High intensity exercise conditioning increases accumulated oxygen deficit of horses

High intensity exercise is associated with production of energy by both aerobic and anaerobic metabolism. Conditioning by repeated exercise increases the maximal rate of aerobic metabolism, aerobic capacity, of horses, but whether the maximal amount of energy provided by anaerobic metabolism, anaerobic capacity, can be increased by conditioning of horses is unknown. We, therefore, examined the effects of 10 weeks of regular (4-5 days/week) high intensity (92+/-3 % VO2max) exercise on accumulated oxygen deficit of 8 Standardbred horses that had been confined to box stalls for 12 weeks. Exercise conditioning resulted in increases of 17% in VO2max (P<0.001), 11% in the speed at which VO2max was achieved (P = 0.019) and 9% in the speed at 115% of VO2max (P = 0.003). During a high speed exercise test at 115% VO2max, sprint duration was 25% longer (P = 0.047), oxygen demand was 36% greater (P<0.001), oxygen consumption was 38% greater (P<0.001) and accumulated oxygen deficit was 27% higher (P = 0.040) than values before conditioning. VLa4 was 33% higher (P<0.05) after conditioning. There was no effect of conditioning on blood lactate concentration at the speed producing VO2max or at the end of the high speed exercise test. The rate of increase in muscle lactate concentration was greater (P = 0.006) in horses before conditioning. Muscle glycogen concentrations before exercise were 17% higher (P<0.05) after conditioning. Exercise resulted in nearly identical (P = 0.938) reductions in muscle glycogen concentrations before and after conditioning. There was no detectable effect of conditioning on muscle buffering capacity. These results are consistent with a conditioning-induced increase in both aerobic and anaerobic capacity of horses demonstrating that anaerobic capacity of horses can be increased by an appropriate conditioning programme that includes regular, high intensity exercise. Furthermore, increases in anaerobic capacity are not reflected in blood lactate concentrations measured during intense, exhaustive exercise or during recovery from such exercise.     

Retrieval of a patent ductus arteriosus coil following embolisation to the right subclavian artery

A two-month-old female Tibetan terrier was re-presented with an incomplete closure of the patent ductus arteriosus. Following a second attempt to close the shunt by coil embolisation, arterial embolisation occurred. The successful removal of the embolised coil is described.     

Neurological dysfunction in three dogs and one cat following attenuation of intrahepatic portosystemic shunts

Neurological dysfunction is an uncommon complication following extrahepatic portosystemic shunt ligation. Three dogs and one cat are described that developed neurological signs within 21 to 42 hours of attenuation of intrahepatic portosystemic shunts. None of these cases had biochemical evidence of hepatic encephalopathy postoperatively. Two dogs died during management of status epilepticus following aspiration of food. One dog died six months postoperatively. The cat had persistent neurological dysfunction at discharge, but was alive and had recovered most of its neurological function at the time of writing, 37 months after surgery. This report demonstrates the potential for animals with intrahepatic portosystemic shunts to develop postoperative neurological signs and highlights the difficulty of managing such cases. Two dogs had both intrahepatic and extrahepatic portosystemic shunts. Large intestinal malrotation (partial situs inversus) may have been linked to the development of a portosystemic shunt in the remaining dog.     

Neurogenesis in a young dog with epileptic seizures

Epileptic seizures can lead to various reactions in the brain, ranging from neuronal necrosis and glial cell activation to focal structural disorganization. Furthermore, increased hippocampal neurogenesis has been documented in rodent models of acute convulsions. This is a report of hippocampal neurogenesis in a dog with spontaneous epileptic seizures. A 16-week-old epileptic German Shepherd Dog had marked neuronal cell proliferation (up to 5 mitotic figures per high-power field and increased immunohistochemical expression of proliferative cell nuclear antigen) in the dentate gyrus accompanied by microglial and astroglial activation. Some granule cells expressed doublecortin, a marker of immature neurons; mitotically active cells expressed neuronal nuclear antigen. No mitotic figures were found in the brain of age-matched control dogs. Whether increased neurogenesis represents a general reaction pattern of young epileptic dogs should be investigated.     

Surgical management of a subepiglottic thyroglossal duct cyst in a dog

A 2 yr old dog presented for dysphagia and coughing secondary to a 4 cm × 4 cm turgid subepiglottic mass. Cervical radiographs, an esophagram, and computed tomography confirmed the presence of a cystic mass that was not intimately associated with any surrounding structures. An incisional biopsy confirmed the cystic nature of the mass and helped to rule out a malignancy. A marginal surgical excision was performed via a ventral approach. Histopathology of the mass was consistent with a thyroglossal duct cyst. This is the first report of a thyroglossal duct cyst in this location in a dog. There was no recurrence of clinical signs 14 mo after surgery.     

Regulatory pathways controlling the endovascular invasive trophoblast cell lineage

Hemochorial placentation is characterized by trophoblast-directed uterine spiral artery remodeling. The rat and human both possess hemochorial placentation and exhibit remarkable similarities regarding the depth of trophoblast invasion and the extent of uterine vascular modification. In vitro and in vivo research methodologies have been established using the rat as an animal model to investigate the extravillous/invasive trophoblast lineage. With these research approaches, two signaling pathways controlling the differentiation and invasion of the trophoblast cell lineage have been identified: i) hypoxia/hypoxia inducible factor and ii) phosphatidylinositol 3-kinase/AKT/Fos like antigen 1. Dissection of these pathways has facilitated identification of fundamental regulators of the invasive trophoblast cell lineage.     

LDSO: a program to simulate pedigrees and molecular information under various evolutionary forces

Simulations are a major tool to evaluate new statistical methods and optimize experimental designs in the genomic era. However, this can only be achieved when the simulations are close enough to reality, as well as diverse enough to be realistic. For mapping studies, it is thus critical to re-create as much as possible the forces generating linkage (mutation, random drift, changes in population sizes, selection and pedigree structure) and the mechanisms producing trait genetic architecture (additivity, dominance, epistasis). We present here a computer program (ldso) simulating these phenomena. Optional outputs provide statistics on the linkage disequilibrium (LD) structure and the identity by descent between chromosomal segments, facilitating further data analyses. Furthermore, ldso enables the simulation of genomic data in known pedigrees, which sticks as precisely as possible to recent population history and structures of the long-range LD, allowing optimization of fine-mapping strategies.