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  1. Article ; Online: Identification of a new genetic variant (G231N, E232T, N235D) of peptidylarginine deiminase from

    Bereta, Grzegorz P / Strzelec, Karolina / Łazarz-Bartyzel, Katarzyna / Dziedzic-Kowalska, Agata / Nowakowska, Zuzanna / Krutyhołowa, Anna / Bielecka, Ewa / Kantyka, Tomasz / Grabiec, Aleksander M / Kaczmarzyk, Tomasz / Chomyszyn-Gajewska, Maria / Potempa, Jan / Gawron, Katarzyna

    Frontiers in immunology

    2024  Volume 15, Page(s) 1355357

    Abstract: Chronic periodontitis (CP), an inflammatory disease of periodontal tissues driven by a dysbiotic subgingival bacterial biofilm, is also associated with several systemic diseases, including rheumatoid arthritis (RA). ...

    Abstract Chronic periodontitis (CP), an inflammatory disease of periodontal tissues driven by a dysbiotic subgingival bacterial biofilm, is also associated with several systemic diseases, including rheumatoid arthritis (RA).
    MeSH term(s) Humans ; Protein-Arginine Deiminases/genetics ; Protein-Arginine Deiminases/metabolism ; Porphyromonas gingivalis ; Peptides ; Periodontium/metabolism ; Chronic Periodontitis/genetics
    Chemical Substances Protein-Arginine Deiminases (EC 3.5.3.15) ; Peptides
    Language English
    Publishing date 2024-03-21
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2024.1355357
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Host and bacterial factors linking periodontitis and rheumatoid arthritis.

    Krutyhołowa, Anna / Strzelec, Karolina / Dziedzic, Agata / Bereta, Grzegorz P / Łazarz-Bartyzel, Katarzyna / Potempa, Jan / Gawron, Katarzyna

    Frontiers in immunology

    2022  Volume 13, Page(s) 980805

    Abstract: Observations from numerous clinical, epidemiological and serological studies link periodontitis with severity and progression of rheumatoid arthritis. The strong association is observed despite totally different aetiology of these two diseases, ... ...

    Abstract Observations from numerous clinical, epidemiological and serological studies link periodontitis with severity and progression of rheumatoid arthritis. The strong association is observed despite totally different aetiology of these two diseases, periodontitis being driven by dysbiotic microbial flora on the tooth surface below the gum line, while rheumatoid arthritis being the autoimmune disease powered by anti-citrullinated protein antibodies (ACPAs). Here we discuss genetic and environmental risk factors underlying development of both diseases with special emphasis on bacteria implicated in pathogenicity of periodontitis. Individual periodontal pathogens and their virulence factors are argued as potentially contributing to putative causative link between periodontal infection and initiation of a chain of events leading to breakdown of immunotolerance and development of ACPAs. In this respect peptidylarginine deiminase, an enzyme unique among prokaryotes for
    MeSH term(s) Anti-Citrullinated Protein Antibodies/genetics ; Anti-Citrullinated Protein Antibodies/immunology ; Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/immunology ; Autoantibodies/genetics ; Autoantibodies/immunology ; Humans ; Periodontitis/complications ; Periodontitis/genetics ; Periodontitis/immunology ; Periodontitis/microbiology ; Porphyromonas gingivalis/enzymology ; Porphyromonas gingivalis/genetics ; Protein-Arginine Deiminases/genetics ; Protein-Arginine Deiminases/immunology
    Chemical Substances Anti-Citrullinated Protein Antibodies ; Autoantibodies ; Protein-Arginine Deiminases (EC 3.5.3.15)
    Language English
    Publishing date 2022-08-25
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.980805
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Apoptosis in Autoimmunological Diseases, with Particular Consideration of Molecular Aspects of Psoriasis.

    Krawczyk, Agata / Miśkiewicz, Joanna / Strzelec, Karolina / Wcisło-Dziadecka, Dominika / Strzalka-Mrozik, Barbara

    Medical science monitor : international medical journal of experimental and clinical research

    2020  Volume 26, Page(s) e922035

    Abstract: Apoptosis is a natural physiological process involving programmed cell death. Thanks to this process, it is possible to maintain the homeostasis of the body and the immune system. Dysfunctions of this mechanism lead to development of autoimmune diseases ... ...

