Breed- and trait-specific associations define the genetic architecture of calving performance traits in cattle.

Reducing the incidence of both the degree of assistance required at calving, as well as the extent of perinatal mortality (PM) has both economic and societal benefits. The existence of heritable genetic variability in both traits signifies the presence of underlying genomic variability. The objective of the present study was to locate regions of the genome, and by extension putative genes and mutations, that are likely to be underpinning the genetic variability in direct calving difficulty (DCD), maternal calving difficulty (MCD), and PM. Imputed whole-genome single-nucleotide polymorphism (SNP) data on up to 8,304 Angus (AA), 17,175 Charolais (CH), 16,794 Limousin (LM), and 18,474 Holstein-Friesian (HF) sires representing 5,866,712 calving events from descendants were used. Several putative quantitative trait loci (QTL) regions associated with calving performance both within and across dairy and beef breeds were identified, although the majority were both breed- and trait-specific. QTL surrounding and encompassing the myostatin (MSTN) gene were associated (P < 5 × 10-8) with DCD and PM in both the CH and LM populations. The well-known Q204X mutation was the fifth strongest association with DCD in the CH population and accounted for 5.09% of the genetic variance in DCD. In contrast, none of the 259 segregating variants in MSTN were associated (P > × 10-6) with DCD in the LM population but a genomic region 617 kb downstream of MSTN was associated (P < 5 × 10-8). The genetic architecture for DCD differed in the HF population relative to the CH and LM, where two QTL encompassing ZNF613 on Bos taurus autosome (BTA)18 and PLAG1 on BTA14 were identified in the former. Pleiotropic SNP associated with all three calving performance traits were also identified in the three beef breeds; 5 SNP were pleiotropic in AA, 116 in LM, and 882 in CH but no SNP was associated with more than one trait within the HF population. The majority of these pleiotropic SNP were on BTA2 surrounding MSTN and were associated with both DCD and PM. Multiple previously reported, but also novel QTL, associated with calving performance were detected in this large study. These also included QTL regions harboring SNP with the same direction of allele substitution effect for both DCD and MCD thus contributing to a more effective simultaneous selection for both traits.

Maternal distress in late pregnancy alters obstetric outcomes and the expression of genes important for placental glucocorticoid signalling.

The experience of maternal distress in pregnancy is often linked with poorer obstetric outcomes for women as well as adverse outcomes for offspring. Alterations in placental glucocorticoid signalling and subsequent increased fetal exposure to cortisol have been suggested to underlie this relationship. In the current study, 121 pregnant women completed the Perceived Stress Scale, State Trait Anxiety Inventory and Edinburgh Postnatal Depression Scale in the third trimester of pregnancy. Placental samples were collected after delivery. Maternal history of psychiatric illness and miscarriage were significant predictors of poorer mental health in pregnancy. Higher anxiety was associated with an increase in women delivering via elective Caesarean Section, and an increase in bottle-feeding. Birth temperature was mildly reduced among infants of women with high levels of depressive symptomology. Babies of mothers who scored high in all stress (cumulative distress) measures had reduced 5-min Apgar scores. High cumulative distress reduced the expression of placental HSD11B2 mRNA and increased the expression of placental NR3C1 mRNA. These data support a role for prenatal distress as a risk factor for altered obstetric outcomes. The alterations in placental gene expression support a role for altered placental glucocorticoid signalling in the relationship between maternal prenatal distress and adverse outcomes.

Potential long-term risks associated with maternal aging (the role of the mitochondria).

The mean age at which women create families in Western society is increasing. This is in spite of the fact that reproduction in later life is subject to various difficulties, such as the lower probability of conception in relation to maternal age, the increase in spontaneous pregnancy loss, and higher obstetric risk. In this review of recent data, we suggest that a fourth effect, the decrease in lifespan of children in relation to the age of conception of the mother, can be added to the list. We discuss this effect in relation to the transmission of the mitochondria exclusively through the female germ line and the effect of age on this organelle. Data from our own studies and the animal literature as a whole suggest that this effect could be due to the transmission of damaged mitochondrial DNA, and further indicate that the effect is more widespread than previously considered.

