Renal carcinoma in a captive Edwards Lory (Trichoglossus haematodus capistratus).
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Biomedical subjects
Publications and source records attributed to G B Hubbard.
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A squamous cell carcinoma of the prepuce and penis with metastases to the inguinal lymph nodes and lung occurred in a rhesus monkey (Macaca mulatta). The primary tumor consisted of eroded nodular masses at the mucocutaneous junction of the prepuce and in the epithelium of the prepuce and penis.
An adult female Macaca fascicularis developed anorexia and minimal fecal production. Abdominal palpation was unrewarding. Rectal palpation revealed a rectal stricture and a large soft tissue mass in the area of the uterus. Clinical pathology tests were within normal limits. Exploratory surgery and histopathology confirmed a diagnosis of endometriosis.
An epizootic of sialodacryoadenitis was identified in 10-week-old rats 5 days after they were housed with a group of older rats. The young rats generally did not develop the characteristic clinical signs of sialodacryoadenitis, but they did have typical histologic lesions of sialodacryoadenitis in Harderian, lacrimal, and salivary glands. The lesions were variable in distribution and severity, and chronic lesions persisted in the Harderian glands of the rats.
Aeromonas hydrophila caused severe disease in a group of Xenopus laevis within 3 weeks of receipt. The primary clinical signs were marked pallor of the skin, petechiation, lethargy, anorexia, and edema. The duration of the outbreak was approximately 45 days during which time 21 frogs became sick and 18 died, despite tetracycline therapy. Pale skin, subcutaneous edema and hemorrhages, ascites, and pale livers were seen at necropsy. Aeromonas hydrophila was isolated from skin, and the same organism was isolated in pure culture from skeletal muscle. Tetracycline treatment via stomach tube was effective if given early in the course of the disease. The outbreak was controlled by removing sick frogs, feeding twice per week, changing the water several hours after feeding, and maintaining the frogs where the ambient temperature was 22 degrees C or lower. The pallor of the skin and general malaise were produced experimentally by crowding normal frogs, changing the water infrequently, and increasing ambient temperatures. Mild disease was reproduced experimentally by subcutaneous injection of Aeromonas hydrophila into apparently healthy frogs.
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Ten dogs were fed diets high in phosphorus and low in calcium to induce secondary hyperparathyroidism, with ten dogs fed a standard diet as controls. At the end of the feeding period, all dogs were necropsied. Because of an apparent increase in mineral deposits in the kidneys of hyperparathyroid dogs, the amount and characteristics of these mineral deposits were compared. The dogs in the test groups had larger and more widely disseminated deposits. Five additional dogs were nephrectomized unilaterally, fed the test diet and euthanized at three-month intervals. In these dogs, the amount of renal mineral increased until six months after the start of the test diet, but dit not appreciably change between six and 15 months postdiet. When compared to controls, the test dog kidneys in this second experiment had a greater amount and wider distribution of renal mineralization and tubular dilatation.
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Effects of nutritional secondary hyperparathyroidism and dietary calcium supplementation on bone healing were determined. Groups (n = 4) of 5 mature male dogs each were fed the following diets: group 1, control diet (0.48% Ca, 0.43% P); group 2, test diet (0.12% Ca, 1.14% P): group 3, control diet plus calcium; group 4, test diet plus calcium. The dietary calcium supplementation was calcium gluconate. Lesions were induced in the right tibial cortex by trephinization. Within the time limitations of this study, it was determined that nutritional secondary hyperparathyroidism does not inhibit bone healing and that dietary calcium supplementation does not aid bone healing.
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Dietary restriction (DR) slows the rate of aging in laboratory rodents but the mechanism of action is unknown. DR is known to induce beneficial effects in a variety of tissues and organ systems. DR also maintains high levels of physical activity over the life span. We tested the hypothesis that lifelong physical activity is an important component of the anti-aging action of DR. Male specific pathogen-free Fischer 344 rats were divided into 4 groups at 6 weeks of age: A: fed old libitum; AE: fed ad libitum and in cages with running wheels; B: fed 60% ad libitum; BE: fed 60% ad libitum and in cages with running wheels. Running activity and spontaneous cage activity were measured over 24 hours and over the life span. Metabolic rate was measured indirectly by analysis of air entering and leaving cages. AE rats exhibited low levels of running activity and ran very little beyond 6 months of age. In contrast, BE rats sustained high running levels even after all A and AE rats had died. High levels of wheel running did not decrease spontaneous cage activity. Median life span (50% survival) was in the order A = AE < B < BE. Ten percent survival was in the order A = AE < B = BE. BE rats had greatest median life span and also highest specific metabolic rate. Exercise and DR altered pathology: At death BE rats had a high incidence of cardiomyopathy, whereas A and AE rats had high incidence of chronic nephropathy and pituitary tumors. The data indicate that increased physical activity is probably not an important factor in the action of DR on aging.
