ABSTRACT
Background/Aims@#Intralesional steroid injections have been administered as prophylaxis for stenosis after esophageal endoscopic submucosal dissection. However, this method carries a risk of potential complications such as perforation because a fine needle is used to directly puncture the postoperative ulcer. We devised a new method of steroid intralesional infusion using a spray tube and evaluated its efficacy and safety. @*Methods@#Intralesional steroid infusion using a spray tube was performed on 27 patients who underwent endoscopic submucosal dissection for superficial esophageal cancer with three-quarters or more of the lumen circumference resected. The presence or absence of stenosis, complications, and the number of endoscopic balloon dilations (EBDs) performed were evaluated after treatment. @*Results@#Although stenosis was not observed in 22 of the 27 patients, five patients had stenosis and dysphagia requiring EBD. The stenosis in these five patients was relieved after four EBDs. No complications related to intralesional steroid infusion using the spray tube were observed. @*Conclusions@#Intralesional steroid infusion using a spray tube is a simple and safe technique that is adequately effective in preventing stenosis Clinical trial number (UMIN000037567).
ABSTRACT
Objective To monitor the systemic gene expression profile in a murine model of li-popolysaccharide (LPS)-induced acute lung injury by the recently modified long serial analysis of gene expression (SAGE) so as to discuss the molecular mechanism of acute lung injury. Methods Acute lung injury was induced by intra-tracheal injection of LPS (25 mg/kg). Control mice were given normal saline in same volume. Animals were killed at 24 hours after the administration of LPS and lungs were harvested en bloc for SAGE study. Results A total of 24 670 tags representing 12 168 transcripts in the control mice and 26 378 tags representing 13 397 transcripts in the mice with lung injury were identified respectively. There were 11 transcripts increased more than 10 folds, 107 transcripts 5-10 folds and 2 121 transcripts 2-5 folds in the LPS-treated mice. But seven transcripts decreased to 1/10, 87 transcripts to 1/10-1/5 and 1 571 transcripts to 1/5-1/2. The most overexpressed genes in the lung injury mice mainly included serum amyloid A 3, metallothionein 2, lipocalin 2, cyclin-dependent kinase inhibitor 1A, lactate dehydrogenase 1 , melatonin receptor, SI00 calcium-binding protein A9 and natriuretic pep-tide precursor. Mitogen activated protein kinase 3, serum albumin, complement component 1 inhibitor, and ATP synthase were underexpressed in the lung injury mice. Conclusion The changes of various genes as well as some unreported genes have been confirmed in the LPS-induced acute lung injury. Further studies of these unreported genes are beneficial to better understanding the mechanism of acute lung injury and may provide useful markers for clinical diagnosis.