HMGB1 promotes a p38MAPK associated non-infectious inflammatory response pathway in human fetal membranes.

OBJECTIVE: Spontaneous preterm birth (PTB) and preterm prelabor rupture of membranes (pPROM) are major pregnancy complications often associated with a fetal inflammatory response. Biomolecular markers of this fetal inflammatory response to both infectious and non-infectious risk factors and their contribution to PTB and pPROM mechanism are still unclear. This study examined fetal membrane production, activation and mechanistic properties of high mobility group box 1 (HMGB1) as a contributor of the non-infectious fetal inflammatory response. MATERIALS AND METHODS: HMGB1 transcripts and active HMGB1 were profiled in fetal membranes and amniotic fluids collected from PTB and normal term birth. In vitro, normal term not in labor fetal membranes were exposed to lipopolysaccharide (LPS) and water soluble cigarette smoke extract (CSE). HMGB1-transcripts and its protein concentrations were documented by RT-PCR and ELISA. Recombinant HMGB1 treated membranes and media were subjected to RT-PCR for HMGB1 receptors, mitogen activated protein kinase pathway analysis, cytokine levels, and Western blot for p38MAPK. RESULTS: HMGB1 expression and its active forms were higher in PTB and pPROM than normal term membranes and amniotic fluid samples. Both LPS and CSE enhanced HMGB1 expression and release in vitro. Fetal membrane exposure to HMGB1 resulted in increased expression of TLR2 and 4 and dose-dependent activation of p38MAPK-mediated inflammation. CONCLUSIONS: HMGB1 increase by fetal membrane cells in response to either oxidative stress or infection can provide a positive feedback loop generating non-infectious inflammatory activation. Activation of p38MAPK by HMGB1 promotes development of the senescence phenotype and senescence associated sterile inflammation. HMGB1 activity is an important regulator of the fetal inflammatory response regardless of infection.

Does asymptomatic carriage of FV Leiden and FII prothrombin mutations in heterozygous configuration pose an increased risk of thrombembolic complications in the course of pregnancy, labor and puerperium?

OBJECTIVE: To evaluate the course of pregnancy and puerperium in asymptomatic carriers of FV Leiden and FII prothrombin mutation in heterozygous configuration in terms of risk of thrombembolic disease (TED) and late pregnancy complications. To evaluate whether global prophylactic LMWH administration during pregnancy benefits these women. METHODS: We monitored the incidence of thrombembolic events and severe late pregnancy complications in 473 asymptomatic carriers of FV Leiden and FII prothrombin mutation in heterozygous configuration. In 253 women, preventive LMWH application was introduced already during pregnancy. In 220 women, the application of LMWH was commenced as late as on the delivery day. In both groups application of LMWH continued during the puerperium. RESULTS: The incidence of TED in the whole group of carriers of thrombophylic mutations accounted for 0.19%. The incidence of severe late pregnancy complications was low - 2.5% compared with general population of pregnant women (6.4%). CONCLUSIONS: No direct causal relationship was established between asymptomatic carriage of Leiden and prothrombin mutation in heterozygous configuration and the occurrence of severe late pregnancy complications. There was no benefit from general LMWH prophylaxis started as early as pregnancy in these women and thus we consider it unnecessary.

Genetic contributions to labor pain and progress.

Studies on genetic contributions to labor analgesia have essentially evaluated the µ-opioid receptor gene (OPRM1), with some evidence that p.118A/G of OPRM1 influences the response to neuraxial opioids. As for labor progress, the ß2-adrenergic receptor gene (ADRB2) is associated with preterm labor and delivery, and impacts the course of labor. Taken together though, there is no evidence that pharmacogenetic testing is needed or beneficial in the context of obstetric anesthesia; however, realizing the influence of genetic variants on specific phenotypes provides the rationale for a more cautious interpretation of clinical studies that attempt to find a dose-regimen that fits all.