    Abstract Apoptosis is a natural physiological process involving programmed cell death. Thanks to this process, it is possible to maintain the homeostasis of the body and the immune system. Dysfunctions of this mechanism lead to development of autoimmune diseases such as psoriasis; these diseases are chronic and treatment is extremely difficult. In psoriasis (a skin disease), apoptosis disorders are manifested by keratinocyte proliferation dysfunction. Autoimmune diseases coexisting with psoriasis include multiple sclerosis, autoimmune thyroid disease, and diabetes, but the common pathogenesis of these diseases is not fully understood. Given the heterogenous nature and chronic and recurrent course of psoriasis, the selection of an effective therapeutic strategy is still a problem. This literature review was focused on the process of apoptosis as a factor in the development of autoimmune diseases, with particular emphasis on psoriasis. The work also includes a review of therapeutic methods of psoriasis based on the latest literature.
    MeSH term(s) Apoptosis/immunology ; Apoptosis Regulatory Proteins/immunology ; Autoimmune Diseases/immunology ; Diabetes Mellitus, Type 1/immunology ; Graves Disease/immunology ; Hashimoto Disease/immunology ; Humans ; Inflammatory Bowel Diseases/immunology ; Multiple Sclerosis/immunology ; Psoriasis/immunology ; Psoriasis/therapy ; Tumor Necrosis Factor-alpha/immunology
    Chemical Substances Apoptosis Regulatory Proteins ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2020-06-22
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1439041-3
    ISSN 1643-3750 ; 1234-1010
    ISSN (online) 1643-3750
    ISSN 1234-1010
    DOI 10.12659/MSM.922035
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4924: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article: Gene-repaired iPS cells as novel approach for patient with

    Fus-Kujawa, Agnieszka / Mendrek, Barbara / Bajdak-Rusinek, Karolina / Diak, Natalia / Strzelec, Karolina / Gutmajster, Ewa / Janelt, Kamil / Kowalczuk, Agnieszka / Trybus, Anna / Rozwadowska, Patrycja / Wojakowski, Wojciech / Gawron, Katarzyna / Sieroń, Aleksander L

    Frontiers in bioengineering and biotechnology

    2023  Volume 11, Page(s) 1205122

    Abstract: Introduction: ...

    Abstract Introduction:
    Language English
    Publishing date 2023-06-30
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2719493-0
    ISSN 2296-4185
    ISSN 2296-4185
    DOI 10.3389/fbioe.2023.1205122
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Clinics and genetic background of hereditary gingival fibromatosis.

    Strzelec, Karolina / Dziedzic, Agata / Łazarz-Bartyzel, Katarzyna / Grabiec, Aleksander M / Gutmajster, Ewa / Kaczmarzyk, Tomasz / Plakwicz, Paweł / Gawron, Katarzyna

    Orphanet journal of rare diseases

    2021  Volume 16, Issue 1, Page(s) 492

    Abstract: Background: Hereditary gingival fibromatosis (HGF) is a rare condition characterized by slowly progressive overgrowth of the gingiva. The severity of overgrowth may differ from mild causing phonetic and masticatory issues, to severe resulting in ... ...

    Abstract Background: Hereditary gingival fibromatosis (HGF) is a rare condition characterized by slowly progressive overgrowth of the gingiva. The severity of overgrowth may differ from mild causing phonetic and masticatory issues, to severe resulting in diastemas or malposition of teeth. Both, autosomal-dominant and autosomal-recessive forms of HGF are described. The aim of this review is a clinical overview, as well as a summary and discussion of the involvement of candidate chromosomal regions, pathogenic variants of genes, and candidate genes in the pathogenesis of HGF. The loci related to non-syndromic HGF have been identified on chromosome 2 (GINGF, GINGF3), chromosome 5 (GINGF2), chromosome 11 (GINGF4), and 4 (GINGF5). Of these loci, pathogenic variants of the SOS-1 and REST genes inducing HGF have been identified in the GINGF and the GINGF5, respectively. Furthermore, among the top 10 clusters of genes ranked by enrichment score, ATP binding, and fibronectin encoding genes were proposed as related to HGF.
    Conclusion: The analysis of clinical reports as well as translational genetic studies published since the late'90s indicate the clinical and genetic heterogeneity of non-syndromic HGF and point out the importance of genetic studies and bioinformatics of more numerous unrelated families to identify novel pathogenic variants potentially inducing HGF. This strategy will help to unravel the molecular  mechanisms as well as uncover specific targets for novel and less invasive therapies of this rare, orphan condition.
    MeSH term(s) Fibromatosis, Gingival/genetics ; Genetic Background ; Genetic Heterogeneity ; Humans ; Pedigree
    Language English
    Publishing date 2021-11-24
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2225857-7
    ISSN 1750-1172 ; 1750-1172
    ISSN (online) 1750-1172
    ISSN 1750-1172
    DOI 10.1186/s13023-021-02104-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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