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Find video protocols related to scientific articles indexed in Pubmed.
Potential celiac children: 9-year follow-up on a gluten-containing diet.
Am. J. Gastroenterol.
PUBLISHED: 02-28-2014
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Potential celiac disease (CD) is defined by the presence of serum anti-tissue-transglutaminase (anti-TG2) antibodies and normal duodenal mucosa. The major clinical problem is the management of asymptomatic patients and how to predict the development of villous atrophy. This prospective longitudinal cohort study describes the natural history of potential CD up to 9 years and explores risk factors associated with the development of mucosal damage.
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Autophagy genes variants and paediatric Crohn's disease phenotype: a single-centre experience.
Dig Liver Dis
PUBLISHED: 02-10-2014
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Little evidence demonstrating the correlation between several single nucleotide polymorphisms and a specific phenotype of Crohn's disease has been reported in children. We investigated the relationship between autophagy genes variants and clinical features in our children with Crohn's disease.
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Celiac disease in the Mediterranean area.
BMC Gastroenterol
PUBLISHED: 01-30-2014
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The World Gastroenterology Organization recommends developing national guidelines for the diagnosis of Celiac Disease (CD): hence a profile of the diagnosis of CD in each country is required. We aim to describe a cross-sectional picture of the clinical features and diagnostic facilities in 16 countries of the Mediterranean basin. Since a new ESPGHAN diagnostic protocol was recently published, our secondary aim is to estimate how many cases in the same area could be identified without a small intestinal biopsy.
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Oversecretion of Soluble CTLA-4 in Various Autoimmune Diseases Overlapping Celiac Disease.
Genet Test Mol Biomarkers
PUBLISHED: 10-19-2013
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Aim: To evaluate the levels of soluble CTLA-4 (sCTLA-4) in sera of celiac disease (CD) patients with overlapping autoimmune diseases (OAD; diabetes mellitus, autoimmune thyroid diseases, inflammatory bowel diseases, and autoimmune polyendocrine syndromes). Methods: Sera from Italian patients with CD were obtained and enzyme-linked immunosorbent assay was used to measure sCTLA-4. Results: Consistently high serum sCTLA-4 levels were observed in CD (13.20?ng/mL, p<0.0001) and OAD (19.48?ng/mL, p<0.0001) compared to normal controls. A significant increase in the level of serum sCTLA-4 was observed in OAD (p=0.0273) compared to CD alone. At variance, no significant difference in the sCTLA-4 levels was observed when single OAD were compared. Conclusion: The present study shows for the first time a statistically significant increase of serum sCTLA-4 levels in CD patients with associated autoimmune disease (namely, CD and OAD) versus patients with CD alone. Previously, the potential genetic associations of several CTLA-4 polymorphisms to susceptibility to autoimmune diseases have been described, although the relationship between CTLA-4 polymorphisms and the ability to produce the soluble form is not fully clarified. CTLA-4 is a strong actor in the adaptive response: our data give supportive evidence of the common background of autoimmune diseases.
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An undigested gliadin peptide activates innate immunity and proliferative signaling in enterocytes: the role in celiac disease.
Am. J. Clin. Nutr.
PUBLISHED: 08-21-2013
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On ingestion of gliadin, the major protein component of wheat and other cereals, the celiac intestine is characterized by the proliferation of crypt enterocytes with an inversion of the differentiation/proliferation program. Gliadins and A-gliadin peptide P31-43, in particular, act as growth factors for crypt enterocytes in patients with celiac disease (CD). The effects of gliadin on crypt enterocyte proliferation and activation of innate immunity are mediated by epidermal growth factors (EGFs) and innate immunity mediators [interleukin 15 (IL15)].
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Immunoregulatory pathways are active in the small intestinal mucosa of patients with potential celiac disease.
Am. J. Gastroenterol.
PUBLISHED: 01-23-2013
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Potential celiac disease (CD) relates to subjects with a normal small intestinal mucosa who are at increased risk of developing CD as indicated by positive CD-associated serology. The objective of this study was to investigate in the small intestinal mucosa of such patients the state of immunological activation with special emphasis on immunoregulatory circuits.
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The Pediatric Symptom Checklist as screening tool for neurological and psychosocial problems in a paediatric cohort of patients with coeliac disease.
Acta Paediatr.
PUBLISHED: 01-23-2013
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To screen for neurological and behavioural disorders in a paediatric cohort of patients with coeliac disease (CD) in order to detect possible differences related to compliance with gluten-free diet (GFD).
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A Celiac Cellular Phenotype, with Altered LPP Sub-Cellular Distribution, Is Inducible in Controls by the Toxic Gliadin Peptide P31-43.
