Folic acid supplementation does not decrease stillbirths and congenital malformations in a guide dog colony.

OBJECTIVES: To investigate if maternal folic acid supplementation (5 mg) is associated with a reduction of cleft palates, umbilical hernias, stillbirths and caesarean sections in a guide dog breeding colony. MATERIALS AND METHODS: Labrador retrievers, golden retrievers and Labrador/golden Crosses from the breeding colony of a professional guide dog training organisation were eligible for inclusion. Dams in the treatment group (n = 137) received 5 mg oral folic acid supplementation daily from the start of pro-oestrous through day 40 of gestation. A historical control group (n = 134) was selected from the previous calendar year for comparison. A logistic regression model identified the relative risk of disease (cleft palates, umbilical hernias, stillbirths and caesarean sections) for puppies whose dams did or did not receive folic acid supplementation. RESULTS: A total of 1917 puppies (890 control, 1027 treatment; from 294 litters) were produced during the entire study period, with 994 puppies (494 control, 500 treatment; from 144 litters) born to the subset of dams (n = 72) who produced litters during both the control and treatment periods. All 95% highest posterior densities of relative risk included 1.0, failing to detect differences between the treatment and control groups on incidence rate of cleft palate (control: 2.25%; treatment: 2.34%), umbilical hernias (control: 1.91%; treatment: 3.12%), stillbirths (control: 3.26%; treatment: 2.92%) and caesarean sections (control: 1.45%; treatment: 1.28%). CLINICAL SIGNIFICANCE: There was no observable reduction of cleft palate, umbilical hernia, stillbirth or caesarean section associated with folic acid supplementation during pregnancy in the study colony. For a domestic dog cohort with a low tendency of hereditary malformations, such as this study colony, 5 mg dietary folic acid supplementation should not be expected to drastically improve or eradicate these diseases.

A missense mutation in damage-specific DNA binding protein 2 is a genetic risk factor for ocular squamous cell carcinoma in Belgian horses.

BACKGROUND: Belgian horses are commonly affected with ocular squamous cell carcinoma (SCC), the most common cancer of the equine eye. A missense mutation in damage-specific DNA binding protein 2 (DDB2 c.1013C>T, p.Thr338Met) has been established as a recessive genetic risk factor for ocular SCC in the Haflinger breed. A sample of Belgian horses with unknown SCC phenotype was shown to possess this variant at a similar frequency to the Haflinger breed. Retrospective studies indicate that chestnut coat colour may predispose to the development of SCC. OBJECTIVES: To determine if DDB2 c.1013C>T is a risk factor for ocular SCC in a strictly phenotyped sample of Belgian horses. To investigate associations between coat colour loci genotypes and ocular SCC. STUDY DESIGN: Retrospective and prospective case identification, genetic investigation. METHODS: Genomic DNA was isolated from blood, hair or formalin-fixed paraffin-embedded tissue from 25 Belgian horses with histologically confirmed ocular SCC and 18 unaffected Belgian horses. Association testing of 34 single nucleotide variants from 11 genomic loci and genotyping for DDB2 c.1013C>T and coat colour alleles were performed. Exons of DDB2 were sequenced in four cases and two controls. Associations were analysed by Chi-square or Fisher's exact tests and relative risk was calculated. RESULTS: Homozygosity for DDB2 c.1013C>T was significantly associated with ocular SCC (P = 7.4 × 10-7 ). Seventy-six per cent of affected horses were homozygous for the variant. Relative risk for homozygous horses developing SCC was 4.0 (P = 1.0 × 10-4 ). Sequencing DDB2 did not identify a variant more concordant with disease phenotype. An association between disease and coat colour loci was not identified. MAIN LIMITATIONS: Phenotyping was determined at a single timepoint. Each included horse genotyped as chestnut, so association with this MC1R variant could not be investigated. CONCLUSIONS: A missense variant, DDB2 c.1013C>T, p.Thr338Met, is a risk factor for ocular SCC in Belgian horses. A genetic risk test is commercially available.

Genetic investigation of equine recurrent uveitis in Appaloosa horses.

