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  1. Book ; Online ; E-Book: Wheat syndromes

    Schuppan, Detlef / Gisbert-Schuppan, Kristin

    how wheat, gluten and ATI cause inflammation, IBS and autoimmune diseases

    2019  

    Author's details Detlef Schuppan, Kristin Gisbert-Schuppan
    Keywords Gastroenterology ; Medicine ; Immunology
    Subject code 616.33
    Language English
    Size 1 Online-Ressource (XV, 142 Seiten)
    Publisher Springer
    Publishing place Cham
    Publishing country Switzerland
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT021585985
    ISBN 978-3-030-19023-1 ; 9783030190224 ; 3-030-19023-4 ; 3030190226
    DOI 10.1007/978-3-030-19023-1
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book: Tägliches Brot: Krank durch Weizen, Gluten und ATI

    Schuppan, Detlef / Gisbert-Schuppan, Kristin

    2018  

    Author's details Detlef Schuppan, Kristin Gisbert-Schuppan
    Keywords Gluten ; Weizen ; ATI ; Nahrungsmittelallergie ; Nahrungsmittelunverträglichkeit ; Lebensmittelallergie ; Lebensmittelunverträglichkeit ; Weizenallergie ; Glutenunverträglichkeit ; Brot ; Reizdarm ; Reizdarmsyndrom ; Zöliakie ; Mehlallergie ; Amylase-Trypsin-Inhibitoren ; Unverträglichkeit ; Weizenprodukt
    Subject ATI ; ATIs ; Amylase-Trypsin-Inhibitor ; Alpha-Amylase-Trypsin-Inhibitoren ; α-Amylase-Trypsin-Inhibitoren ; Wheat amylase trypsin inhibitors ; Klebereiweiss ; Kleberproteine ; Weizenerzeugnis ; Weizen ; Getreideallergie ; Coeliakie ; Heubner-Herter-Krankheit ; Herter-Infantilismus ; Intestinaler Infantilismus
    Subject code 610
    Language German
    Size XIII, 144 Seiten, mit 30 farbigen Abbildungen, 23.5 cm x 15.5 cm
    Publisher Springer
    Publishing place Berlin
    Publishing country Germany
    Document type Book
    HBZ-ID HT019660634
    ISBN 978-3-662-56043-3 ; 3-662-56043-7 ; 9783662560440 ; 3662560445
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    Vcl available for loan (reading room) Lesesaal EG Gesundheitsliteratur

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  3. Article ; Online: Further Progress to Quantify Histological Damage in Patients With Celiac Disease.

    Schuppan, Detlef / Rostami, Kamran

    Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association

    2024  

    Language English
    Publishing date 2024-01-24
    Publishing country United States
    Document type Editorial
    ZDB-ID 2119789-1
    ISSN 1542-7714 ; 1542-3565
    ISSN (online) 1542-7714
    ISSN 1542-3565
    DOI 10.1016/j.cgh.2024.01.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Serum connective tissue markers as predictors of advanced fibrosis in patients with chronic hepatitis B and D.

    Seven, Gülseren / Karatayli, Senem Ceren / Köse, S Kenan / Yakut, Mustafa / Kabaçam, Gökhan / Törüner, Murat / Heper, Aylin Okçu / Voelker, Michael / Erden, Esra / Bozdayi, A Mithat / Uzunalımoğlu, Ozden / Bozkaya, Hakan / Yurdaydin, Cihan / Schuppan, Detlef

    The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology

    2011  Volume 22, Issue 3, Page(s) 305–314

    Abstract: ... hepatitis B and D. All patients had compensated liver disease. Using the METAVIR score, advanced disease was ... In conclusion, advanced liver fibrosis in chronic hepatitis B and D may be predicted with use of these two ...

