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  1. Buch ; Dissertation / Habilitation: Osteoprotegerin und Adiponektin in der Pathogenese der experimentellen Autoimmunmyokarditis

    Stroikova, Vera / Kaya, Ziya

    2019  

    Körperschaft Universität Heidelberg
    Verfasserangabe vorgelegt von Vera Stroikova ; Doktorvater: Herr Prof. Dr. med. Ziya Kaya
    Sprache Deutsch
    Umfang 75 Blätter, Illustrationen, Diagramme, 30 cm
    Erscheinungsort Heidelberg
    Erscheinungsland Deutschland
    Dokumenttyp Buch ; Dissertation / Habilitation
    Dissertation / Habilitation Dissertation, Ruprecht-Karls-Universität Heidelberg, 2020
    HBZ-ID HT020632364
    Datenquelle Katalog ZB MED Medizin, Gesundheit

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  2. Buch ; Dissertation / Habilitation: Beteiligung der Laktatdehydrogenase B an der Troponin I induzierten Autoimmunmyokarditis

    Salbach, Christian / Kaya, Ziya

    2021  

    Körperschaft Universität Heidelberg
    Verfasserangabe vorgelegt von Christian Arne Salbach ; Doktorvater: Herr Prof. Dr. med. Ziya Kaya
    Sprache Deutsch
    Umfang 104 Blätter, Illustrationen, Diagramme, 30 cm
    Erscheinungsort Heidelberg
    Erscheinungsland Deutschland
    Dokumenttyp Buch ; Dissertation / Habilitation
    Dissertation / Habilitation Dissertation, Ruprecht-Karls-Universität Heidelberg, 2022
    HBZ-ID HT021740134
    Datenquelle Katalog ZB MED Medizin, Gesundheit

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  3. Buch ; Dissertation / Habilitation: Die Beteiligung des Immunoproteasoms und der Laktatdehydrogenase B an der Pathogenese der Autoimmunmyokarditis

    Bockstahler, Mariella / Fricker, Gert / Kaya, Ziya

    2018  

    Körperschaft Universität Heidelberg
    Verfasserangabe vorgelegt von M.Sc. Molekulare Biotechnologie Mariella Alexandra Bockstahler
    Sprache Deutsch
    Umfang Seite A-N, 110, XX Seiten, Illustrationen, Diagramme, 30 cm
    Erscheinungsort Heidelberg
    Erscheinungsland Deutschland
    Dokumenttyp Buch ; Dissertation / Habilitation
    Dissertation / Habilitation Dissertation, Ruprecht-Karls-Universität Heidelberg, 2018
    Anmerkung Zusammenfassungen in deutscher und englischer Sprache
    HBZ-ID HT020364079
    Datenquelle Katalog ZB MED Medizin, Gesundheit

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  4. Buch ; Dissertation / Habilitation: Trends bei der Implantation von Herzschrittmachern

    Kaya, Ziya

    Analyse eines 4-Jahres-Zeitraumes an 43865 Patienten

    1998  

    Verfasserangabe Ziya Kaya
    Sprache Deutsch
    Umfang 77 Bl. : graph. Darst.
    Dokumenttyp Buch ; Dissertation / Habilitation
    Dissertation / Habilitation Ulm, Univ., Diss., 1998
    HBZ-ID HT010406433
    Datenquelle Katalog ZB MED Medizin, Gesundheit

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  5. Artikel ; Online: Cardiac Troponin I autoantibodies and their potential role in cardiac remodelling.

    Salbach, Christian / Kaya, Ziya

    EBioMedicine

    2019  Band 48, Seite(n) 11–12

    Mesh-Begriff(e) Autoantibodies/immunology ; Autoantigens/immunology ; Humans ; Myocardium/immunology ; Myocardium/metabolism ; Troponin I/immunology ; Ventricular Remodeling/immunology
    Chemische Substanzen Autoantibodies ; Autoantigens ; Troponin I
    Sprache Englisch
    Erscheinungsdatum 2019-09-14
    Erscheinungsland Netherlands
    Dokumenttyp Letter
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2019.09.005
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: No Evidence for Myocarditis or Other Organ Affection by Induction of an Immune Response against Critical SARS-CoV-2 Protein Epitopes in a Mouse Model Susceptible for Autoimmunity.

