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    Browsing Center for Celiac Research by Subject "Celiac Disease"

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    Now showing items 21-40 of 76

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        Celiac Disease in at Risk Groups in Southern California

        Pietzak, Michelle; Wolfe, Adam; Rongey, Christine; Monarch, Elaine; Bergwerk, Ari; Duh, Glenn; Naon, Hillel; Quiros, Antonio; Sinatra, Frank Raymond, M.D.; Yamaga, Ardath; et al. (2002)
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        Celiac Disease In Egypt: Preliminary Results Of A Pilot Screening Study In Schoolchildren

        Catassi, C. (Carlo); Abu-Zakry, Mona; Kryszak, Deborah; Fasano, Alessio (2004-05)
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        Comparison of Intestinal Tissue Damage and HLA Haplotypes Between American and Italian Celiac Disease Patients

        Drago, Sandro; Fornaroli, Fabiola; Sdepanian, Vera; Di Pierro, Mariarosaria; Kryszak, Deborah; Sewell, Palestine; Madeiros, Lisa; Horvath, Karoly, M.D.; Pietzak, Michelle; Catassi, C. (Carlo); et al. (2002)
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        Composition and Dynamic Changes of Gut Microbia in HLA DQ2/DQ8 Positive Babies at Risk of Celiac Disease: Preliminary Results

        Sellitto, Maria; Kryszak, Deborah; Bhatti, Bushra; Sturgeon, Craig; Puppa, Elaine L.; Ravel, Jacques, Ph.D.; Fasano, Alessio (2009)
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        DDW Meet the Professor Lunch, "Celiac Disease"

        Fasano, Alessio (2008-05-19)
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        Differences in HLA DQ2/DQ8 Haplotype and FOXP3 Gene Expression Between Celiac and Non-Celiac Down Syndrome Patients

        Serena, Gloria; Libreri, Davide; Sturgeon, Craig; Kryszak, Deborah; Lammers, Karen M.; Fasano, Alessio (2011)
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        Dilated Cardiomyopathy and Type 1 Diabetes in a Patient with Celiac Disease

        Gelfond, Daniel; Fasano, Alessio (2006)
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        Early Feeding Practices and their Impact on Development of Celiac Disease

        Fasano, Alessio; Catassi, C. (Carlo) (2010-10)
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        Effect Of the Gluten Free Diet on Serum Zonulin Levels and Autoimmune Biomarkers in Both Treated and Untreated Celiac Disease Patients

        Kryszak, Deborah; Neri, Elena; Palese, Teresa; Sapone, Anna; Counts, Donald R.; Not, Tarcisio; Catassi, C. (Carlo); Fasano, Alessio (2005)
        Background: It is well known that Celiac Disease (CD) can be associated with other autoimmune diseases (AD). It is however still unclear whether the CD-associated risk of other AD is related to ongoing gluten ingestion or simply depends on common genetic background. Zonulin, which is responsible for the modulation of intestinal permeability, is up regulated in CD and other AD, such as Type 1 diabetes. Our hypothesis is that the loss of barrier function secondary to zonulin increase in CD can be involved in the high risk for AD co-morbidity. Aim: To establish the changes of serum zonulin levels and serum autoimmune antibodies in patients with newly diagnosed CD and after treatment with the gluten-free diet (GFD). Patients and Methods: They were 54 patients diagnosed with CD (20 M and 34 F; mean age: 39y; biopsy-proven: 42/54). Associated AD were found in 8 subjects (2 Type 1 diabetes, 1 Graves’s disease, 5 rheumatoid arthritis). Serum samples were collected at diagnoses and after a mean period of 17 months of GFD (range 10-49). All serum samples were measured for auto-antibodies related to CD (anti-transglutaminase - tTG, anti-endomysial - EMA), Type 1 diabetes (IA-2: tyrosine phosphates, IAA: anti-insulin antibodies, GAD: glutamic acid decarboxilase), thyroiditis (TPO: thyreoperoxidase antibodies, TG: thyreoglobulin antibodies), and zonulin levels. Results: at CD diagnosis increased serum zonulin were found in 76 % and auto-antibodies were detected in 39 % (TPO: 21.7%, TG 19.6%, GAD 6.5%, ICA 4.4% and IA-2 2.5 %). After GFD, EMA and zonulin remained altered in 13% of patients, and tTG in 35% of the subjects. Some auto-antibodies decreased (TPO: 10.9%, GAD 4.4%), while other remained unchanged (TG 23.9%, ICA 4.4%, and IA-2 2.2 %). Seven out of 53 patients did not start the GFD. These subjects had altered zonulin, EMA, and tTG and 14% of them were auto-antibodies positive. In these subjects, both zonulin levels and serum auto-antibodies did not change at the follow-up evaluation. Conclusions: Untreated CD typically show zonulin up-regulation and increased prevalence of serum auto-antibodies. After treatment with GFD, serum zonulin levels tend to normalize, a situation that is associated with a decreased prevalence of some auto-antibodies (especially TPO). These results indirectly suggest that recovery of the intestinal barrier function can decrease the risk of associated autoimmune phenomena. These results also suggest that if the GFD is implemented early (less 30 years of age) the auto-antibodies will seroconvert, suggesting a possible protective roll against autoimmunity co-morbidity, if CD is diagnosed early and started on a GFD.
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        Elevated levels of Neuronal Tissue Transglutaminase (tTG) 6 in tTG 2 positive Schizophrenic Subjects

