Comparison between haplotype-based and individual snp-based genomic predictions for beef fatty acid profile in Nelore cattle
JOURNAL OF ANIMAL BREEDING AND GENETICS
Authors: Braga Feitosa, Fabieli Loise; Cravo Pereira, Angelica Simone; Amorim, Sabrina Thaise; Peripolli, Elisa; de Oliveira Silva, Rafael Medeiros; Braz, Camila Urbano; Ferrinho, Adrielle Matias; Schenkel, Flavio Schramm; Brito, Luiz Fernando; Espigolan, Rafael; de Albuquerque, Lucia Galvao; Baldi, Fernando
The aim of this study was to evaluate the genomic predictions using the single-step genomic best linear unbiased predictor (ssGBLUP) method based on SNPs and haplotype markers associated with beef fatty acids (FAs) profile in Nelore cattle. The data set contained records from 963 Nelore bulls finished in feedlot (+/- 90 days) and slaughtered with approximately 24 months of age. Meat samples from the Longissimus dorsi muscle were taken for FAs profile measurement. FAs were quantified by gas chromatography using a SP-2560 capillary column. Animals were genotyped with the high-density SNP panel (BovineHD BeadChip assay) containing 777,962 markers. SNPs with a minor allele frequency and a call rate lower than 0.05 and 0.90, respectively, monomorphic, located on sex chromosomes, and with unknown position were removed from the data set. After genomic quality control, a total of 469,981 SNPs and 892 samples were available for subsequent analyses. Missing genotypes were imputed and phased using the FImpute software. Haplotype blocks were defined based on linkage disequilibrium using the Haploview software. The model to estimate variance components and genetic parameters and to predict the genomic values included the random genetic additive effects, fixed effects of the contemporary group and the age at slaughter as a linear covariate. Accuracies using the haplotype-based approach ranged from 0.07 to 0.31, and those SNP-based ranged from 0.06 to 0.33. Regression coefficients ranged from 0.07 to 0.74 and from 0.08 to 1.45 using the haplotype- and SNP-based approaches, respectively. Despite the low to moderate accuracies for the genomic values, it is possible to obtain genetic progress trough selection using genomic information based either on SNPs or haplotype markers. The SNP-based approach allows less biased genomic evaluations, and it is more feasible when taking into account the computational and operational cost underlying the haplotypes inference.
Fas ligand neutralization attenuates hypertension, endothelin-1, and placental inflammation in an animal model of HELLP syndrome
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
Authors: Gibbens, Jacob; Spencer, Shauna-Kay; Solis, Lucia; Bowles, Teylor; Kyle, Patrick B.; Szczepanski, Jamie L.; Dumas, John Polk; Robinson, Reanna; Wallace, Kedra
Neutralization of FasL is linked to suppression of hypertension, placental inflammation, and endothelin system activation in an animal model of hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome. During HELLP syndrome the placenta has been reported to serve as the primary source of Fas ligand (FasL), which has an impact on inflammation and hypertension during pregnancy and is dysregulated in women with severe pre-eclampsia and HELLP syndrome. We hypothesize that neutralization of FasL during pregnancy in an animal model of HELLP syndrome decreases inflammation and placental apoptosis, improves endothelial damage, and improves hypertension. On gestational day (GD) 12, rats were chronically infused with placental antiangiogenic factors sFlt-1 and sEng to induce HELLP syndrome. To neutralize FasL, MFL4 or FasL antibody was infused into a subset of HELLP or normal pregnant rats on GD13. IgG infusion into another group of NP and HELLP rats on GD13 was used as a control for FasL antibody, and all rats were euthanized on GD19 after blood pressure measurement. Plasma and placentas were collected to assess inflammation, apopto-sis, and the degree of placental debris activation of endothelial cells. Administration of MFL4 to HELLP rats significantly decreased blood pressure compared with untreated HELLP rats and HELLP rats infused with IgG and improved the biochemistry of HELLP syn-drome. Both circulating and placental FasL were significantly atten-uated in response to MFL4 infusion, as were levels of placental and circulating TNFa when compared with untreated HELLP rats and HELLP rats infused with IgG. Endothelial cells exposed to placental debris and media from HP + MFL4 rats secreted significantly less endothelin-1 compared with stimulated endothelial cells from HELLP placentas. Neutralization of FasL is associated with decreased MAP and improvement in placental inflammation and endothelial damage in an animal model of HELLP syndrome.