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Found 5 results

  1. Celiac.com 06/15/2010 - A clinical team conducted a functional analysis of celiac risk loci, and found that SH2B3 offers protection against bacterial infection. The team included Alexandra Zhernakova, Clara C. Elbers, Bart Ferwerda, Jihane Romanos, Gosia Trynka, Patrick C. Dubois, Carolien G.F. de Kovel, Lude Franke, Marije Oosting, Donatella Barisani, Maria Teresa Bardella, the Finnish Celiac Disease Study Group, Leo A.B. Joosten, Paivi Saavalainen, David A. van Heel, Carlo Catassi, Mihai G. Netea, and Cisca Wijmenga. Celiac disease has a fairly high morbidity, yet it is prevalent in Western populations at rates of of 1%–2%. So far, scientists don't understand why the celiac disease phenotype is so common despite its obvious negative impact on human health. This is especially true when one considers that doctors only developed a gluten-free diet to treat celiac disease in the 1950's. The research team scientists hypothesize that the high prevalence of celiac disease might suggest that the process of natural selection favors genes that trigger celiac disease, and thus, that the gene may convey some evolutionary advantage to those who inherit them. The study group included 8,154 controls from four European populations, and 195 individuals from a North African population. By examining haplotype lengths using the integrated haplotype score (iHS) method, the team looked at selection signatures for ten confirmed celiac-associated loci in several genome-wide data sets. They found consistent indications of positive selection for celiac-associated derived alleles in three loci: IL12A, IL18RAP, and SH2B3. For the SH2B3 risk allele, they also found a variation in allele frequency distribution (Fst) between HapMapphase II populations. Functional investigation of the effect of the SH2B3 genotype in response to lipopolysaccharide and muramyl dipeptide showed that carriers of the SH2B3 rs3184504*A risk allele provided more robust triggering of the NOD2 recognition pathway. This suggests that SH2B3 plays a role in protection against bacteria infection, and it provides a possible explanation for the selective sweep on SH2B3, which occurred sometime between 1,200 and 1,700 years ago. Source: AJHG - 2010, 04 May. doi:10.1016/j.ajhg.2010.05.004
  2. Celiac.com 12/26/2012 - Currently, researchers have found forty separate gene sites that they associate with celiac disease. They classify all of these sies as "low-penetrance," with the exception of the high-risk genotypes in the HLA-DQA1 and HLA-DQB1 genes, which are necessary, but not sufficient to cause the disease. So far, their efforts to find more such sites have been prevented by the strong effects from the known HLA loci and the genetically complex nature of the major histocompatibility complex (MHC). A research team wanted to test the hypothesis that additional celiac disease gene sites exist within the extended major histocompatibility complex (xMHC). The research team included Richard Ahn, Yuan Chun Ding, Joseph Murray, Alessio Fasano, Peter H. R. Green, Susan L. Neuhausen, and Chad Garner. They are variously affiliated with the Department of Epidemiology, University of California Irvine, Irvine, California, the Department of Population Sciences at eh Beckman Research Institute of City of Hope in Duarte, California, the Department of Medicine and Immunology at The Mayo Clinic in Rochester, Minnesota, the Center for Celiac Research at the University of Maryland School of Medicine in Baltimore, Maryland, and the Celiac Disease Center at Columbia University in New York, New York. To follow up on the hypothesis, they looked at a collection of single nucleotide polymorphisms, frequently called SNPs (pronounced “snips”), which are the most common type of genetic variation among people. For their study, the research team analyzed a set of 1898 SNPs for association across the 7.6 Mb xMHC region in 1668 patients with confirmed celiac disease, and 517 non-celiac control subjects. The researchers used what is called conditional recursive partitioning to create a marker of known HLA-DQA1 and HLA-DQB1 high-risk genotypes that was included in the association analysis to account for their effects. After accounting for the known effects, they used a linkage disequilibrium-based grouping procedure to estimate the number of independent celiac disease loci present in the xMHC. They found strong statistical evidence for four new independent celiac disease loci within the classic MHC region. This was the first time researchers have conducted a comprehensive association analysis of the xMHC in celiac disease that specifically accounts for the known HLA disease genotypes and the genetic complexity of the region. Source: PLoS One. 2012;7(5):e36926. Epub 2012 May 17.
