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Genetics of Human and Canine Dilated Cardiomyopathy.

Simpson S, Edwards J, Ferguson-Mignan TF, Cobb M, Mongan NP, Rutland CS - Int J Genomics (2015)

Bottom Line: In human studies of DCM there are more than 50 genetic loci associated with the disease.In this review the aetiology, epidemiology, and clinical characteristics of canine DCM are examined, along with highlighting possible different subtypes of canine DCM and their potential relevance to human DCM.Finally the current position of genetic research into canine and human DCM, including the genetic loci, is identified and the reasons many studies may have failed to find a genetic association with canine DCM are reviewed.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Medicine and Health Sciences, School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington Campus, Loughborough LE12 5RD, UK.

ABSTRACT
Cardiovascular disease is a leading cause of death in both humans and dogs. Dilated cardiomyopathy (DCM) accounts for a large number of these cases, reported to be the third most common form of cardiac disease in humans and the second most common in dogs. In human studies of DCM there are more than 50 genetic loci associated with the disease. Despite canine DCM having similar disease progression to human DCM studies into the genetic basis of canine DCM lag far behind those of human DCM. In this review the aetiology, epidemiology, and clinical characteristics of canine DCM are examined, along with highlighting possible different subtypes of canine DCM and their potential relevance to human DCM. Finally the current position of genetic research into canine and human DCM, including the genetic loci, is identified and the reasons many studies may have failed to find a genetic association with canine DCM are reviewed.

No MeSH data available.


Related in: MedlinePlus

χ2goodness of fit tests: contingency tables Df = 1, α err prob = 0.05, and power (1 − β err prob) = 0.8.
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fig1: χ2goodness of fit tests: contingency tables Df = 1, α err prob = 0.05, and power (1 − β err prob) = 0.8.

Mentions: The majority of studies undertaken with the aim of identifying causal genetic variants of canine DCM have only utilised small samples (5–40 individuals) which is unlikely to be large enough to detect an effect. To establish appropriate study sizes and indicate the effect size that can be detected in published studies G∗Power 3.1.7 Chi-squared goodness of fit tests were used (using the methods from [72]). This takes known input parameters, including sample size, and calculates estimated effect sizes based on assumed power and can be used to indicate minimum sample size for prescribed power, alpha error rate, and effect size. This was done to indicate minimum sample sizes needed to detect various effect sizes (Figure 1).


Genetics of Human and Canine Dilated Cardiomyopathy.

Simpson S, Edwards J, Ferguson-Mignan TF, Cobb M, Mongan NP, Rutland CS - Int J Genomics (2015)

χ2goodness of fit tests: contingency tables Df = 1, α err prob = 0.05, and power (1 − β err prob) = 0.8.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4525455&req=5

fig1: χ2goodness of fit tests: contingency tables Df = 1, α err prob = 0.05, and power (1 − β err prob) = 0.8.
Mentions: The majority of studies undertaken with the aim of identifying causal genetic variants of canine DCM have only utilised small samples (5–40 individuals) which is unlikely to be large enough to detect an effect. To establish appropriate study sizes and indicate the effect size that can be detected in published studies G∗Power 3.1.7 Chi-squared goodness of fit tests were used (using the methods from [72]). This takes known input parameters, including sample size, and calculates estimated effect sizes based on assumed power and can be used to indicate minimum sample size for prescribed power, alpha error rate, and effect size. This was done to indicate minimum sample sizes needed to detect various effect sizes (Figure 1).

Bottom Line: In human studies of DCM there are more than 50 genetic loci associated with the disease.In this review the aetiology, epidemiology, and clinical characteristics of canine DCM are examined, along with highlighting possible different subtypes of canine DCM and their potential relevance to human DCM.Finally the current position of genetic research into canine and human DCM, including the genetic loci, is identified and the reasons many studies may have failed to find a genetic association with canine DCM are reviewed.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Medicine and Health Sciences, School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington Campus, Loughborough LE12 5RD, UK.

ABSTRACT
Cardiovascular disease is a leading cause of death in both humans and dogs. Dilated cardiomyopathy (DCM) accounts for a large number of these cases, reported to be the third most common form of cardiac disease in humans and the second most common in dogs. In human studies of DCM there are more than 50 genetic loci associated with the disease. Despite canine DCM having similar disease progression to human DCM studies into the genetic basis of canine DCM lag far behind those of human DCM. In this review the aetiology, epidemiology, and clinical characteristics of canine DCM are examined, along with highlighting possible different subtypes of canine DCM and their potential relevance to human DCM. Finally the current position of genetic research into canine and human DCM, including the genetic loci, is identified and the reasons many studies may have failed to find a genetic association with canine DCM are reviewed.

No MeSH data available.


Related in: MedlinePlus