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Biomedical subjects

T G Terrell

Publications and source records attributed to T G Terrell.

30 records · Page 2Linked to original sources
PubMed1977

Polyclonal gammopathies associated with chronic diseases in nonhuman primates.

Serum samples collected from clinically healthy rhesus macaques (Macaca mulatta) were compared with serums from animals diagnosed as having malignant lymphoma, atypical tuberculosis, progressive multifocal leukoencephalopathy, or more than 1 of these. Electrophoretic analyses of serum proteins (in grams per deciliter) indicated that mean values in a clinically normal group were as follows--total protein, 8.30; albumin, 4.07; alpha-globulin, 0.85; beta-globulin, 2.23; and gamma-globulin, 1.15. In macaques with malignant lymphoma, mean values were--total protein, 7.60; albumin, 2.72; alpha-globulin, 0.91; beta-globulin, 1.71; and gamma-globulin, 2.23. In macaques with atypical tuberculosis, these values were 8.47, 2.92, 0.84, 2.18, and 2.52, respectively, and those with progressive multifocal leukoencephalopathy, 9.06, 4.01, 6.71, 2.42, and 1.93. Where multiple serum samples were available from 1 macaque for analysis, gamma-globulin values were increased before clinical disease was apparent. Evaluation of serums from macaques may be used as a means of detecting preclinical lymphoproliferative disease.

Animals↗
PubMed1977

Lymphocyte subpopulations in spontaneous disease of rhesus macaques.

The immunologic status of rhesus macaques (Macaca mulatta) with naturally occurring disease was evaluated by determining the percentages of B and T lymphocytes and mitogen responsiveness of lymphocytes in peripheral blood and lymph nodes. The B lymphocytes were identified by the presence of cell surface immunoglobulin and receptors for complement. The T lymphocytes were identified by their ability to form spontaneous rosettes with sheep red blood cells. Rhesus macaques with idiopathic or primary amyloidosis had normal lymphocyte characteristics. Peripheral blood lymphocytes from rhesus macaques with atypical tuberculosis had decreased percentages of spontaneous rosette-forming cells and depressed responses to concanavalin A, and those with chronic diarrhea or chronic arthritis were also found to have abnormal peripheral blood lymphocyte characteristics. The percentage of B and T lymphocytes in normal lymph nodes was variable, making simultaneous histologic examination necessary for evaluation of diseased animals.

Amyloidosis↗
PubMed1976

Idiopathic hypoparathyroidism in a dog.

Idiopathic hypoparathyroidism in a 3-year-old dog was manifested clinically as periodic episodes of depression, vomiting, and tetanic convulsions. Hypocalcemia and hyperphosphatemia were detected late in the course of the illness, but the dog died before corrective measures could be instituted. The pathologic features were similar to those reported in dogs in which hypoparathyroidism was induced by injection of homologous parathyroid tissue, thus suggesting an auto-immune pathogenesis.

Animals↗
PubMed1975

Fibrous osteodystrophy in an opossum.

A free living opossum (Didelphis marsupialis) was found to have severe fibrous osteodystrophy of the maxilla and mandibles. No significant lesions were found in the kidneys, ruling out an etiology of renal secondary hyperparathyroidism. An etiology of primary phperthyroidism or nutritional secondary hyperparathyroidism is suggested.

Animals↗
PubMed1973

Pathology of Bolivian hemorrhagic fever in the rhesus monkey.

Gross and microscopic lesions associated with Bolivan hemorrhagic fever virus infection in the rhesus monkey were studied in 10 animals which died following inoculation. Gross lesions included skin rash, lymphadenopathy, splenomegaly, meningeal edema, hydropericardium and enlarged friable livers. Hemorrhagic manifestations of the infection were not consistently observed, but hemorrhages were present in the skin, heart, brain and nares in some monkeys. Histopathologic lesions were fairly consistent. Hepatic necrosis with the presence of acidophilic hyaline bodies, necrotizing enteritis, epithelial necrosis and adrenal cortical necrosis were present in all monkeys. Those monkeys which died after the seventeenth day of infection had nonsupurative meningoencephalitis; lymphoid necrosis was present in 3 monkeys that died after day 18. Other microscopic lesions included myocardial degeneration, lymphoid and reticuloendothelial cell hyperplasia and lymphoid depletion. Most of the histopathologic lesions described in human autopsy material were reproduced; however, the necrosis in the skin and oral mucosa, mucosa of the gastrointestinal tract and the adrenal cortex have not been described in man. Despite these apparent discrepancies the results of this investigation indicate that the rhesus monkey is a good experimental model for the study of Bolivian hemorrhagic fever infection.

Adrenal Glands↗
PubMedDate not supplied

Issues with biotechnology products in toxicologic pathology.

The emergence of the biotechnology industry and introduction of drugs derived from recombinant DNA technology has generated many new issues in approaches to preclinical safety evaluation and extrapolation of results to risk assessment in humans. Products or therapeutic approaches for consideration include hormones, growth factors, cytokines, monoclonal antibodies, vaccines, blood products, antisense, and gene therapy. In many instances the application of standard safety tests conventionally used for small molecules are of limited value or are inappropriate. Studies should be designed to answer specific scientific questions rather than simply to fulfill regulatory requirements. Special consideration must be given to study design and species selection in terms of biological activity and species specificity, implications of immunological responses in the animal studies, and effects of systemic administration of molecules at clinically relevant doses. A full understanding of the clinical relevance of toxicological and pathologic findings associated with administration of these molecules to laboratory animals requires definition of the pathogenic mechanism of lesion induction.

Animals↗