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Found 4 results

  1. Celiac.com 02/28/2018 - In an effort to discover more genes that trigger type 1 diabetes, a team of researchers recently conducted a large, prospective study of children at risk for type 1 diabetes. The end goal is to reveal more targets for treating or even preventing the disease. The research team included A Sharma, X Liu, D Hadley, W Hagopian, WM Chen, S Onengut-Gumuscu, C Törn, AK Steck, BI Frohnert, M Rewers, AG Ziegler, Å Lernmark, J Toppari, JP Krischer, B Akolkar, SS Rich, JX She; and TEDDY Study Group. The team identified six new chromosomal regions in young people who have already developed type 1 diabetes, or who have started making antibodies against their insulin-producing cells, often a step toward full-blown diabetes that requires lifelong insulin therapy. Their analysis of 5,806 individuals, which is published in the Journal of Autoimmunity, also confirms three regions already associated with one of those related conditions. The team observed two top autoantibodies. The first, called IAA, acts directly against insulin. The second, called GADA, acts against the enzyme glutamate decarboxylase, which regulates the insulin-producing beta cells in the pancreas. According to Dr. She, about 90 percent of patients with type 1 diabetes start with one of the autoantibodies, and many patients eventually end up with both. The second autoantibody may surface in a few days or even years later. They began this study with 176,586 SNPs, or single nucleotide polymorphisms. Nucleotides are basic building blocks of our genetic information. According to Sharma, the SNPs evaluated by TEDDY scientists were already linked with other autoimmune conditions like rheumatoid arthritis or celiac disease, but not type 1 diabetes. The researchers figured out which of these SNPs are different in TEDDY participants with type 1 diabetes versus those with Islet cell autoantibodies versus those with neither. Previous research has shown that the genes associated with IA and actual type 1 diabetes can differ. Dr. She says that even though clinicians regard Islet cell autoantibodies (IA) as a red flag for type 1 diabetes, not every child with IA goes on to develop diabetes, though multiple autoantibodies definitely increase that risk. The team notes that it is possible that the genes that promote IA development may differ from those that lead to full-blown disease progression. She says that this is the first study of gene identification for any disease to use this sort of longitudinal information. She add that this and other studies by the TEDDY research group help to clarify the search for important non-HLA genes by adding the "time to disease" perspective. Source: J Autoimmun. 2018 Jan 5. pii: S0896-8411(17)30739-4. doi: 10.1016/j.jaut.2017.12.008. The researchers are variously affiliated with the Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA; Division of Biostatistics and Data Science, Department of Population Health Sciences, Medical College of Georgia, Augusta University, Augusta, GA, US; the Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL, USA; the Division of Population Health Sciences and Education, St George's University of London, London, United Kingdom; the Pacific Northwest Research Institute, Seattle, WA, USA; the Center for Public Health Genomics, University of Virginia, Charlottesville, VA, USA; the Department of Clinical Sciences, Lund University/CRC, Malmö, Sweden; the Barbara Davis Center for Childhood Diabetes, University of Colorado, Denver, Aurora, CO, USA; the Institute of Diabetes Research, Helmholtz Zentrum München, Munich-Neuherberg, Germany; Klinikum rechts der Isar, Technische Universität München, Munich-Neuherberg, Germany; Forschergruppe Diabetes e.V., Munich-Neuherberg, Germany; the Department of Pediatrics, Turku University Hospital, Turku, Finland; the National Institutes of Diabetes and Digestive and Kidney Disorders, National Institutes of Health, Bethesda, MD, USA; and the Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA.
