GSTM1 polymorphism is related to risks of nasopharyngeal cancer and laryngeal cancer: a meta-analysis.

BACKGROUND: Accumulating data have reported that GSTM1 polymorphism may be related to nasopharyngeal cancer (NPC) and laryngeal cancer (LC). This meta-analysis was performed to investigate the relationship between GSTM1 polymorphism and risks of NPC and LC. METHODS: Pubmed, Embase, and China National Knowledge Infrastructure (CNKI) databases were searched for potential articles. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to evaluate the relationship of GSTM1 polymorphism with the risks of NPC and LC. I2>50% or P<0.05 indicates significant heterogeneity. When heterogeneity existed, the random-effects model was used to pool data, otherwise, the fixed-effects model was adopted. Publication bias was detected by Begg's funnel plot and Egger's regression. Quality of each study was evaluated by Newcastle-Ottawa Scale. RESULTS: Thirty-two eligible articles were included. Pooled outcome suggested the significant relationship of GSTM1 null genotype with increased risk of LC (OR =1.28, 95% CI =1.05-1.54). Compared with hospital-based (HB) population, GSTM1 null genotype was also related to increased risk of LC (OR =1.38, 95% CI =1.06-1.80). Positive relationship of GSTM1 null genotype with enhanced risk of NPC was observed (OR =1.43, 95% CI =1.26-1.63). A similar trend was also observed in the subgroup analysis by source of control (population-based [PB]: OR =1.39, 95% CI =1.18-1.63; HB: OR =1.52, 95% CI =1.22-1.89). CONCLUSION: GSTM1 null genotype is related to increased risk of NPC and LC.

Effects of lentiviral vector-mediated TRADD expression on the inhibition of hypertrophic scar formation.

The tumor necrosis factor receptor-associated death domain protein (TRADD) regulates cell proliferation and apoptosis via tumor necrosis factor alpha (TNF-α)-mediated signaling pathways. Low levels of TRADD expression may result in the excessive proliferation of hypertrophic scar fibroblasts (HSFb). This study investigated the effects of a lentiviral vector carrying the human tradd gene on the proliferation, apoptosis and type I collagen synthesis of HSFb and embryonic fibroblasts (EFb) and further explored the resulting effects on hypertrophic scars (HS). We utilized cytoimmunofluorescence and Western blotting to confirm the expression of TRADD in HSFb and EFb. A PLVX-TRADD-EGFP lentivirus was prepared and transfected into EFb and HSFb, and then the expression of a TRADD-GFP-FLAG fusion protein was detected in HSFb and EFb. After stimulation with 10 ng/mL TNF-α, cell proliferation, apoptosis, and the synthesis of type I collagen were assessed. Our results show that the expression level of TRADD was significantly lower in HSFb than in EFb. A biologically active PLVX-TRADD-EGFP lentivirus was constructed and transfected into HSFb and EFb. The TRADD-GFP-FLAG fusion protein was effectively expressed in HSFb and EFb. Either alone or in combination with 10 ng/mL TNF-α, the PLVX-TRADD-EGFP lentivirus inhibited proliferation, caused a G2/M phase arrest, induced the appearance of a sub-G1 apoptotic peak and inhibited the secretion of type I collagen by HSFb without significantly affecting EFb. These results suggest that the low expression of TRADD in HSFb is a principal reason for their excessive proliferation. The transfection of a PLVX-TRADD-EGFP lentivirus led to the normal expression of TRADD in HSFb. When combined with 10 ng/mL TNF-α, a PLVX-TRADD-EGFP lentivirus transfection could inhibit cell proliferation, promote apoptosis, and reduce the secretion of type I collagen in HSFb, thereby reducing HS formation.

Plastic tube-assisted gastroscopic removal of embedded esophageal metal stents: a case report.

A patient with stent embedding after placement of an esophageal stent for an esophagobronchial fistula was treated with an ST-E plastic tube inserted into the esophagus to the upper end of the stent using gastroscopy. The gastroscope was guided into the esophagus through the ST-E tube, and an alligator forceps was inserted into the esophagus through the ST-E tube alongside the gastroscope. Under gastroscopy, the stent wire was grasped with the forceps and pulled into the ST-E tube. When resistance was met during withdrawal, the gastroscope was guided further to the esophageal section where the stent was embedded. Biopsy forceps were guided through a biopsy hole in the gastroscope to the embedded stent to remove silicone membranes and connection threads linking the Z-shaped wire mesh. While the lower section of the Z-shaped stent was fixed by the biopsy forceps, the alligator forceps were used to pull the upper section of the metal wire until the Z-shaped metal loops elongated. The wire mesh of the stent was then removed in stages through the ST-E tube. Care was taken to avoid bleeding and perforation. Under the assistance of an ST-E plastic tube, an embedded esophageal metal stent was successfully removed with no bleeding or perforation. The patient experienced an uneventful recovery after surgery. Plastic tube-assisted gastroscopic removal of embedded metal stents can be minimally invasive, safe, and effective.