Dogs exhibit a wide variety of coat color types, and many genes have been identified that control pigment production, appearance, and distribution. Some breeds, such as the Nova Scotia Duck Tolling Retriever (NSDTR), exhibit variation in pheomelanin pigment intensity that is not explained by known genetic variants. A genome-wide association study comparing light red to dark red in the NSDTR identified a significantly associated region on canine chromosome 15 (CFA 15:23 Mb–38 Mb). Coverage analysis of whole genome sequence data from eight dogs identified a 6 kb copy number variant (CNV) 152 kb upstream of KITLG. Genotyping with digital droplet PCR (ddPCR) confirmed a significant association between an increased copy number with the dark-red coat color in NSDTR (p = 6.1 × 10−7). The copy number of the CNV was also significantly associated with coat color variation in both eumelanin and pheomelanin-based Poodles (p = 1.5 × 10−8, 4.0 × 10−9) and across other breeds. Moreover, the copy number correlated with pigment intensity along the hair shaft in both pheomelanin and eumelanin coats. KITLG plays an important role in melanogenesis, and variants upstream of KITLG have been associated with coat color variation in mice as well as hair color in humans consistent with its role in the domestic dog.

Simple SummaryNeonatal foals must pass key milestones for survival such as standing and sucking from the mare shortly after birth. A condition known as neonatal maladjustment syndrome (NMS), or “dummy foal syndrome”, is characterized by failure to stand, suck, and follow their mare, putting them at risk of malnourishment, infection, and death. NMS had been presumed to be exclusively caused by low oxygen in the foal during the perinatal period. More recently, however, our group demonstrated the presence of neuroactive steroids in foals that exhibited the altered behavior and consciousness characteristic of the disorder. It has been hypothesized that signaling the transition from the in utero unconscious state to extrauterine consciousness may involve labor-induced physical compression (squeezing). During normal birth, foals experience such physical compression for approximately 20 min during stage-2 labor. Current medical treatments for NMS are symptomatic and supportive, which may require 2–7 days of veterinary care. Anecdotal evidence demonstrated that a novel physical compression (squeeze method) that applies 20 min of sustained pressure to the chest of neonatal foals exhibiting this syndrome might rapidly hasten recovery. This survey compares reported outcomes of medical therapy alone to this squeeze procedure with or without medical therapy. The results revealed some foals that received the squeeze procedure recovered faster than those that received medical therapy only.AbstractHorses are a precocious species that must accomplish several milestones that are critical to survival in the immediate post-birth period for their survival. One essential milestone is the successful transition from the intrauterine unconsciousness to an extrauterine state of consciousness or awareness. This transition involves a complex withdrawal of consciousness inhibitors and an increase in neuroactivating factors that support awareness. This process involves neuroactive hormones as well as inputs related to factors such as cold, visual, olfactory, and auditory stimuli. One factor not previously considered in this birth transition is a yet unreported direct neural reflex response to labor-induced physical compression of the fetus in the birth canal (squeezing). Neonatal maladjustment syndrome (NMS) is a disorder of the newborn foal characterized by altered behavior, low affinity for the mare, poor awareness of the environment, failure to bond to the mother, abnormal sucking, and other neurologically-based abnormalities. This syndrome has been associated with altered events during birth, and was believed to be caused exclusively by hypoxia and ischemia. However, recent findings revealed an association of the NMS syndrome with the persistence of high concentrations of in utero neuromodulating hormones (neurosteroids) in the postnatal period. Anecdotal evidence demonstrated that a novel physical compression (squeeze) method that applies 20 min of sustained pressure to the thorax of some neonatal foals with this syndrome might rapidly h...

Background Oral administration of magnesium and boron might have a beneficial effect on headshaking behavior in horses. Objective Evaluate the effects of oral magnesium alone or in combination with boron on headshaking behavior in affected horses. Animals Twelve geldings (6 healthy controls and 6 affected). Methods Prospective randomized controlled dietary trial over 42 days in 12 horses (6 horses diagnosed with trigeminal‐mediated headshaking and 6 unaffected healthy controls). All horses received a hay diet and were randomized into 3 treatment groups: pelleted feed combination (PF), pelleted feed combination with magnesium (M), and pelleted feed combination with magnesium‐boron (MB) with a week washout of hay only between treatments. Headshaking behavior and biochemical blood variables were assessed at baseline (hay only) and then after each week of supplementation. Results All 3 diet interventions increased blood ionized and total magnesium. Groups M and MB further increased Mg 2+ when compared to PF. Horses receiving treatments had a significant reduction in headshaking behavior, as measured by incidence rate ratio (IRR), when compared to unsupplemented hay diet (44% for PF, IRR, 0.558; CI, 0.44, 0.72; P < .001; 52% for M, IRR, 0.476; CI, 0.37, 0.62; P < .001; and 64% for MB, IRR, 0.358; CI, 0.27, 0.48; P < .001). Conclusions and Clinical Importance Magnesium in combination with boron had the greatest decrease in headshaking. Oral supplementation with magnesium or magnesium in combination with boron should be considered in horses affected with headshaking.

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BackgroundThe carrier status of lavender foal syndrome (LFS), cerebellar abiotrophy (CA), severe combined immunodeficiency (SCID), and occipitoatlantoaxial malformation (OAAM1) in foals with juvenile idiopathic epilepsy (JIE) is unknown.Hypothesis/ObjectivesTo determine the carrier status of LFS, CA, SCID, and OAAM1 in foals with JIE.AnimalsTen foals with JIE.Materials and MethodsArchived DNA samples were tested for known genetic mutations causing LFS, CA, SCID, and OAAM1. The inclusion criteria consisted of having been diagnosed with JIE by ruling out other causes of seizures in foals and supported by electroencephalographic examination.ResultsTen Egyptian Arabian horses (5 females and 5 males) were phenotyped as foals with JIE by electroencephalography (EEG). All foals were negative for the genetic mutations that cause LFS, CA, SCID, and OAAM1 except for 1 foal that was a carrier of CA.Conclusions and Clinical ImportanceJuvenile idiopathic epilepsy of Egyptian Arabian foals and LFS appear to be phenotypically and genetically distinct disorders. There was no apparent association between JIE and LFS, CA, SCID, and OAAM1.