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Biomedical subjects

J Beech

Publications and source records attributed to J Beech.

At least 73 records · Page 4Linked to original sources

Differential regulation of a Thy-1 gene in transgenic mice.

We have generated Thy-1.1-transgenic Thy-1.2 mice to study the developmental expression of the Thy-1 gene in detail by transcriptional and immunological methods. In brain, the expression of the injected gene was identical to that of the endogenous gene in a tissue- and development-specific manner. In lymphoid tissue, the transferred gene was also expressed correctly in the early phases of T-cell lineage development; however, as the T cells matured, the transcription of the transferred gene, but not the endogenous gene, was suppressed. This result shows that different regulatory elements are used to express the Thy-1 gene in early and late lymphoid development.

Age Factors↗

Genetic studies of neuraxonal dystrophy in the Morgan.

A naturally occurring disease condition, neuraxonal dystrophy, was identified in 27 male and 15 female Morgans, many of which were closely related. Five-generation pedigrees were constructed for 33 of these horses and were compared with those for 29 randomly selected age- and sex-matched Morgans. Their mean coefficient of inbreeding was not statistically different (P greater than 0.1, 1 tailed t test; P less than 0.001, median test). Breeding of 2 severely affected and 2 normal stallions to 2 severely affected, 3 mildly affected, and 6 normal mares produced 10 mildly affected, 8 suspect affected, and 6 normal offspring. Breeding 4 normal stallions to 17 normal mares produced 22 normal offspring. Neuraxonal dystrophy seems to have a familial component, although neither a simple dominant not recessive mode of inheritance could be demonstrated. The condition could be inherited in a polygenic mode or as a dominant disorder with variable expression.

Animals↗

Equine intravenous glucose tolerance test: glucose and insulin responses of healthy horses fed grain or hay and of horses with pituitary adenoma.

Intravenous glucose tolerance testing (0.5 g/kg of body weight) was done on 2 groups of healthy horses maintained with hay (group 1, n = 5) and with hay plus grain supplementation (group 2, n = 5) and on a group of horses with clinically diagnosed pituitary adenoma (group 3, n = 10). Healthy horses showed an immediate increase of plasma glucose concentration after the IV glucose injection, with return of values to base line in 1 hour. Group 3 horses showed resting hyperglycemia and a delayed return of glucose values to base line (3 hours). Group 3 horses showed resting hyperinsulinemia and a feeble (nonsignificant) response to the glycemic stimulus, with gradual decrease of insulin values to base line. In addition to the apparently reduced tissue sensitivity to insulin in group 3 horses, as evidenced by hyperglycemia, hyperinsulinemia, and protracted glucose and insulin curves, the initial decrease in the insulin/glucose ratio indicates that there was secretory deficiency in response to acute IV glucose loading.

Adenoma↗

Endocrinologic, hematologic, and heart rate changes in swimming horses.

Two identical experiments, using Standardbred and Thoroughbred horses (experiment A, n = 31; experiment B, n = 17) on a swimming regimen, were performed 1 week apart to evaluate short-term heart rate, hematologic, and endocrinologic changes. Horses were placed in 4 categories based on duration of swimming (1 to 5, greater than 5 to 10, greater than 10 to 15, and greater than 15 minutes). Heart rate, PCV, and plasma concentrations of total protein, cortisol triiodothyronine, thyroxine, insulin, and glucose of each horse were evaluated before, immediately after, and 1 hour after swimming. For experiment A, there was a main effect of time of sampling on PCV, total protein, triiodothyronine, thyroxine, and insulin. There was a main effect of duration of swimming on insulin concentration and an interaction of duration of swimming and time of blood collection on heart rate and cortisol concentration. For experiment B, there was a main effect of time of blood collection on all the variables except glucose.

Animals↗

Respiratory problems in foals.

Despite major advances in our knowledge and ability to treat respiratory diseases in neonatal foals, neonatal respiratory medicine is still in its infancy. It is hoped that this article may serve as a guideline for diagnosis and treatment. Specific antibiotic regimens and emergency procedures are covered in other articles in this symposium. Because management factors play a critical role in the pathogenesis of respiratory disease, education of clients as to their importance would help both prophylactically and therapeutically. The necessity of very careful monitoring of neonates, which is critical to early detection of disease, should be stressed. As respiratory diseases can be fulminant and rapidly fatal, it is imperative not to delay diagnosis and therapy. Thorough examination and implementation of appropriate diagnostic techniques, as well as prompt early referral to a more sophisticated facility when indicated, would prevent many deaths. Although sophisticated support systems are vital for survival of some of these foals, good basic intensive nursing care combined with selection of appropriate drug therapy very early in the course of the disease is all that many foals require and can significantly improve survival rates.

