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Biomedical subjects

D H Gribble

Publications and source records attributed to D H Gribble.

At least 19 recordsLinked to original sources

Diagnostic testing for pituitary pars intermedia dysfunction in horses.

Pituitary pars intermedia dysfunction is a slowly progressive disorder that afflicts most breeds of horses. Because it shares features with human Cushing disease, it has been referred to as equine Cushing disease. A variety of tests of pituitary-adrenocortical function were performed on horses with evidence of pituitary pars intermediate dysfunction, and results were compared with those in healthy control horses. Diurnal variations in plasma cortisol concentration were not statistically different between control horses and those with pituitary pars intermedia dysfunction. An ACTH stimulation (1 U of natural ACTH gel/kg of body weight, IM) test or a combined dexamethasone suppression test (10 mg, IM) and ACTH stimulation (100 mg of synthetic ACTH, IV) test also failed to distinguish horses with pituitary pars intermedia dysfunction from control horses. A significant (P < 0.001) dose-related suppression of cortisol concentration in response to increasing doses (5, 10, 20, and 40 micrograms/kg) of dexamethasone was observed in control horses but not in those with pituitary pars intermedia dysfunction. On the basis of plasma cortisol concentration, the dexamethasone suppression test, using 40 micrograms/kg, whether initiated at 5 PM with sample collection at 15 (8 AM) and 19 (12 PM) hours after dexamethasone administration, or initiated at 12 AM with sample collection at 8 (8 AM), 12 (12 PM), 16 (4 PM), 20 (8 PM), and 24 (12 AM) hours after dexamethasone administration, reliably distinguished between control horses and those with pituitary pars intermedia dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

Mortality of harbor seal pups at different sites in the inland waters of Washington.

We examined the mortality rates and causes of death of harbor seal (Phoca vitulina) pups in three regions of the inland waters of Washington (USA) in 1984. One hundred eight pups were collected during 239 searches of the shoreline areas near harbor seal haulout sites or through public reports. Minimum neonatal (up to 1 mo after birth) mortality rates at these regions ranged from 12% to 26% of the pups born. Neonatal mortality was highest in the Strait of Juan de Fuca; 33 of the estimated 105 (31%) pups born at the primary site died. Causes of death varied by location. In southern Puget Sound predation by coyotes (Canis latrans) was the primary cause of death, accounting for eight of 43 (19%) of the dead pups examined; starvation was the next most common cause of death. Mortality at study sites in the Strait of Juan de Fuca was related to premature parturition; 19 of 49 (39%) of the pups found dead were born prematurely. Nine species of bacteria were identified in samples taken from 42 pups; Proteus sp. and Escherichia coli were the most common.

Animals↗

Nephrotoxicity of sodium arsenate in dogs.

Nephrotoxicity of sodium arsenate was evaluated in dogs to determine the pathophysiologic basis for renal lesions caused by this heavy metal. Examination of biopsy specimens indicated that the low dose of the As salt (0.73 mg/kg of body weight) produced histologic changes consisting of mild degeneration and vacuolation of renal tubular epithelium. Vacuolation involved mainly the ascending thick portion of the nephron. Clinical pathologic changes were not demonstrable at this dosage level according to glomerular filtration rate (creatinine clearance), fractional reabsorption of sodium, potassium, and chloride; plasma osmolar and free water clearance; and urinalysis. The medium dose (7.33 mg/kg) resulted in alterations determined by urinalysis, but did not markedly affect other clinical pathologic measurements. Histopathologic changes were equal to or greater than those seen with the low dose. Tubular necrosis was observed in the cortical portion of the nephron and the ascending thick limb. The high dose (14.66 mg/kg) consistently produced marked changes in all parameters evaluated. Clinical pathologic alterations were compatible with acute tubular necrosis involving all segments of the nephron. Histologically, moderate glomerular sclerosis and severe tubular necrosis were observed. During recovery from the high dose of As, a gradual compensatory healing process was observed that was evident in all clinical pathologic parameters and was confirmed from sequential renal biopsy specimens.

Animals↗

Malignant lymphoma in macaques: a clinicopathologic study of 45 cases.

Malignant lymphoma was diagnosed in 42 rhesus macaques (Macaca mulatta) and 3 stumptail macaques (M. arctoides) between February 1969 and December 1977. The distribution of tumor masses in the tissues of individual animals varied widely. Solitary tumor masses were present in 14 animals and multiple masses in the remaining 31 animals. Visceral lymph nodes, gastrointestinal tract, heart, and kidneys were most commonly affected. Peripheral lymph nodes were rarely involved. Most malignant lymphomas were of an undifferentiated cell type, although tumors of histiocytic, lymphocytic, poorly differentiated, and mixed lymphocytic and histiocytic cell types were also observed. Concurrent bacterial and/or viral infections were evident in 30 of the 45 macaques with malignant lymphoma. Amyloidosis was present in 9 animals. This high incidence of malignant lymphoma suggested that their immune responses were abnormal. The development of malignant lymphoma in the macaques may have been secondary to or enhanced by immunodeficiency.