    Abstract Background/aims: Liver biopsy to assess fibrosis is invasive and prone to sampling error. While algorithms of serum markers to predict fibrosis stage have been described for chronic hepatitis C, these cannot be applied equally well to hepatitis B.
    Methods: We therefore determined 9 serum fibrosis markers, liver biochemical tests and ultrasound parameters in 109 consecutive adult patients with chronic hepatitis B and D. All patients had compensated liver disease. Using the METAVIR score, advanced disease was defined as fibrosis stage ≥F2, and active inflammation as grade ≥A2. A gold standard was created considering splenomegaly and/or platelets <150,000 as indicators of advanced fibrosis irrespective of histology. Area under receiver operating characteristics curves was used for assessment of single markers and odds ratio for their combinations.
    Results: Patients with advanced disease were older, had lower albumin, higher gamma glutamyl transferase and lower platelet. Levels of 6 of the 9 fibrosis markers, tissue inhibitor of metalloproteinases-1, procollagen type III aminoterminal propeptide, matrix metalloproteinase-2, laminin, hyaluronan and collagen IV correlated with advanced fibrosis. Markers useful for fibrosis prediction also predicted marked inflammation. Using the gold standard, age, prothrombin time, gamma glutamyl transferase and albumin were independent predictors of fibrosis with odds ratio's of 3.11, 4.18, 3.35 and 5.25, respectively. Their combined use predicted fibrosis with an odds ratio of 228.8. Tissue inhibitor of metalloproteinases-1 and hyaluronan were powerful predictors of fibrosis (Odds ratio's of 8.65 and 8.38). Their combined use revealed an odds ratio of 28.6, when compared with the gold standard.
    Conclusion: In conclusion, advanced liver fibrosis in chronic hepatitis B and D may be predicted with use of these two fibrosis markers.
    MeSH term(s) Adult ; Analysis of Variance ; Biomarkers/blood ; Biopsy ; Female ; Hepatitis B, Chronic/blood ; Hepatitis B, Chronic/diagnostic imaging ; Hepatitis D, Chronic/blood ; Hepatitis D, Chronic/diagnostic imaging ; Humans ; Hyaluronic Acid/blood ; Liver Cirrhosis/blood ; Liver Cirrhosis/diagnostic imaging ; Liver Function Tests ; Logistic Models ; Male ; Predictive Value of Tests ; ROC Curve ; Tissue Inhibitor of Metalloproteinase-1/blood ; Ultrasonography
    Chemical Substances Biomarkers ; Tissue Inhibitor of Metalloproteinase-1 ; Hyaluronic Acid (9004-61-9)
    Language English
    Publishing date 2011-08-01
    Publishing country Turkey
    Document type Journal Article
    ZDB-ID 1340275-4
    ISSN 2148-5607 ; 1300-4948
    ISSN (online) 2148-5607
    ISSN 1300-4948
    DOI 10.4318/tjg.2011.0217
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: How Future Pharmacologic Therapies for Celiac Disease Will Complement the Gluten-Free Diet.

    Discepolo, Valentina / Kelly, Ciarán P / Koning, Frits / Schuppan, Detlef

    Gastroenterology

    2024  

    Abstract: The only proven treatment for celiac disease is adherence to a strict, lifelong, gluten-free diet. However, complete dietary gluten avoidance is challenging and a substantial number of patients do not respond fully, clinically, or histologically, despite ...

    Abstract The only proven treatment for celiac disease is adherence to a strict, lifelong, gluten-free diet. However, complete dietary gluten avoidance is challenging and a substantial number of patients do not respond fully, clinically, or histologically, despite their best efforts. As celiac disease is common and its central pathophysiology is well elucidated, it has become attractive for drug development to address the limitations of dietary treatment. Most efforts address nonresponsive celiac disease, defined as continued symptoms and/or signs of disease activity despite a gluten-free diet, including the more severe forms of refractory celiac disease, types I and II. An increasing spectrum of therapeutic approaches target defined mechanisms in celiac disease pathogenesis and some have advanced to current phase 2 and 3 clinical studies. We discuss these approaches in terms of potential efficiency, practicability, safety, and need, as defined by patients, regulatory authorities, health care providers, and payors.
    Language English
    Publishing date 2024-04-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2024.02.050
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 572: Show issues

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  6. Article ; Online: Macrophages and platelets in liver fibrosis and hepatocellular carcinoma.