PLoS ONE
PUBLISHED: 01-01-2013
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Celiac disease (CD) is a frequent inflammatory intestinal disease, with a genetic background, caused by gliadin-containing food. Undigested gliadin peptides P31-43 and P57-68 induce innate and adaptive T cell-mediated immune responses, respectively. Alterations in the cell shape and actin cytoskeleton are present in celiac enterocytes, and gliadin peptides induce actin rearrangements in both the CD mucosa and cell lines. Cell shape is maintained by the actin cytoskeleton and focal adhesions, sites of membrane attachment to the extracellular matrix. The locus of the human Lipoma Preferred Partner (LPP) gene was identified as strongly associated with CD using genome-wide association studies (GWAS). The LPP protein plays an important role in focal adhesion architecture and acts as a transcription factor in the nucleus. In this study, we examined the hypothesis that a constitutive alteration of the cell shape and the cytoskeleton, involving LPP, occurs in a cell compartment far from the main inflammation site in CD fibroblasts from skin explants. We analyzed the cell shape, actin organization, focal adhesion number, focal adhesion proteins, LPP sub-cellular distribution and adhesion to fibronectin of fibroblasts obtained from CD patients on a Gluten-Free Diet (GFD) and controls, without and with treatment with A-gliadin peptide P31-43. We observed a "CD cellular phenotype" in these fibroblasts, characterized by an altered cell shape and actin organization, increased number of focal adhesions, and altered intracellular LPP protein distribution. The treatment of controls fibroblasts with gliadin peptide P31-43 mimics the CD cellular phenotype regarding the cell shape, adhesion capacity, focal adhesion number and LPP sub-cellular distribution, suggesting a close association between these alterations and CD pathogenesis.
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Enterocyte proliferation and signaling are constitutively altered in celiac disease.
PLoS ONE
PUBLISHED: 01-01-2013
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Celiac disease (CD) occurs frequently, and is caused by ingestion of prolamins from cereals in subjects with a genetic predisposition. The small intestinal damage depends on an intestinal stress/innate immune response to certain gliadin peptides (e.g., A-gliadin P31-43) in association with an adaptive immune response to other gliadin peptides (e.g., A-gliadin P57-68). Gliadin and peptide P31-43 affect epithelial growth factor receptor (EGFR) signaling and CD enterocyte proliferation. The reason why the stress/innate immune and proliferative responses to certain gliadin peptides are present in CD and not in control intestine is so far unknown. The aim of this work is to investigate if, in CD, a constitutive alteration of enterocyte proliferation and signaling exists that may represent a predisposing condition to the damaging effects of gliadin. Immunofluorescence and immunohistochemistry were used to study signaling in CD fibroblasts and intestinal biopsies. Western blot (WB) analysis, immunoprecipitation, and quantitative PCR were also used. We found in CD enterocytes enhancement of both proliferation and Epidermal Growth Factor Receptor (EGFR)/ligand system. In CD enterocytes and fibroblasts we found increase of the phosphorylated downstream signaling molecule Extracellular Signal Regulated Kinase (ERK); block of the ERK activation normalizes enterocytes proliferation in CD mucosa. In conclusion the same pathway, which gliadin and gliadin peptide P31-43 can interfere with, is constitutively altered in CD cells. This observation potentially explains the specificity of the damaging effects of certain gliadin peptides on CD intestine.
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Gene expression profile of peripheral blood monocytes: a step towards the molecular diagnosis of celiac disease?
PLoS ONE
PUBLISHED: 01-01-2013
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Celiac disease (CD) is a multifactorial autoimmune disease induced by ingestion of gluten in genetically predisposed individuals. Despite technological progress, the diagnosis of CD is still based on duodenal biopsy as it was 50 years ago. In this study we analysed the expression of CD-associated genes in small bowel biopsies of patients and controls in order to explore the multivariate pathway of the expression profile of CD patients. Then, using multivariant discriminant analysis, we evaluated whether the expression profiles of these genes in peripheral blood monocytes (PBMs) differed between patients and controls.
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Potential celiac patients: a model of celiac disease pathogenesis.
PLoS ONE
PUBLISHED: 03-23-2011
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Potential celiacs have the celiac type HLA, positive anti-transglutaminase antibodies but no damage at small intestinal mucosa. Only a minority of them develops mucosal lesion. More than 40 genes were associated to Celiac Disease (CD) but we still do not know how those pathways transform a genetically predisposed individual into an affected person. The aim of the study is to explore the genetic features of Potential CD individuals.
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Gliadin-mediated proliferation and innate immune activation in celiac disease are due to alterations in vesicular trafficking.
PLoS ONE
PUBLISHED: 01-18-2011
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Damage to intestinal mucosa in celiac disease (CD) is mediated both by inflammation due to adaptive and innate immune responses, with IL-15 as a major mediator of the innate immune response, and by proliferation of crypt enterocytes as an early alteration of CD mucosa causing crypts hyperplasia. We have previously shown that gliadin peptide P31-43 induces proliferation of cell lines and celiac enterocytes by delaying degradation of the active epidermal growth factor receptor (EGFR) due to delayed maturation of endocytic vesicles. IL-15 is increased in the intestine of patients affected by CD and has pleiotropic activity that ultimately results in immunoregulatory cross-talk between cells belonging to the innate and adaptive branches of the immune response. Aims of this study were to investigate the role of P31-43 in the induction of cellular proliferation and innate immune activation.