Characterization of the myometrial transcriptome in women with an arrest of dilatation during labor.

OBJECTIVE: The molecular basis of failure to progress in labor is poorly understood. This study was undertaken to characterize the myometrial transcriptome of patients with an arrest of dilatation (AODIL). STUDY DESIGN: Human myometrium was prospectively collected from women in the following groups: (1) spontaneous term labor (TL; n=29) and (2) arrest of dilatation (AODIL; n=14). Gene expression was characterized using Illumina® HumanHT-12 microarrays. A moderated Student's t-test and false discovery rate adjustment were used for analysis. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) of selected genes was performed in an independent sample set. Pathway analysis was performed on the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway database using Pathway Analysis with Down-weighting of Overlapping Genes (PADOG). The MetaCore knowledge base was also searched for pathway analysis. RESULTS: (1) Forty-two differentially expressed genes were identified in women with an AODIL; (2) gene ontology analysis indicated enrichment of biological processes, which included regulation of angiogenesis, response to hypoxia, inflammatory response, and chemokine-mediated signaling pathway. Enriched molecular functions included transcription repressor activity, heat shock protein (Hsp) 90 binding, and nitric oxide synthase (NOS) activity; (3) MetaCore analysis identified immune response chemokine (C-C motif) ligand 2 (CCL2) signaling, muscle contraction regulation of endothelial nitric oxide synthase (eNOS) activity in endothelial cells, and triiodothyronine and thyroxine signaling as significantly overrepresented (false discovery rate <0.05); (4) qRT-PCR confirmed the overexpression of Nitric oxide synthase 3 (NOS3); hypoxic ischemic factor 1A (HIF1A); Chemokine (C-C motif) ligand 2 (CCL2); angiopoietin-like 4 (ANGPTL4); ADAM metallopeptidase with thrombospondin type 1, motif 9 (ADAMTS9); G protein-coupled receptor 4 (GPR4); metallothionein 1A (MT1A); MT2A; and selectin E (SELE) in an AODIL. CONCLUSION: The myometrium of women with AODIL has a stereotypic transcriptome profile. This disorder has been associated with a pattern of gene expression involved in muscle contraction, an inflammatory response, and hypoxia. This is the first comprehensive and unbiased examination of the molecular basis of an AODIL.

Familial risk of obstetric anal sphincter injuries: registry-based cohort study.

OBJECTIVE: To investigate the aggregation of obstetric anal sphincter injuries (OASIS) in relatives. DESIGN: Population-based cohort study. SETTING: The Medical Birth Registry of Norway from 1967 to 2008. POPULATION: All singleton, vertex-presenting infants weighing 500 g or more. Through linkage by national identification numbers, 393 856 mother-daughter pairs, 264 675 mother-son pairs, 134 889 mothers whose sisters later became mothers, 132 742 fathers whose brothers later became fathers, 131 702 mothers whose brothers later became fathers and 88 557 fathers whose sisters later became mothers were provided. METHODS: Comparison of women with and without a history of OASIS in their relatives. MAIN OUTCOME MEASURE: Relative risk of OASIS after a previous OASIS in the family. RESULTS: The risk of OASIS was increased if the woman's mother or sister had OASIS in a delivery (aRR 1.9, 95% CI 1.6-2.3; aRR 1.7, 95% CI 1.6-1.7, respectively). If OASIS occurred in one brother's partner at delivery, the risk of OASIS in the next brother's partner was modestly increased (aRR 1.2, 95% CI 1.1-1.4). If OASIS occurred in one sister at delivery, the risk of OASIS in the brother's partner was also increased a little (aRR 1.2, 95% CI 1.1-1.4). However, there was no excess occurrence in sisters whose brothers' partners had previously had OASIS (aRR 1.1, 95% CI 0.9-1.3). CONCLUSIONS: There appears to be increased familial aggregation of OASIS. These risks are stronger through the maternal rather than the paternal line of transmission, suggesting a strong genetic role that shapes aggregation of OASIS within families. These observations must be cautiously interpreted because of bias from unmeasured confounding factors may have impacted the findings.

