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Atrophic gastritis pathology,extreme diets actors,diet for weight loss in telugu,dieting tips to lose weight fast in urdu - Within Minutes

Marshall BJ, Warren JR.1984Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Serial Analysis for Microarray from Non-tumor adjacent mucosa [NTAM] and and chronic gastritis controls.
Gastric mucosal atrophy: interobserver consistency using new criteria for classification and grading.
For the purpose of this chapter, we will focus only on chronic gastritis due to its relevance to gastric cancer. Among the causes of chronic gastritis are chronic bile reflux, stress, certain autoimmune disorders and bacterial infection, primarily Helicobacter pylori. Since 1870, both human and veterinary pathologists have described the presence of tiny curved bacteria within gastric mucosa, but the organisms were dismissed as irrelevant contaminants [1, 2]. Farinati, 2011Operative Link for Gastritis Assessment gastritis staging incorporates intestinal metaplasia subtyping. Kim, 2003Aberrant CpG island hypermethylation of chronic gastritis, in relation to aging, gender, intestinal metaplasia, and chronic inflammation. Subsequently, accurate morphological data were gathered by pathologic examination of autopsy material [5] and, later, of endoscopic biopsy specimens. As a result, distinct types and patterns of gastritis were recognized, which led to the conception, presentation, dismissal, and replacement of many different classification systems.2. Histological classification and grading of gastritisFor the purpose of this chapter we decided to divided chronic gastritis in into two main categories, namely non-atrophic and atrophic gastritis [6].


The main purpose of this classification is to individualize high-risk gastritis subgroup that subsequently might develop to gastric cancer. The extent and site of the atrophic changes significantly correlate with cancer risk [6, 7]. Two main types of atrophic gastritis can be recognized, one characterized by the loss of glands, accompanied by fibrosis or fibromuscular proliferation in the lamina propria, and the other characterized by the replacement of the normal mucosa into an intestinal type of mucosa [i.e. The first can be assessed with the new Operative Link for Gastritis Assessment [OLGA] staging system for atrophy risk assessment [9] which ranks the risk of gastric cancer according to the extension and severity of gastric atrophy [Fig.
Cross-sectional descriptive studies and follow-up trials have consistently supported a strong association between OLGA stages and IM histochemical phenotypes, where IM of small intestinal type [type I] significantly prevailed in low-risk atrophic stages and high-risk OLGA stages were associated with IM of types II and III [6]. Accordingly, epidemiological studies have shown that degree of severity for non-metaplastic atrophy influences the prevalence of IM and that the severity of IM influences the prevalence of dysplasia [12]. Thus, gastritis, and gastric cancer premalignant conditions should be understood as a disturbance in the balance between tumor suppressor genes and oncogenes.
Epigenetic bases of gastritisEpigenetic processes control the packaging and function of the human genome and contribute to normal development and disease [27]. DNA methylation and gastritisThere are limited reports on DNA methylation analysis in gastritis and premalignant lesions of gastric cancer.
Kang et al [40] tested five genes [p16, hMLH1, DAP-kinase, THBS1, and TIMP-3] in a series of 64 carcinomas and 179 premalignant conditions [69 chronic gastritis, 49 IM and 61 gastric adenomas] to identify two different classes of methylation patterns, preferential methylation of THBS-1 and TIMP-3 in chronic gastritis and IM and preferential methylation of hMLH1 and p16 in intestinal metaplasia, displasia and gastric cancer. A subsequent study identified specific patterns of DNA methylation associated with aging after testing 11 genes in 268 premalignant gastritis [41].


Histological evaluation after the treatment, showed chronic inactive gastritis in most of the cases. This methylated circulating cell-free DNA offers the opportunity for non-invasive detection of gastric cancer and premalignant gastritis.
This data suggest that cagA and vacA virulence determinants are significantly associated with DNA methylation of a specific gene, RPRM in high-risk gastritis [49]. Thus, the posibility to detect DNA methylation of RPRM as a cell-free DNA in plasma in combination with H.pylori strains might opening the oportunity for a non-invasive detection of high-risk premalignant gastritis.
Integration of histological and DNA methylation features of gastritisAlthough histological assessment of gastritis to search for premalignant conditions for the development of gastric cancer has been proposed [6] and epigenetic markers based on DNA methylation are associated with this progression [50], no integrative approach has been explore up to date for this two disparate fields.
Recently, we have integrated histological together with in-situ molecular features to demonstrate that overexpression of p73 was probably the most important marker to identified high-risk premalignant gastritis [51]. Taken together these findings suggest that DNA methylation might play a role in gastritis and premalignant condition in both ways, inactivating or activating tumor-related genes by hypermethylation or demethylation of promoter region of specific genes, respectively. Specific DNA methylation changes might play a major role in premalignant gastritis and might be associated with H.
Integrative analysis of histological features of premalignant conditions with overexpression of specific genes such as p73 by demethylation might be important to identified the best biomarkers for high-risk premalignant gastritis for the development of gastric cancer.



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