Preparation of iodine containing diamond-like carbon films by trifluoroiodomethane

Iodine containing diamond-like carbon (DLC) films were prepared by a plasma-enhanced chemical vapor deposition process using a mixture of trifluoroiodomethane (CF3I) and acetylene (C2H2) as plasma gas. The resulting films contain iodine throughout but are mostly fluorine free. Even though the precursor contains more fluorine than iodine, fluorine is only present in larger concentrations in the surface and interface region. The films are smooth, show a decreased hardness and a higher contact angle as compared to iodine free DLC films

Properties of iodine containing diamond-like carbon films prepared by plasma source ion implantation

The addition of halogens to diamond-like carbon (DLC) films provides attractive film properties, e.g. a hydrophobic surface combined with an improved corrosion protection. The use of iodine is of interest in this regard because of its additional marked influence on the band gap and therefore on the optical properties of the film. Instead of solid iodine, the gaseous precursor trifluoroiodomethane (CF3I) was used to prepare iodine containing DLC films. In contrast to our earlier experiments, a lower voltage was used in the plasma based preparation process thereby extending the iodine concentration range. The film properties, such as halogen content, bonding, water contact angle and corrosion protection were evaluated. The iodine containing DLC films are suitable to be deposited on polymer materials

Cooperative effects of aminopeptidase N (CD13) expressed by nonmalignant and cancer cells within the tumor microenvironment

Processes that promote cancer progression such as angiogenesis require a functional interplay between malignant and nonmalignant cells in the tumor microenvironment. The metalloprotease aminopeptidase N (APN; CD13) is often overexpressed in tumor cells and has been implicated in angiogenesis and cancer progression. Our previous studies of APN-null mice revealed impaired neoangiogenesis in model systems without cancer cells and suggested the hypothesis that APN expressed by nonmalignant cells might promote tumor growth. We tested this hypothesis by comparing the effects of APN deficiency in allografted malignant (tumor) and nonmalignant (host) cells on tumor growth and metastasis in APN-null mice. In two independent tumor graft models, APN activity in both the tumors and the host cells cooperate to promote tumor vascularization and growth. Loss of APN expression by the host and/or the malignant cells also impaired lung metastasis in experimental mouse models. Thus, cooperation in APN expression by both cancer cells and nonmalignant stromal cells within the tumor microenvironment promotes angiogenesis, tumor growth, and metastasis