Equine recurrent uveitis (ERU) is characterized by intraocular inflammation that often leads to blindness in horses. Appaloosas are more likely than any other breed to develop insidious ERU, distinguished by low-grade chronic intraocular inflammation, suggesting a genetic predisposition. Appaloosas are known for their white coat spotting patterns caused by the leopard complex spotting allele (LP) and the modifier PATN1. A marker linked to LP on ECA1 and markers near MHC on ECA20 were previously associated with increased ERU risk. This study aims to further investigate these loci and identify additional genetic risk factors. A GWAS was performed using the Illumina Equine SNP70 BeadChip in 91 horses. Additive mixed model approaches were used to correct for relatedness. Although they do not reach a strict Bonferroni genome-wide significance threshold, two SNPs on ECA1 and one SNP each on ECA12 and ECA29 were among the highest ranking SNPs and thus warranted further analysis (P = 1.20 × 10-5 , P = 5.91 × 10-6 , P = 4.91 × 10-5 , P = 6.46 × 10-5 ). In a second cohort (n = 98), only an association with the LP allele on ECA1 was replicated (P = 5.33 × 10-5 ). Modeling disease risk with LP, age and additional depigmentation factors (PATN1 genotype and extent of roaning) supports an additive role for LP and suggests an additive role for PATN1. Genotyping for LP and PATN1 may help predict ERU risk (AUC = 0.83). The functional role of LP and PATN1 in ERU development requires further investigation. Testing samples across breeds with leopard complex spotting patterns and a denser set of markers is warranted to further refine the genetic components of ERU.

Maternal omega-3 polyunsaturated fatty acid supplementation on offspring hip joint conformation.

Unsaturated omega-3 fatty acids, especially docosahexaenoic acid (DHA), when fed to dogs improves cognitive and neurological development. Supplementation with omega-3 fatty acids such as DHA and eicosapentaenoic acid (EPA) has also been associated with lipid peroxidation, which in turn has been implicated in reduced body weight and altered bone formation. To assess the impact of omega-3 fatty acid supplementation on skeletal growth, diets containing three levels of DHA and EPA (0.01 and 0.01%, 0.14 and 0.12%, and 0.21 and 0.18%, respectively) were fed to bitches during gestation and lactation with puppies also supplemented through weaning. Thus, the subjects studied were the puppies supplemented with DHA and EPA through gestation and early postnatal life. The hip joint conformation of the puppies (n = 676) was recorded at adulthood using two radiographic, non-invasive evaluations. In this population, females had higher hip distraction indices (DI) than males. Males from the lower two levels of DHA and EPA supplementation had significantly smaller hip DI than all females and males from the highest DHA and EPA supplementation. In contrast, there were no diet effects on anatomical indicators of hip joint conformation and no visible arthritic changes. These data suggest that dietary supplementation of DHA and EPA during gestation and the perinatal period to weaning does not adversely influence hip joint formation of dogs.

Cardiac adaptations in SCNT newborn cloned calves during the first month of life assessed by echocardiography.

The aim of this study was to compare cardiac morphology in newborn and month-old control and cloned calves. A total of 10 in vivo-derived (IVD) control (five Holstein, five Hereford) and seven cloned (five Holstein, two Hereford) calves were subjected to echocardiographic examination, including 2D, M-mode, spectral and color flow Doppler evaluation at Day 1 (mean 26.3 h) and Day 30 (mean 29.2 days) after birth. Echocardiographic measurements were compared between control and cloned calves, and between Hereford and Holstein control calves of the same age. At Day 1 and at Day 30 after birth, left ventricular free wall (LVFW) and interventricular septal (IVS) thicknesses were greater in Holstein calves than Hereford calves. Several indices of myocardial wall thickness were increased in cloned versus control calves at Day 1 after birth, and included systolic LVFW thickness, systolic right ventricular free wall (RVFW) thickness, diastolic LVFW thickness, diastolic RVFW thickness and diastolic IVS thickness (p < 0.05). Differences between cloned and non-cloned calves were no longer evident at Day 30 after birth. The apparent disappearance of the cloning effect on cardiac structures may reflect the influence of placenta on fetal cardiac morphology, suggestive of a placental hemodynamic role in fetal cardiac muscle development. Differences seen in clones at birth spontaneously resolved by Day 30 of age, after organ development recovery from cardiovascular abnormalities of presumed placental origin. Echocardiographic measurements should provide useful data for research and clinical evaluation of high-risk neonatal calves of both breeds and from clones of the same breed.

Long-term genetic selection reduced prevalence of hip and elbow dysplasia in 60 dog breeds.

