Publications by authors named "Etsuko Kishimoto"
Article Synopsis
- * The study involved 2,962 patients in Japan, using upper gastrointestinal endoscopy to assess various conditions related to GERD and to analyze the correlation of symptoms using the FSSG and GSRS scoring systems.
- * Results indicate that FSSG and GSRS scores are effective in diagnosing the severity of reflux esophagitis, with FSSG scores linked to mucosal atrophy and GSRS scores relating to the functionality of the gastroesophageal flap.
Background: Nonalcoholic fatty liver disease is characterized by excessive hepatic fat accumulation. Some individuals frequently present elevated gamma-glutamyl transferase (GGT) levels without fatty liver ultrasound images and other abnormal liver enzymes levels. However, whether these individuals are at an elevated risk for developing fatty liver is unclear.
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- The study investigates how Helicobacter pylori infection affects adiponectin levels, a protein linked to metabolic syndrome, in humans.
- Out of 456 patients tested for H. pylori, those who received successful eradication therapy showed significantly increased levels of total adiponectin after 12 weeks.
- The findings suggest that eliminating H. pylori might help raise adiponectin levels, potentially aiding in the prevention of metabolic syndrome, particularly in Japanese individuals.
A 50-year-old female became aware of skin yellowing and consulted another hospital where she was diagnosed intraoperatively with duodenal cancer because of lymph node metastases around the aorta. Endoscopy revealed type IIa + IIc cancer distal to the duodenal papilla, and biopsy allowed a diagnosis of well-differentiated adenocarcinoma. Computed tomography revealed a large number of lymph node metastases around the aorta and in the left supraclavicular cavity.
View Article and Find Full Text PDFProtection of the small intestine from mucosal injury induced by nonsteroidal anti-inflammatory drugs including acetylsalicylic acid is a critical issue in the field of gastroenterology. Polaprezinc an anti-ulcer drug, consisting of zinc and L-carnosine, provides gastric mucosal protection against various irritants. In this study, we investigated the protective effect of polaprezinc on acetylsalicylic acid-induced apoptosis of the RIE1 rat intestinal epithelial cell line.
View Article and Find Full Text PDFOxidative stress-induced posttranslational modification of TRPV1 expressed in esophageal epithelial cells.
Am J Physiol Gastrointest Liver Physiol
August 2011
Human esophageal epithelium is continuously exposed to physical stimuli or to gastric acid that sometimes causes inflammation of the mucosa. Transient receptor potential vanilloid 1 (TRPV1) is a nociceptive, Ca(2+)-selective ion channel activated by capsaicin, heat, and protons. It has been reported that activation of TRPV1 expressed in esophageal mucosa is involved in gastroesophageal reflux disease (GERD) or in nonerosive GERD symptoms.
View Article and Find Full Text PDFBackground: To protect the small intestine from mucosal injury induced by nonsteroidal anti-inflammatory drugs is one of the critical issues in the field of gastroenterology. Polaprezinc (PZ), a gastric muco-protecting agent, has been widely used for the treatment of gastric ulcer and gastritis for its unique effects, such as its strong reactive oxygen species (ROS)-quenching effect. The aim of this study was to clarify the mechanism by which indomethacin-induced small intestinal mucosal injury occurs, by using a rat intestinal epithelial cell line (RIE-1).
View Article and Find Full Text PDFBackground/aims: Protecting intestinal mucosa from nonsteroidal anti-inflammatory drugs is still an unsolved problem. It has been revealed that apoptosis in epithelial cells as a result of mitochondrial injury is an important pathogenesis in indomethacin-induced gastric mucosal injury. In this study, we revealed the effect of overexpressed heat-shock protein 70 (HSP70) in indomethacin-induced apoptosis and oxidative stress.
View Article and Find Full Text PDFBackground: The precise pathogenic mechanism of nonsteroidal antiinflammatory drug-induced small intestinal injury is still unknown. In the present study, we investigated the mechanism by which indomethacin induced mucosal injury by using an in vitro model of small intestine.
Methods: The colon cancer cell line Caco-2, exhibiting a small intestinal phenotype starting as a crypt cell and differentiating to a villous phenotype, and RIE, a rat intestinal epithelial cell line, were employed.