This study investigated the accuracy of direct genomic breeding values (DGV) using a genomic BLUP model, genomic enhanced breeding values (GEBV) using a one-step blending approach, and GEBV using a selection index blending approach for 15 traits of Nordic Red Cattle. The data comprised 6,631 bulls of which 4,408 bulls were genotyped using Illumina Bovine SNP50 BeadChip (Illumina, San Diego, CA). To validate reliability of genomic predictions, about 20% of the youngest genotyped bulls were taken as test data set. Deregressed proofs (DRP) were used as response variables for genomic predictions. Reliabilities of genomic predictions in the validation analyses were measured as squared correlations between DRP and genomic predictions corrected for reliability of DRP, based on the bulls in the test data sets. A set of weighting (scaling) factors was used to construct the combined relationship matrix among genotyped and nongenotyped bulls for one-step blending, and to scale DGV and its expected reliability in the selection index blending. Weighting (scaling) factors had a small influence on reliabilities of GEBV, but a large influence on the variation of GEBV. Based on the validation analyses, averaged over the 15 traits, the reliability of DGV for bulls without daughter records was 11.0 percentage points higher than the reliability of conventional pedigree index. Further gain of 0.9 percentage points was achieved by combining information from conventional pedigree index using the selection index blending, and gain of 1.3 percentage points was achieved by combining information of genotyped and nongenotyped bulls simultaneously applying the one-step blending. These results indicate that genomic selection can greatly improve the accuracy of preselection for young bulls in Nordic Red population, and the one-step blending approach is a good alternative to predict GEBV in practical genetic evaluation program.

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This paper studies whether cows with originally lower somatic cell count (SCC) are more susceptible to clinical mastitis (CM) than cows with higher somatic cell count, and evaluates the correlations between CM, SCC, and milk yield. Data were extracted from the Finnish national milk-recording database and from the health recording system. First and second lactation records of 87,861 Ayrshire cows calving between January 1998 and December 2000 were included. Traits studied were incidence of CM, test-day SCC, and test-day milk yield before and following CM. Genetic parameters were estimated using multitrait REML with a sire model. Results did not indicate that cows with genetically low SCC would be more susceptible to CM. The genetic correlation between CM in the first and second lactation was reasonably high (0.73), suggesting that susceptibility to mastitis remains similar across lactations. The genetic correlation between CM and milk yield traits was positive (from 0.38 to 0.56), confirming the genetic antagonism between production and udder health traits. The genetic correlation between SCC and milk was positive in the first lactation, but negative, or near zero in the second lactation. This indicates that breeding for lower SCC might not affect milk production in later lactations. The results of this study support the use of SCC as an indicator of mastitis and a tool for selection for mastitis resistance.

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Data on 23,196 cows were extracted from the Finnish system for recording health data and merged with information on SCS and 305-d milk production to study 1) the genetic and phenotypic correlations of clinical mastitis (within 150 d postpartum) and SCS across the first three lactations and 2) the genetic relationships between the traits for individual lactations. (Co)variance components were estimated using linear multitrait REML and the expectation-maximization algorithm. Heritability estimates for separate lactations were distinctly higher for somatic cell score (0.14 to 0.19) than for clinical mastitis (0.02 to 0.05). Genetic correlations of the same traits among different lactations were positive and moderate to high, suggesting that, in practice, clinical mastitis and SCS can be considered as the same traits for different lactations. Genetic correlations of clinical mastitis and SCS varied from 0.37 for first lactation to 0.68 for third lactation, implying that clinical mastitis and SCC monitor different aspects of udder health. A clear, antagonistic genetic association existed between clinical mastitis and milk production, but the genetic correlation of SCS and milk production did not differ from 0.