Canine hip dysplasia (CHD) and elbow dysplasia (ED) impact the health and welfare of all dogs. The first formally organized assessment scheme to improve canine health centered on reducing the prevalence of these orthopedic disorders. Phenotypic screening of joint conformation remains the currently available strategy for breeders to make selection decisions. The present study evaluated the efficacy of employing phenotypic selection on breed improvement of hips and elbows using the Orthopedic Foundation for Animals complete database spanning the 1970-2015 time period. Sixty breeds having more than 1000 unique hip evaluations and 500 elbow evaluations (1,056,852 and 275,129 hip and elbow records, respectively) were interrogated to derive phenotypic improvement, sex and age at time of assessment effects, correlation between the two joints, heritability estimates, estimated breeding values (EBV), and effectiveness of maternal/paternal selection. The data demonstrated that there has been overall improvement in hip and elbow conformation with a reduction in EBV for disease liability, although the breeds differed in the magnitude of the response to selection. Heritabilities also differed substantially across the breeds as did the correlation of the joints; in the absence of a universal association of these differences with breed size, popularity, or participation in screening, it appears that the breeds themselves vary in genetic control. There was subtle, though again breed specific, impact of sex and older ages on CHD and ED. There was greater paternal impact on a reduction of CHD. In the absence of direct genetic tests for either of these two diseases, phenotypic selection has proven to be effective. Furthermore, the data underscore that selection schemes must be breed specific and that it is likely the genetic profiles will be unique across the breeds for these two conditions. Despite the advances achieved with phenotypic selection, incorporation of EBVs into selection schemes should accelerate advances in hip and elbow improvement.

Partitioning of feed intake into maintenance and gain in growing beef cattle: Evaluation of conventional and Bayesian analyses.

The robustness of efficiency estimates depends on theoretical consistency of models from which those estimates are developed; functional forms of the variables must be globally consistent with theoretical properties regarding feed utilization for maintenance and gain in growing and finishing cattle. Model parameter estimates and their dimensions must be unique or estimates of feed utilization and gain will not reflect reality. A linear equation commonly used to estimate daily DMI by the th individual animal (ADFI), based on mean weight and gain during a feeding period, was evaluated to determine if that model was correctly specified and if the vector predicted ADFI differed from the vector observed ADFI. Three independently gathered data sets were evaluated using a multiple linear regression model; variability described by that model failed to capture observed variability in the data (lack of fit, < 0.10), and predicted ADFI differed from observed ( < 0.05); for 1 of the 3 data sets, residuals were not normally distributed ( < 0.001). Functional forms of the variables in the first model evaluated, characterizing ADFI required for maintenance ( × BW) and gain ( × ADG), were consistent with neither published empirical nor theoretical relationships among ADFI, BW, and ADG. Parameter estimates determined for that linear model were not BLUE. Better fits among final BW, initial BW, and ADFI were found for a first-order relationship, in which final BW was a function of initial BW and ADFI, as indicated by > 0.90. The linear model and, to a lesser degree, the first nonlinear model lacked theoretical and global consistency. A second nonlinear model, which described retained energy as a function of ME intake, best fit the data, and functional forms of variables describing ME intake at maintenance and the efficiency of ME utilization for gain were consistent with theoretical estimates found in the literature. Changes in feed intake and live BW in linear and nonlinear models failed to adequately describe efficiencies of metabolic processes, which are better characterized by changes in retained energy as a function of ME intake in nonlinear models.

Ten inherited disorders in purebred dogs by functional breed groupings.

BACKGROUND: Analysis of 88,635 dogs seen at the University of California, Davis Veterinary Medical Teaching Hospital from 1995 to 2010 identified ten inherited conditions having greater prevalence within the purebred dog population as compared to the mixed-breed dog population: aortic stenosis, atopy/allergic dermatitis, gastric dilatation volvulus (GDV), early onset cataracts, dilated cardiomyopathy, elbow dysplasia, epilepsy, hypothyroidism, intervertebral disk disease (IVDD), and hepatic portosystemic shunt. The objective of the present study was to ascertain if disorders with higher prevalence in purebreds were restricted to particular breed group classifications within the purebred population, specifically the American Kennel Club breed grouping or groups with genomic similarities based upon allele sharing. For each disorder, healthy controls seen at the hospital during that same time period were matched for age, weight, and sex to each affected dog to determine risk of disease presentation in the purebred group as compared to that of the mixed-breed population. To enhance reliability of the analyses, sampling of matched healthy to affected dogs was repeated 50 times. For each comparison, the purebred subgroups to mixed-breed odds ratio was determined as was the mean P value used to test this ratio. RESULTS: For aortic stenosis, GDV, early onset cataracts, dilated cardiomyopathy, elbow dysplasia, epilepsy, and portosystemic shunt, most purebred groups were not statistically distinct from the mixed-breed population with higher prevalence in purebreds restricted to distinct subsets of purebred dogs. The conditions of atopy/allergic dermatitis, hypothyroidism, and IVDD were more pervasive across the purebred population with many groups having higher prevalence than the mixed-breed population. The prevalence of IVDD in purebred terrier groups was statistically lower than that observed for mixed-breed dogs. CONCLUSIONS: The results offer an assessment of the distribution of inherited disorders within purebred dogs and illustrate how mixed-breed and subpopulations of purebred dogs do not differ statistically in prevalence for certain disorders. Some disorders appear linked to common ancestors providing insight into disease allele origin whereas others may be due to selection for common structural morphology. Knowledge of the origin of a condition may aid in reducing its prevalence in the dog population as a whole.