Obstetric complications in early psychosis: relation with family history of psychosis.

The people classified as being at ultra-high risk (UHR) of developing psychosis are expected to share many risk factors for psychosis with the patients diagnosed with schizophrenia, including an enhanced incidence of obstetric complications (OCs). This study set out to investigate the incidence and correlates of OCs in a sample of patients accessing an early intervention center. Patients' mothers were asked whether they had suffered from any somatic complication during pregnancy from a list of OCs with potential direct relevance to the physical wellbeing of the offspring. Out of 86 patients diagnosed with first-episode psychosis, 20 (23%) cases were positive for the occurrence of severe OCs, as reported by their mothers during an interview; out of 83 UHR patients, 21 (25%) cases were positive for OCs. OCs were more common in individuals with a family history of psychosis than in those without such a history. OCs might interact with genetic vulnerability to increase the risk of psychosis. Lack of comparison to healthy controls is a limitation that decreases the value of these findings.

[Incidence of hereditary thrombophilia in women with pregnancy loss in multi-center studies in Poland]. / Czestosc wystepowania trombofilii wrodzonej u kobiet z utrata ciaz w wieloosrodkowych badaniach w Polsce.

AIM: The aim of this study was to estimate the prevalence of factor V Leiden and prothrombin gene G20210A mutation among women with pregnancy loss in Poland. MATERIAL AND METHODS: we analyzed a group of 396 women (mean age of 30.4 (+/- 4.6) years), who experienced at least one pregnancy loss. Patients were recruited from 6 academic centers (Poznan, Bialystok, Lublin, Wroclaw Bydgoszcz, Gdansk), and were divided into the following groups: 122 patients with 3 episodes of early recurrent pregnancy loss (group 1), 87 patients with late pregnancy loss (group 2) and 46 patients with intrauterine pregnancy loss (group 3). Patients who did not fulfill the above inclusion criteria were divided into additional groups. 50 healthy women (mean age of 29.2 (+/- 4.5) years), having at least one child, constituted the control group. Factor V Leiden mutation and prothrombin G20210A gene mutation were examined in all 396 women with pregnancy loss and 50 controls. For molecular analysis peripheral blood was tested. Genome DNA isolation from lymphocyte was performed with commercial assay QIAampDNA Blood Mini Kit. RESULTS: Among 396 women with unexplained loss of at least one pregnancy 36 (9.1%) were carriers of inherited thrombophilia. Factor V Leiden mutation was present in 29 women (73%), prothrombin gene mutation G20210A in 6 (1.5%) and in 1 (0.3%) patient both mutations were detected. No coagulation defects were found in the control group. Factor V Leiden mutations was the most common disorder (21.7%) in patients with intrauterine demise and was significantly higher than in the group of women with early recurrent and late losses, p<0.011 and p<0,006 respectively The frequency of G20210 A prothrombin gene mutation did not differ substantially between the examined groups; the highest number (2.6%) was found in women with early and late pregnancy losses, and the lowest number (0.8%) was seen in women with early recurrent miscarriages. CONCLUSION: Factor V Leiden screening should be performed, regardless of negative history of thrombosis, in patients who experienced intrauterine fetal demise or recurrent early miscarriages.

Polwarth and Texel ewe parturition duration and its association with lamb birth asphyxia.