  2. Celiac.com 06/26/2007 - The results of a study recently published in the online science journal Nature Genetics have revealed a previously unknown genetic risk factor for celiac disease. An international team of researchers set out to study the genetic causes of intestinal inflammatory disorders. When the study began, it was well known that individuals with celiac disease have specific tissue types that identify wheat proteins. Why healthy individuals with the same tissue type failed to develop celiac symptoms or celiac disease remained unknown, and was a key question the team set out to answer. The team was led David van Heel, Professor of Gastrointestinal Genetics at Queen Mary, University of London. The Human Genome Project and the Hap Map Project played key support roles in the study. The results show that a protective DNA sequence in a specific gene segment, generally found in healthy individuals are missing in people with celiac disease. The research team evaluated genome data of 778 individuals with celiac disease and 1,422 controls non-celiacs within the British, Irish and Dutch populations. Key DNA Sequence Missing in Celiacs Researchers discovered that, compared to people with celiac disease, healthy people more commonly have a DNA sequence in the interleukin-2 and interleukin-21 gene region that protects against celiac disease. Interleukin-2 and interleukin-21 are cytokine proteins that are secreted by white blood cells, and which control inflammation. In people with celiac disease, the protective DNA sequence most likely leads to lesser amounts of these cytokines being produced, which weakens the defense against intestinal inflammation. Breakthrough in Better Understanding Risk Factors for Development of Celiac Disease About 1 in 133 people develop the disease, but, so far, predicting those at risk to develop the disease has been haphazard at best. Present methods of genetic testing can only narrow down the search to about 30% of the general population. These results give doctors a means to discover what further genetic risk factors leave people vulnerable to developing celiac disease. Queen Mary, University of London Press Release - Public release date: 10-Jun-2007 health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
  3. - Genetic Digestive Disorder Affects an Estimated One in 250 Americans - Celiac.com 02/26/2003 - WOODLAND HILLS, Calif., Feb. 19, 2003/PRNewswire -- Results from a new study may lead to the first medical treatment for celiac disease, a hereditary digestive disease that can damage the small intestine and interfere with the absorption of nutrients from food. Celiac disease sufferers cannot tolerate gluten, a protein that is found in wheat, barley and rye. Celiac disease affects an estimated one in 250 Americans, mostly those of European descent, and there is no known medical treatment or cure. Zengen, Inc. researchers discovered that a synthetic form of alpha-Melanocyte-Stimulating Hormone (alpha-MSH) has an anti-inflammatory effect in celiac mucosa, the inside lining of the intestinal tract that absorbs food into the body. A naturally occurring molecule, alpha-MSH modulates inflammatory and immune responses. Data confirming the presence of alpha-MSH in celiac mucosa suggests the presence of a local reaction of the molecule to control the inflammatory response elicited by gliadin. Gliadin is the sub fraction of gluten that acts as a toxin or poison in people with celiac disease; it causes an immune reaction, resulting in damage to the small intestine and an inability to digest and absorb nutrients necessary for health and growth (malabsorption). The findings, Anti-Inflammatory Effects of alpha-Melanocyte-Stimulating Hormone in Celiac Intestinal Mucosa, appear in the February 20, 2003 issue of NeuroImmunoModulation, the official journal of the International Society for Neuroimmunomodulation. Our research suggests that locally-produced alpha-MSH modulates inflammation and perhaps limits epithelial damage in patients with celiac disease, stated James M. Lipton, Ph.D., study investigator, chief scientific officer and director of Zengen. We are particularly excited by these findings as these data, coupled with abundant evidence of the anti-inflammatory and anti-infective activity of Zengens novel molecules based on alpha-MSH, further validate our research and development efforts in numerous areas including celiac disease. These positive results will be used to guide further advancements toward clinical use of the molecules. The study used human celiac mucosa cells in culture. Researchers collected duodenal biopsy pairs from 53 adult celiac patients (34 untreated patients and 19 celiac patients on a gluten-free diet) and 14 normal subjects and conducted three series of experiments in order to determine: (1) mucosal immunoreactivity for alpha-MSH and melanocortin receptors (MCRs), and gene expression of alpha-MSH precursor pro-opiomelanocortin and MCRs; (2) alpha-MSH and inflammatory cytokine production by duodenal specimens in vitro, and the influence of synthetic alpha-MSH on such cytokine production, and; (3) the influence of stimulation with gliadin on alpha-MSH and cytokine production in vitro and the effect of alpha-MSH on gliadin-stimulated cytokine production. Results suggest a localized anti-inflammatory influence based on alpha-MSH and its receptors: duodenal mucosa showed evidence of alpha-MSH and two of its receptor subtypes, MC1R and