Determining the heritable component of dairy cattle foot lesions.

Lameness and hoof health affect dairy cows as an animal welfare issue, in decreased milk production, and in premature culling. Selection schemes for dairy cattle focus on sire contribution to milk production, with little consideration of the cow's physical structure or disease probability. On 3 commercial California dairies, 6 phenotypic binary hoof traits that contribute to lameness were recorded: white line disease, sole ulcer, other claw horn lesions, foot rot (interdigital phlegmon), foot warts (digital dermatitis), and other lesions. Monthly lactation records were collected from December 2006 to April 2009 with weekly observations of hoof lesions for lame and dry cows. In addition to hoof lesion information, data on cows (n=5,043) included parentage, birth date, freshening date, lactation number, and date of lameness diagnosis. The prevalence of hoof lesions ranged from a low of 2.2% (foot rot) to a high of 17.1% (foot warts). The farm environment increased the odds ratio depending upon the lesion. Lameness was more common in early lactation and as lactation number increased. Using a threshold model, heritabilities and repeatabilities were estimated for each binary trait. The heritability for risk varied by lesion, with the higher estimates being 0.40 (95% confidence interval: 0.20-0.67) for digital dermatitis and 0.30 (95% confidence interval: 0.08-0.63) for sole ulcer. Including terms to account for cow productivity on either a 305-d mature-equivalent basis or a per-lactation basis had minimal effect on the heritability estimates, suggesting that selection for hoof health is not correlated with response to selection for greater milk production and that improvement could be made for both traits. The genetic component lends support for further genetic studies to identify loci contributing to some of the lesion phenotypes such as foot warts or sole ulcers, 2 of the top 3 causes of lameness in dairy cattle.

Pedigree analysis and exclusion of alpha-tocopherol transfer protein (TTPA) as a candidate gene for neuroaxonal dystrophy in the American Quarter Horse.

BACKGROUND: Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (NAD/EDM) is a neurodegenerative disorder affecting young horses of various breeds that resembles ataxia with vitamin E deficiency in humans, an inherited disorder caused by mutations in the alpha-tocopherol transfer protein gene (TTPA). To evaluate variants found upon sequencing TTPA in the horse, the mode of inheritance for NAD/EDM had to be established. HYPOTHESIS: NAD/EDM in the American Quarter Horse (QH) is caused by a mutation in TTPA. ANIMALS: 88 clinically phenotyped (35 affected [ataxia score ≥2], 53 unaffected) QHs with a diagnosis of NAD/EDM with 6 affected and 4 unaffected cases confirmed at postmortem examination. PROCEDURES: Pedigrees and genotypes across 54,000 single nucleotide polymorphism (SNP) markers were assessed to determine heritability and mode of inheritance of NAD/EDM. TTPA sequence of exon/intron boundaries was evaluated in 2 affected and 2 control horses. An association analysis was performed by 71 SNPs surrounding TTPA and 8 SNPs within TTPA that were discovered by sequencing. RT-PCR for TTPA was performed on mRNA from the liver of 4 affected and 4 control horses. RESULTS: Equine NAD/EDM appears to be inherited as a polygenic trait and, within this family of QHs, demonstrates high heritability. Sequencing of TTPA identified 12 variants. No significant association was found using the 79 available variants in and surrounding TTPA. RT-PCR yielded PCR products of equivalent sizes between affected cases and controls. CONCLUSIONS AND CLINICAL IMPORTANCE: NAD/EDM demonstrates heritability in this family of QHs. Variants in TTPA are not responsible for NAD/EDM in this study population.

