Search PubMed⌕ Search

Biomedical subjects

J T Robertson

Publications and source records attributed to J T Robertson.

At least 55 records · Page 3Linked to original sources
PubMed1994

Surgical repair of iatrogenic soft palate defects in two horses.

A 4-year-old Thoroughbred filly was referred for evaluation of a soft palate defect that had been created several weeks earlier during surgical correction of epiglottic entrapment, performed transorally. Surgical correction of the defect was performed via mandibular symphysiotomy. At 85 days after repair, the horse raced successfully. A 2-year-old Thoroughbred filly was admitted for evaluation and treatment of epiglottic entrapment. The soft palate was lacerated during transnasal division of the entrapping membrane. A 2-cm full-thickness soft palate laceration was repaired transorally.

Animals↗
PubMed1994

Humoral hypercalcemia of malignancy associated with ameloblastoma in a horse.

Humoral hypercalcemia of malignancy was evident in a horse that had a locally invasive ameloblastoma of the left hemimandible. Surgical removal of the neoplasm resulted in prompt return of serum calcium and parathyroid hormone concentrations to within reference limits. The tumor contained parathyroid hormone-related protein, as demonstrated by immunohistochemistry and western blot analysis. It is likely that production of this protein by the neoplasm was important in the pathogenesis of the hypercalcemia. The case represented a sporadic form of humoral hypercalcemia of malignancy attributable to an uncommon epithelial neoplasm, and indicated that humoral hypercalcemia of malignancy can develop with neoplasms in horses.

Ameloblastoma↗
PubMed1994

Heterogeneity of subcellular localization of p53 protein in human glioblastomas.

Immunohistochemical analysis of the p53 protein in human glioblastomas with known genetic profiles of p53 mutations and allele losses on chromosome 17p demonstrated a heterogeneous pattern of subcellular compartmentalization of the p53 protein. Tumors with a single wild type copy of the p53 gene but with allelic deletions on chromosome 17p exhibit nuclear and/or cytoplasmic accumulation of p53, whereas tumors with both copies of the wild type gene and no allele losses on chromosome 17 do not accumulate p53. Glioblastomas with one normal and one mutated copy of the p53 gene and allelic deletions on 17p distal to p53, on the other hand, show predominantly cytoplasmic staining, probably originating from the wild type p53 protein. Furthermore, tumors with mutations in the same codon of p53 display quite different intracellular distribution suggesting that, in addition to the genotype of p53, the intracellular microenvironment of a particular tumor is important in determining the subcellular localization of the p53 protein.

Base Sequence↗
PubMed1994

Respiratory emergencies in the adult horse.

Responding to an equine respiratory emergency requires rapid localization of the problem and appropriate choices for therapy. Localizing the cause of respiratory distress is aided by history and thorough physical examination. When examining the patient, one must focus on the presenting signs as indicators of URT or LRT dysfunction. Table 3 summarizes the characteristic presenting signs based on respiratory tract location and suggests the initial treatment course indicated. Respiratory distress in the absence of signs related to the pulmonary system suggests inadequate oxygen delivery secondary to a nonpulmonary problem such as shock or severe anemia, which is just as compromising to the animal but requires an entirely different therapeutic approach (see Allen and Schertel, this issue). Thus, localization of the source of respiratory distress is always the first step in determining successful treatment.

Animals↗
PubMed1994

Effect of sternothyrohyoid myectomy on upper airway mechanics in normal horses.

The effect of transection of the sternothyroideus and sternohyoideus muscles on upper airway mechanics was investigated in exercising horses. Upper airway mechanics of six Standardbred horses were measured at rest and during exercise before and 24 h and 2 wk after sternothyrohyoid myectomy. Transnasal tracheal and pharyngeal catheters connected to differential pressure transducers were used to measure tracheal and pharyngeal pressures. A pneumotachograph mounted on the rostral end of an airtight face mask was used to measure airflow. Horses ran at 50, 75, and 100% of maximal O2 consumption on a treadmill. Twenty-four hours after sternothyrohyoid myectomy, no significant difference was detected in tracheal, pharyngeal, or translaryngeal inspiratory and expiratory pressures and impedances, inspiratory and expiratory flows, and respiratory frequency. Two weeks after sternothyrohyoid myectomy, there was a statistically significant increase in translaryngeal inspiratory pressure (P = 0.035) and tracheal inspiratory pressure (P = 0.032) compared with preoperative measurements. Two weeks after sternothyrohyoid myectomy, there was a statistically significant increase in translaryngeal inspiratory resistance (P = 0.017) and tracheal inspiratory resistance (P = 0.023) compared with preoperative values. Increased translaryngeal and tracheal inspiratory pressures and resistances after sternothyrohyoid myectomy suggest that the sternothyroideus and sternohyoideus muscles act to increase or maintain upper airway patency and stability in normal horses.

