ABSTRACT
Objective To summarize the diagnosis and treatment experience of the pancreatic fistula secondary to abdominal operations.Methods The clinical data of 27 patients with pancreatic fistula due to abdominal operations were analyzed retrospectively.Results 25 patients were diagnosed by the amylase concentration of the drainage fluid and 2 patients were diagnosed by the percutaneous puncture fluid amylase concentration.Four patients underwent percutaneous puncture drainage by BS-guide.Five patients underwent re.operation drainage.Enteral feeding,total parenteral nutrition,total parenteral plus oral nutrition were applied to 15,6 and 6 patients,respectively.Altogether 3 patients died,all of these patients were in the total parenteral nutrition group.13 cases were discharged with draining tubes,including 2 patients who developed Dseudocyst and received surgical treatment,and the others 1 1 patients were discharged with tubes for(9.0±3.2)months.The mean hospital stays for oral feeding,jejunum tube nutrition and total parenteral nutrition groups were(36.3±10.2)d,(57.6±17.3)d and(63.3±33.4)d,respectively;and difference was statistically significant(F=3.49,P=0.049).The mean hospital stays for patients with or without somatostatin treatment were(53.5±20.3)d and(51.5 ±21.0)d,and difference was not statistically significant(t=0.207,P=0.838).Conclusions hereasingthe understanding ofpancreaticfistula,adequate drainage and rational nutrition phyed a key role in impmving the treatment effects of pancreatic fistula.
ABSTRACT
Objective To investigate the apoptosis of HepG2 cells and their sensitivities to the ciglitazone after inhibiting the activity of nuclear factor-kappa B (NF-kB) by NF-kB decoy oligonucleotide. Methods After transfecting HepG2 cells with NF-kB decoy oligonucleotide, the activity of NF-kB was observed by electrophonetic mobility shift assay and the protein expression of Bcl-2 and Fas by Western blot. The transfected and untransfected HepG2 cells were processed with 100 umol/L of ciglitazone for 1 to 4 days, and the growth curve and cell cycle of HepG2 cells were observed. Results After transfecting NF-kB decoy oligonucleotide to HepG2 cells, the activity of the NF-kB was inhibited, the Bcl-2 protein expression decreased and the Fas protein expression increased. The inhibition effect of the ciglitazone on the growth of HepG2 ceils was strengthened and more HepG2 cells were arrested at G1/G0 phase. Conclusions NF-kB decoy oligonucleotide could accelerate the apoptosis of HepG2 cells and enhance the inhibition effect of ciglitazone on HepG2 proliferation, the mechanism of which might be attributable to the increased expression of Fas protein and the decreased expression of Bcl-2 protein after NF-kB decoy oligonucleotide inhibiting the activity of NF-kB.