Treatment with recombinant equine follicle stimulating hormone (reFSH) followed by recombinant equine luteinizing hormone (reLH) increases embryo recovery in superovulated mares.

The dynamics of ovarian follicular development depend on a timely interaction of gonadotropins and gonadal feedback in the mare. The development and efficacy of genetically cloned recombinant equine gonadotropins (reFSH and reLH) increase follicular activity and induce ovulation, respectively, but an optimum embryo recovery regimen in superovulated mares has not been established. The objective of this study was to determine if treatment with reFSH followed by reLH would increase the embryo per ovulation ratio and the number of embryos recovered after superovulation in mares. Sixteen estrous cycling mares of light horse breeds (4-12 years) were randomly assigned to one of two groups: Group 1; reFSH (0.65mg)/PBS (n=8) and Group 2; reFSH (0.65mg)/reLH (1.5mg) (n=8). On the day of a 22-25mm follicle post-ovulation mares were injected IV twice daily with reFSH for 3 days (PGF(2α) given IM on the second day of treatment) and once per day thereafter until a follicle or cohort of follicles reached 29mm after which either PBS or reLH was added and both groups injected IV twice daily until the presence of a 32mm follicles, when reFSH was discontinued. Thereafter, mares were injected three times daily IV with only PBS or reLH until a majority of follicles reached 35-38mm when treatment was discontinued. Mares were given hCG IV (2500IU) to induce ovulation and bred. Embryo recovery was performed on day 8 day post-treatment ovulation. Daily jugular blood samples were collected from the time of first ovulation until 8 days post-treatment ovulation. Blood samples were analyzed for LH, FSH, estradiol, progesterone and inhibin by validated RIA. Duration of treatment to a ≥35mm follicle(s) and number of ovulatory size follicles were similar between reFSH/reLH and reFSH/PBS treated mares. The number of ovulations was greater (P<0.01) in the reFSH/reLH group, while the number of anovulatory follicles was less (P<0.05) compared to the reFSH/PBS group. Number of total embryos recovered were greater in reFSH/reLH mares than in the reFSH/PBS mares (P≤0.01). The embryo per ovulation ratio tended to be greater (P=0.07) in the reFSH/reLH mares. Circulating concentrations of estradiol, inhibin, LH and progesterone were not statistically different between groups. Plasma concentrations of FSH were less (P<0.01) in the reFSH/reLH treated mares on days 0, 1, 4, 6, 7 and 8 post-treatment ovulation. In summary, reFSH with the addition of reLH, which is critical for final follicular and oocyte maturation, was effective in increasing the number of ovulations and embryos recovered, as well as reduce the number of anovulatory follicles, making this a more viable option than treatment with reFSH alone. Further evaluation is needed to determine the dose and regimen of reFSH/reLH to significantly increase the embryo per ovulation ratio.

Feedlot efficiency implications on greenhouse gas emissions and sustainability.

The term sustainable has many meanings, but in agriculture it generally refers to some balance between environmental, social, and economic goals. The objective of this project was to quantify inputs and outputs to assess the sustainability implications of 2 feedlot cattle management systems: Never Ever 3 (NE3) and a conventional (CON) system using metabolic modifiers. Angus-cross steers (n=104) were stratified by BW (337 kg ± 17) and randomly assigned to 4 pens per treatment group. The NE3 cattle received no feed additives or implants, whereas CON were implanted with 100 mg of trenbolone acetate and 14 mg of estradiol benzoate on d 1 and 70, and were additionally fed monensin [330 mg/(animal·d)] and tylosin phosphate [90 mg/(animal·d)] in their ration throughout the course of the study, and ractopamine hydrochloride at 254 mg/(animal·d) for the last 29 d on feed. Cattle were shipped on a constant average pen weight basis (596 kg ± 32 BW). The CON cattle had greater ADG (1.81 vs. 1.35 kg, P < 0.01) and were on feed fewer days (146 vs. 188 d, P < 0.01) than the NE3 cattle. No significant differences were observed in HCW (P = 0.072) or dressing percentage (P=0.62) between treatments (P > 0.05); however, CON carcasses averaged larger ribeye area (87 vs. 80 cm(2), P < 0.01), greater Warner-Bratzler shear force measurement (WBSF; 3.46 vs. 3.19 kg, P < 0.01), and smaller USDA marbling score (5.4 vs. 6.2, P < 0.01), and less backfat thickness (1.64 vs. 1.84 cm, P < 0.05) and yield grade (3.38 vs. 3.95, P < 0.01) than NE3 carcasses. Overall, CON cattle consumed 393 kg less DM in the feedlot (1,250 vs. 1,643 kg; P < 0.05). No treatment effects were observed for daily methane (CH(4); P=0.62) or nitrous oxide (N(2)O; P=0.7) emissions per steer. Assuming a constant emission rate on a DMI basis throughout the course of the feedlot trial, CON feedlot management resulted in a 31% decrease in emissions per finished steer compared with NE3 management. Expressing CH(4) emissions on a carbon dioxide equivalent (CO(2)-eq) basis revealed a 1.10-kg CO(2)-eq difference per kilogram BW gain (5.02 kg of NE3 vs. 3.92 kg of CON) between the 2 feedlot management systems. Although the metabolic modifiers resulted in additional costs for the CON treatment group, the cost per kilogram of feedlot BW gain was significantly less ($1.12/kg vs. $1.35/kg; P < 0.05) than NE3. Both production systems satisfied some sustainability criteria, although neither concurrently fulfilled all of the environmental, social, and economic goals of agricultural sustainability.