The objective of the present study was to test the hypothesis that parturition duration is related to birth asphyxia in lambs and that asphyxia affects newborn lamb viability and vigor. Two sire and dam genotypes (Texel: TX; Polwarth: PW) and their crosses were represented in the study. Eighty lambs (25 PW sire × PW dam, 13 TX × TX, 25 TX × PW, and 17 PW × TX) born to 69 grazing ewes were used. At birth, the log10 length of the second stage of parturition, birth weight, placental weight, and several body measurements were recorded on all lambs, and jugular blood samples were analyzed with the i-Stat Portable Clinical Analyzer (Abbott, Montevideo, Uruguay). A modified Apgar viability score at birth and lamb behavior during their first hour of life were recorded. Brain weight, muscle:bone ratio, and bone density were recorded in 20 male lambs (5 from each breed group) that were euthanized and dissected 24 h after birth. Data were analyzed by linear regression, least squares ANOVA, and ordinal and binary logistic regressions. Mean blood gas and acid-base variables were 7.21 ± 0.09 for pH, 18.4 ± 9.8 mmHg for partial pressure of oxygen, 53 ± 12.5 mmHg for partial pressure of carbon dioxide, and -4 ± 5.1 mmol/L for extracellular fluid base excess. Parturition duration increased with birth weight (P < 0.001) and was shorter in TX ewes (P < 0.001), female lambs (P < 0.05), twins (P < 0.09), and twin females (sex × litter size interaction, P < 0.02). Twenty-six (32.9%) lambs were born asphyxiated (pO2 < 10 mmHg or pH <7.1). Parturition duration increased the risk of asphyxia (P < 0.001), decreased the viability score (P < 0.001), and increased the latency to suckle the udder (P < 0.05). Twin-born lambs presented at birth a 16-fold greater risk of asphyxia (P < 0.01) and reduced placental efficiency (P < 0.05). Texel-sired lambs appeared immature at birth, with less bone density (P < 0.05), smaller brain (P < 0.05), shorter forelimbs (P < 0.05), greater anterior (P < 0.001) and posterior (P < 0.05) neck circumference, and greater muscle:bone ratio (P < 0.05). Immaturity may explain greater TX biotype survival. Together these results demonstrate that a relationship exists between parturition duration, neonatal viability and behavior, and acid-base balance values in single- and twin-born lambs, suggesting that birth asphyxia is an important risk factor in perinatal lamb mortality.

Perinatal complications in unaffected sisters of anorexia nervosa patients: testing a covariation model between genetic and environmental factors.

Although perinatal complications are hypothesized to be risk factors for the development of anorexia nervosa (AN), no study to date explored this issue using a discordant sibling design. This type of design allows to explore whether the risk for obstetric complications is itself a consequence of the genetic vulnerability for AN (covariation model) or whether obstetric complications increase the risk of AN independently of (additive model), or in interaction with (interaction model), the disorder's genetic liability. The presence of perinatal complications was assessed through review of the obstetric records of 60 AN subjects, 60 unaffected sisters, and 70 healthy subjects. Unaffected sisters and healthy controls were compared in relation to perinatal characteristics and complications. There was no evidence for an elevated rate of complications in unaffected siblings of AN patients. Mothers with a positive psychiatric history tended to have more perinatal complications. Perinatal complications seem to be independent risk factors that may interact with, but are not caused by, familial risk factors for AN. In terms of prevention, a particular attention should be paid to mothers with a lifetime history of psychiatric disorders.

Hereditary thrombophilia and recurrent pregnancy loss: a retrospective cohort study of pregnancy outcome and obstetric complications.

BACKGROUND: The association among hereditary thrombophilia, recurrent pregnancy loss (RPL) and obstetric complications is yet uncertain. The objective of the study was to assess the prognostic value of the factor V Leiden (FVL) and prothrombin (PT) mutations for the subsequent chance of live birth for women with RPL. METHODS: Pregnancy outcome was recorded in a retrospective cohort of 363 women with a minimum of three consecutive pregnancy losses (early miscarriage, late miscarriage or stillbirth/neonatal death) who were not treated with anticoagulation therapy. RESULTS: Of the 363 women, 29 were FVL-mutation carriers and 6 were PT-mutation carriers. The unadjusted live birth rate was 45.7% in FVL/PT carriers versus 63.4% in FVL/PT non-carriers, P = 0.04. The adjusted odds ratio for live birth in FVL/PT carriers was 0.48 (95% CI = 0.23-1.01), P = 0.05. Among the obstetric complications, only excessive bleeding was found to be associated with FVL/PT mutations. CONCLUSIONS: In the unadjusted analysis, FVL and PT mutations have a negative prognostic impact on the live birth rate in women with RPL; however, when adjusting for significant covariates, the results no longer reach statistical significance. Strong conclusions on the association between obstetric complications and hereditary thrombophilia cannot be drawn from this study. Whether anticoagulation therapy would improve the prognosis in women with RPL and FVL/PT mutations remains to be documented in large randomized controlled trials.