    Ignatz, Rebecca Maria / Zirkenbach, Vanessa Antje / Kaya, Mansur / Stroikova, Vera / Öttl, Renate / Frey, Norbert / Kaya, Ziya

    International journal of molecular sciences

    2023  Band 24, Heft 12

    Abstract: ... ...

    Abstract After
    Mesh-Begriff(e) Mice ; Humans ; Animals ; SARS-CoV-2 ; Autoimmunity ; COVID-19 ; Myocarditis/etiology ; Epitopes ; Post-Acute COVID-19 Syndrome ; Peptides ; Autoimmune Diseases/etiology ; Inflammation
    Chemische Substanzen Epitopes ; Peptides
    Sprache Englisch
    Erscheinungsdatum 2023-06-08
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24129873
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel: Exploration of Analgesia with Tramadol in the Coxsackievirus B3 Myocarditis Mouse Model

    Pinkert, Sandra / Kespohl, Meike / Kelm, Nicolas / Kaya, Ziya / Heuser, Arnd / Klingel, Karin / Beling, Antje

    Viruses. 2021 June 24, v. 13, no. 7

    2021  

    Abstract: Infection of mice with Coxsackievirus B3 (CVB3) triggers inflammation of the heart and this mouse model is commonly used to investigate underlying mechanisms and therapeutic aspects for viral myocarditis. Virus-triggered cytotoxicity and the activity of ... ...

    Abstract Infection of mice with Coxsackievirus B3 (CVB3) triggers inflammation of the heart and this mouse model is commonly used to investigate underlying mechanisms and therapeutic aspects for viral myocarditis. Virus-triggered cytotoxicity and the activity of infiltrating immune cells contribute to cardiac tissue injury. In addition to cardiac manifestation, CVB3 causes cell death and inflammation in the pancreas. The resulting pancreatitis represents a severe burden and under such experimental conditions, analgesics may be supportive to improve the animals’ well-being. Notably, several known mechanisms exist by which analgesics can interfere with the immune system and thereby compromise the feasibility of the model. We set up a study aiming to improve animal welfare while ensuring model integrity and investigated how tramadol, an opioid, affects virus-induced pathogenicity and immune response in the heart. Tramadol was administered seven days prior to a CVB3 infection in C57BL/6 mice and treatment was continued until the day of analysis. Tramadol had no effect on the virus titer or viral pathogenicity in the heart tissue and the inflammatory response, a hallmark of myocardial injury, was maintained. Our results show that tramadol exerts no disruptive effects on the CVB3 myocarditis mouse model and, therefore, the demonstrated protocol should be considered as a general analgesic strategy for CVB3 infection.
    Schlagwörter analgesia ; analgesics ; animal welfare ; cell death ; cytotoxicity ; heart ; immune response ; immune system ; inflammation ; mice ; myocarditis ; pancreas ; pancreatitis ; pathogenicity ; viral load
    Sprache Englisch
    Erscheinungsverlauf 2021-0624
    Erscheinungsort Multidisciplinary Digital Publishing Institute
    Dokumenttyp Artikel
    ZDB-ID 2516098-9
    ISSN 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v13071222
    Datenquelle NAL Katalog (AGRICOLA)

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  8. Artikel ; Online: Increase of Cardiac Autoantibodies Against Beta-2-adrenergic Receptor During Acute Cellular Heart Transplant Rejection.

