Coating and functionalization of high density ion track structures by atomic layer deposition

In this study flexible TiO 2 coated porous Kapton membranes are presented having electron multiplication properties. 800 nm crossing pores were fabricated into 50 m thick Kapton membranes using ion track technology and chemical etching. Consecutively, 50 nm TiO 2 films were deposited i nto the pores of the Kapton membranes by atomic layer deposition using Ti( i OPr) 4 and water as precursors at 250 °C. The TiO 2 films and coated membranes were studied by scanning electro n microscopy (SEM), X - ray diffraction (XRD) and X - ray reflectometry (XRR). Au metal electrod e fabrication onto both sides of the coated foils was achieved by electron beam evaporation. The electron multipliers were obtained by joining 3 two coated membranes separated by a conductive spacer. The results show that electron multiplication can be achie ved using ALD - coated flexible ion track polymer foils

Cervical squamous carcinoma cells are resistant to the combined action of tumor necrosis factor-α and histamine whereas normal keratinocytes undergo cytolysis

<p>Abstract</p> <p>Background</p> <p>Previous reports showed that mast cells can typically be found in the peritumoral stroma of cervix carcinomas as well as in many other cancers. Both histamine and TNF-α are potent preformed mast cell mediators and they can act simultaneously after release from mast cells. Thus, the effect of TNF-α and histamine on cervical carcinoma cell lines was studied.</p> <p>Methods and results</p> <p>TNF-α alone induced slight growth inhibition and cell cycle arrest at G0/G1 phase in SiHa cells, but increased their migration. Histamine alone had no effect on cells. In addition, TNF-α and histamine in combination showed no additional effect over that by TNF-α alone, although SiHa cells were even pretreated with a protein synthesis inhibitor. Furthermore, TNF-α-sensitive ME-180 carcinoma cells were also resistant to the combination effect of TNF-α and histamine. In comparison, TNF-α or histamine alone induced growth inhibition in a non-cytolytic manner in normal keratinocytes, an effect that was further enhanced to cell cytolysis when both mediators acted in combination. Keratinocytes displayed strong TNF receptor (TNFR) I and II immunoreactivity, whereas SiHa and ME-180 cells did not. Furthermore, cervix carcinoma specimens revealed TNF-α immunoreactivity in peritumoral cells and carcinoma cells. However, the immunoreactivity of both TNFRs was less intense in carcinoma cells than that in epithelial cells in cervical specimens with non-specific inflammatory changes.</p> <p>Conclusion</p> <p>SiHa and ME-180 cells are resistant to the cytolytic effect of TNF-α and histamine whereas normal keratinocytes undergo cytolysis, possibly due to the smaller amount of TNFRs in SiHa and ME-180 cells. In the cervix carcinoma, the malignant cells may resist this endogenous cytolytic action and TNF-α could even enhance carcinoma cell migration.</p