Implementing biosecurity measures on dairy farms in Ireland

peer-reviewedDairy farms in Ireland are expanding in preparation for a new era of unrestricted milk production with the elimination of the European Union (EU) production quotas in 2015. Countries experiencing a changing agricultural demographic, including farm expansion, can benefit from documenting the implementation of on-farm biosecurity. The objectives of this study were to document and describe influences on biosecurity practices and related opinions on dairy farms. A representative response rate of 64% was achieved to a nationwide telesurvey of farmers. A 20% discrepancy was found between self-declared and truly ‘closed’ herds indicating a lack of understanding of the closed herd concept. Although >72% of farmers surveyed considered biosecurity to be important, 53% stated that a lack of information might prevent them from improving their biosecurity. Logistic regression highlighted regional, age, and farm-size related differences in biosecurity practices and opinions towards its implementation. Farmers in the most dairy cattle dense region were three times more likely to quarantine purchased stock than were their equivalents in regions where dairy production was less intense (P = 0.012). Younger farmers in general were over twice as likely as middle-aged farmers to implement biosecurity guidelines (P = 0.026). The owners of large enterprises were almost five times more likely to join a voluntary animal health scheme (P = 0.003), and were over three times more likely to pay a premium price for health accredited animals (P = 0.02) than were those farming small holdings. The baseline data recorded in this survey will form the basis for more detailed sociological and demographic research which will facilitate the targeting of future training of the farming community in biosecurity

Clinically driven analysis reveals gene-socioeconomic status interaction influencing periodontal disease in the electronic health record-linked Generation Scotland: Scottish Family Health Study (GS: SFHS) cohort.

Introduction Heritability (proportion of trait variation attributable to genetic factors) is not a fixed property. It can vary across different social settings and environments. Exploration of gene-environment interaction has been limited by lack of large sample sizes. Biobanks linked to electronic health records pose a solution to this sample size problem. Objectives and Approach Social inequalities in periodontal health have been well documented in the dental scientific literature. However, gene-socioeconomic status interaction has yet to be examined. We identified 2,192 cases and 11,525 controls from linked electronic periodontal treatment records within the Generation Scotland: Scottish Family Health Study (GS: SFHS) (www.generationscotland.org). The measure of socioeconomic status used was the Scottish Index of Multiple Deprivation. The objective of this study was to investigate the gene-socioeconomic status interaction within this data. A reaction norm model was used to evaluate the presence of a gene-socioeconomic status interaction in the statistical software ASReml. Results We estimated the heritability of periodontal disease at 10.42% (95% confidence interval 5.97-14.88%). Socioeconomic status modified the heritability of periodontal disease. The heritability of was 13.37%, 0.14% and 11.70% in areas of high, moderate and low deprivation respectively; indicating the occurrence of a gene-socioeconomic status interaction with periodontal disease. These results indicate that socioeconomic status explains a large portion of genetic variation in periodontal disease risk. This information suggests that effective intervention and prevention programs for periodontal disease should involve socioeconomic aspects in their planning, implementations and evaluation. For instance, interventions targeted to reduce smoking in more deprived subjects with a genetic predisposition to periodontal disease could enhance the effect of health promotion strategies in reducing risk. Conclusion/Implications This study presents contemporary evidence in a large population based cohort that gene-socioeconomic interaction leads to the progression of periodontal disease. This information may lead to the development of better preventative strategies for clinical dentistry

A case-control study in an Orcadian population investigating the relationship between human plasma N-glycans and metabolic syndrome.

Background: Alterations in glycosylation patterns have long been known to reflect changes in cell metabolism. In this study, we investigated the relationship between human N-glycan profiles and metabolic syndrome. Method: Between 2005 and 2011, 2,155 individuals from the Orkney Islands (UK) were recruited and biological material, alongside phenotypic measures were collected. Individual N-glycan profiles were measured in plasma using weak anion exchange high performance liquid chromatography and calibrated hydrophilic interaction liquid chromatography. Pre-specified criteria were used to identify 564 cases with metabolic syndrome and 1475 controls. We applied logistic regression to test for association between this binary outcome against measured plasma N-glycans. We also assessed the correlation between N-glycan traits and individual components of metabolic syndrome and compared this to results found in similar analyses based in Chinese and Croatian populations. Results: 21 N-glycan traits were found to be associated with either an increased or a decreased likelihood of participants having metabolic syndrome, including monosialylated plasma N-glycans (OR of 1.49 (95%CI 1.33, 1.67), q=1.26E-12) and core fucosylated plasma N-glycans (OR of 0.81(95% CI 0.72-0.90), q=7.75E-4). Notably, consistent results in both sections of this analysis demonstrated the protective association of higher levels of core fucosylated N-glycans. Conclusion: Our results demonstrate that metabolic syndrome is associated with an alteration in plasma N-glycosylation patterns. The metabolic role of core fucosylated N-glycans is of particular interest for future study