An exploratory model for G x E interaction on hippocampal volume in schizophrenia; obstetric complications and hypoxia-related genes.

BACKGROUND: Smaller hippocampal volume has repeatedly been reported in schizophrenia patients. Obstetric complications (OCs) and single nucleotide polymorphism (SNP) variation in schizophrenia susceptibility genes have independently been related to hippocampal volume. We investigated putative independent and interaction effects of severe hypoxia-related OCs and variation in four hypoxia-regulated schizophrenia susceptibility genes (BDNF, DTNBP1, GRM3 and NRG1) on hippocampal volume in schizophrenia patients and healthy controls. METHODS: Clinical assessment, structural MRI scans, and blood samples for genotyping of 32 SNPs were obtained from 54 schizophrenia patients and 53 control subjects. Information on obstetric complications was collected from original birth records. RESULTS: Severe OCs were related to hippocampal volume in both patients with schizophrenia and healthy control subjects. Of the 32 SNPs studied, effects of severe OCs on hippocampal volume were associated with allele variation in GRM3 rs13242038, but the interaction effect was not specific for schizophrenia. SNP variation in any of the four investigated genes alone did not significantly affect hippocampal volume. CONCLUSIONS: The findings suggest a gene-environment (G x E) interaction between GRM3 gene variants and severe obstetric complications on hippocampus volume, independent of a diagnosis of schizophrenia. Due to the modest sample size, the results must be considered preliminary and require replication in independent samples.

Effects of labor on placental expression of superoxide dismutases in preeclampsia.

A decreased antioxidant activity for superoxide dismutases (SODs) in the placenta was reported in preeclampsia (PE). However, it is unclear if this reduced enzymatic activity can be attributed to a specific SOD isoform. Moreover, the specific spatial SOD expression in the placenta and the impact of the mode of delivery on the latter are still lacking. There are three known SOD isoforms: SOD1 (cytosolic), SOD2 (mitochondrial) and SOD3 (extracellular). Our main objective was to characterize by RT-PCR, western blot and immunolocalization, the expression of SOD1, SOD2, and SOD3 in placentas of normotensive (n = 23) and PE pregnancies (n = 25) according to the presence or absence of labor, the sampling site (peri-insertion, mid-disc and periphery) and the placental layer: amnion-chorion, villi, and maternal side layer (MS). In absence of labor (cesarean), SOD1 expression in the placental villi and MS was lower in PE than in controls (p < 0.049). In presence of labor (vaginal deliveries), SOD1 expression in the amnion-chorion only was higher in PE than controls (p = 0.014). Additionally, SOD2 and SOD3 expression in presence of labor were higher in all three layers in PE than controls, with a strong positive correlation between these two SODs (mRNA; r > 0.65, p < 0.008). The sampling site and gestational age had no effect on SOD expression within the placenta. In this study, we showed that the reported decrease for SOD activity in PE may be attributed to SOD1 in absence of labor. Also, this is the first study characterizing specific SOD isoforms according to the mode of delivery. We demonstrated in PE that labor upregulates SOD1 in fetal membranes as well as SOD2 and SOD3 in the whole placenta.

Quantitative trait loci mapping of calving and conformation traits on Bos taurus autosome 18 in the German Holstein population.