    Casari, Martina / Siegl, Dominik / Deppermann, Carsten / Schuppan, Detlef

    Frontiers in immunology

    2023  Volume 14, Page(s) 1277808

    Abstract: During fibrosis, (myo)fibroblasts deposit large amounts of extracellular matrix proteins, thereby replacing healthy functional tissue. In liver fibrosis, this leads to the loss of hepatocyte function, portal hypertension, variceal bleeding, and increased ...

    Abstract During fibrosis, (myo)fibroblasts deposit large amounts of extracellular matrix proteins, thereby replacing healthy functional tissue. In liver fibrosis, this leads to the loss of hepatocyte function, portal hypertension, variceal bleeding, and increased susceptibility to infection. At an early stage, liver fibrosis is a dynamic and reversible process, however, from the cirrhotic stage, there is significant progression to hepatocellular carcinoma. Both liver-resident macrophages (Kupffer cells) and monocyte-derived macrophages are important drivers of fibrosis progression, but can also induce its regression once triggers of chronic inflammation are eliminated. In liver cancer, they are attracted to the tumor site to become tumor-associated macrophages (TAMs) polarized towards a M2- anti-inflammatory/tumor-promoting phenotype. Besides their role in thrombosis and hemostasis, platelets can also stimulate fibrosis and tumor development by secreting profibrogenic factors and regulating the innate immune response, e.g., by interacting with monocytes and macrophages. Here, we review recent literature on the role of macrophages and platelets and their interplay in liver fibrosis and hepatocellular carcinoma.
    MeSH term(s) Humans ; Carcinoma, Hepatocellular/pathology ; Esophageal and Gastric Varices/metabolism ; Esophageal and Gastric Varices/pathology ; Liver Neoplasms/pathology ; Gastrointestinal Hemorrhage ; Liver Cirrhosis ; Macrophages ; Fibrosis
    Language English
    Publishing date 2023-12-05
    Publishing country Switzerland
    Document type Journal Article ; Review ; 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.2023.1277808
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Measurement of Reactive Oxygen and Nitrogen Species in Living Cells Using the Probe 2',7'-Dichlorodihydrofluorescein.

    Dornas, Waleska / Schuppan, Detlef

    Bio-protocol

    2021  Volume 11, Issue 24, Page(s) e4279

    Abstract: Reactive oxygen species and reactive nitrogen species (RONS) are involved in programmed cell death in the context of numerous degenerative and chronic diseases. In particular, the ability of cells to maintain redox homeostasis is necessary for an ... ...

    Abstract Reactive oxygen species and reactive nitrogen species (RONS) are involved in programmed cell death in the context of numerous degenerative and chronic diseases. In particular, the ability of cells to maintain redox homeostasis is necessary for an adaptive cellular response to adverse conditions that can cause damage to proteins and DNA, resulting in apoptosis and genetic mutations. Here, we focus on the 2',7'-dichlorodihydrofluorescein diacetate (DCFH
    Language English
    Publishing date 2021-12-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2833269-6
    ISSN 2331-8325 ; 2331-8325
    ISSN (online) 2331-8325
    ISSN 2331-8325
    DOI 10.21769/BioProtoc.4279
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: [No title information]

    Stölzel, Ulrich / Schuppan, Detlef

    Deutsche medizinische Wochenschrift (1946)

    2021  Volume 146, Issue 23, Page(s) 1578–1579

    Title translation Erwiderung auf den Leserbrief zum Beitrag „Neue Therapieoption für akute hepatische Porphyrien“.
    MeSH term(s) Humans ; Porphobilinogen Synthase ; Porphyrias, Hepatic
    Chemical Substances Porphobilinogen Synthase (EC 4.2.1.24)
    Language German
    Publishing date 2021-11-26
    Publishing country Germany
    Document type Letter ; Comment
    ZDB-ID 200446-x
    ISSN 1439-4413 ; 0012-0472
    ISSN (online) 1439-4413
    ISSN 0012-0472
    DOI 10.1055/a-1585-8256
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Co-factors, Microbes, and Immunogenetics in Celiac Disease to Guide Novel Approaches for Diagnosis and Treatment.

