Irradiation-induced telomerase activity and gastric cancer risk: a case-control analysis in a Chinese Han population

<p>Abstract</p> <p>Background</p> <p>Telomerase expression is one of the characteristics of gastric cancer (GC) cells and telomerase activity is frequently up-regulated by a variety of mechanisms during GC development. Therefore, we hypothesized that elevated levels of activated telomerase might enhance GC risk due to increased propagation of cells with DNA damage, such as induced by γ-radiation.</p> <p>Methods</p> <p>To explore this hypothesis, 246 GC cases and 246 matched controls were recruited in our case-control study. TRAP-ELISA was used to assess the levels of telomerase activity at baseline and after γ-radiation and the γ-radiation-induced telomerase activity (defined as after γ-irradiation/baseline) in cultured peripheral blood lymphocytes (PBLs).</p> <p>Results</p> <p>Our data showed that there was no significant difference for the baseline telomerase activity between GC cases and controls (10.17 ± 7.21 <it>vs. </it>11.02 ± 8.03, <it>p </it>= 0.168). However, after γ-radiation treatment, γ-radiation-induced telomerase activity was significantly higher in the cases than in the controls (1.51 ± 0.93 <it>vs</it>. 1.22 ± 0.66, <it>p </it>< 0.001). Using the median value of γ-radiation-induced telomerase activity in the controls as a cutoff point, we observed that high γ-radiation-induced telomerase activity was associated with a significantly increased GC risk (adjusted odds ratio, 2.45; 95% confidence interval, 1.83-3.18). Moreover, a dose response association was noted between γ-radiation-induced telomerase activity and GC risk. Age, but not sex, smoking and drinking status seem to have a modulating effect on the γ-radiation-induced telomerase activities in both cases and controls.</p> <p>Conclusion</p> <p>Overall, our findings for the first time suggest that the increased γ-radiation-induced telomerase activity in PBLs might be associated with elevated GC risk. Further confirmation of this association using a prospective study design is warranted.</p

Reduced expression of N-Myc downstream-regulated gene 2 in human thyroid cancer

<p>Abstract</p> <p>Background</p> <p><it>NDRG</it>2 (N-Myc downstream-regulated gene 2) was initially cloned in our laboratory. Previous results have shown that <it>NDRG</it>2 expressed differentially in normal and cancer tissues. Specifically, <it>NDRG</it>2 mRNA was down-regulated or undetectable in several human cancers, and over-expression of <it>NDRG</it>2 inhibited the proliferation of cancer cells. <it>NDRG</it>2 also exerts important functions in cell differentiation and tumor suppression. However, it remains unclear whether <it>NDRG</it>2 participates in carcinogenesis of the thyroid.</p> <p>Methods</p> <p>In this study, we investigated the expression profile of human <it>NDRG</it>2 in thyroid adenomas and carcinomas, by examining tissues from individuals with thyroid adenomas (n = 40) and carcinomas (n = 35), along with corresponding normal tissues. Immunohistochemistry, quantitative RT-PCR and western blot methods were utilized to determine both the protein and mRNA expression status of Ndrg2 and c-Myc.</p> <p>Results</p> <p>The immunostaining analysis revealed a decrease of Ndrg2 expression in thyroid carcinomas. When comparing adenomas or carcinomas with adjacent normal tissue from the same individual, the mRNA expression level of <it>NDRG</it>2 was significantly decreased in thyroid carcinoma tissues, while there was little difference in adenoma tissues. This differential expression was confirmed at the protein level by western blotting. However, there were no significant correlations of <it>NDRG</it>2 expression with gender, age, different histotypes of thyroid cancers or distant metastases.</p> <p>Conclusion</p> <p>Our data indicates that <it>NDRG</it>2 may participate in thyroid carcinogenesis. This finding provides novel insight into the important role of <it>NDRG2 </it>in the development of thyroid carcinomas. Future studies are needed to address whether the down-regulation of <it>NDRG</it>2 is a cause or a consequence of the progression from a normal thyroid to a carcinoma.</p

Magnetoelectric interaction and transport behaviours in magnetic nanocomposite thermoelectric materials

How to suppress the performance deterioration of thermoelectric materials in the intrinsic excitation region remains a key challenge. The magnetic transition of permanent magnet nanoparticles from ferromagnetism to paramagnetism provides an effective approach to finding the solution to this challenge. Here, we have designed and prepared magnetic nanocomposite thermoelectric materials consisting of BaFe12O19 nanoparticles and Ba0.3In0.3Co4Sb12 matrix. It was found that the electrical transport behaviours of the nanocomposites are controlled by the magnetic transition of BaFe12O19 nanoparticles from ferromagnetism to paramagnetism. BaFe12O19 nanoparticles trap electrons below the Curie temperature (TC) and release the trapped electrons above the TC, playing an ‘electron repository’ role in maintaining high figure of merit ZT. BaFe12O19 nanoparticles produce two types of magnetoelectric effect—electron spiral motion and magnon-drag thermopower—as well as enhancing phonon scattering. Our work demonstrates that the performance deterioration of thermoelectric materials in the intrinsic excitation region can be suppressed through the magnetic transition of permanent magnet nanoparticles