Adrenergic beta-Agonists↗

Hormonal response to thyrotropin-releasing hormone in healthy horses and in horses with pituitary adenoma.

Cortisol, triiodothyronine (T3), thyroxine (T4), insulin, and glucose responses to thyrotropin-releasing hormone (TRH) were evaluated in 12 healthy, mature horses and in 7 horses and 4 ponies with clinical signs of pituitary adenoma (PA). Within 1 hour after TRH administration, the increase in T3 and T4 was similar in healthy horses and animals with PA. Plasma cortisol in the group with PA increased (P less than 0.05) within 0.25 hours after TRH administration, and remained increased for 1.5 hours. In the control group, a significant increase in plasma cortisol concentrations did not develop after TRH administration. Plasma glucose and insulin concentrations were higher in animals with PA than in the healthy horses throughout the experiment (6 hours).

Adenoma↗

Bacterial isolates from tracheobronchial aspirates of healthy horses.

Of tracheobronchial aspirates from 50 clinically healthy Thoroughbred racehorses, 4 (8%) had aerobic bacteria with recognized pathogenicity, 12 (24%) contained transient bacterial isolates, and 37 (74%) had no bacterial growth. Of tracheobronchial aspirates from 36 pastured, nonracing racehorses, 3 (8%) had bacteria with recognized pathogenicity, 23 (64%) contained transient bacteria, and 10 (28%) had no bacterial growth. Anaerobes were not isolated from 12 of 12 pastured horses. Transient bacteria were isolated more often in the pastured horses.

Animals↗

Congenital nuclear cataracts in the Morgan horse.

Nuclear cataracts were found in 2 groups of related Morgan horses. The cataracts were finely reticulated central spherical translucencies that sometimes extended to the region of the posterior "Y" suture. The cataracts were not associated with other ocular defects and did not impair vision. In 1 group of 8 horses, 5 were affected; in the other group, 6 of 8 were affected. Although a pattern of inheritance could not be determined, the familial distribution of the cataracts supported the conclusion that the defect was a heritable disorder.

Animals↗

Lymphosarcoma and associated immune-mediated hemolytic anemia and thrombocytopenia in horses.

Three horses with equine lymphosarcoma were examined because of clinical signs including chronic weight loss, respiratory distress, peripheral edema, and chronic colic. Clinicopathologic findings included evidence of an immune-mediated hemolytic anemia. Immune-mediated thrombocytopenia also was diagnosed in 1 of the horses and suspected in another. One horse died in spite of treatment, 1 died 5 hours after surgical removal of a tumor encircling the jejunum, and 1 was euthanatized because of deteriorating condition. Necropsy of each horse revealed extensive neoplastic infiltration of peripheral lymph nodes and abdominal or thoracic viscera with neoplastic lymphocytes.

Anemia, Hemolytic, Autoimmune↗

Neuroaxonal dystrophy of the accessory cuneate nucleus in horses.

Data were collected from 37 horses with a neurologic disability and compared to a group of 34 normal horses. Affected horses had neuroaxonal dystrophy, gliosis, vacuoles, and sometimes pigment localized to the accessory cuneate nuclei with minimal or no changes in the spinal cord and no changes in the proximal peripheral nerves. The focal nature of the change and usual absence of significant light microscopic spinal cord or peripheral nerve changes are different than previously described equine neuropathologic conditions.

Age Factors↗

Pharmacokinetic disposition of theophylline in horses after intravenous administration.

The pharmacokinetics of theophylline were determined in 6 healthy horses after a single IV administration of 12 mg of aminophylline/kg of body weight (equivalent to 9.44 mg of theophylline/kg). Serum theophylline was measured after the IV dose at 0.25, 0.5, 1, 2, 4, 6, 8, 12, and 15 hours. Serum concentration plotted against time on semilogarithmic coordinates, indicated that theophylline in 5 horses was best described by a 2-compartment open model and in 1 horse by a 1-compartment open model. The following mean pharmacokinetic values were determined; elimination half-life = 11.9 hours, distribution half-life = 0.495 hours, apparent specific volume of distribution = 0.885 +/- 0.075 L/kg, apparent specific volume of central compartment = 0.080 L/kg, and clearance = 51.7 +/- 11.2 ml/kg/hr. Three horses with reversible chronic obstructive pulmonary disease were serially given 1, 3, 6, 9, 12, and 15 mg of aminophylline/kg in single IV doses (equivalent to 0.8, 2.4, 4.7, 7.1, 9.44, and 11.8 mg of theophylline/kg, respectively). The horses were exposed to a dusty barn until they developed clinical signs of respiratory distress and were then given the aminophylline. Effects of increasing doses on different days were correlated with clinical signs, blood pH, and blood gases. The 3 horses had a decrease in the severity of clinical signs after the 9, 12, or 15 mg doses of aminophylline/kg. The horses at 0.5 hour after dosing had a significant decrease in PaCO2 (43.6 +/- 5.5 to 39.4 +/- 6.7 mm of Hg, P less than 0.001) and a significant increase in blood pH (7.38 +/- 0.017 to 7.41 +/- 0.023, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

Pharmacokinetics of ticarcillin in the horse after intravenous and intramuscular administration.