  3. Celiac.com 06/23/2010 - A team of researchers evaluated the possibility of diagnosing celiac disease using quantitative analysis of videocapsule endoscopy images. The team included Edward J. Ciaccioa, Christina A. Tennysonb, Suzanne K. Lewisb, Suneet, Krishnareddy, Govind Bhagat, and Peter H.R. Green. They are variously associated with the Department of Pharmacology, Department of Medicine, Department of Pathology, Columbia University College of Physicians and Surgeons in New York. Images taken with videocapsule endoscopy can be useful for diagnosing celiac disease, but their interpretation is highly subjective. Quantitative disease markers might help to determine the degree of villous atrophy and efficacy of treatment. The team gathered capsule endoscopy images from a group of 11 celiac patients with small bowel pathology, and from a group of 10 control patients. Images had a resolution of 576×576 pixels, with 256 grayscale tones, and a frame-rate of 2 s−1. The team measured over 10×10 pixel sub-images for pixel brightness and image texture. They then averaged the results for for 56×56 sub-images per frame. For each patient, the team took measurements at from five locations in the proximal to distal small intestine. At each location, they figured measurements using 200 consecutive image frames (100 s). For classification with a nonlinear discriminant function, they computed mean frame-to-frame pixel brightness, image texture, periodicity in brightness, and estimated wall motion or intestinal motility. By pooling the data, the team found that images from the celiac group showed greater texture than did images from control group (p < 0.001). Images from the celiac disease group exhibited more frame-to-frame brightness variation as well (p = 0.032). Celiac patients showed longer dominant period of brightness in celiacs (p = 0.001), which may indicate reduced motility. Markers for three-dimensional nonlinear classification of celiacs versus controls showed sensitivity of 92.7% and specificity of 93.5%. Both celiac patients and control subjects showed an approximately linear association between dominant period and small intestinal transit time (r2 = 0.42 and r2 =0 .55, respectively). The results show that videocapsule images can be used to reveal villous atrophy throughout the small intestine, and to distinguish individuals with celiac disease from individuals without mucosal atrophy. Source: Science Direct. doi:10.1016/j.cmpb.2010.02.005
  4. Celiac.com 12/28/2009 - A team of researchers recently set out to compare continual monitoring of intraepithelial lymphocyte immunophenotype and clonality against snapshot analysis in the surveillance of refractory celiac disease. The research team was made up of H. Liu, R. Brais, A. Lavergne-Slove, Q. Jeng, K. Payne K, H. Ye, Z. Liu, J. Carreras, Y. Huang, C. M. Bacon, R. Hamoudi, V. Save, L. Venkatraman, P. G. Isaacson, J. Woodward, and M. Q. Du of Addenbrooke's Hospital, Cambridge, UK. Often, people with refractory celiac disease suffer from abnormal immunophenotype and monoclonality of intraepithelial lymphocytes (IELs). No good studies have been done to compare the utility of continual monitoring of IEL immunophenotype and clonality in monitoring refractory celiac disease (RCD). To address this deficiency, and to gather some data for comparison, the team used CD3e/CD8 double immunohistochemistry and PCR-based clonality analysis of the rearranged TCR genes to evaluate diagnostic and follow-up biopsies from 33 people with proven celiac disease, 7 with suspected refractory celiac disease, 41 with proven refractory celiac disease, and 20 with enteropathy associated T-cell lymphoma (including 11 evolved from RCD). The team found aberrant immunophenotype (CD3epsilon(+)CD8(-) IEL >/=40%) and monoclonality in occasional celiac disease biopsies, either transiently in celiac patients not following a gluten free diet, or in those who later developed refractory celiac disease, suspected RCD, or enteropathy associated T-cell lymphoma (EATL). By comparison, they found aberrant immunophenotype and monoclonality respectively in 30 of 41 (73%) and 24 of 37 (65%) biopsies at the time of diagnosis for refractory celiac disease. Among the patients with refractory celiac disease showed no such abnormalities in their diagnostic biopsies, 8 of 10 (80%) and 5 of 11 (45%) cases showed aberrant immunophenotype and monoclonality respectively upon follow-up. Whether found in initial or follow-up biopsies, the ongoing development of both aberrant immunophenotype and monoclonality is a common facet of refractory celiac disease. One key point was that the presence of both persistent monoclonality and aberrant immunophenotype, especially <>/=>80% CD3epsilon(+)CD8(-) IEL, was a strong predictor of enteropathy associated T-cell lymphoma development in patients with RCD (P=0.001). From these findings, the team found concludes that the continual monitoring of both immunophenotype and clonality of IEL is superior to snapshot analysis for diagnosis and follow-up of refractory celiac disease, and could provide a useful tool for surveillance of patients at risk of developing EATL. Source: Gut. 2009 Dec 8.
  5. Celiac.com 09/25/2008 - Mucosal inflammation of the small intestine, coupled with damage to intestinal villi, is a classic indication of celiac disease. Recently, doctors have begun to embrace the idea that some patients with positive celiac blood tests may have mucosal lesions that are too small to appear on routine histopathological analysis. In the first study of its kind, a team of researchers based in Ireland set out to analyze enterocyte morphology and cytoskeletal structures using a high content analysis technology. The research team was made up of doctors Bashir M. Mohamed, Conleth Feighery, Yvonne Williams, Anthony Davies, Dermot Kelleher, Yuri Volkov, Jacinta Kelly and Mohamed Abuzakouk. The team examined duodenal biopsies from 14 untreated and 10 treated celiac patients and from 20 non-celiac control subjects. They also investigated tissue sections from six study group subjects before and after the development of gluten-sensitive enteropathy. The research team used an anti-α-tubulin antibody to conduct immunohistochemical studies on paraffin-embedded tissue sections. They found important differences in enterocyte morphology and intracellular cytoskeletal structures in the patients with proven celiac disease and those in the study group. Moreover, the team observed that these changes existed in the study group prior to any indication of enteropathy, as determined by standard microscopy. This is the first time researchers have used high content analysis to show specific details of enterocyte morphology. Such an approach permits doctors to quantitatively analyze enterocyte intracellular structure from standard biopsy samples and allows for detection of minute changes that develop before the classic histological lesion. This process could become important for improving the diagnosis of celiac disease. If doctors can spot celiac-related intestinal lesions before they develop, they can begin to prevent celiac disease before it develops and thereby save lives. Central European Journal of Biology Volume 3, Number 3 / September, 2008
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