Hironori Oki

Assessment of autonomic nervous function by power spectral analysis of heart rate variability in the horse

We studied power spectral analysis of heart rate (HR) variability in the horse, with the hypothesis that the quantitative information provided by the spectral analysis of HR variability reflects the interaction between sympathetic and parasympathetic regulatory activities. For this purpose, electrocardiogram, blood pressure (BP) and respiratory (Resp) waveform were simultaneously recorded from Thoroughbred horses (3-5 years old) and analyzed by power spectrum. There were two major spectral components at low-frequency (LF) and high-frequency (HF) bands for HR variability. The peak of Resp variability clearly occurred at the HF range. In contrast to Resp variability, the power spectra of BP variability occurred at lower frequencies. The maximum coherence between HR and Resp variabilities and HR and BP variabilities occurred at approximately 0.15 and approximately 0.03 Hz, respectively. These relationships were similar to the ensemble spectra. On the basis of these data, we have defined two frequency bands of interest: LF (0.01-0.07 Hz) and HF (0.07-0.6 Hz). Therefore, we believe that power spectral analysis of HR variability provides a very powerful technique for assessing autonomic nervous activity in the horse.

Estimation of heritability for superficial digital flexor tendon injury by Gibbs sampling in the Thoroughbred racehorse

The superficial digital flexor tendon (SDFT) injury causes considerable wastage of racing Thoroughbreds. In this study, the heritability of SDFT injury of the forelimbs was estimated in the Thoroughbred racehorses based on the Bayesian analysis with Gibbs sampling using threshold animal models. New horse patients of SDFT injury at the age of 2-5 years accommodated in the training centers in 2005 were used for the analyses. Based on clinical data of 8198 horses, heritability of SDFT was estimated to be the order of 0.17 (posterior mode) to 0.19 +/- 0.05 (posterior mean +/- posterior SD).

A genome-wide scan for tying-up syndrome in Japanese Thoroughbreds.

Tying-up syndrome, also known as recurrent exertional rhabdomyolysis in Thoroughbreds, is a common muscle disorder for racehorses. In this study, we performed a multipoint linkage analysis using LOKI based on the Bayesian Markov chain Monte Carlo method using 5 half-sib families (51 affected and 277 nonaffected horses in total), and a genome-wide association study (GWAS) using microsatellites (144 affected and 144 nonaffected horses) to map candidate regions for tying-up syndrome in Japanese Thoroughbreds. The linkage analysis identified one strong L-score (82.45) between the loci UCDEQ411 and COR058 (24.9-27.9 Mb) on ECA12. The GWAS identified two suggestive genomic regions on ECA12 (24.9-27.8 Mb) and ECA20 (29.3-33.5 Mb). Based on both results, the genomic region between UCDEQ411 and TKY499 (24.9-27.8 Mb) on ECA12 was the most significant and was considered as a candidate region for tying-up syndrome in Japanese Thoroughbreds.

Demographic Analysis of Breeding Structure in Japanese Thoroughbred Population

To investigate the breeding structure in the Japanese Thoroughbred population, we applied a demographic analysis to the populations of foals produced from 1978 to 2005. The migration rate estimated from the proportion of foals produced by imported breeding horses was around 40% over the investigated period. After early 1990s, the migration rate through stallions imported from USA sharply increased. The average generation interval was within range of 10.5–11.5 years. The longer generation interval of Thoroughbred was considered to be a reflection of the fact that Thoroughbred horses begin breeding only after completing their performance in races. After the peak of 729 in 1993, the number of sires of foals progressively declined to 358 in 2005. Although the coefficient of variation of the progeny number of sires was within range of 1.0–1.2 until early 1990s, it gradually increased and reached the value of 1.6–1.7 in recent years. The effective number of sires consistently decreased after the peak of 302.6 in 1992, and reached 120–130 in recent years, which is 25–30% of the actual number of sires. In parallel, the demographic estimate of the effective population size declined after early 1990s. The main cause of the observed change in the breeding structure was inferred to be the intensive use of a limited number of stallions for breeding.

Gene dropping analysis of ancestral contributions and allele survival in Japanese thoroughbred population.

Genetic contributions of nine historically important ancestors and allelic diversity in the Japanese Thoroughbred population were examined by applying the gene dropping simulation to the foals produced from 1978 to 2005. Full pedigree records traced to ancestors (base animals) born around 1890 were used for the simulation. Alleles originated from some of the historically important ancestors were found to be at risk of future extinction, although their genetic contributions to the foal population have increased during the last three decades. The proportion of surviving alleles to the total alleles assigned to the base animals was 8.0% in the foal population in 2005, suggesting that a large part of genetic variability contained in the base animals is extinct in the current population.

Estimation models for the morbidity of the horses infected with equine influenza virus.

Estimation formulas for the morbidity of horses infected with equine influenza virus by linear regression, logistic regression and probit transformation were developed, using data from the outbreak at the Sha Tin Racing Track in Hong Kong in 1992. Using these formulas, we estimated the equine influenza virus morbidity rates at training centers belonging to the Japan Racing Association (JRA) in October 1997 and in October 1998. In 1998 JRA started a new vaccination program, and every horse must now be vaccinated twice per year. At that time, the vaccine included two US lineage virus strains, the A/equine/Kentucky/81 strain and the A/equine/La Plata/93 (LP93) strain, against equine type-2 influenza viruses; it did not include any EU lineage virus strains, such as A/equine/Suffolk/89 (SF89). Comparing the geometric mean (GM) values of hemagglutination inhibition (HI) titers between the LP93 strain and the SF89 strain in 1997 and in 1998, they both rose significantly at every age (p<0.05) by Wilcoxon test. Calculations by the simulation models show the morbidity rates for LP93 diminished from 0.439 (linear), 0.423 (logistic) and 0.431 (probit) to 0.276 (linear), 0.265 (logistic) and 0.271 (probit), respectively. On the other hand, the estimated morbidity rates for SF89 diminished only slightly from 0.954 (linear), 0.932 (logistic) and 0.944 (probit) to 0.946 (linear), 0.914 (logistic) and 0.927 (probit), respectively. Our simulation models could estimate the effect of the vaccine on each of the equine virus strains represented by the morbidity of infected horses. Thus, they are useful for vaccine evaluation.