ABSTRACT
BACKGROUND: Transplantation of primary hepatocytes (PH) has been shown to provide metabolic support during acute liver failure. However, PH are known to be subject to necrosis in the peritoneal cavity. This is because cell-cell interaction plays an important role in their survival, but the peritoneal cavity can not provide such an environment. We tried to improve the survival of PH by simultaneously transplanting nonparenchymal liver cells (NPL). METHODS: PH from normal Wistar rats, either alone (10(9) cells/kg, group 1, n=10) or mixed with NPL (5x10(8) cells/kg, group 2, n=10) were transplanted into the peritoneal cavity of hyperbilirubinemic Gunn rats which are congenitally devoid of bilirubin glucuronidation. Liver cells from Gunn rats were transplanted as a control. RESULTS: Bilirubin glucuronides (BG) were detected in the bile of both group 1 and 2 rats collected at 6 hours after transplantation, and reached peak levels in 4 days. However, in the third and fourth week, BG could be detected only in group 2 animals. The serum bilirubin levels were decreased by 12.1~18.9% of basal levels in the second and third week for group 2 rats, but decreased by 15.1% only in the second week for the group 1 rats. Using in situ hybridization, albumin mRNA positive cells could be detected until the fourth week for the group 2 animals, but only until the second week for the group 1 rats. CONCLUSIONS: PH start functioning in a short time after intraperitoneal transplantation and simultaneous transplantation of NPL with PH can prolong the survival and function of transplanted hepatocytes.
Subject(s)
Animals , Rats , Bile , Bilirubin , Cell Transplantation , Glucuronides , Hepatocytes , Hydrogen-Ion Concentration , In Situ Hybridization , Liver Failure, Acute , Liver , Necrosis , Peritoneal Cavity , Rats, Gunn , Rats, Wistar , RNA, MessengerABSTRACT
Colonic ischemia is the most prevalent form of gastrointestinal ischemia and causes 3~9% of all acute lower intestinal bleeding. Most common cause is known to be cardiac embolus. A 67-year-old female patient presented with rectal bleeding. The patient had cerebral infarction 15 days ago. A colonoscopy showed a large ulcer with hemorrhage in the rectum. Computed tomography showed deep vein thrombosis from the left popliteal vein to infrarenal inferior vena cava. Transthoracic echocardiography was carried out, but no abnormal feature was found. Then, transesophageal echocardiography, with agitated saline contrast to find out a right to left shunt, was performed, patent foramen ovale was found. This patient was treated with anticoagulation and inferior vena cava filtering. We suggest this ischemic colitis may be due to arterial embolization from deep vein thrombosis through PFO.
Subject(s)
Aged , Female , Humans , Cerebral Infarction , Colitis, Ischemic , Colon , Colonoscopy , Dihydroergotamine , Echocardiography , Echocardiography, Transesophageal , Embolism , Foramen Ovale, Patent , Hemorrhage , Ischemia , Popliteal Vein , Rectum , Ulcer , Vena Cava, Inferior , Venous ThrombosisABSTRACT
BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infection is the cause of peptic ulcer diseases, and gastric cancer. Hydrolysis of urea generating ammonia may cause cytotoxic effects on the gastric epithelium. The ammonia may induce the synthesis of epidermal growth factor (EGF) in gastric epithelium as an adaptive cytoprotective mechanism. The first aim was to examine the concentration of ammonia and EGF in gastric juice before and after H. pylori eradication in functional dyspepsia patients. The second aim was to examine the correlation among ammonia concentration, EGF concentration, and inflammatory score of gastritis. METHODS: The concentration of ammonia and EGF were measured by ELISA. The grade and severity of gastritis were measured according to the updated Sydney system. RESULTS: The concentration of ammonia in gastric juice was much higher in the H. pylori positive subjects (10,787 +/- 6,584 micro mol/L) than in the negative subjects (2,339 +/- 1,158 micro mol/L, p<0.0001). The concentrations of EGF in gastric juice was much higher in the positive subjects (1,462 +/- 393 pg/mL) than in the negative subjects (1,088 +/- 499 pg/mL, p<0.005). The concentration of ammonia and EGF in gastric juice showed significant correlation (r=0.63, p<0.0001). The concentrations of ammonia and histologic severities showed significant correlation (r=0.41, p<0.0001). Moreover, the level of EGF in gastric juice and histologic severities showed positive correlation (r=0.20, p<0.005). CONCLUSIONS: As the concentration of ammonia in gastric juices increased, the concentration of EGF was also increased in functional dyspepsia with H. pylori infection. The concentration of EGF in gastric juice may play a role in the adaptive cytoprotection in H. pylori- induced gastritis.