Necrotizing meningoencephalitis of Pug dogs associates with dog leukocyte antigen class II and resembles acute variant forms of multiple sclerosis.

Necrotizing meningoencephalitis (NME) is a disorder of Pug Dogs that appears to have an immune etiology and high heritability based on population studies. The present study was undertaken to identify a genetic basis for the disease. A genome-wide association scan with single tandem repeat (STR) markers showed a single strong association near the dog leukocyte antigen (DLA) complex on CFA12. Fine resolution mapping with 27 STR markers on CFA12 further narrowed association to the region containing DLA-DRB1, -DQA1 and, -DQB1 genes. Sequencing confirmed that affected dogs were more likely to be homozygous for specific alleles at each locus and that these alleles were linked, forming a single high risk haplotype. The strong DLA class II association of NME in Pug Dogs resembles that of human multiple sclerosis (MS). Like MS, NME appears to have an autoimmune basis, involves genetic and nongenetic factors, has a relatively low incidence, is more frequent in females than males, and is associated with a vascularly orientated nonsuppurative inflammation. However, NME of Pug Dogs is more aggressive in disease course than classical human MS, appears to be relatively earlier in onset, and involves necrosis rather than demyelination as the central pathobiologic feature. Thus, Pug Dog encephalitis (PDE) shares clinical features with the less common acute variant forms of MS. Accordingly, NME of Pug Dogs may represent a naturally occurring canine model of certain idiopathic inflammatory disorders of the human central nervous system.

Influence of genetic architecture on contemporary local evolution in the soapberry bug, Jadera haematoloma: artificial selection on beak length.

Little is known about the influence of genetic architecture on local adaptation. We investigated the genetic architecture of the rapid contemporary evolution of mouthparts, the flight polymorphism and life history traits in the soapberry bug Jadera haematoloma (Hemiptera) using laboratory selection. The mouthparts of these seed-feeding bugs have adapted in 40-50 years by decreasing in length following novel natural selection induced by a host switch to the seeds of an introduced tree with smaller fruits than those of the native host vine. Laboratory selection on beak length in both an ancestral population feeding on the native host and a derived population feeding on the introduced host reveals genetic variance allowing a rapid response (heritabilities of 0.51-0.87) to selection for either longer or shorter beaks. This selection resulted in reverse evolution by restoring long beaks in the derived population and forward evolution by re-creating short beaks in the ancestral bugs. There were strong genetic correlations (0.68-0.84) in both populations between beak lengths and the frequency of flight morphs, with short beaks associated with short wings. The results reveal a genetically interrelated set of adaptive multivariate traits including both beak length and flight morph. This suite of traits reflects host plant patchiness and seeding phenology. Weaker evidence suggests that egg mass and early egg production may be elements of the same suite. Reversible or forward evolution thus may occur in a broad set of genetically correlated multivariate traits undergoing rapid contemporary adaptation to altered local environments.

The efficacy of recombinant equine follicle stimulating hormone (reFSH) to promote follicular growth in mares using a follicular suppression model.

