Estimation of genetic variation in residual variance in female and male broiler chickens

In breeding programs, robustness of animals and uniformity of end product can be improved by exploiting genetic variation in residual variance. Residual variance can be defined as environmental variance after accounting for all identifiable effects. The aims of this study were to estimate genetic variance in residual variance of body weight, and to estimate genetic correlations between body weight itself and its residual variance and between female and male residual variance for broilers. The data sets comprised 26 972 female and 24 407 male body weight records. Variance components were estimated with ASREML. Estimates of the heritability of residual variance were in the range 0.029 (s.e.50.003) to 0.047 (s.e.50.004). The genetic coefficients of variation were high, between 0.35 and 0.57. Heritabilities were higher in females than in males. Accounting for heterogeneous residual variance increased the heritabilities for body weight as well. Genetic correlations between body weight and its residual variance were 20.41 (s.e.50.032) and 20.45 (s.e.50.040), respectively, in females and males. The genetic correlation between female and male residual variance was 0.11 (s.e.50.089), indicating that female and male residual variance are different traits. Results indicate good opportunities to simultaneously increase the mean and improve uniformity of body weight of broilers by selection

Heterogeneity of genetic parameters for calving difficulty in Holstein heifers in Ireland

Calving difficulty is a trait that greatly affects animal welfare, herd profitability, and the amount of labor required by cattle farmers. It is influenced by direct and maternal genetic components. Selection and breeding strategies can optimize the accuracy of genetic evaluations and correctly emphasize calving difficulty in multiple-trait indices provided there are accurate estimates of genetic parameters. In Ireland, large differences exist in the age at which heifers first give birth to calves. The objective of this study was to estimate genetic parameters for calving difficulty in first-parity Holsteins and to determine whether these differed with age of the heifer at calving. Transformed calving difficulty records for 18,798 Holstein heifers, which calved between January 2002 and May 2006, were analyzed using univariate, multitrait, and random regression linear sire-maternal grandsire models. The model that 1) fitted a second-order random regression of dam age at first parity for the direct component, 2) treated the maternal component as a single trait regardless of dam age, and 3) fitted a single residual variance component was optimal. Heritabilities for direct (0.13) and maternal (0.04) calving difficulty were significantly different from zero. These 2 components were moderately negatively correlated (¿0.47). Estimates of direct genetic variance and heritability were heterogeneous along the dam age trajectory, decreasing initially with dam age before subsequently increasing. Heritability estimates ranged between 0.11 and 0.37 and were higher for records with younger and older dams at parturition. Genetic correlations between the direct components of calving difficulty decreased from unity to 0.5 with increasing distance between dam ages at parturition. The results of this study indicated that heterogeneity of direct genetic variance existed for calving difficulty, depending on dam age at first parturition

Shock-induced termination of reentrant cardiac arrhythmias: comparing monophasic and biphasic shock protocols

In this article, we compare quantitatively the efficiency of three different protocols commonly used in commercial defibrillators. These are based on monophasic and both symmetric and asymmetric biphasic shocks. A numerical one-dimensional model of cardiac tissue using the bidomain formulation is used in order to test the different protocols. In particular, we performed a total of 4.8 × 10(6) simulations by varying shock waveform, shock energy, initial conditions, and heterogeneity in internal electrical conductivity. Whenever the shock successfully removed the reentrant dynamics in the tissue, we classified the mechanism. The analysis of the numerical data shows that biphasic shocks are significantly more efficient (by about 25%) than the corresponding monophasic ones. We determine that the increase in efficiency of the biphasic shocks can be explained by the higher proportion of newly excited tissue through the mechanism of direct activation.journal article2013 Decimporte

Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980�2015: a systematic analysis for the Global Burden of Disease Study 2015