    Salbach, Christian / Schlegel, Philipp / Stroikova, Vera / Helmschrott, Matthias / Mueller, Anna-Maria / Weiß, Christel / Giannitsis, Evangelos / Frey, Norbert / Raake, Philip / Kaya, Ziya

    Transplantation

    2024  

    Abstract: Background: Acute cellular rejection (ACR) in heart transplant (HTx) recipients may be accompanied by cardiac cell damage with subsequent exposure to cardiac autoantigens and the production of cardiac autoantibodies (aABs). This study aimed to evaluate ... ...

    Abstract Background: Acute cellular rejection (ACR) in heart transplant (HTx) recipients may be accompanied by cardiac cell damage with subsequent exposure to cardiac autoantigens and the production of cardiac autoantibodies (aABs). This study aimed to evaluate a peptide array screening approach for cardiac aABs in HTx recipients during ACR (ACR-HTx).
    Methods: In this retrospective single-center observational study, sera from 37 HTx recipients, as well as age and sex-matched healthy subjects were screened for a total of 130 cardiac aABs of partially overlapping peptide sequences directed against structural proteins using a peptide array approach.
    Results: In ACR-HTx, troponin I (TnI) serum levels were found to be elevated. Here, we could identify aABs against beta-2-adrenergic receptor (β-2AR: EAINCYANETCCDFFTNQAY) to be upregulated in ACR-HTx (intensities: 0.80 versus 1.31, P = 0.0413). Likewise, patients positive for β-2AR aABs showed higher TnI serum levels during ACR compared with aAB negative patients (10.0 versus 30.0 ng/L, P = 0.0375). Surprisingly, aABs against a sequence of troponin I (TnI: QKIFDLRGKFKRPTLRRV) were found to be downregulated in ACR-HTx (intensities: 3.49 versus 1.13, P = 0.0025). A comparison in healthy subjects showed the same TnI sequence to be upregulated in non-ACR-HTx (intensities: 2.19 versus 3.49, P = 0.0205), whereas the majority of aABs were suppressed in non-ACR-HTx.
    Conclusions: Our study served as a feasibility analysis for a peptide array screening approach in HTx recipients during ACR and identified 2 different regulated aABs in ACR-HTx. Hence, further multicenter studies are needed to evaluate the prognostic implications of aAB testing and diagnostic or therapeutic consequences.
    Sprache Englisch
    Erscheinungsdatum 2024-05-21
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 208424-7
    ISSN 1534-6080 ; 0041-1337
    ISSN (online) 1534-6080
    ISSN 0041-1337
    DOI 10.1097/TP.0000000000005062
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Exploration of Analgesia with Tramadol in the Coxsackievirus B3 Myocarditis Mouse Model.

    Pinkert, Sandra / Kespohl, Meike / Kelm, Nicolas / Kaya, Ziya / Heuser, Arnd / Klingel, Karin / Beling, Antje

    Viruses

    2021  Band 13, Heft 7

    Abstract: Infection of mice with Coxsackievirus B3 (CVB3) triggers inflammation of the heart and this mouse model is commonly used to investigate underlying mechanisms and therapeutic aspects for viral myocarditis. Virus-triggered cytotoxicity and the activity of ... ...