Airway Resistance↗
PubMed1994

Acute subdural hematoma: nonsurgical management of selected patients.

There is a current trend toward nonsurgical therapy for small, minimally symptomatic acute subdural hematomas (ASDH), but data supporting such a scheme have been lacking. We evaluated 83 patients with minimally symptomatic ASDH (Glasgow Coma Scale scores of 11-15) and found 58 managed nonsurgically (70%) and 25 managed with craniotomy (30%). Patients managed without surgery had a lower incidence of focal neurologic deficits (12% vs. 40%; p < .01), open cisterns (90% vs. 28%; p < .001), and small (< or = 1 cm) ASDHs (92% vs. 62%; p < .001). Ninety-three percent of patients managed nonsurgically had functional recovery compared with 84% of patients with craniotomy. Age and injury Severity Score were significantly associated with patient outcome. Timing of surgery had no association with outcome. Six percent of patients managed nonsurgically developed chronic SDH requiring craniotomy. We conclude that unless the hematoma is causing clinical evidence of intracranial hypertension or significant neurologic dysfunction, there appears to be no advantage in evacuating the clot. Selected patients with ASDH and GCS scores of 11-15 can safely be managed without craniotomy.

Acute Disease↗
PubMed1993

Surgical treatment of cervical stenotic myelopathy in horses: 73 cases (1983-1992).

Seventy-three horses with cervical stenotic myelopathy underwent cervical vertebral interbody fusion (n = 63) or dorsal laminectomy (n = 10). Neurologic function improved in 77% of horses, and 46% of horses achieved athletic function (racing, race training, or pleasure riding) after cervical vertebral interbody fusion for static and dynamic spinal cord compressive lesions. Neurologic status improved in 4 of 10 horses after dorsal decompression for static compressive spinal cord lesions. The duration of clinical signs prior to surgical intervention was shorter for horses that achieved athletic function or improved by at least 2 neurologic grades than for horses that did not improve in neurologic status or improved 1 neurologic grade after cervical vertebral interbody fusion. The number of cervical spinal cord compressive lesions and age of horses did not affect the long-term surgical outcome of cervical vertebral interbody fusion. Seroma formation, implant failure, right laryngeal hemiplegia, and colitis were nonfatal complications associated with cervical vertebral interbody fusion. Dorsal laminectomy and cervical vertebral interbody fusion of static compressive lesions of the caudal cervical vertebral column were associated with fatal postoperative complications, including vertebral body fracture, spinal cord edema, and implant failure.

Animals↗
PubMed1993

Mass spectrometric analysis of opioid and tachykinin neuropeptides in non-secreting and ACTH-secreting human pituitary adenomas.

In a study to test the hypothesis that defects in the metabolism of neuropeptides might be a contributing factor to human anterior pituitary tumor formation, the proenkephalin A, proopiomelanocortin (POMC), and tachykinin systems, which produce methionine enkephalin (ME), beta-endorphin (BE), and substance P (SP), respectively, were measured in patients who had a wide variety of pituitary tumors. Mass spectrometry was used to optimize the level of molecular specificity of the ME and BE analytical measurements, and radioimmunoassay was used to measure SP-like immunoreactivity (SP-li). Compared to data obtained from pituitaries from post-mortem controls, the non-secreting tumors contained a significantly lower amount of the POMC neuropeptide, BE. The lower ME level was not significant. However, two adrenocorticotrophic hormone (ACTH)-secreting tumors contained ME, BE, and SP-li amounts that were much higher than both the controls and nonsecreting tumors. These data suggest that a hypometabolism of the POMC precursor may be operating in non-secreting tumors, and that a hypermetabolism of the proenkephalin A, POMC, and tachykinin precursors may be operating in two ACTH-secreting tumors. These data demonstrate that mass spectrometry plays a critical role in the study of human pituitary tumors.

Adenoma↗
PubMed1993

Ubiquitin marks the reactive swellings of diffuse axonal injury.

