The initial growth process of CNWs was investigated with and Without O(2) gas addition to a C(2)F(6) capacitively Coupled plasma with H radical injection. In the case of the CNW synthesis without the addition of O(2) gas, scanning electron microscopy (SEM). transmission electron microscopy, x-ray photoelectron spectroscopy (XPS). and Raman spectroscopy revealed that a 10-nm-thick interface layer composed of nanoislands wits formed selleck on a Si substrate approximately I min
prior to CNW formation. In contrast. with O(2) gas addition. SEM and XPS revealed that an interface layer was not formed and that CNWs were grown directly from nanoislands. Moreover. Raman spectroscopy suggested that the interface layer was composed of amorphous Fludarabine clinical trial carbon and that O(2) gas addition during CNW growth is effective for achieving a high graphitization of CNWs. Therefore. O(2) gas addition has the effect of reducing the amorphicity and disorder of CNWs and controlling CNW nucleation. (C) 2009 American Institute of Physics. [doi:10.1063/1.3253734]“
“Background-Familial history is a strong risk factor for coronary
artery disease (CAD), especially for early-onset myocardial infarction (MI). Several genes and chromosomal regions have been implicated in the genetic cause of coronary artery disease/MI, mostly through the discovery of familial mutations implicated in hyper-/hypocholesterolemia by linkage studies and single nucleotide polymorphisms by genome-wide association studies. Except for a few examples (eg, PCSK9), the role of low-frequency genetic variation (minor allele frequency [ MAF]) approximate to 0.1%-5% on MI/coronary artery disease predisposition has not been extensively investigated.
Methods and Results-We selected 68 candidate genes and sequenced their exons (394 kb) in 500 early-onset MI cases and 500 matched controls, all of French-Canadian ancestry, using solution-based
capture in pools of nonindexed DNA samples. In these regions, we identified 1852 single nucleotide variants (695 novel) and captured 85% of the variants with MAF >= 1% found by the 1000 PLX4032 supplier Genomes Project in Europe-ancestry individuals. Using gene-based association testing, we prioritized for follow-up 29 low-frequency variants in 8 genes and attempted to genotype them for replication in 1594 MI cases and 2988 controls from 2 French-Canadian panels. Our pilot association analysis of low-frequency variants in 68 candidate genes did not identify genes with large effect on MI risk in French Canadians.
Conclusions-We have optimized a strategy, applicable to all complex diseases and traits, to discover efficiently and cost-effectively DNA sequence variants in large populations. Resequencing endeavors to find low-frequency variants implicated in common human diseases are likely to require very large sample size. (Circ Cardiovasc Genet. 2012;5:547-554.