Linkage, linkage disequilibrium, and combined linkage and linkage disequilibrium analyses were performed to map quantitative trait loci (QTL) affecting calving and conformation traits on Bos taurus autosome 18 (BTA18) in the German Holstein population. Six paternal half-sib families consisting of a total of 1,054 animals were genotyped on 28 genetic markers in the telomeric region on BTA18 spanning approximately 30 Mb. Calving traits, body type traits, and udder type traits were investigated. Using univariately estimated breeding values, maternal and direct effects on calving ease and stillbirth were analyzed separately for first- and further-parity calvings. The QTL initially identified by separate linkage and linkage disequilibrium analyses could be confirmed by a combined linkage and linkage disequilibrium analysis for udder composite index, udder depth, fore udder attachment, front teat placement, body depth, rump angle, and direct effects on calving ease and stillbirth. Concurrence of QTL peaks and a similar shape of restricted log-likelihood ratio profiles were observed between udder type traits and for body depth and calving traits, respectively. Association analyses were performed for markers flanking the most likely QTL positions by applying a mixed model including a fixed allele effect of the maternally inherited allele and a random polygenic effect. Results indicated that microsatellite marker DIK4234 (located at 53.3 Mb) is associated with maternal effects on stillbirth, direct effects on calving ease, and body depth. A comparison of effects for maternally inherited DIK4234 alleles indicated a favorable, positive correlation of maternal and direct effects on calving. Additionally, the association of maternally inherited DIK4234 marker alleles with body depth implied that conformation traits might provide the functional background of the QTL for calving traits. For udder type traits, the strong coincidence of QTL peaks and the position of the QTL in a region previously reported to harbor QTL for somatic cell score indicated that effects of QTL for udder type traits might be correlated with effects of QTL for udder health traits on BTA18. Our results suggest that loci in the middle to telomeric region on BTA18 with effect on conformation traits may also contribute to the genetic variance of calving and udder health traits. Further analyses are required to identify the causal mutations affecting conformation and calving traits and to investigate the correlation of effects for loci associated with conformation, calving, and udder health traits.

Genetic relationships among calving ease, gestation length, and calf survival to weaning in the Asturiana de los Valles beef cattle breed.

The aim of this paper was to estimate the genetic relationships among calving ease (CE), calf survival (CS), and gestation length (GL) to assess the possibility of including this information in beef cattle breeding programs. A total of 35,395 field records were available for CE, 30,684 for GL, and 36,132 for CS from the Asturiana de los Valles beef cattle breed. The 3 traits were analyzed as traits of the calf fitting a multivariate linear mixed model. Estimates of heritability (+/-SE) for the direct genetic effects (CEd, GLd, and CSd) were 0.325 +/- 0.022, 0.331 +/- 0.026, and 0.226 +/- 0.018, respectively, whereas the estimates for maternal genetic effects (CEm, GLm, and CSm) were 0.066 +/- 0.018, 0.066 +/- 0.017, and 0.034 +/- 0.011. The estimates for the ratio of permanent environmental variance to phenotypic variance were CEc 0.090 +/- 0.011, GLc 0.066 +/- 0.011, and CSc 0.024 +/- 0.007. Genetic correlations between direct, maternal genetic, or permanent environmental effects involving CE and GL were, in general, positive and moderate, whereas those involving CE and CS were high. All were significant except for the pair CEm-GLm (0.277 +/- 0.172). Correlations between GL and CS were nonsignificant. Genetic correlations for CEd-CEm, GLd-GLm, and CSd-CSm were negative and high, ranging from -0.461 +/- 0.120 for GLd-GLm to -0.821 +/- 0.145 for CSd-CSm. The genetic correlations for CEd-CSm and for CSd-CEm were negative, significant, and high, whereas that for GLd-CEm was moderate (-0.323 +/- 0.124) and that for GLd-CSm was nonsignificant. The genetic correlations for GLm with the direct effects of the other traits were non-significant. Strong selection for CE will result in a significant correlated response in CS. Therefore, CE can be considered an early indicator of CS performance. The benefit of using GL as a correlated trait in a genetic evaluation with CE and CS seems limited.