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Silicon dioxide films were grown by low-temperature anneal in O2 on substrates of CoSi2 lines or disks. The leakage current through SiO2 films grown on CoSi2 lines have a strong dependence on the O2 anneal temperature, while those grown on CoSi2 disks have a weak dependence on anneal temperature. This difference is due to the shape of the oxide grown on the CoSi2. Oxide films were found to grow in a convex shape on CoSi2 disks, being much thicker in the middle of the disk than on the edge. Oxide films grown on CoSi2 lines had relatively uniform thickness across the width of the line. [ABSTRACT FROM AUTHOR]

Activating BRAF or NRAS mutations have been found in 80% of human sporadic melanomas, but only one of these genetic alterations could be detected in each tumour. This suggests that BRAF and NRAS ‘double mutants’ may not provide advantage for tumour growth, or may even be selected against during tumorigenesis. However, by applying mutant-allele-specific-amplification-PCR method to short-term melanoma lines, one out of 14 tumours was found to harbour both BRAFV600E and the activating NRASQ61R mutations. On the other hand, analysis of 21 melanoma clones isolated by growth in soft agar from this tumour indicated that 16/21 clones harboured a BRAFV600E, but were wild-type for NRAS, whereas the remaining had the opposite genotype (NRASQ61R/wild-type BRAF). When compared to BRAFV600E clones, NRASQ61R clones displayed reduced growth in soft agar, but higher proliferative ability in vitro in liquid medium and even in vivo after grafting into SCID/SCID mice. These data suggest that NRAS and BRAF activating mutations can coexist in the same melanoma, but are mutually exclusive at the single-cell level. Moreover, the presence of NRASQ61R or BRAFV600E is associated with distinct in vitro and in vivo growth properties of neoplastic cells.Oncogene (2006) 25, 3357–3364. doi:10.1038/sj.onc.1209379; published online 6 February 2006 [ABSTRACT FROM AUTHOR]

Sodalites and sulfatic sodalites in holocrystalline K-feldspar-rich ejecta from the Somma-Vesuvius volcanic complex, Italy, have been characterized by combined chemical, structural and spectroscopic analyses. Sodalite has a relatively homogeneous chemical composition, with the ubiquitous presence of CO2-3 and H2O/OH-. The sulfatic sodalites are isomorphous and have cage structures which can contain a wide variety of anions, molecular species and cations. Molecular CO2 and H2O/OH- are present in sulfatic sodalites, instead of the CO2-3 anions that are present in sodalite sensu stricto. The cell dimensions of the all of the studied sodalite samples are very similar, the sulfatic sodalite cell dimensions are more variable. Structure refinement of a distinctly green sample confirms the P4̅3n space group. Metasomatic magma-derived fluids that are rich in H2O, CO2, Cl and S are believed to be responsible for the genesis of the relatively late-stage phases which form the ejecta containing the sodalite-group minerals. [ABSTRACT FROM AUTHOR]

Background Malignant melanoma (MM) is the most aggressive skin cancer. Most MMs are sporadic, and in this setting an association with mismatch repair (MMR) gene mutations, typical of hereditary nonpolyposis colorectal cancer (HNPCC) tumours, has been proposed. Objectives To characterize clinically and/or by molecular biology the patients with MM belonging to a cohort of 60 kindreds with HNPCC. Methods Patients with HNPCC with a diagnosis of MM were studied by immunohistochemistry (IHC) on tumour tissue using antibodies to MLH1, MSH2, p16, β-catenin and E-cadherin, and by direct sequencing of MMR genes on germline DNA, and BRAF and NRAS on somatic DNA extracted from MM. Results Nine cutaneous MMs were detected in the tumour spectrum of eight families with HNPCC. The median age at diagnosis was 46 years. In one HNPCC family the diagnosis of MM was made in two first-degree relatives fitting the clinical definition of familial melanoma. IHC and sequencing analysis showed an MSH2 mutation in one patient with MM. Conclusions Dermatological surveillance should be recommended to families in which MM is diagnosed in at least one member, especially at a young age. The combination of MMR gene mutations and abnormalities of p16 or other molecular pathways is needed to induce melanocytic carcinogenesis in a familial setting as well as in sporadic MM. [ABSTRACT FROM AUTHOR]