    Abstract Infection of mice with Coxsackievirus B3 (CVB3) triggers inflammation of the heart and this mouse model is commonly used to investigate underlying mechanisms and therapeutic aspects for viral myocarditis. Virus-triggered cytotoxicity and the activity of infiltrating immune cells contribute to cardiac tissue injury. In addition to cardiac manifestation, CVB3 causes cell death and inflammation in the pancreas. The resulting pancreatitis represents a severe burden and under such experimental conditions, analgesics may be supportive to improve the animals' well-being. Notably, several known mechanisms exist by which analgesics can interfere with the immune system and thereby compromise the feasibility of the model. We set up a study aiming to improve animal welfare while ensuring model integrity and investigated how tramadol, an opioid, affects virus-induced pathogenicity and immune response in the heart. Tramadol was administered seven days prior to a CVB3 infection in C57BL/6 mice and treatment was continued until the day of analysis. Tramadol had no effect on the virus titer or viral pathogenicity in the heart tissue and the inflammatory response, a hallmark of myocardial injury, was maintained. Our results show that tramadol exerts no disruptive effects on the CVB3 myocarditis mouse model and, therefore, the demonstrated protocol should be considered as a general analgesic strategy for CVB3 infection.
    Mesh-Begriff(e) Analgesia/methods ; Animals ; Coxsackievirus Infections/complications ; Disease Models, Animal ; Enterovirus B, Human/pathogenicity ; Heart/drug effects ; Heart/virology ; Male ; Mice ; Mice, Inbred C57BL ; Myocarditis/drug therapy ; Myocarditis/virology ; Tramadol/pharmacology ; Tramadol/therapeutic use ; Viral Load/drug effects ; Virus Replication/drug effects
    Chemische Substanzen Tramadol (39J1LGJ30J)
    Sprache Englisch
    Erscheinungsdatum 2021-06-24
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v13071222
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Effect of SARS-CoV-2 mRNA-Vaccine on the Induction of Myocarditis in Different Murine Animal Models.

    Zirkenbach, Vanessa A / Ignatz, Rebecca M / Öttl, Renate / Cehreli, Zeynep / Stroikova, Vera / Kaya, Mansur / Lehmann, Lorenz H / Preusch, Michael R / Frey, Norbert / Kaya, Ziya

    International journal of molecular sciences

    2023  Band 24, Heft 5

    Abstract: In the course of the SARS-CoV-2 pandemic, vaccination safety and risk factors of SARS-CoV-2 mRNA-vaccines were under consideration after case reports of vaccine-related side effects, such as myocarditis, which were mostly described in young men. However, ...

    Abstract In the course of the SARS-CoV-2 pandemic, vaccination safety and risk factors of SARS-CoV-2 mRNA-vaccines were under consideration after case reports of vaccine-related side effects, such as myocarditis, which were mostly described in young men. However, there is almost no data on the risk and safety of vaccination, especially in patients who are already diagnosed with acute/chronic (autoimmune) myocarditis from other causes, such as viral infections, or as a side effect of medication and treatment. Thus, the risk and safety of these vaccines, in combination with other therapies that could induce myocarditis (e.g., immune checkpoint inhibitor (ICI) therapy), are still poorly assessable. Therefore, vaccine safety, with respect to worsening myocardial inflammation and myocardial function, was studied in an animal model of experimentally induced autoimmune myocarditis. Furthermore, it is known that ICI treatment (e.g., antibodies (abs) against PD-1, PD-L1, and CTLA-4, or a combination of those) plays an important role in the treatment of oncological patients. However, it is also known that treatment with ICIs can induce severe, life-threatening myocarditis in some patients. Genetically different A/J (most susceptible strain) and C57BL/6 (resistant strain) mice, with diverse susceptibilities for induction of experimental autoimmune myocarditis (EAM) at various age and gender, were vaccinated twice with SARS-CoV-2 mRNA-vaccine. In an additional A/J group, an autoimmune myocarditis was induced. In regard to ICIs, we tested the safety of SARS-CoV-2 vaccination in PD-1
    Mesh-Begriff(e) Male ; Animals ; Humans ; Mice ; Mice, Inbred C57BL ; Myocarditis ; COVID-19 Vaccines ; CTLA-4 Antigen ; SARS-CoV-2 ; Programmed Cell Death 1 Receptor ; COVID-19 ; Inflammation ; Drug-Related Side Effects and Adverse Reactions ; Antibodies ; Models, Animal ; RNA, Messenger ; Vaccination
    Chemische Substanzen COVID-19 Vaccines ; CTLA-4 Antigen ; Programmed Cell Death 1 Receptor ; Antibodies ; RNA, Messenger
    Sprache Englisch
    Erscheinungsdatum 2023-03-06
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24055011
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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