Methods: The study subjects were 43 patients, who underwent exchange of a PEG button or tube, 20-French or more in diameter. After PD-0332991 in vivo PEG buttons or tubes were extracted
from the gastrostomy tract, an ultrathin endoscope was inserted through the gastrostomy tract. The stomach and the duodenal bulb were observed and the esophagus was observed in retrograde passage. A new PEG button or tube was then inserted. The rate of successful insertion into the esophagus and duodenal bulb, the observation of the gastrostomy site in retroversion in the stomach, and the endoscopic findings were analyzed. Results: Ninety-nine examinations were carried out. The esophagus could be observed in 95 (96.0%), the duodenum in 92 (92.9%) and the gastrostomy site in the stomach in all. Gastric polyps were detected in four patients, gastric erosions find more in two, reflux esophagitis in two, polypoid lesion at the gastrostomy tract in two, gastric ulcer scar in one, duodenal ulcer scar in one, early gastric cancer in one and recurrent esophageal cancer in one. Neither discomfort nor complications occurred during transgastrostomic endoscopy. Conclusions: Observation of the upper gastrointestinal tract by transgastrostomic endoscopy using an ultrathin endoscope during a gastrostomy button or tube replacement may be useful and safe. “
“Bone marrow–derived mesenchymal stem cells (MSCs) have therapeutic
potential in liver injury, but the signals responsible for MSC localization to sites of injury and initiation of differentiation are not known. Adenosine concentration is increased at sites of cellular injury and inflammation, and Selleck MG-132 adenosine is known to signal a variety of cellular changes. We
hypothesized that local elevations in the concentration of adenosine at sites of tissue injury regulate MSC homing and differentiation. Here we demonstrate that adenosine does not induce MSC chemotaxis but dramatically inhibits MSC chemotaxis in response to the chemoattractant hepatocyte growth factor (HGF). Inhibition of HGF-induced chemotaxis by adenosine requires the A2a receptor and is mediated via up-regulation of the cyclic adenosine monophosphate (AMP)/protein kinase A pathway. This results in inhibition of cytosolic calcium signaling and down-regulation of HGF-induced Rac1. Because of the important role of Rac1 in the formation of actin stress fibers, we examined the effect of adenosine on stress fiber formation and found that adenosine inhibits HGF-induced stress fiber formation. In addition, we found that adenosine induces the expression of some key endodermal and hepatocyte-specific genes in mouse and human MSCs in vitro. Conclusion: We propose that the inhibition of MSC chemotaxis at sites of high adenosine concentration results in localization of MSCs to areas of cellular injury and death in the liver.