Background Improving survival and extending the longevity of life for all populations requires timely, robust evidence on local mortality levels and trends. The Global Burden of Disease 2015 Study (GBD 2015) provides a comprehensive assessment of all-cause and cause-specific mortality for 249 causes in 195 countries and territories from 1980 to 2015. These results informed an in-depth investigation of observed and expected mortality patterns based on sociodemographic measures. Methods We estimated all-cause mortality by age, sex, geography, and year using an improved analytical approach originally developed for GBD 2013 and GBD 2010. Improvements included refinements to the estimation of child and adult mortality and corresponding uncertainty, parameter selection for under-5 mortality synthesis by spatiotemporal Gaussian process regression, and sibling history data processing. We also expanded the database of vital registration, survey, and census data to 14�294 geography�year datapoints. For GBD 2015, eight causes, including Ebola virus disease, were added to the previous GBD cause list for mortality. We used six modelling approaches to assess cause-specific mortality, with the Cause of Death Ensemble Model (CODEm) generating estimates for most causes. We used a series of novel analyses to systematically quantify the drivers of trends in mortality across geographies. First, we assessed observed and expected levels and trends of cause-specific mortality as they relate to the Socio-demographic Index (SDI), a summary indicator derived from measures of income per capita, educational attainment, and fertility. Second, we examined factors affecting total mortality patterns through a series of counterfactual scenarios, testing the magnitude by which population growth, population age structures, and epidemiological changes contributed to shifts in mortality. Finally, we attributed changes in life expectancy to changes in cause of death. We documented each step of the GBD 2015 estimation processes, as well as data sources, in accordance with Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER). Findings Globally, life expectancy from birth increased from 61·7 years (95 uncertainty interval 61·4�61·9) in 1980 to 71·8 years (71·5�72·2) in 2015. Several countries in sub-Saharan Africa had very large gains in life expectancy from 2005 to 2015, rebounding from an era of exceedingly high loss of life due to HIV/AIDS. At the same time, many geographies saw life expectancy stagnate or decline, particularly for men and in countries with rising mortality from war or interpersonal violence. From 2005 to 2015, male life expectancy in Syria dropped by 11·3 years (3·7�17·4), to 62·6 years (56·5�70·2). Total deaths increased by 4·1 (2·6�5·6) from 2005 to 2015, rising to 55·8 million (54·9 million to 56·6 million) in 2015, but age-standardised death rates fell by 17·0 (15·8�18·1) during this time, underscoring changes in population growth and shifts in global age structures. The result was similar for non-communicable diseases (NCDs), with total deaths from these causes increasing by 14·1 (12·6�16·0) to 39·8 million (39·2 million to 40·5 million) in 2015, whereas age-standardised rates decreased by 13·1 (11·9�14·3). Globally, this mortality pattern emerged for several NCDs, including several types of cancer, ischaemic heart disease, cirrhosis, and Alzheimer's disease and other dementias. By contrast, both total deaths and age-standardised death rates due to communicable, maternal, neonatal, and nutritional conditions significantly declined from 2005 to 2015, gains largely attributable to decreases in mortality rates due to HIV/AIDS (42·1, 39·1�44·6), malaria (43·1, 34·7�51·8), neonatal preterm birth complications (29·8, 24·8�34·9), and maternal disorders (29·1, 19·3�37·1). Progress was slower for several causes, such as lower respiratory infections and nutritional deficiencies, whereas deaths increased for others, including dengue and drug use disorders. Age-standardised death rates due to injuries significantly declined from 2005 to 2015, yet interpersonal violence and war claimed increasingly more lives in some regions, particularly in the Middle East. In 2015, rotaviral enteritis (rotavirus) was the leading cause of under-5 deaths due to diarrhoea (146�000 deaths, 118�000�183�000) and pneumococcal pneumonia was the leading cause of under-5 deaths due to lower respiratory infections (393�000 deaths, 228�000�532�000), although pathogen-specific mortality varied by region. Globally, the effects of population growth, ageing, and changes in age-standardised death rates substantially differed by cause. Our analyses on the expected associations between cause-specific mortality and SDI show the regular shifts in cause of death composition and population age structure with rising SDI. Country patterns of premature mortality (measured as years of life lost YLLs) and how they differ from the level expected on the basis of SDI alone revealed distinct but highly heterogeneous patterns by region and country or territory. Ischaemic heart disease, stroke, and diabetes were among the leading causes of YLLs in most regions, but in many cases, intraregional results sharply diverged for ratios of observed and expected YLLs based on SDI. Communicable, maternal, neonatal, and nutritional diseases caused the most YLLs throughout sub-Saharan Africa, with observed YLLs far exceeding expected YLLs for countries in which malaria or HIV/AIDS remained the leading causes of early death. Interpretation At the global scale, age-specific mortality has steadily improved over the past 35 years; this pattern of general progress continued in the past decade. Progress has been faster in most countries than expected on the basis of development measured by the SDI. Against this background of progress, some countries have seen falls in life expectancy, and age-standardised death rates for some causes are increasing. Despite progress in reducing age-standardised death rates, population growth and ageing mean that the number of deaths from most non-communicable causes are increasing in most countries, putting increased demands on health systems. Funding Bill & Melinda Gates Foundation. © 2016 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY licens

Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980�2015: a systematic analysis for the Global Burden of Disease Study 2015