The efficacy of a recently engineered single chain recombinant equine follicle stimulating hormone (reFSH) was investigated in estrous cycling mares whose gonadotropins and follicular activity had been suppressed by concurrent treatment with progesterone and estradiol (P&E). Time of estrus was synchronized in 15 estrous cycling mares during the breeding season with prostaglandins F(2alpha) (PGF(2alpha)). The day after ovulation, mares were treated once daily with P&E for 14 days. Mares received a second injection of PGF(2alpha) on day 6 of the synchronized estrous cycle to induce luteolysis. On day 8 post-ovulation mares were randomly assigned to three groups: small dose reFSH-treatment group (0.5mg reFSH IV, twice daily); large dose reFSH-treatment group (0.85mg reFSH IV twice daily); control group (saline IV, twice daily). reFSH treatment occurred concurrently with the last week of P&E treatment. After a follicle or cohort of follicles reached 35mm in diameter, mares were injected with 0.75mg of recombinant equine luteinizing hormone (reLH) to induce ovulation. Post-treatment ovulation was assessed. Daily blood samples were collected for analysis of FSH, LH, estradiol, progesterone, and inhibin by radioimmunoassay (RIA). On the first day of reFSH/saline treatment, blood samples were collected periodically from 1h prior to treatment to 6h post-injection via an indwelling jugular catheter to determine acute changes in FSH concentrations. Monitoring of follicular activity, estrus, and ovulation was performed daily by utilizing a stallion and transrectal ultrasonography. A difference (por=35mm follicles (days 16-21) than controls. Mares treated with reFSH, at either dose, took less time (average: 2.95+/-0.42 days) to develop 2-3 times more pre-ovulatory follicles than control mares (7.8+/-0.51 days) (p

Amyloidosis in black-footed cats (Felis nigripes).

A high prevalence of systemic amyloidosis was documented in the black-footed cat (Felis nigripes) based on a retrospective review of necropsy tissues (n = 38) submitted as part of ongoing disease surveillance. Some degree of amyloid deposition was present in 33 of 38 (87%) of the examined cats, and amyloidosis was the most common cause of death (26/38, 68%). Amyloid deposition was most severe in the renal medullary interstitium (30/33, 91%) and glomeruli (21/33, 63%). Other common sites included the splenic follicular germinal centers (26/31, 84%), gastric lamina propria (9/23, 39%), and intestinal lamina propria (3/23, 13%). Amyloid in all sites stained with Congo red, and in 13 of 15 (87%) cats, deposits had strong immunoreactivity for canine AA protein by immunohistochemistry. There was no association with concurrent chronic inflammatory conditions (P = .51), suggesting that amyloidosis was not secondary to inflammation. Adrenal cortical hyperplasia, a morphologic indicator of stress that can predispose to amyloid deposition, was similarly not associated (P = .09) with amyloidosis. However, adrenals were not available from the majority of cats without amyloidosis; therefore, further analysis of this risk factor is warranted. Heritability estimation suggested that amyloidosis might be familial in this species. Additionally, tissues from a single free-ranging black-footed cat had small amounts of amyloid deposition, suggesting that there could be a predilection for amyloidosis in this species. Research to identify the protein sequence of serum amyloid A (SAA) in the black-footed cat is needed to further investigate the possibility of an amyloidogenic SAA in this species.

Hereditary hydrocephalus internus in a laboratory strain of golden hamsters ( Mesocricetus auratus).

Golden hamsters of one common laboratory strain had a high incidence of hydrocephalus internus. When a severity score of hydrocephalus was used, a major autosomal recessive locus could be identified. However, when a binary score (hydrocephalus, no hydrocephalus) was used, no such major locus could be detected and results of test matings were not consistent with Mendelian inheritance. Golden hamsters with severe forms of hydrocephalus had a dorsally compressed and ventrally intact hippocampus. Implications for the behavior and well-being of affected hamsters are unknown but researchers using this strain should be aware of the likely presence of hydrocephalus.

Meta-analysis of factors affecting carcass characteristics of feedlot steers.