A Case-control study in an Orcadian population investigating the rRelationship between human plasma N-glycans and metabolic syndrome

Background: Alterations in glycosylation patterns have long been known to reflect changes in cell metabolism. In this study, we investigated the relationship between human N-glycan profiles and metabolic syndrome. Method: Between 2005 and 2011, 2,155 individuals from the Orkney Islands (UK) were recruited and biological material, alongside phenotypic measures were collected. Individual N-glycan profiles were measured in plasma using weak anion exchange high performance liquid chromatography and calibrated hydrophilic interaction liquid chromatography. Pre-specified criteria were used to identify 564 cases with metabolic syndrome and 1475 controls. We applied logistic regression to test for association between this binary outcome against measured plasma N-glycans. We also assessed the correlation between N-glycan traits and individual components of metabolic syndrome and compared this to results found in similar analyses based in Chinese and Croatian populations. Results: 21 N-glycan traits were found to be associated with either an increased or a decreased likelihood of participants having metabolic syndrome, including monosialylated plasma N-glycans (OR of 1.49 (95%CI 1.33, 1.67), q=1.26E-12) and core fucosylated plasma N-glycans (OR of 0.81(95% CI 0.72-0.90), q=7.75E-4). Notably, consistent results in both sections of this analysis demonstrated the protective association of higher levels of core fucosylated N-glycans. Conclusion: Our results demonstrate that metabolic syndrome is associated with an alteration in plasma N-glycosylation patterns. The metabolic role of core fucosylated N-glycans is of particular interest for future study

Birth weight associations with DNA methylation differences in an adult population

The Developmental Origins of Health and Disease (DOHaD) theory predicts that prenatal and early life events shape adult health outcomes. Birth weight is a useful indicator of the foetal experience and has been associated with multiple adult health outcomes. DNA methylation (DNAm) is one plausible mechanism behind the relationship of birth weight to adult health. Through data linkage between Generation Scotland and historic Scottish birth cohorts, and birth records held through the NHS Information and Statistics Division, a sample of 1,757 individuals with available birth weight and DNAm data was derived. Epigenome-wide association studies (EWAS) were performed in two independently generated DNAm subgroups (n(Set1) = 1,395, n(Set2) = 362), relating adult DNAm from whole blood to birth weight. Meta-analysis yielded one genome-wide significant CpG site (p = 5.97x10(−9)), cg00966482. There was minimal evidence for attenuation of the effect sizes for the lead loci upon adjustment for numerous potential confounder variables (body mass index, educational attainment, and socioeconomic status). Associations between birth weight and epigenetic measures of biological age were also assessed. Associations between lower birth weight and higher Grim Age acceleration (p((FDR)) = 3.6x10(−3)) and shorter DNAm-derived telomere length (p((FDR)) = 1.7x10(−3)) are described, although results for three other epigenetic clocks were null. Our results provide support for an association between birth weight and DNAm both locally at one CpG site, and globally via biological ageing estimates

Characterisation of an inflammation-related epigenetic score and its association with cognitive ability

BACKGROUND: Chronic systemic inflammation has been associated with incident dementia, but its association with age-related cognitive decline is less clear. The acute responses of many inflammatory biomarkers mean they may provide an unreliable picture of the chronicity of inflammation. Recently, a large-scale epigenome-wide association study identified DNA methylation correlates of C-reactive protein (CRP)-a widely used acute-phase inflammatory biomarker. DNA methylation is thought to be relatively stable in the short term, marking it as a potentially useful signature of exposure. METHODS: We utilise a DNA methylation-based score for CRP and investigate its trajectories with age, and associations with cognitive ability in comparison with serum CRP and a genetic CRP score in a longitudinal study of older adults (n = 889) and a large, cross-sectional cohort (n = 7028). RESULTS: We identified no homogeneous trajectories of serum CRP with age across the cohorts, whereas the epigenetic CRP score was consistently found to increase with age (standardised β = 0.07 and 0.01) and to do so more rapidly in males compared to females. Additionally, the epigenetic CRP score had higher test-retest reliability compared to serum CRP, indicating its enhanced temporal stability. Higher serum CRP was not found to be associated with poorer cognitive ability (standardised β = - 0.08 and - 0.05); however, a consistent negative association was identified between cognitive ability and the epigenetic CRP score in both cohorts (standardised β = - 0.15 and - 0.08). CONCLUSIONS: An epigenetic proxy of CRP may provide a more reliable signature of chronic inflammation, allowing for more accurate stratification of individuals, and thus clearer inference of associations with incident health outcomes