Background Improving survival and extending the longevity of life for all populations requires timely, robust evidence on local mortality levels and trends. The Global Burden of Disease 2015 Study (GBD 2015) provides a comprehensive assessment of all-cause and cause-specific mortality for 249 causes in 195 countries and territories from 1980 to 2015. These results informed an in-depth investigation of observed and expected mortality patterns based on sociodemographic measures. Methods We estimated all-cause mortality by age, sex, geography, and year using an improved analytical approach originally developed for GBD 2013 and GBD 2010. Improvements included refinements to the estimation of child and adult mortality and corresponding uncertainty, parameter selection for under-5 mortality synthesis by spatiotemporal Gaussian process regression, and sibling history data processing. We also expanded the database of vital registration, survey, and census data to 14�294 geography�year datapoints. For GBD 2015, eight causes, including Ebola virus disease, were added to the previous GBD cause list for mortality. We used six modelling approaches to assess cause-specific mortality, with the Cause of Death Ensemble Model (CODEm) generating estimates for most causes. We used a series of novel analyses to systematically quantify the drivers of trends in mortality across geographies. First, we assessed observed and expected levels and trends of cause-specific mortality as they relate to the Socio-demographic Index (SDI), a summary indicator derived from measures of income per capita, educational attainment, and fertility. Second, we examined factors affecting total mortality patterns through a series of counterfactual scenarios, testing the magnitude by which population growth, population age structures, and epidemiological changes contributed to shifts in mortality. Finally, we attributed changes in life expectancy to changes in cause of death. We documented each step of the GBD 2015 estimation processes, as well as data sources, in accordance with Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER). Findings Globally, life expectancy from birth increased from 61·7 years (95 uncertainty interval 61·4�61·9) in 1980 to 71·8 years (71·5�72·2) in 2015. Several countries in sub-Saharan Africa had very large gains in life expectancy from 2005 to 2015, rebounding from an era of exceedingly high loss of life due to HIV/AIDS. At the same time, many geographies saw life expectancy stagnate or decline, particularly for men and in countries with rising mortality from war or interpersonal violence. From 2005 to 2015, male life expectancy in Syria dropped by 11·3 years (3·7�17·4), to 62·6 years (56·5�70·2). Total deaths increased by 4·1 (2·6�5·6) from 2005 to 2015, rising to 55·8 million (54·9 million to 56·6 million) in 2015, but age-standardised death rates fell by 17·0 (15·8�18·1) during this time, underscoring changes in population growth and shifts in global age structures. The result was similar for non-communicable diseases (NCDs), with total deaths from these causes increasing by 14·1 (12·6�16·0) to 39·8 million (39·2 million to 40·5 million) in 2015, whereas age-standardised rates decreased by 13·1 (11·9�14·3). Globally, this mortality pattern emerged for several NCDs, including several types of cancer, ischaemic heart disease, cirrhosis, and Alzheimer's disease and other dementias. By contrast, both total deaths and age-standardised death rates due to communicable, maternal, neonatal, and nutritional conditions significantly declined from 2005 to 2015, gains largely attributable to decreases in mortality rates due to HIV/AIDS (42·1, 39·1�44·6), malaria (43·1, 34·7�51·8), neonatal preterm birth complications (29·8, 24·8�34·9), and maternal disorders (29·1, 19·3�37·1). Progress was slower for several causes, such as lower respiratory infections and nutritional deficiencies, whereas deaths increased for others, including dengue and drug use disorders. Age-standardised death rates due to injuries significantly declined from 2005 to 2015, yet interpersonal violence and war claimed increasingly more lives in some regions, particularly in the Middle East. In 2015, rotaviral enteritis (rotavirus) was the leading cause of under-5 deaths due to diarrhoea (146�000 deaths, 118�000�183�000) and pneumococcal pneumonia was the leading cause of under-5 deaths due to lower respiratory infections (393�000 deaths, 228�000�532�000), although pathogen-specific mortality varied by region. Globally, the effects of population growth, ageing, and changes in age-standardised death rates substantially differed by cause. Our analyses on the expected associations between cause-specific mortality and SDI show the regular shifts in cause of death composition and population age structure with rising SDI. Country patterns of premature mortality (measured as years of life lost YLLs) and how they differ from the level expected on the basis of SDI alone revealed distinct but highly heterogeneous patterns by region and country or territory. Ischaemic heart disease, stroke, and diabetes were among the leading causes of YLLs in most regions, but in many cases, intraregional results sharply diverged for ratios of observed and expected YLLs based on SDI. Communicable, maternal, neonatal, and nutritional diseases caused the most YLLs throughout sub-Saharan Africa, with observed YLLs far exceeding expected YLLs for countries in which malaria or HIV/AIDS remained the leading causes of early death. Interpretation At the global scale, age-specific mortality has steadily improved over the past 35 years; this pattern of general progress continued in the past decade. Progress has been faster in most countries than expected on the basis of development measured by the SDI. Against this background of progress, some countries have seen falls in life expectancy, and age-standardised death rates for some causes are increasing. Despite progress in reducing age-standardised death rates, population growth and ageing mean that the number of deaths from most non-communicable causes are increasing in most countries, putting increased demands on health systems. Funding Bill & Melinda Gates Foundation. © 2016 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY licens