Serum and peritoneal fluid concentrations of ticarcillin were measured in 10 healthy adult horses from 0.5 to 8 hours after IV or IM administration of 44 mg/kg of body weight. After IV injection, the serum concentration at 30 minutes was 104.3 +/- 6.1 mg/L and the mean peak peritoneal fluid concentration (61.4 +/- 29.0 mg/L) occurred 2 hours after injection. The peak serum (28.3 +/- 5.5 mg/L) and the peak peritoneal fluid concentrations (19.2 +/- 6.0 mg/L) occurred 2 hours after the IM injection. Ticarcillin (greater than or equal to 2 mg/L) persisted in serum and peritoneal fluid for 6 hours after IV injection and 8 hours after IM injection. The half-life of ticarcillin was 0.94 hour after IV injection and the bioavailability of ticarcillin administered IM was 64.9%.

Absorption↗

Disseminated intravascular coagulation in six horses.

Disseminated intravascular coagulation (DIC) was diagnosed as a secondary disease in 6 horses. Four horses had localized and/or systemic sepsis, one horse had disseminated neoplasia, and one had idiopathic ulcerative enteropathy. The diagnosis of DIC was based on the finding of at least 3 of 4 abnormalities: thrombocytopenia, prolonged prothrombin time, prolonged activated partial thromboplastin time, and a high concentration of fibrinolytic degradation products. The most common clinical signs other than those attributable to the primary disease process were abnormal hemorrhage (4 hours) and venous thrombosis (4 horses). All horses eventually died or were euthanatized because of the severity of the primary disease.

Animals↗

The distribution of Thy-1 antigen in the P.N.S. of the adult rat.

The distribution of the cell surface glycoprotein Thy-1 in the P.N.S. of adult rats was examined using immunohistochemical and experimental techniques. In the hypoglossal nerve the pattern of Thy-1 labelling suggested the antigen was on the plasma membrane of all axons, not only in their major myelinated course but also on their fine terminal branches and at the motor end plate itself. Similarly in other peripheral nerves examined [phrenic and vagus nerves, dorsal and ventral roots, and both the preganglionic and postganglionic trunks of the superior cervical ganglion (SCG) and the submandibular ganglion] Thy-1 was always associated with axons, but the resolution obtained with immunohistochemical techniques was not in itself sufficient to exclude the possibility that the antigen was on the surface of the ensheathing Schwann cell where it apposed the axons. However, in the hypoglossal nerve the antigen was found to accumulate proximal to a ligation of the nerve, suggesting it was made by the neurons and transported down the nerve by axoplasmic flow. This impression was supported by examining neuronal cell bodies in the SCG, dorsal root ganglia and submandibular ganglion, all of which contain readily detectable cytoplasmic Thy-1. In the SCG this cytoplasmic antigen was shown to include the pool of newly synthesized Thy-1. It was increased by treatment of the ganglion with colchicine, and decreased by cycloheximide. Conversely, treatment of hypoglossal nerve trunk with colchicine did not lead to the appearance of the antigen around the non-neuronal perikarya. It is therefore concluded that in those parts of the adult rat P.N.S. examined, Thy-1 is made by neurons and occurs generally on the plasma membrane of axons.

Animals↗

Pharmacokinetics of phenytoin (diphenylhydantoin) in horses.

The pharmacokinetics of the anti-convulsant phenytoin were investigated in clinically healthy horses after oral (p.o.) and intravenous (i.v.) administration. A single dose of phenytoin (8.8 mg/kg body weight) was given i.v. as a bolus to nine horses and one horse received 13.2 mg/kg. A two-compartment open model was used to describe the disposition of phenytoin. Four of the horses that received an i.v. dose (three at 8.8 mg/kg and one at 13.2 mg/kg) were then given the same dose 3 days later by the oral route. Phenytoin achieved a peak concentration in serum within 1-4 h after p.o. administration and was poorly absorbed with a bioavailability of 34.5 +/- 8.6%. Oral dosage regimens were calculated on the basis of a dosing interval of 8 h to provide average serum steady-state concentrations of 5 and 10 micrograms/ml for phenytoin.

Animals↗