Animals↗

Effect of pyrrolizidine alkaloid-induced hepatic disease on plasma amino acid patterns in the horse.

Plasma amino acid patterns were studied in 6 clinically normal adult horses during the course of hepatic disease induced by feeding them plants containing pyrrolizidine alkaloids. At death, there were significant (P less than 0.01) increases in glutamine, proline, tyrosine, asparagine, lysine, histidine, alanine, phenylalanine, methionine, aspartic acid, and ornithine values. There were no significant changes in glycine, valine, isoleucine tryptophan, and arginine values. There were significant (P less than 0.01) decreases in citrulline. Ammonia increased 4-fold. Alpha-Aminoadipic acid and alpha-aminobutyric acid were not detectable in the plasma of clinically normal horses, but were in the plasma of horses with severe hepatic disease. The ratio of branched chain amino acids (isoleucine + leucine + valine) to phenylalanine plus tyrosine progressively decreased from a normal of +/- 0.5 to 1.3 +/- 0.3 (mean +/- SD) just prior to death. The relative changes in plasma amino acid pattern in horses with hepatic diseases seem similar to those changes occurring in man and other animals with hepatic disease.

2-Aminoadipic Acid↗

Canine hyperadrenocorticism: pretreatment clinical and laboratory evaluation of 117 cases.

The physical findings, clinical signs, age, breed and sex distributions, and laboratory data of 117 dogs with untreated Cushing's syndrome were reviewed. Poodles, Dachshunds, and Boxers of all ages were found to be at increased risk, as were dogs of all breeds greater than or equal to 6 years old. Polydipsia, polyuria, progressive bilaterally symmetric alopecia, and abdominal distention were the most frequently observed clinical signs and physical findings. Lymphopenia, eosinopenia, above normal values of serum alkaline phosphatase, serum cholesterol, and sulfobromphthalein dye retention, and below normal urine specific gravity were the most frequent abnormalities found in the laboratory data. About 50% of the dogs had urinary tract infections. Final diagnosis was established on the basis of abnormally high plasma corticosteroid values in response to an intramuscular injection of adrenocorticotropic hormone.

17-Ketosteroids↗

Vitamin D intoxication and the pathogenesis of vitamin D nephropathy in the dog.

Dogs given excess vitamin D (500 or 1,000 micrograms/kg of body weight each day for 1 to 3 weeks were observed for clinical and pathologic changes of increased blood pressure and of characteristic nephropathy associated with vitamin D toxicosis or hypercalcemia. Serum calcium and serum urea nitrogen (UN) increased throughout the treatment period, but serum phosphorus remained within the normal range. Plasma renin activity increased markedly. Blood pressure showed only insignificnat changes (P = greater than 0.05). Gross and microscopic examination of the kidneys suggested vascular-oriented changes with an ischemic basis. Glomerular vascular poles showed hypertrophy and hyperplasia of juxtaglomerular cells. Ultrastructually, an increase in the number of secretory granules was noticed in these cells. A hypothesis regarding the mechanism of renal injury during vitamin D toxicosis is presented.

Animals↗

Blood pressure measurement in the dog.

An indirect method of blood pressure measurement was evaluated in 169 dogs, including 114 that were hospitalized because of a variety of diseases, 10 clinically normal dogs presented for neutering, and 45 privately owned, clinically normal dogs. Measurements correlated well with values obtained by simultaneous direct arterial puncture. Normotension was considered to be 130 to 180 mm of Hg, systolic, and 60 to 95 mm of Hg, diastolic. As a group, 20 dogs with advanced renal disease had significant (P less than 0.001) hypertension, compared with the groups of clinically normal dogs. Of 94 dogs with a variety of diseases exclusive of renal disease, 10 had hypertension and 2 had hypotension.

Animals↗

Isolation of simian virus 40 from rhesus monkeys (Macaca mulatta) with spontaneous progressive multifocal leukoencephalopathy.

Isolates of virus from the brain tissue of two naturally occurring cases of progressive multifocal leukoencephalopathy in rhesus monkeys (Macaca mulatta) have been characterized. Both isolates were demonstrated to be simian virus 40 (SV40) by serological tests and analysis of cleavage fragments of viral deoxyribonucleic acid produced by restriction endonuclease from Haemophilus influenzae. SV40 virions and the nonvirion T antigen were demonstrated in the brain lesions of one monkey by the fluorescent antibody staining technique. SV40 was not demonstrated in the brain of normal rhesus monkeys from the same colony with use of the same methods of viral isolation or demonstration of antigen.

Animals↗

A mucocutaneous disease in the dog, resembling pemphigus vulgaris in man.

A chronic mucocutaneous disease was diagnosed in 3 dogs. Clinically, the disease was characterized by erosions and ulcerations of the oral mucosa, various mucocutaneous junctions, and the skin. Histologically, there was acantholysis or a separation of the epithelial cells from one another, resulting in the formation of clefts and bullae. Based on clinical and laboratory findings, the disease seemed to be the canine equivalent of pemphigus vulgaris (PV) in man.

Acantholysis↗