Merging and characterising phenotypic data on conventional and rare traits from dairy cattle experimental resources in three countries

peer-reviewedThis study set out to demonstrate the feasibility of merging data from different experimental resource dairy populations for joint genetic analyses. Data from four experimental herds located in three different countries (Scotland, Ireland and the Netherlands) were used for this purpose. Animals were first lactation Holstein cows that participated in ongoing or previously completed selection and feeding experiments. Data included a total of 60 058 weekly records from 1630 cows across the four herds; number of cows per herd ranged from 90 to 563. Weekly records were extracted from the individual herd databases and included seven traits: milk, fat and protein yield, milk somatic cell count, liveweight, dry matter intake and energy intake. Missing records were predicted with the use of random regression models, so that at the end there were 44 weekly records, corresponding to the typical 305-day lactation, for each cow. A total of 23 different lactation traits were derived from these records: total milk, fat and protein yield, average fat and protein percentage, average fat-to-protein ratio, total dry matter and energy intake and average dry matter intake-to-milk yield ratio in lactation weeks 1 to 44 and 1 to 15; average milk somatic cell count in lactation weeks 1 to 15 and 16 to 44; average liveweight in lactation weeks 1 to 44; and average energy balance in lactation weeks 1 to 44 and 1 to 15. Data were subsequently merged across the four herds into a single dataset, which was analysed with mixed linear models. Genetic variance and heritability estimates were greater (P,0.05) than zero for all traits except for average milk somatic cell count in weeks 16 to 44. Proportion of total phenotypic variance due to genotype-by-environment (sire-by-herd) interaction was not different (P.0.05) from zero. When estimable, the genetic correlation between herds ranged from 0.85 to 0.99. Results suggested that merging experimental herd data into a single dataset is both feasible and sensible, despite potential differences in management and recording of the animals in the four herds. Merging experimental data will increase power of detection in a genetic analysis and augment the potential reference population in genome-wide association studies, especially of difficult-to-record traits.European Commission Seventh Research Framework Program (Grant Agreement KBBE-211708, RobustMilk project); RERAD grant to Scottish Agricultural Colleg

Genome-wide associations for fertility traits in Holstein–Friesian dairy cows using data from experimental research herds in four European countries

peer-reviewedGenome-wide association studies for difficult-to-measure traits are generally limited by the sample population size with accurate phenotypic data. The objective of this study was to utilise data on primiparous Holstein–Friesian cows from experimental farms in Ireland, the United Kingdom, the Netherlands and Sweden to identify genomic regions associated with traditional measures of fertility, as well as a fertility phenotype derived from milk progesterone profiles. Traditional fertility measures investigated were days to first heat, days to first service, pregnancy rate to first service, number of services and calving interval (CI); post-partum interval to the commencement of luteal activity (CLA) was derived using routine milk progesterone assays. Phenotypic and genotypic data on 37 590 single nucleotide polymorphisms (SNPs) were available for up to 1570 primiparous cows. Genetic parameters were estimated using linear animal models, and univariate and bivariate genome-wide association analyses were undertaken using Bayesian stochastic search variable selection performed using Gibbs sampling. Heritability estimates of the traditional fertility traits varied from 0.03 to 0.16; the heritability for CLA was 0.13. The posterior quantitative trait locus (QTL) probabilities, across the genome, for the traditional fertility measures were all ,0.021. Posterior QTL probabilities of 0.060 and 0.045 were observed for CLA on SNPs each on chromosome 2 and chromosome 21, respectively, in the univariate analyses; these probabilities increased when CLA was included in the bivariate analyses with the traditional fertility traits. For example, in the bivariate analysis with CI, the posterior QTL probability of the two aforementioned SNPs were 0.662 and 0.123. Candidate genes in the vicinity of these SNPs are discussed. The results from this study suggest that the power of genome-wide association studies in cattle may be increased by sharing of data and also possibly by using physiological measures of the trait under investigation.European Union Seventh Research Framework Programme (Grant Agreement KBBE-211708, RobustMilk project