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Potential celiac disease in type 1 diabetes: a multicenter study.
Diabetes Res. Clin. Pract.
PUBLISHED: 01-15-2011
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To describe the prevalence of potential celiac disease (pot-CD) in young patients with type 1 diabetes mellitus (T1DM) and characterize their clinical features.
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Intestinal deposits of anti-tissue transglutaminase IgA in childhood celiac disease.
Dig Liver Dis
PUBLISHED: 01-05-2011
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High serum levels of anti-tissue-transglutaminase-2 IgA antibodies (anti-TG2), which are produced and deposited in the intestine, characterize celiac disease.
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The PreventCD Study design: towards new strategies for the prevention of coeliac disease.
Eur J Gastroenterol Hepatol
PUBLISHED: 10-29-2010
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PreventCD (www.preventcd.com) is a European multicentre study, which studies the influence of infant nutrition, and that of genetic, immunologic and environmental factors, on the risk of developing coeliac disease (CD). The hypothesis is that it is possible to induce tolerance to gluten by introducing small quantities of gluten to infants, preferably while they are still being breast-fed, and that this might also reduce the risk for related autoimmune disorders.
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Safety for patients with celiac disease of baked goods made of wheat flour hydrolyzed during food processing.
Clin. Gastroenterol. Hepatol.
PUBLISHED: 09-21-2010
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Celiac disease (CD) is characterized by an inflammatory response to wheat gluten, rye, and barley proteins. Fermentation of wheat flour with sourdough lactobacilli and fungal proteases decreases the concentration of gluten. We evaluated the safety of daily administration of baked goods made from this hydrolyzed form of wheat flour to patients with CD.
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Natural history of potential celiac disease in children.
Clin. Gastroenterol. Hepatol.
PUBLISHED: 05-13-2010
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The presence of celiac disease-associated autoantibodies (antiendomysium and antitissue transglutaminase [anti-TG2]) with normal jejunal mucosa indicate potential celiac disease. We performed a prospective, 3-year cohort study to determine the natural history of potential celiac disease in children.
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Gliadin peptide P31-43 localises to endocytic vesicles and interferes with their maturation.
PLoS ONE
PUBLISHED: 03-24-2010
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Celiac Disease (CD) is both a frequent disease (1:100) and an interesting model of a disease induced by food. It consists in an immunogenic reaction to wheat gluten and glutenins that has been found to arise in a specific genetic background; however, this reaction is still only partially understood. Activation of innate immunity by gliadin peptides is an important component of the early events of the disease. In particular the so-called "toxic" A-gliadin peptide P31-43 induces several pleiotropic effects including Epidermal Growth Factor Receptor (EGFR)-dependent actin remodelling and proliferation in cultured cell lines and in enterocytes from CD patients. These effects are mediated by delayed EGFR degradation and prolonged EGFR activation in endocytic vesicles. In the present study we investigated the effects of gliadin peptides on the trafficking and maturation of endocytic vesicles.
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Italian paediatricians approach to coeliac disease diagnosis.
J. Pediatr. Gastroenterol. Nutr.
PUBLISHED: 07-11-2009
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The aim of this study was to investigate the current implementation of the 1990 ESPGHAN criteria for the diagnosis of celiac disease (CD) in Italy to form a foundation for their revision. From September 2006 to March 2007 a nationwide questionnaire concerning current diagnostic methods was sent by mail to 54 Italian centres for the diagnosis of CD, which were distributed across the entire national territory. The questionnaire investigated the tests performed, diagnostic criteria currently used, and the management of some special cases in each centre. Eighty percent of the centres use anti-tissue transglutaminase to diagnose CD and anti-endomysium antibodies to confirm the results. Fifty-five percent still use anti-gliadin antibodies. A total of 87.5% of centres perform HLA typing, especially in first-degree relatives and in unclear diagnosis. Regarding histology, 67.5% of centres consider an infiltrative lesion consistent with diagnosis of CD. The majority of centres (85%) use the 1990 ESPGHAN criteria for both symptomatic and asymptomatic patients, but 80% do not perform a second biopsy in asymptomatic cases or a gluten challenge in children younger than 2 years of age. Furthermore, most centres (72.5%) do not prescribe a gluten-free diet to asymptomatic patients with positive serology and normal bowel architecture (ie, potential cases), but they do program a careful follow-up. In conclusion, ESPGHAN criteria are widely followed by Italian CD centres. However, their revision may be useful, but it should be evidence based. Large, multicentre studies are greatly needed.
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Majority of children with type 1 diabetes produce and deposit anti-tissue transglutaminase antibodies in the small intestine.
Diabetes
PUBLISHED: 04-28-2009
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Anti-tissue transglutaminase (TG2) antibodies are the serological marker of celiac disease. Given the close association between celiac disease and type 1 diabetes, we investigated the production and deposition of anti-TG2 antibodies in the jejunal mucosa of type 1 diabetic children.
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.