Recently, cytoskeletal changes associated with abnormally phosphorylated tau protein were demonstrated in neurons and glial cells of two aged baboons (Papio). The present study examines the effects of age on the development of tau pathology in baboons. Brains of 50 baboons ranging in age from 1 to 30 years were categorized into four age groups: Group I: 1-10 years [n = 9], group II: 11-20 years [n = 13], group III: 21-25 years [n = 17], group IV: 26-30 years [n = 11]). Whole hemisphere sections (100 microm) were examined using phosphorylation-dependent anti-tau antibodies. Cytoskeletal changes were completely absent in animals of group I. In group II four animals (31%) exhibited cytoskeletal changes which were rated as mild or moderate. In group III abnormal tau was found in 12 brains (71%) ranging in severity from mild to severe. Finally, in group IV 10 out of 11 animals (91%) exhibited some degree of tau pathology which was rated as severe in 4 animals (36%). A statistically significant relationship was found between advancing age and progression of tau pathology in baboons. In conclusion, the present findings underline the value of the baboon as a potential nonhuman primate model for age-related tau pathology afflicting the human brain.
Ubiquitin and alpha B-crystallin belong to a class of proteins which are overexpressed in a variety of human neuropathological conditions associated with increased cellular stress. In this study we have examined the brains of aged rhesus monkeys (Macaca mulatta; n = 10, mean age: 29.7 years) using antibodies against the stress proteins ubiquitin, alpha B-crystallin, and heat shock protein 27 (hsp27). Here, we demonstrate an increased expression of ubiquitin, alpha B-crystallin, and hsp27 in spheroid bodies predominantly localized in the globus pallidus and pars reticulata of the substantia nigra. A portion of the pallido-nigral spheroids also contained ferric iron as highlighted by Perls' staining. On the basis of these findings we advance the hypothesis that expression of ubiquitin, alpha B-crystallin, and hsp27 in pallido-nigral spheroids of aged rhesus monkeys represents a stress response possibly related to increased iron-mediated oxidative stress.
Corneal tumours were induced in almost 100% of grey, short-tailed South American opossums (Monodelphis domestica) exposed three times weekly to ultraviolet radiation (UVR) for periods of a year or more. Five tumours, representing the morphological spectrum of UVR-induced corneal tumours (two fibrosarcomas, one malignant fibrous histiocytoma, one putative haemangiosarcoma, and one squamous cell carcinoma overlying a sarcoma), were assayed immunohistochemically for reactivity with antibodies against the intermediate filaments vimentin, smooth muscle actin (alpha isoform), muscle-specific actins (alpha and gamma isoforms), desmin and cytokeratin, and with antibodies against the vascular endothelial marker von Willebrand factor. The squamous cell carcinoma was cytokeratin-positive. Other tumours were cytokeratin-negative and vimentin-positive. Three tumours had scattered individual cells and groups of cells immunoreactive with antibodies against smooth muscle actin and muscle-specific actins; two tumours (a fibrosarcoma and the malignant fibrous histiocytoma) had small numbers of desmin-positive cells. The putative haemangiosarcoma contained two populations of neoplastic cells, von Willebrand factor-positive vascular endothelial cells and smooth muscle actin-positive spindle cells. It was concluded (1) that UVR-induced corneal tumours may be composed of cells derived from resident epithelial cells, immigrant vascular endothelial cells, or fibroblast-like cells of unknown origin, and (2) that such tumours may contain more than one neoplastic cell type.
OBJECTIVE: Microvascular abnormalities have been postulated in the pathogenesis of chagasic cardiomyopathy. The objective of this study was to evaluate the relationship between coronary microcirculation and systolic function impairment in baboons with Chagas disease using myocardial contrast echocardiography (MCE). METHODS: Seventeen seropositive (5 males, 12 females; mean age 20 years) and 13 age- and gender-matched seronegative baboons underwent MCE using intravenous octafluoropropane human albumin microspheres. Color-coding was used to enhance tissue contrast in assessing regional myocardium uniformity and texture. Dipyridamole (0.54 mg/kg) was given to a subset of 4 animals to challenge coronary flow reserve. Systolic indices included left ventricular fractional shortening, velocity of circumferential fiber shortening, and left and right ventricular ejection fractions. RESULTS: Four of the 17 (24%) seropositive primates had decreased fractional shortening (25 +/- 8% vs. 40 +/-5%, p <.005), velocity of circumferential fiber shortening (1.05 +/- 0.36 circ/s vs. 1.84 +/- 0.23 circ/s, p <.0001), and reduced right ventricular ejection fraction (44 +/- 9% vs. 54 +/- 4%, p <.05) compared to other seropositive animals. Seropositive and seronegative groups showed no significant differences on the coronary microcirculation pattern as evaluated by MCE, including the 4 baboons with systolic function impairment. Moreover, coronary flow vasoreactivity resulted in a significant increase in myocardial flow as detected by color-coding masking. CONCLUSIONS: Chagasic heart disease is present in 24% of seropositive baboons spontaneously infected with Trypanosoma cruzi. MCE reveals a discrepancy between coronary microcirculation at rest and alterations in myocardial contractility, suggesting preservation of the microvascular integrity in this unique animal model.