Stents for benign and malignant esophageal strictures.

This paper presents commentaries on endotherapy for esophageal perforation/leaks; treatment of esophageal perforation; whether esophageal stents should be used for treating benign esophageal strictures; what determines the optimal stenting period in benign esophageal strictures/leaks; how to choose an esophageal stent; how a new fistula secondary to an esophageal stent should be treated; which strategy should be adopted when a fistula of a cervical anastomosis occurs; intralesional steroids for refractory esophageal strictures; balloon and bougie dilators for esophageal strictures and predictors of response to dilation; whether refractory strictures from different etiologies respond differently to endotherapy; surgical therapy of benign esophageal strictures; and whether stenoses following severe esophageal burns should be treated by esophageal resection or esophageal bypass.

In vitro study on the mechanisms of action of a novel phytotherapeutic compound against human hepatoma cells.

HepG2 human hepatoma cells were incubated for 24 or 48 h with various concentrations of YHK solution. After 24 h incubation, cell proliferation and cytotoxicity were determined by 3-(4,5-dimethylthiazol-2- yl)-5-(3- carboxymethoxyphenyl)-2-(4-sulfophenyl)-2Htetrazolium (MTT) assay. Cytotoxicity or necrosis was expressed as lactate dehydrogenase (LDH) release. After exponential growth phase HepG2 cells were treated with different doses of YHK and apoptosis was assessed by using an Annexin V-FITC kit. Further, oxidative stress was measured by dichlorofluorescein-diacetate (DCFH-DA) assay. As compared to control, YHK-treated cultures showed a significant time-course decrease of the proliferation rate of HepG2 cell growth (p < 0.01). This is likely to be due to an enhanced cytotoxicity (MTT and LDH tests) (p < 0.001). On the other hand, YHK showed in vitro to significantly enhance the oxidative stress of HepG2 cell (p < 0.01) while also markedly increasing apoptosis at 72 h with cells G2/M phase arrest (p < 0.01). These data suggest that YHK seem to modulate the extrinsic and intrinsic regulators of apoptosis and sensitize tumour cells to apoptosis. These preliminary data are worth interest when considering that this nutraceutical has been shown in vitro and in vivo to exert protective anti-tumour effect by redox statusmodulating and immuno-regulatory actions. Given its lack of toxicity so far reported, such natural product might represent an effective nutritional supplement in a number of pathological conditions where a chemopreventive strategy is planned.