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Ceramide has been suggested as an important mediator of the effects of extracellular agonists on cell growth inhibition, differentiation, apoptosis. However the biochemical sign aling mechanism involved in transducing the effects of ceramide on leukemia cell differentiation is still unclear. In these respects, we examined the regulatory effects of ceramide on c-jun gene expression during differentiation. In U-937 cells. ceramide increased c-jun mRNA levels in a time-dependent manner. The half life, of c-jun mRNA was 30 min. In contrast, inhibition of protein synthesis with cycloheximide in the absence, of transcription with actinomycin D increased the half-life of c-jun mRNA in ceramide-treated U-937 cells to more than 90 min. In order to examine whether ceramide-inhibited c-jun gene expression is regulated through ceramide-activated protein phosphatase (CAPP), a direct target for the action of ceramide, okadaic acid were treated to the cells. Okadaic acid inhibited enhancement of c-jun mRNA induced by C2-ceramide in a dose-dependent manner. These results suggested that ceramide increases c-jun mRNA level during differentiation in U-937 cells and regulates the gene expression on posttranscriptional level. In addition, we provide the evidence that CAPP is involved in ceramide-induced c-jun gene expression in U-937 cells.
The orifice of duodenal papilla is only about 1 mm in diameter. As much as 2,000 ml of bile and pancreatic juice pass through its sphincter zone into the duodenum each day. Since the sphincter of Oddi regulates the flow of bile and pancreatic juice, a disorder of the sphincter can disturb the smooth outflow of bile and pancreatic juice and produce secondary abnormalities in the biliary tract or the exocrine pancreas. Recently, pressure dynamics of the sphincter of Oddi have been reported in variaus pancreatobilfary diseases, butt the physiology and pathophysiology of the sphincter of Oddi and pancreatic duetal pressure have been poorly investigated in patients with chronic pancreatitis. The present study was undertaken to compare tlfe sphincter of Oddi and pancreatic duct pressures in 7 patients with chronic pancreatitis anal in 8 normal controls and to determine whether pressure differences exist in patients subdivided by the findings of endoscopic retrograde pancreatograms(ERP). The following results were obtained: 1) The basal pressure of phasic contractions of pancreatic duct sphincter in patients with chronic pancreatitis(18.8±16.0 mmHg) was significantly higher than that in normal contrals(5.4±2.3 mmHg). There were no statistically significant adiffereaces in main pancreatic duct pressure, and peak pressure, frequency, duration and direction of propagation of phasic contractions of pancreatic duct sphincter between the patients with chronic pancreatitis and normal controls. 2) When the patients with chronic pancreatitis ware subdivided into 3 groups according to ERP findings, the pressure of main pancreatic duct and basal pressure of phasic contractions of pancreatic duct sphincter in group B(focally abnormal side branches in pancreas tail) were remarkably higher than those of group A(segmental stenosis at pancreatic head with poststenotic dilatation) and group C(diffuse abnormalities in entire pancreatic duct). In conclusion, the abnormalities of motility in pancreatic duct sphincter and the different manometric findings among each group subdivided by ERP findings in patients with chronic pancreatitis may suggest the important role of motility of pancreatic duct sphincter in the pathogenesis of chronic pancreatitis, however further studies in more cases will be required.
Desferrioxamine (DFO), an iron chelator, has been sbown to have antiproliferative activity in a variety of malignant cells including hepatocellular carcinoma. The antiproliferative effect of DFO's known to be caused by decreased activity of ribonucleotide reductase, a key enzyme in DNA synthesis. This study was conducted to investigate the effect Of DFO on the DNA synthesis of cultured hepatoma cells. The proliferation of hepatocellular carcinoma (Hep 3B) as well as hepatoblastoma (Hep G2) cells was measured by trypan blue dye exclusion method and the DNA synthesis was measured by [^3H] thymidine incorporation. The results obtained were as follows: The proliferation of hepatoma cells was slightly inhibited by 2 ug/ml and markedly inhibited by 6 ug/ml of DFO. This antiproliferative effect was not enhanced any more by higher dose of DFO. The percent viability of Hep 3B and Hep G2 cells was above 90%. after 96 hours of incubation with 60 ug/ml of DFO and that of Hep 3B and Hep G2 cells was 88.0% and 89.6% respectively after l6 hours of culture with 120 ug/ml of DFO. DNA synthesis of hepatoma ceils was decreased by DFO in a dose dependent manner up to 20 ug/ ml. The decrease of DNA synthesis was not enhanced any more by higher dose of DFO. In conclusion, the antiproliferative effect of DFO on cultured human hepatoma cell lines was caused by the inhibition of DNA synthesis rather than by direct cytocidal effect.
Doppler ultrasonography, which provides noninvasive evaluation of bloodflow patterns has used widely in cardiovascular diseases. Recently intratumoral Doppler signal has been analysed to evaluate intra and peritumoral blood flow and to differentiate malignant from benign neoplasm. Hepatocellular carcinomas have characteristic vascular appearance including arteriovenous shunts that aid in their diagnosis and Doppler ultrasonography allows recognition of these arteriovenous shunts. But Doppler ultrasonographic observation of arterio-portal fistula involving relatively large branch of portal vein is very rare. We present a 55-year-old female patient with hepatocellular carcinoma showing characteristic Doppler signal consistant with intrahepatic arterio-portal fistula which was confirmed by hepatic arteriography. After transarterial embolization with Gelfoam this high velocity flow signal was clisappeared.
Femoropopliteal (FP) artery-in stent restenosis (ISR) is a daunting management problemthat we continue to face. FP artery-ISR rates after primary stent implantation are relativelyhigh. Although repeat FP artery-ISR and the need for additional interventions remain alltoo common, little consensus exists regarding the best treatment algorithm. In this article,we review the limitations of the currently used devices for the endovascular treatment of FPartery-ISR and discuss which strategies are the most effective and safe