Little is known about the involvement of Smad-related molecules in the regulation of the Transforming Growth Factor (TGF)-beta signaling pathway during hepatocarcinogenesis, particularly with respect to preneoplastic lesions of a rat liver. The aims of this study were to investigate the localizations and temporal expressions of TGF-beta Receptor Type 1 (TGR1) and Smads during the promotion stage of chemical hepatocarcinogenesis in rats. We investigated expressions and localizations of TGR1, Smad2, Smad4, and Smad7 by using semi-quantitative RT-PCR and immunohistochemistry in preneoplastic lesions during rat chemical hepatocarcinogenesis induced by Solt and Farber's method. The down-regulation of TGR1, Sma-d2, and Smad4 was evident during the later steps of the promotion stage of chemical hepatocarcinogenesis. In contrast with other Smads, increased Smad7 expression was evident during the later steps of the promotion stage. Also immunohistochemistry revealed that the main site of TGR1, Smad2, Smad4, and Smad7 expression was mainly in hepatocytes of the preneoplastic lesions of a rat liver. Dysregulation of the downstream effectors of TGF-beta such as TGR1, Smad2, Smad4 and, Smad7 might contribute to the progression of preneoplastic lesions during chemical hepatocarcinogenesis in a rat.
Activin Receptors, Type I/*biosynthesis ; Animals ; Apoptosis ; DNA-Binding Proteins/*biosynthesis ; Disease Progression ; Glutathione Transferase/metabolism ; Immunohistochemistry ; In Situ Nick-End Labeling ; Liver/metabolism ; Liver Neoplasms/chemically induced ; Male ; Peptides/chemistry ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Transforming Growth Factor beta/*biosynthesis ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Time Factors ; Trans-Activators/*biosynthesis

BACKGROUND: Propofol can be used to provide general anesthesia or sedation. The objectives of this study were to assess propofol as sedative agents for outpatient GI endoscopy, amnestic effects, hemodynamic state and oxygenation during the procedure. METHODS: From April and June 2000, 50 patients scheduled outpatient gastrointestinal endoscopy were enrolled in this study. 30 healthy outpatients requesting sedation at diagnostic gastroscopy were received a bolus dose of propofol 2.5 mg/kg and compared with 20 patients with non-sedation. Pulse rate, blood-pressure and arterial oxygen saturation was monitored. RESULTS: Statistically significant decrease in arterial oxygen saturation were observed since 5 min after endoscopy in patients receiving propofol (p=0.006). Patients receiving sedative endoscopy, pulse rate during endoscopy was significantly increased compared with propofol group (p=0.009). Patients receiving propofol are more tolerable than patients with non-sedative endoscopy (p=0.001), therefore all patients receiving propofol wanted the same sedative endoscopy in their next endoscopy. CONCLUSION: Propofol is believed to be a useful, safe sedative agent for upper gastrointestinal endoscopy with satisfactory sedation and conditions. However, due to its untoward effect of hypoxia, careful monitoring is recommended.
Anesthesia, General ; Anoxia ; Conscious Sedation* ; Endoscopy ; Endoscopy, Gastrointestinal* ; Gastroscopy ; Heart Rate ; Hemodynamics ; Humans ; Outpatients ; Oxygen ; Propofol*