Ubiquitin is a protein that targets proteins for non-lysosomal degradation. It has been found to be present in a number of inclusions characteristic of neurodegenerative diseases. Using the fluid percussion model of closed head injury in the cat, a well-established model of diffuse axonal injury (DAI), we now report that the reactive axonal swellings and the retraction balls produced in this model stain positively with anti-ubiquitin immunohistochemistry. Furthermore, the affected axons become ubiquitin positive quickly (within the first 6 h after injury). Anti-ubiquitin immunohistochemistry compares well with the recently reported ability of antibodies to low molecular weight neurofilament proteins to demonstrate reactive axonal change in DAI, and it could provide additional clues to the pathogenesis of axonal transection.

Animals↗
PubMed1993

Early assessment of neurologic deficits in the fluid percussion model of brain injury.

This study was designed to quantify the early neurologic effects of brain injury elicited by fluid percussion to the dura of cats. Propofol was used for surgical anesthesia because recovery in normal animals from an intravenous infusion was found to be nearly complete within 2 h of cessation and absolutely complete by 4 h. In addition, a cat coma scale (CCS) was developed that reflects normal (CCS, 14) to moribund (CCS, 3) behavior. The CCS values at 6 h were compared with the force of injury expressed in atmospheres (atm), maximum blood pressure change, and gross neuropathology to ascertain which parameter might best account for the behavior observed after brain injury. The results showed that decreasing neurologic scores correlated well with increasing atmospheres of injury (Pearson's r 0.71, p < 0.001) but not with the rise in systolic blood pressure caused by the trauma (n = 29). Coma scores did correlate with the cross sectional area of ponto-mesencephalic lesions (Pearson's r = 0.51, p < 0.01) and proved to be significantly different in animals grouped according to lesion size of less or more than 3 mm in length (t test, p < 0.01). Thus the CCS and the pharmacologic properties of propofol permit an early analysis of the neurologic status in the feline fluid percussion model of brain injury. These procedures could facilitate the evaluation of early biochemical changes that affect behavior and of therapies designed to ameliorate the deleterious effects of head injury.

Anesthesia↗
PubMed1993

Plasma constituents during incremental treadmill exercise in intact and splenectomised horses.

Six intact and 6 splenectomised mares were given an incremental exercise test on a treadmill to examine the fluid and electrolyte changes associated with exercise and the role of the spleen in these changes. Blood samples were obtained at rest and at the end of each 1-min step of the test. Exercise at 7 m/sec caused significant (P < 0.05) increases in plasma osmolality (intact, +9.9%; splenectomised, +6.2%), plasma protein concentration (intact, +15.8%; splenectomised, +11.4%), and plasma K+ concentration (intact 46%; splenectomised, +57%). Plasma Na+ concentration did not increase significantly (P > 0.05) in either group (intact = 2.7%; splenectomised, = 3.5%). This appears to be the first record of substantial changes of these constituents during short-term exercise, even before the onset of visible sweat losses. The changes in the concentration of plasma protein suggest that short-term exercise causes a decrease in plasma volume. The changes in the concentration and content of sodium suggest that this is an isotonic shift of fluid. The increase in plasma potassium concentration appears to be due to haemoconcentration as well as an increase in the content of potassium within the vascular compartment.

Animals↗
PubMed1993

Role of decreased plasma volume in hematocrit alterations during incremental treadmill exercise in horses.

Six intact (IN) and six splenectomized (SP) mares were subjected to an incremental exercise test to examine the role of decreases in plasma volume (PV) in the changes in hematocrit (Hct) normally seen with exercise. Each horse underwent an incremental exercise test in which it ran on a treadmill up a fixed incline of 6 degrees. The test started at a speed of 4 m/s, and speed was increased 1 m/s each min until heart rate reached a plateau. Blood samples were obtained at rest and at the end of the 4, 5, 6, and 7 m/s steps of the exercise test. Resting PV was greater (P < 0.05) in the IN group (28.6 +/- 0.5 liters) compared with SP horses (22.7 +/- 2.2 liters). Exercise produced a significant increase in Hct in both groups of horses; however, the increases were greater (P < 0.05) at all exercise intensities in IN compared with SP horses. Hct increased rapidly during the first step (4 m/s) in the exercise test in the IN animals. After this, Hct increased slowly in IN horses, and values for the 5, 6, and 7 m/s steps paralleled the changes observed in the SP horses. Corrected Hct values were then used to calculate the relative change in PV. Exercise produced a significant decrease in PV in both groups of horses; however, there were no differences (P > 0.05) between the groups when IN horses (-13 +/- 3 and -18 +/- 2%) were compared with SP horses (-14 +/- 4 and -17 +/- 4%) at the 6 and 7 m/s steps of the exercise test.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Cocaine-induced platelet defects.

