No Abstract Available.
Protein-Serine-Threonine Kinases* ; Receptors, Cell Surface* ; Transforming Growth Factor beta*

Current evidences have expended the concept that chronic inflammation might play a crucial role in the development and progression of colorectal cancer. For instance, chronic ulcerative colitis (UC) is associated with a 10- to 40-fold increased risk of developing colorectal cancer (CRC) compared to the general population. However, the specific mechanistic link between chronic inflammation and carcinogenesis in colon has not been integrated into molecular understanding. In this current review, we will provide an update on the molecular pathogenesis of colitis-associated colorectal cancer, focused on 1) the differences of molecular mechanism between the colitis-associated colorectal cancer (CAC) and the sporadic colorectal cancer (SCC), 2) the plausible and contributive role of chronic inflammation in colon carcinogenesis, and 3) lessons learned from colitis-associated animal model. Understanding of molecular pathogenic mechanism underlying the colitis-associated colorectal cancer will facilitate the development of novel treatment strategies for prevention of colitis-associated colorectal cancer.
Carcinogenesis* ; Colitis, Ulcerative ; Colon* ; Colorectal Neoplasms ; Inflammation* ; Inflammatory Bowel Diseases ; Models, Animal

No abstract availble.
Animals ; *Cell Line ; *Helicobacter Infections ; *Helicobacter pylori ; Humans

Gastrointestinal hemangioma is a relatively uncommon benign vascular tumor that can occur anywhere in the gastrointestinal tract. It is the second most common vascular lesion of the colon and a clinically important entity because of the possibility of massive hemorrhage when complicated. In gross appearance, hemangioma presents variously as a pedunculated, subpedunculated, or flat elevated lesion similar to a submucosal tumor. A typical case of hemangioma is relatively easy to diagnose because the lesion presents as translucent blue-purple vessels under the mucosa. However, it can be difficult to diagnose in some cases, especially if it does not have its usual characteristic color or is covered with normal mucosa. We incidentally found a colonic hemangioma that had the unusual appearance of a pedunculated polypoid lesion with normal mucosa. It was misdiagnosed as a pedunculated polyp with a long, thick neck and treated by using an endoscopic mucosal resection.
Caves ; Colon ; Gastrointestinal Tract ; Hemangioma ; Hemangioma, Cavernous ; Hemorrhage ; Mucous Membrane ; Neck ; Polyps

No abstract available.
Helicobacter pylori* ; Helicobacter*

No abstract available.
Helicobacter pylori* ; Helicobacter*

No abstract available.
Capsule Endoscopy*

BACKGROUND/AIMS: Transforming growth factor-beta (TGF-β) is a cytokine implicated in the susceptibility, development, and progression of gastrointestinal cancer and certain other neoplasms. In the later stages of cancer, TGF-β not only acts as a bystander of host-immune response, but also contributes to cell growth, invasion, and metastasis. In the current study, we generated gastric mucosal cells that stably express Smad7, and explored the Helicobacter pylori-associated biological changes between mock-transfected and Smad7-transfected RGM1 cells. METHODS: RGM1 cells stably transfected with Smad7 were infected with H. pylori, and molecular changes in apoptotic markers and inflammatory mediators were examined. Several candidate genes were explored in Smad7-overexpressing cells after H. pylori infection. RESULTS: Overexpression of Smad7 in RGM1 cells significantly increased the H. pylori-induced cytotoxicity compared to mock-transfected cells. Exaggerated increases in inflammatory mediators, cyclooxygenase 2, inducible NO synthase, and augmented apoptosis were noted in Smad7-overexpressing cells, whereas mitigated heme oxygenase 1 was noted in Smad7- overexpressing cells. These phenomena were reversed in cells transfected with Smad7 siRNA. CONCLUSIONS: These data suggest that inhibition of Smad7 is a possible target for mitigating H. pylori-associated inflammation.
Apoptosis ; Cyclooxygenase 2 ; Gastritis ; Gastrointestinal Neoplasms ; Helicobacter pylori ; Helicobacter* ; Heme Oxygenase-1 ; Inflammation ; Neoplasm Metastasis ; Nitric Oxide Synthase ; RNA, Small Interfering ; Transforming Growth Factor beta

Recently, gastric Helicobacter pylori (H. pylori) colonization has been shown to affect the expression of leptin and ghrelin, hormones that control appetite and satiety. Gastric leptin, produced by chief and parietal cells and released in response to meals, may play a role in weight gain after eradication of H. pylori infection, whereas ghrelin, produced by X/A-like enteroendocrine cells in oxyntic gland, is released during fasting, and suppressed by feeding and leptin. Whether either that H. pylori genes represent microbial contributions to the complement of thrifty genes of humans, or that H. pylori disappearance plays a role in adiposity remains to be determined. Simply, ghrelin-leptin might tango in body weight regulation, gastric inflammation, and gastric motility. In the current review about the possible role of ghrelin in gastric inflammation, we found that high serum albumin condition decreased ghrelin expression, whereas serum albumin deprivation significantly increased ghrelin expression, however, of which regulation was abolished after H. pylori infection. Ghrelin significantly attenuated the inflammatory stimuli imposed after H. pylori, shown with inactivation of phospho-extracellular signal-regulated kinase (p-ERK) and nuclear factor-KappaB (NF-KappaB)-DNA binding activities. Conclusively, besides orexigenic and weight gaining actions of gastric hormone, ghrelin, it likely endows the stomach the protective effect from exogenous damages.
Amino Acid Sequence ; Appetite Stimulants ; Gastritis/*metabolism/microbiology ; Ghrelin/*blood/chemistry ; Helicobacter Infections/*metabolism ; *Helicobacter pylori ; Humans ; Insulin-Like Growth Factor I/analysis ; Leptin/*blood ; Mitogen-Activated Protein Kinases/metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Neurosecretory Systems/*metabolism ; Peptide Hormones/*blood ; Signal Transduction ; Weight Gain

Patients with hypertrophic cardiography often complain of chest pain and have electrocardioagrams suggesting myocardial damage or ischemia. Some of three patients have associated coronary arterial atherosclerosis. Transmural myocardial infarction may occur in patients with hypertrophic cardiomyopathy in the absence of significant atherosclerosis of the extramural coronary arteries, about which several pathophysiologic exlpanations were discussed. Presented here, a case of 49-year-old man with hypertrophic cardiomyopathy accompanied with myocardial infarction and angiographically normal coronary arteries is reported. Asymmetric septal hypertrophy, characteristic morphologic abnormality of hypertrophic cardiomyopathy, was progressed to dilated cardiomyopathy after the occurrence myocardial infarction.
Atherosclerosis ; Cardiomyopathy, Dilated ; Cardiomyopathy, Hypertrophic* ; Chest Pain ; Coronary Vessels ; Humans ; Ischemia ; Middle Aged ; Myocardial Infarction*