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

No abstract available.
Helicobacter pylori* ; Helicobacter*

No abstract available.
Helicobacter pylori* ; Helicobacter*

No abstract available.
Capsule Endoscopy*

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

Dieulafoy ulcer is an unusual cause of massive, recurrent and frequently fatal gastrointestinal hemorrhage that results from erosion of abnormally large submucosal artery. Although the lesion has been found throughout the gastrointestinal tract, it most commonly occurs in the proximal stomach. Diagnosis depends on the observation of protruding and eroded artery with pulsatile bleeding or adherent thrombus by endoscopy. Even during active bleeding, the endoseopic examination can be negative if intraluminal blood or clots obscure the source of bleeding. If the bleeding has stopped, the small mucosal lesion can be easily overlooked. Unlike peptic ulceration, there is no excavation of the mucosa. A 76-year-old man presented with massive hematemesis and melena. The patient had no previous history of peptic ulcer disease. He did not drink alcohol and use aspirin or NSAIDs. Physical examination revealed a pale, severely diaphoretic male with hypotension and melenic stools. He was found to have hemoglobin 4.0 g/dL and hematocrit 12.7%. We performed emergency endoscopy which showed a pulsatile and bleeding exposed artery without evidence of surrounding ulcerative lesion on the posterior wall of upper body of stomach. Endoscopic ligation using O ring of Stiegman-Goff endoscopic ligator kit was done successfully and the bleeding stopped immediately after ligation. Ten days after treatment, endoscopy showed artificial ulcerative lesion on previous ligated site and no evidence of bleeding. Another endoscopy four days later revealed healing ulcerative lesion. After improvement, the patient was discharged and rebleeding has not occurred to date.
Aged ; Anti-Inflammatory Agents, Non-Steroidal ; Arteries ; Aspirin ; Cytochrome P-450 CYP1A1 ; Diagnosis ; Emergencies ; Endoscopy ; Gastrointestinal Hemorrhage ; Gastrointestinal Tract ; Hematemesis ; Hematocrit ; Hemorrhage ; Humans ; Hypotension ; Ligation* ; Male ; Melena ; Mucous Membrane ; Peptic Ulcer ; Physical Examination ; Stomach ; Thrombosis ; Ulcer*

Heterotopia (of Ectopia) is defined as the occurrence of normal tissue in an abnormal location. Heterotopic gastric mucosa has been found throughout the length of the gastrointestinal tract from oral cavity to the rectum. Curiously, it is extremely rare in the gailbladder, but when it occurs, it tends to cause symptoms of acute cholecystitis in patients under 20 years of age, and chronic cholecystitis and gallstones in older patients. The heterotopic mucosa results in an intramural mass, a polyp or multiloculated gallbladder. A firm diagnosis of gastric heterotopia is based on the presence of fundic or pyrolic mucosa replete with parietal and chief cells. A clear distinction from intestinal rnetaplasia should be made, but at times may be difficult. Potential complications include mucosal ulceration, obstruction, and hemorrhage. Treatment is cholecystectomy. We report a case of gastric heterotopia in the gallbladder of a 35-year-old-man. Ultrasonography showed fatty change of liver with a 1.5 cm-sized polypoid lesion in the gallbladder. Endoscopic retrograde cholangiography showed a small filling defect, revealed by pooling of the dye in the center, in the body of gallbladder. Laparoscopic cholecystectomy was performed. A sessile polypoid leision with central umbilication was seen in the upper body of gallbladder, without gallstones. The microscopic finding of polypoid lesion consisted of gastric pyloric glands with parietal and chief cells. The surrounding mucosa revealed ordinary gallbladder epithelium without any metaplastic change. We report a case of this condition in which there was a separate loculus lined by gastric epithelium.
Cholangiography ; Cholecystectomy ; Cholecystectomy, Laparoscopic ; Cholecystitis ; Cholecystitis, Acute ; Diagnosis ; Epithelium ; Gallbladder* ; Gallstones ; Gastric Mucosa ; Gastrointestinal Tract ; Hemorrhage ; Humans ; Liver ; Mouth ; Mucous Membrane ; Polyps ; Rabeprazole ; Rectum ; Ulcer ; Ultrasonography

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