In this study, adjuvant IFNα-2b did not reduce the postoperative recurrence of viral hepatitis-related HCC. More potent antiviral therapy deserves to be explored for this patient population. This study is registered at ClinicalTrials.gov and carries the identifier NCT00149565.

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Administering PI-88 at 160 mg/d is a safe and well-tolerated dosage that may confer significant clinical benefits for patients with HCC.

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Hepatocyte growth factor (HGF) has been found to stimulate proliferation and migration of human gastric carcinoma cells. Whether the HGF-induced responses are correlated with the expressed level of HGF receptors or the changes of ionic currents is not clear. The present study investigated the effects of HGF on the proliferation and ionic currents of two human gastric adenocarcinoma cell lines, which were found to express different amounts of HGF receptor. Results showed that HGF induced a dose-dependent growth stimulation and accelerated cell cycle progression in SC-M1 cells. In patch clamp study, HGF treatment induced an outward K+ current and increased the slope conductance at -80 mV from 110+/-15 pS/pF to 207+/-15 pS/pF. The HGF-induced K+ current was abolished when tetraethylammonium chloride was added in bathing solution or a low Ca2+ solution was included in the recording pipette. Furthermore, HGF (10 ng/ml) induced an oscillatory Ca2+-activated K+ current with a lag period of 5+/-3 min in SC-M1 cells. In contrast, HGF did not induce mitogenesis, cell cycle progression and changes in ionic currents in KATO-III cells, although this cell line expressed a higher level of HGF receptors than SC-M1 cells did. These findings provide evidence that the activity of Ca2+-activated K+ channel may be involved in the HGF-induced cell proliferation in human gastric cancer cells, but it did not correlate with the density of HGF receptors.

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The effect of the natural compound phenethyl isothiocyanate (PEITC) on cytosolic Ca(2+) concentrations ([Ca(2+)](i)) and viability in MDCK renal cells is unknown. This study explored whether PEITC changed [Ca(2+)](i) in MDCK cells using the Ca(2+)-sensitive fluorescent dye fura-2. PEITC at 200-700 μM increased [Ca(2+)](i) in a concentration-dependent manner. The signal was reduced by removing extracellular Ca(2+). PEITC-induced Ca(2+) influx was inhibited by nifedipine, econazole, SK&F 96365 and protein kinase C modulators. In Ca(2+)-free medium, treatment with the endoplasmic reticulum Ca(2+) pump inhibitor thapsigargin (TG) or 2,5-di-tert-butylhydroquinone (BHQ) inhibited PEITC-induced rise in [Ca(2+)](i). Incubation with PEITC also inhibited TG or BHQ-induced rise in [Ca(2+)](i). Inhibition of phospholipase C with U73122 abolished PEITC-induced rise in [Ca(2+)](i). At 15-75 μM, PEITC decreased viability. The cytotoxic effect of PEITC was enhanced by chelating cytosolic Ca(2+) with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxymethyl ester. Annexin V-FITC data suggest that 20 and 50 μM PEITC induced apoptosis. At 10 and 15 μM, PEITC did not increase reactive oxygen species (ROS) production. Together, in renal tubular cells, PEITC-induced rise in [Ca(2+)](i) by inducing phospholipase C-dependent Ca(2+) release from endoplasmic reticulum and Ca(2+) entry via store-operated Ca(2+) channels. PEITC induced apoptosis in a concentration-dependent, ROS/Ca(2+)-independent manner.

Whole-body leucine and plasma glucose kinetics were simultaneously measured in burned rats after 2 d of total parenteral nutrition (TPN) containing sodium DL-3-hydroxybutyrate or sodium acetate to evaluate the ketone bodies as energy substrates during stress. TPN solutions consisted of dextrose and amino acids [200 kcal/(kg . d); 13 g amino acids/(kg . d)] and contained 34.3 mEq/(kg . d) either as sodium DL-3-hydroxybutyrate (n = 8) or sodium acetate (n = 7). Whole-body leucine appearance, incorporation into protein, release from protein breakdown and oxidation rates, as measured after a constant infusion of L-[1-14C]leucine did not significantly differ between the groups. In contrast, D-[6-3H]glucose appearance rates after constant infusion of this tracer were significantly higher in rats given sodium DL-3-hydroxybutyrate [209.3 +/- 3.8 mumol/(kg body weight . min)] than in those given sodium acetate [162.4 +/- 9.7 mumol/(kg body weight . min)] (P less than 0.01). Since leucine kinetics did not differ, the results suggest that sodium DL-3-hydroxybutyrate infusions increase endogenous glucose production [61.0 +/- 4.6 mumol/(100 kg body weight . min)] by enhancing glucose recycling. However, there was no unique protein-sparing effect of ketone bodies identified during injury.