In addition, we also conducted single-marker regression analysis on markers that were excluded due to segregation distortion, and markers that failed to be grouped with the current linkage groups at an LOD threshold of 4.0 (unlinked).
In the context of QTL fine-mapping, Grapes et al. [ 23] found that single marker regression with 10 markers performed worse than an IBD-method using linkage disequilibrium and linkage analysis information with a haplotype window of 10 markers, but single marker regression performed similarly when 20 markers were used.
Other methods involved multiple regression on markers, with (BL) or without penalization (RR), that both considered the animal additive genetic effect to correct for stratification.
However, the proportion of variance accounted for by the regression on markers is captured in our estimates h M 2 (see Table 1).
In an ordinal regression model, markers of neurological development (cognitive test scores) and stress (emotional stress scores) accounted for approximately 36% of the relationship between breast feeding and social mobility.
In a multinomial logistic regression model, markers of chronic asthma severity (history of hospitalisation for asthma and use of inhaled corticosteroids) were significantly associated with a higher frequency of ED visits (both p<0.05).
Interval mapping improves on the marker regression method by estimating markers (pseudomarkers) in between true markers.
*FM-A: Full model - pedigree-based; FM-RR: Full model - ridge regression with marker data; FM-RRA: Full model - combined ridge regression with markers and pedigree data; FM-L: full model - the least absolute shrinkage and selection operator; FM-LA: full model – combined least absolute shrinkage and selection operator, and pedigree information.
Since the AIL we are using as a test population is relatively densely genotyped we mapped using regression at marker locations in all cases, which also had the effect of halving the time required and eliminating potential worries about the accuracy of assigning genotype probabilities between markers.
In addition, no correlation was detected between histopathologically determined tumour regression and marker expression (Table 3).
