Variation simulation analysis has been used in the design stage to predict such uncertainties, but variation analysis based on rigid body assumptions usually yields over-estimates of the assembly variations.
Paleomagnetic secular variation (PSV) analysis has been employed to constrain the eruption frequency down to the millennium or century timescale, and to identify the eruption pulses in some LIPs (Makinen et al. 1985; Riisager et al. 2003; Knight et al. 2004; Chenet et al. 2008; Pavlov et al. 2011; Courtillot and Fluteau 2014).
Copy number variation (CNV) analysis has had a major impact on the field of medical genetics, providing a mechanism to identify disease-causing genomic alterations in an unprecedented number of diseases and phenotypes.
Although there are few in depth analyses on individual bordetellae loci to determine mechanisms or the selective pressures contributing to variation, previous analysis has shown some evidence for HGT in several loci shared by most strains, such as the Pertussis Toxin assembly locus [ 5].
The use of single-nucleotide polymorphisms (SNPs) as markers of genetic variation for phylogenetic analysis has been described in many studies [ 23– 28].
A computational framework, the exposure variation analysis (EVA), has been suggested to quantify variation [ 11].
Recent genetic evidence conclusively showed that the tumour cell itself is the transmissible agent responsible for CTVT [ 4] and, on the basis of microsatellite and mtDNA variation analysis, it has been possible to estimate the age of CTVT at between 250 and 2,500 years or earlier [ 4, 19].
However, three-dimensional scapular motion analysis has indicated variations in this ratio according to the arm elevation angle.
Comparative genomic analysis has shown variations in different genes between these biotypes (1 ).
The statistical analysis has revealed that variation in agitation from 150 rpm to 200 rpm has no effect on the production of α-amylase and that of protein; whereas such as a variation increases the biomass.
Our pathway analysis has shown that variation in conserved canonical inflammatory pathways underlies genetic susceptibility to T1D, CD, and RA.