A meta-analysis was conducted to assess the effects of biological type (early-moderate or late maturity) and implant status (estrogenic, combination, or nonimplanted; repeats included) on HCW (kg); LM area (cm2); 12th-rib fat thickness (fat thickness, cm); KPH (%), and intramuscular fat (%) at harvest, to provide inputs to an ongoing program for modeling beef cattle growth and carcass quality. Forty-three publications from 1982 to 2004 with consistent intramuscular fat data were evaluated. Two studies were undertaken: 1) with fat thickness as a covariate and 2) with BW as a covariate. The intercept-slope covariance estimate was not statistically different from 0 for LM area (P = 0.11), KPH (P = 0.19), and intramuscular fat (P = 0.74) in study 1, and for LM area (P = 0.44), fat thickness (P = 0.11), KPH (P = 0.19), and intramuscular fat (P = 0.74) in study 2; therefore, a reduced model without a covariance component was fitted for these carcass characteristics. A covariance component was fitted for HCW (P = 0.01, study 1 and P = 0.05, study 2) and for intramuscular fat (P = 0.05, study 2). In study 1, the results for maturity indicated differences between early-moderate and late maturity for HCW (P < 0.01) and LM area (P < 0.01) but no differences for KPH (P = 0.26) and intramuscular fat (P = 0.50); for implant status, an estrogenic or combination implant increased HCW by 2.9% (P = 0.27) or 4.8% (P < 0.01), increased LM area by 3.2% (P = 0.23) or 6.3% (P < 0.01), decreased intramuscular fat by 8.1% (P < 0.01) or 5.4% (P < 0.01), respectively, and decreased KPH by 7.6% (P = 0.34) for estrogenic implants but increased KPH by 1.1% (P = 0.36) for combination implants, compared with nonimplanted steers. In study 2, the results at 600 kg of BW for implant status (implant or nonimplant) indicated no differences for HCW (P = 0.63) and LM area (P = 0.73), but there were differences for fat thickness (P < 0.01), KPH (P < 0.01), and intramuscular fat (P < 0.01); the results for maturity (early-moderate or late maturity) indicated no differences for HCW (P = 0.94), but there were differences for LM area (P < 0.01), fat thickness (P < 0.01), KPH (P < 0.01), and intramuscular fat (P < 0.01). The difference between early-moderate and late maturity (studies 1 and 2) confirmed that frame size accounts for a substantial portion of the variation in carcass composition. Studies 1 and 2 also indicate that implant status had significant effects on carcass quality.

Genetic evaluation of Addison's disease in the Portuguese Water Dog.

BACKGROUND: Addison's disease, also known as hypoadrenocorticism, has been reported in many individual dogs, although some breeds exhibit a greater incidence than the population as a whole. Addison's is presumed to be an autoimmune mediated hereditary defect but the mode of inheritance remains unclear. In particular, the heritability and mode of inheritance have not been defined for the Portuguese Water Dog although Addison's is known to be prevalent in the breed. RESULTS: The analyses present clear evidence that establishes Addison's disease as an inherited disorder in the Portuguese Water Dog with an estimate of heritability of 0.49 (+/- 0.16); there were no differences in risk for disease across sexes (p > 0.49). Further, the complex segregation analysis provides suggestive evidence that Addison's disease in the Portuguese Water Dog is inherited under the control of a single, autosomal recessive locus. CONCLUSION: The high heritability and mode of inheritance of Addison's disease in the Portuguese Water Dog should enable the detection of segregating markers in a genome-wide scan and the identification of a locus linked to Addison's. Though the confirmation of Addison's disease as an autosomal recessive disorder must wait until the gene is identified, breeders of these dogs may wish to keep the present findings in mind as they plan their breeding programs to select against producing affected dogs.

Uveodermatologic (VKH-like) syndrome in American Akita dogs is associated with an increased frequency of DQA1*00201.

The Akita breed of dog is affected by a number of distinct immune-mediated diseases, including thyroiditis, sebaceous adenitis, pemphigus foliaceus, uveitis, polyarthritis, myasthenia gravis, and uveodermatologic (UV) syndrome. UV syndrome is manifested by progressive uveitis and depigmenting dermatitis that closely resembles the human Vogt - Koyanagi - Harada syndrome. This study examined the allelic diversity of the three DLA class II loci (DRB1, DQA1, and DQB1) in the American Akita dog, and the relationship of specific DLA class II alleles to the UV. Low allelic variation was demonstrated within genes of DLA class II. American Akita dogs possessed six of the reported 16 DQA1 alleles, but only eight of 61 reported alleles in DRB1 and nine of 47 reported alleles in DQB1. Almost one-half of American Akita dogs were homozygous for a single allele at DQA1 and up to a quarter at DRB1 and DQB1. DLA-DQA1*00201 was associated with a significantly higher relative risk (RR = 15.3) or odds ratio (OR = 15.99) for UV syndrome than other DLA class II alleles. No significant association was noted with haplotypes of DRB1, DQB1, and DQA1 alleles; DRB1*03201-DQA1*00201 trended toward significance. This study confirmed loss of DLA genetic diversity in the American Akita dog in common with other pure breeds of dog and suggested a role for certain DLA class II gene alleles in the pathogenesis of UV.