MC5R. Further, alpha-MSH and MC1R immunoreactivity was more intense in cell specimens from celiac patients and release of interleukin 6 (a lymphokine that stimulates the inflammatory response) from gliadin-stimulated duodenal mucosa was inhibited by synthetic alpha-MSH. Patients suffering from celiac disease currently have no medical options beyond a lifetime adherence to a strict, gluten-free diet, added Dr. Lipton. Clearly, if we can control the inflammatory responses that are a major part of celiac disease and limit the immunosuppression, this could lead to the first medical treatment to help the millions worldwide suffering from this genetic disease. Zengens novel molecules were developed from more than 25 years of original research in the US, Europe and Asia on peptide molecules derived from alpha-Melanocyte-Stimulating Hormone (alpha-MSH). James Lipton, Ph.D., Zengens chief scientific officer, chairman of the scientific advisory board and director, and his collaborators first demonstrated that alpha-MSH possesses anti-inflammatory properties and uncovered the specific activity of the carboxy-terminal tripeptide region (C-terminal peptide) of the alpha-MSH peptide. These discoveries led to the development of Zengens proprietary peptide molecules, including CZEN 002, a synthetic octapeptide. Zengen is currently conducting phase I/II clinical trials with CZEN 002 in vaginitis. About Celiac Disease According to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the National Institutes of Health (NIH), celiac disease (celiac disease), also known as gluten intolerance, celiac sprue or gluten sensitive enteropathy, affects an estimated one in 250 Americans. Celiac disease is a condition in which there is a chronic reaction to proteins called glutens which causes destruction of the villi in the small intestine, with resulting malabsorption of nutrients. A genetic disease, it may appear at any time in the life of a person with a hereditary predisposition. Celiac disease is often misdiagnosed, symptoms are varied and there is no current medical treatment or cure. Patients who suffer from celiac disease currently have only one alternative -- adherence to a lifetime, gluten-free diet. If left untreated, celiac disease can lead to malabsorption, which, in turn, can lead to malnutrition. Celiac disease is especially serious in children and adolescents, who need adequate nutrition to develop properly. Further, people with celiac disease who dont maintain a strict, gluten-free diet have a greater chance of developing one of several forms of cancer, particularly intestinal lymphoma. Other long-term complications include anemia, diabetes mellitus, hypothyroidism, osteoporosis, seizures and peripheral neuropathy. About Zengen, Inc Zengen, Inc. is a biopharmaceutical company focused on discovering, developing and commercializing innovative products to treat and prevent infection and inflammation through application of its proprietary peptide technologies. Zengens novel molecules offer broad-based anti-infective and anti-inflammatory solutions for multiple diseases and disorders, ranging from yeast infection to transplantation, and have the potential to significantly alter the way these diseases are treated. For more information about Zengen, please visit www.zengen.com. Zengen, Inc. Forward-Looking Statement Disclaimer This announcement may contain, in addition to historical information, certain forward-looking statements that involve risks and uncertainties. Such statements reflect managements current views and are based on certain assumptions. Actual results could differ materially from those currently anticipated as a result of a number of factors. The company is developing several products for potential future marketing. There can be no assurance that such development efforts will succeed, that such products will receive required regulatory clearance or that, even if such regulatory clearance were received, such products would ultimately achieve commercial success. Source: Zengen, Inc.
  4. July 2000 - Chemistry In Britain Summarized by Linda Blanchard Celiac.com 01/10/2001 - The article states that Oxford physicians and scientists did an experiment in which celiac patients who were previously on a gluten-free diet were fed a series of human-made peptides that are copies of portions of the peptide chains that are found in the gliadin portion of wheat. The hope was that by feeding those in the study overlapping partial chains, and then testing their blood for T-cells afterward, they could find which specific portion of the wheat protein set off the immune reaction in celiacs. One single peptide did trigger the reaction. Now that it has been identified, it is hoped that some solutions to the problems caused by celiac disease may become available. Two approaches seem to involve "turning off" the reaction -- its thought that offering a megadose of the particular peptide might turn the immune reaction off. Another method would involve offering a peptide that was very similar to the offending piece of wheat protein -- but just enough different that it might "turn off" the reaction. Another possibility is, of course, genetically modified wheat. It should be possible for scientists to develop a wheat that has a different peptide in the place of the offender, which would hopefully look, taste, and act as wheat does in normal baking without triggering celiac reactions.
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