        Kryszak, Deborah; Choudhary, Somaera; Gregory, Patricia; Eaton, William W.; Cascella, Nicola; Fasano, Alessio (2011)
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        Elevated Levels of Neuronal Tissue Transglutaminase (tTG)6 in AGA-IgA Positive Schizophrenic Subjects

        Fasano, Alessio; Santora, Debby; Choudhary, Somaera; Eaton, William W.; Gregory, Patricia; Cascella, Nicola (2012)
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        Expression of Tight Junction Proteins in Diseases With Compromised Intestinal Barrier Function

        Tripathi, Amit; Clemente, Maria Grazia; Sapone, Anna; Musu, Maria Paola; De Virgiliis, Stefano; Fasano, Alessio (2006)
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        Fact Sheet on Irritable Bowel Syndrome and Celiac Disease

        University of Maryland, Baltimore. School of Medicine. Center for Celiac Disease
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        Food Related Gastrointestinal Diseases: Celiac disease

        Fasano, Alessio (2009)
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        Future options for treatments alternative to the gluten free diet

        Fasano, Alessio (2008)
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        Gliadin Binding to CXCR3 Causes Zonulin Release and Increased Intestinal Permeability

        Lammers, Karen M.; Brownley, Julie; Lu, Ruiliang; Sapone, Anna; Lu, Bao; Gerard, Craig John George, 1954-; Vogel, Stefanie N.; Fasano, Alessio (2006)
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        Gliadin Binding to CXCR3 Induces a MyD88- and G-Coupled Protein Receptor-Dependent Increased Intestinal Permeability and Zonulin Release

        Lammers, Karen M.; Lu, Ruiliang; Brownley, Julie; Sapone, Anna; Lu, Bao; Gerard, Craig John George, 1954-; Vogel, Stefanie N.; Fasano, Alessio (2007-10)
        Background & Premises: Celiac disease (CD) is an auto-immune enteropathy triggered by ingestion of gluten. Gliadin, a component of the grain protein gluten, is known to induce increased intestinal permeability, which is considered an early crucial biological event in the pathogenesis of CD. Zonulin induces tight junction disassembly. It is therefore considered to be involved in CD. In CD: An increased and persistant release of zonulin and a significant increase in intestinal permeability (S. Drago et al. Scand J Gastroenterol. 2006); Apical, but not basolateral, exposure to gliadin led to zonulin release (MG Clemente et al. Gut 2003). We recently identified the chemokine receptor CXCR3 as the receptor to which gliadin binds. Aim: to explore the function of CXCR3 after gliadin binding
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        Gliadin Induces Increased Intestinal Permeability, Zonulin Release, and Occludin Down-Regulation in an Ex-Vivo Human Intestinal Model of Celiac Disease

        Drago, Sandro; El Asmar, Ramzi; Iacono, Giuseppe; Di Pierro, Mariarosaria; Catassi, C. (Carlo); Fasano, Alessio; D’Agate, Cinzia (2003)
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        Gliadin Induces Zonulin Release, Occludin Down-Regulation, and Tight Junctions Disassembly in a Rat Animal Model

        Drago, Sandro; Di Pierro, Mariarosaria; Margaretten, Klara; Thakar, Manjusha; Fasano, Alessio (2001)
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        Gliadin Peptides Induce Increased Caco2 Monolayer Permeability and Tight Junction Protein ZO-1 Redistribution

        El Asmar, Ramzi; Zampini, Lucia; Galeazzi, Tiziana; Thakar, Manjusha; Drago, Sandro; Coppa, Giovanni Valentino; Fasano, Alessio; Catassi, C. (Carlo) (2003)
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