concomitant MTX on ustekinumab (UST) levels and antidrug antibody (ADA) formation in PsA and evaluated consequences in pharmacodynamics and pharmacokinetics.
    Methods: We conducted a post-hoc analysis on 112 PsA serum samples of subjects treated with open-label UST and either concomitant MTX (UST/MTX, n = 58) or placebo (UST/pbo, n = 54) obtained in a randomized (1:1), double-blind, multicentre trial. A validated antibody-binding-based multitiered testing was used to detect ADA and ADA with neutralizing capacity (nADA). The impact of MTX on UST immunogenicity was analysed by comparison of UST/pbo with UST/MTX cohorts at different time points. Patient- and disease-related predispositions for ADA formation were investigated with multiple linear regression analysis. Immunogenicity impact on pharmacokinetics, safety and efficacy was determined by cohort comparison between patients with and without ADA formation.
    Results: Over 52 weeks, 11 UST/pbo- and 19 UST/MTX-treated patients developed ADA (P > 0.05). In the UST/pbo cohort, the visit-dependent UST levels were in the range of 0.047 (0.05) -0.110 (0.07) µg/ml overall, and 0.037 (0.04)-0.091 (0.08) µg/ml in ADA-confirmed subjects. In UST/MTX-treated patients, the UST levels exhibited an intervisit variation in the range of 0.0502 (0.04)-0.106 (0.07) µg/ml overall and 0.029 (0.03)-0.097 (0.07) µg/ml in ADA positive subjects (P > 0.05). At week 52, ADA-confirmed patients did not differ significantly (P > 0.05) in safety or clinical outcomes from ADA-negative patients.
    Conclusion: Concomitant MTX had no significant impact on UST immunogenicity. Furthermore, ADA formation was not associated with impairments in UST safety, efficacy or trough levels.
    Trial registration: ClinicalTrials.gov, https://clinicaltrials.gov, NCT03148860.
    MeSH term(s) Humans ; Methotrexate/therapeutic use ; Antirheumatic Agents/adverse effects ; Ustekinumab/therapeutic use ; Arthritis, Psoriatic/drug therapy ; Arthritis, Psoriatic/chemically induced ; Drug Therapy, Combination ; Treatment Outcome
    Chemical Substances Methotrexate (YL5FZ2Y5U1) ; Antirheumatic Agents ; Ustekinumab (FU77B4U5Z0)
    Language English
    Publishing date 2023-04-14
    Publishing country England
    Document type Randomized Controlled Trial ; Multicenter Study ; Journal Article
    ZDB-ID 1464822-2
    ISSN 1462-0332 ; 1462-0324
    ISSN (online) 1462-0332
    ISSN 1462-0324
    DOI 10.1093/rheumatology/kead177
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    Zs.MO 497: Show issues

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  10. Article ; Online: Human MHC Class II and Invariant Chain Knock-in Mice Mimic Rheumatoid Arthritis with Allele Restriction in Immune Response and Arthritis Association.

    Romero-Castillo, Laura / Li, Taotao / Do, Nhu-Nguyen / Sareila, Outi / Xu, Bingze / Hennings, Viktoria / Xu, Zhongwei / Svensson, Carolin / Oliveira-Coelho, Ana / Sener, Zeynep / Urbonaviciute, Vilma / Ekwall, Olov / Burkhardt, Harald / Holmdahl, Rikard

    Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    2024  , Page(s) e2401513

    Abstract: Transgenic mice expressing human major histocompatibility complex class II (MHCII) risk alleles are widely used in autoimmune disease research, but limitations arise due to non-physiologic expression. To address this, physiologically relevant mouse ... ...

    Abstract Transgenic mice expressing human major histocompatibility complex class II (MHCII) risk alleles are widely used in autoimmune disease research, but limitations arise due to non-physiologic expression. To address this, physiologically relevant mouse models are established via knock-in technology to explore the role of MHCII in diseases like rheumatoid arthritis. The gene sequences encoding the ectodomains are replaced with the human DRB1*04:01 and 04:02 alleles, DRA, and CD74 (invariant chain) in C57BL/6N mice. The collagen type II (Col2a1) gene is modified to mimic human COL2. Importantly, DRB1*04:01 knock-in mice display physiologic expression of human MHCII also on thymic epithelial cells, in contrast to DRB1*04:01 transgenic mice. Humanization of the invariant chain enhances MHCII expression on thymic epithelial cells, increases mature B cell numbers in spleen, and improves antigen presentation. To validate its functionality, the collagen-induced arthritis (CIA) model is used, where DRB1*04:01 expression led to a higher susceptibility to arthritis, as compared with mice expressing DRB1*04:02. In addition, the humanized T cell epitope on COL2 allows autoreactive T cell-mediated arthritis development. In conclusion, the humanized knock-in mouse faithfully expresses MHCII, confirming the DRB1*04:01 alleles role in rheumatoid arthritis and being also useful for studying MHCII-associated diseases.
    Language English
    Publishing date 2024-04-11
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2808093-2
    ISSN 2198-3844 ; 2198-3844
    ISSN (online) 2198-3844
    ISSN 2198-3844
    DOI 10.1002/advs.202401513
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