    Verdu, Elena F / Schuppan, Detlef

    Gastroenterology

    2021  Volume 161, Issue 5, Page(s) 1395–1411.e4

    Abstract: Celiac disease (CeD) is a frequent immune-mediated disease that affects not only the small intestine but also many extraintestinal sites. The role of gluten proteins as dietary triggers, HLA-DQ2 or -DQ8 as major necessary genetic predisposition, and ... ...

    Abstract Celiac disease (CeD) is a frequent immune-mediated disease that affects not only the small intestine but also many extraintestinal sites. The role of gluten proteins as dietary triggers, HLA-DQ2 or -DQ8 as major necessary genetic predisposition, and tissue transglutaminase (TG2) as mechanistically involved autoantigen, are unique features of CeD. Recent research implicates many cofactors working in synergism with these key triggers, including the intestinal microbiota and their metabolites, nongluten dietary triggers, intestinal barrier defects, novel immune cell phenotypes, and mediators and cytokines. In addition, apart from HLA-DQ2 and -DQ8, multiple and complex predisposing genetic factors and interactions have been defined, most of which overlap with predispositions in other, usually autoimmune, diseases that are linked to CeD. The resultant better understanding of CeD pathogenesis, and its manifold manifestations has already paved the way for novel therapeutic approaches beyond the lifelong strict gluten-free diet, which poses a burden to patients and often does not lead to complete mucosal healing. Thus, supported by improved mouse models for CeD and in vitro organoid cultures, several targeted therapies are in phase 2-3 clinical studies, such as highly effective gluten-degrading oral enzymes, inhibition of TG2, cytokine therapies, induction of tolerance to gluten ingestion, along with adjunctive and preventive approaches using beneficial probiotics and micronutrients. These developments are supported by novel noninvasive markers of CeD severity and activity that may be used as companion diagnostics, allow easy-to perform and reliable monitoring of patients, and finally support personalized therapy for CeD.
    MeSH term(s) Animals ; Bacteria/immunology ; Bacteria/pathogenicity ; Celiac Disease/genetics ; Celiac Disease/immunology ; Celiac Disease/microbiology ; Celiac Disease/therapy ; Disease Models, Animal ; Gastrointestinal Microbiome ; Genetic Predisposition to Disease ; Glutens/immunology ; Host-Pathogen Interactions ; Humans ; Immunogenetic Phenomena ; Immunologic Tests ; Intestines/immunology ; Intestines/microbiology ; Intestines/pathology ; Phenotype ; Predictive Value of Tests ; Prognosis ; Risk Factors
    Chemical Substances Glutens (8002-80-0)
    Language English
    Publishing date 2021-08-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2021.08.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The Promise of Novel Therapies to Abolish Gluten Immunogenicity in Celiac Disease.

    Cerf-Bensussan, Nadine / Schuppan, Detlef

    Gastroenterology

    2021  Volume 161, Issue 1, Page(s) 21–24

    MeSH term(s) Animals ; Celiac Disease/etiology ; Celiac Disease/immunology ; Celiac Disease/therapy ; Diet, Gluten-Free ; Disease Models, Animal ; Glutens/adverse effects ; Glutens/immunology ; Glutens/metabolism ; Humans ; Mice
    Chemical Substances Glutens (8002-80-0)
    Language English
    Publishing date 2021-04-20
    Publishing country United States
    Document type Editorial ; Introductory Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2021.04.031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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