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C Schug

Publications and source records attributed to C Schug.

3 recordsLinked to original sources
PubMed2002

Analytical characterization of thin carbon films.

CH(x) films on silicon substrates deposited by a Mesh Hollow Cathode Process (MHC) were analyzed by various techniques. The films were produced with varying deposition times, resulting in thicknesses ranging from ~2-20 nm. X-Ray Reflectivity (XRR) was used to determine the film thicknesses and the deposition rate. A good correlation of measured XRR thicknesses with SIMS sputter depths down to the film-substrate transition was found. An AFM-based nanoscratching technique was applied to test the wear resistance of the thin overcoats. The MHC films reveal slightly decreasing scratch resistance for reduced film thicknesses, which can be explained by a higher fraction of soft interface zones for thinner films. This is in accordance with Raman spectroscopic measurements in the visible spectral range which were carried out to examine the carbon bonding properties. Combined analysis of G peak position and D/G peak intensity ratio indicates a more graphitic structure for film thicknesses less than 10 nm.

Journal Article↗
PubMed2000

A RET double mutation in the germline of a kindred with FMTC.

Activating germline mutations of the RET proto-oncogene are found in more than 90% of families with multiple endocrine neoplasia type 2a (MEN 2a) and familial medullary thyroid carcinoma (FMTC). The majority of patients with these hereditary tumors carry germline mutations that result in the substitution of one of five cysteine residues in exon 10 and 11. Different mutations in exons 13, 14 and 15 affecting non-cysteine residues have also been described but are considered to be rare. We now for the first time report a double mutation of the RET proto-oncogene occurring in the germline of a kindred with FMTC. Both mutations occur within the tyrosine kinase domain in exon 14 and lead to the substitution of valine 804 by methionine and arginine 844 by leucine. Since the double mutated allele cosegregated with the disease and was not identified in 200 unrelated normal probands, we conclude that they represent mutations that predispose the individual to the development of FMTC with a mild phenotype.

Adolescent↗