Relationship between endogenous plasma adrenocorticotropic hormone concentration and reproductive performance in Thoroughbred broodmares.

BACKGROUND: Pituitary pars intermedia dysfunction (PPID) is an endocrine disorder the clinical signs of which include infertility, but few reports have examined the relationship between PPID and reproductive performance in broodmares. HYPOTHESIS/OBJECTIVE: Broodmares with infertility of unknown etiology were screened for PPID using baseline endogenous plasma ACTH concentrations, and its relationship with subsequent reproductive performance was analyzed. ANIMALS: Sixty-seven Thoroughbred broodmares. METHODS: Adrenocorticotropic hormone concentrations were measured in autumn. The broodmares were divided into 3 groups based on endogenous plasma ACTH concentration (low, <50 pg/mL; intermediate 50-100 pg/mL; and high >100 pg/mL) as recommended by the Equine Endocrinology Group. We compared these results with those of other blood tests, clinical examinations, subsequent conception, and frequency of normal delivery. RESULTS: The numbers of horses per group (percentage) were 22 (32.8%), 20 (29.9%), and 25 (37.3%). The mean ± SD ages (years) were 11.1 ± 3.4, 12.1 ± 4.5, and 13.0 ± 4.3, with no significant difference among groups. Mean ± SD plasma cortisol concentrations (µg/dL) were 4.0 ± 1.6, 7.1 ± 1.4, and 7.6 ± 1.9, with the intermediate and high ACTH groups having significantly higher results than the low ACTH group (P < .001). Conception rates were 77.3%, 89.5%, and 56.5% and normal delivery rates were 77.2%, 84.2%, and 43.5% with the percentage of each significantly lower in the high ACTH group (P = .02, P = .008, respectively). CONCLUSIONS AND CLINICAL IMPORTANCE: The study group of infertile broodmares may include horses with PPID. The reproductive performance of the high ACTH group was significantly lower than the other groups. Early diagnosis and treatment of infertile broodmares by screening plasma ACTH concentrations could help improve reproductive performance.

A retrospective study of radiographic abnormalities in the repositories for Thoroughbreds at yearling sales in Japan.

This study aimed to evaluate whether radiographic abnormalities at yearling sales were associated with the failure to start racing at 2-3 years of age. Radiographic abnormalities in the carpal (n=852), tarsal (n=976), metacarpophalangeal (n=1,055), and metatarsophalangeal joints (n=1,031) from 1,082 horses, recorded at yearling sale, were reviewed. Eighty-two horses (7.6%) failed to start racing. Radiographic abnormalities such as wedged or collapsed tarsal bones, irregular lucency of a sagittal ridge at the distal aspect of the distal third metatarsal bone, and proximal dorsal fragmentation of the first phalanx in metatarsophalangeal joints were associated with failure to start racing in these horses. In the follow-up survey of 12 horses with one or more these radiographic abnormalities, the horses failed to start racing due to reasons unrelated to these radiographic abnormalities such as pelvic fractures (2 horses), fracture of a distal phalanx (1 horse), cervical stenotic myelopathy and proximal sesamoid fracture (1 horse), superficial digital flexor tendonitis (2 horses), laryngeal hemiplegia (1 horse), economic problems (2 horses) and unknown causes (3 horses). Although radiographic abnormalities at yearling sales can be associated with failure to start racing at 2-3 years of age, these radiographically detected abnormalities might not necessarily cause that failure.

A retrospective study of radiographic abnormalities in the repositories of 2-year-old Thoroughbred in-training sales in Japan.

This study aimed to evaluate the influence of radiographic abnormalities of 2-year-old Thoroughbred horses that were listed at in-training sales in Japan, on whether they started to race or not at 2-3 years of age. Radiographs of 850 2-year-old Thoroughbreds in the in-training sales repository from 2007 to 2010 were reviewed, and 26 categories of radiographic abnormalities were found. Forty-three horses (5.1%, 43/850) did not start a race at 2-3 years of age. In accordance with the racing results for this age category, as determined by Fisher's exact test and multiple logistic regression analysis, none of the radiographic abnormalities were significantly related to failure to start a race. At 2 years of age, 198 horses (23.3%, 198/850) did not start a race. Horses with enlargement of the proximal sesamoid bones in the fore (9 of 19 horses) and hind limbs (5 of 9 horses) did not start a race at the age of 2 years, and fewer of these horses (fore, P=0.021; hind, P=0.030) started a race at the age of 2 years compared with the population of horses without these radiographic abnormalities. These results suggest that identification of radiographic enlargement of the proximal sesamoid bones during training sales could derail the racing debut of horses at the age of 2 years. However, this might not necessarily indicate a poor prognosis and resulting in retirement from racing at 2-3 years of age.

Adenomyosis with severe inflammation in the uterine cervix in a dog.

A dog with purulent vulval discharge was found to have many cysts containing purulent mucus in the uterine cervix. The uterine horns did not contain any pus. Histological examination revealed a cervical adenomyosis infiltrated by many neutrophils. After an ovariohysterectomy including the whole cervix, the dog recovered well.

The myelin vacuolation (mv) rat with a null mutation in the attractin gene.

We recently found a spontaneous tremor mutant in an outbred colony of Sprague-Dawley rats. The tremor behavior was exhibited from around 3 weeks of age and inherited as an autosomal recessive trait. The mutant rats had variously sized vacuoles in the neuropil and white matter throughout the central nervous system, especially in the brain stem, cerebellum, and spinal cord. Ultrastructurally these vacuoles mainly consisted of splitting of myelin lamella both in the periaxonal and intermyelinic spaces. Linkage analysis using intercross progeny between the myelin vacuolation (mv) rat, named after the pathologic characteristics, and normal control rat strains showed that the mv phenotypes were cosegregated with polymorphic markers adjacent to the Atrn (Attractin, formerly zi [zitter]) locus on rat chromosome 3. A test for allelism suggested that the mv mutation was a new allele in ATRN: In comparison with a marked decrease of Atrn(zi)/Arn(zi), Northern blot analysis revealed no expression of Atrn mRNA in the brain of the mv rats. Finally, a genomic deletion including exon 1 of the mv rats was detected by genomic and sequence analyses. Discovery of the rat null mutation Atrn(mv), different from Atrn(zi), provides a new animal model for studying the functions of the attractin protein.