BACKGROUND AND PURPOSE: Numerous studies have demonstrated an association between acute cardiac events, cerebrovascular accidents, and cocaine use. The underlying mechanisms leading to these complications have not been well defined. Using various in vitro model systems, it has been reported that cocaine, up to or greater than an order of magnitude of the lethal dose, causes either inhibitory or proaggregatory effects on platelet function. METHODS: To address these reported discrepancies, we examined the effect of cocaine and its carrier on the activation and aggregation of human platelets in vitro. RESULTS: We found that cocaine inhibited platelet aggregation when platelets were challenged with ADP, collagen, or arachidonic acid. This inhibition was due to a direct effect on fibrinogen binding to the activated platelet. Cocaine also caused the dissociation of preformed platelet aggregates. At these same concentrations, cocaine did not inhibit agonist-mediated increases in cytosolic calcium or inhibit platelet shape change, suggesting that its effect on platelet aggregation was a selective process and not due to a total destruction of platelet function. Interestingly, the organization of the cytoskeleton of activated platelets, a secondary event critical to cell receptor clustering and clot retraction, was disrupted by cocaine treatment. In addition, alterations in platelet protein electrophoretic patterns were observed on preincubation of platelets with cocaine. CONCLUSIONS: We conclude that cocaine may have a direct inhibitory effect on the ability of platelets to participate in thrombus formation. The contribution of this effect as an underlying mechanism of sudden death in cocaine abusers is unknown.

Adenosine Diphosphate↗
PubMed1993

Expression of the vascular permeability factor/vascular endothelial growth factor gene in central nervous system neoplasms.

Expression of the vascular permeability factor/vascular endothelial growth factor (VEGPF) gene was investigated in human central nervous system (CNS) neoplasms and normal brain. Adsorption of capillary permeability activity from human glioblastoma multiforme (GBM) cell conditioned medium and GBM cyst fluids by anti-VEGPF antibodies demonstrated that VEGPF is secreted by GBM cells and is present in sufficient quantities in vivo to induce vascular permeability. Cloning and sequencing of polymerase chain reaction-amplified GBM and normal brain cDNA demonstrated three forms of the VEGPF coding region (567, 495, and 363 nucleotides), corresponding to mature polypeptides of 189, 165, and 121 amino acids, respectively. VEGPF mRNA levels in CNS tumors vs. normal brain were investigated by the RNase protection assay. Significant elevation of VEGPF gene expression was observed in 81% (22/27) of the highly vascular and edema-associated CNS neoplasms (6/8 GBM, 8/8 capillary hemangioblastomas, 6/7 meningiomas, and 2/4 cerebral metastases). In contrast, only 13% (2/15) of those CNS tumors that are not commonly associated with significant neovascularity or cerebral edema (2/10 pituitary adenomas and 0/5 nonastrocytic gliomas) had significantly increased levels of VEGPF mRNA. The relative abundance of the forms of VEGPF mRNA was consistent in tumor and normal brain: VEGPF495 > VEGPF363 > VEGPF567. In situ hybridization confirmed the presence of VEGPF mRNA in tumor cells and its increased abundance in capillary hemangioblastomas. Our results suggest a significant role for VEGPF in the development of CNS tumor neovascularity and peritumoral edema.

Base Sequence↗
PubMed1993

The reduction of postlaminectomy peridural fibrosis in rabbits by a carbohydrate polymer.

Spinal peridural fibrosis following total laminectomy in New Zealand White rabbits was significantly decreased by the intraoperative application of GT1587, a semi-synthetic carbohydrate polymer. The application of a similar polymer, GT1043, or phosphate-buffered saline (PBS) was not as effective. Laminectomies were performed at L-2 and L-4 in 25 rabbits. Absorbable gelatin sponge soaked with GT1043, GT1587, or PBS was applied in a blinded fashion to the operative sites, with untreated (sham) laminectomy sites serving as controls. Animals were sacrificed after 2 or 4 weeks. The extent of peridural fibrosis was evaluated by gross microdissection and histological analysis. Dense scar formation and dural adhesions were evident at both time intervals in the sham- and PBS-treated laminectomy sites. The sites treated with GT1587 showed significantly decreased peridural scar formation and dural adhesions, whereas GT1043 treatment caused modest reduction of scar formation at only the 2-week examination. The healing of skin and lumbosacral fascia was not affected by treatment of the laminectomy site with GT1587. These results suggest that GT1587 may prove beneficial in preventing postlaminectomy dural adhesions and peridural fibrosis in humans.

Animals↗