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Biomedical subjects

N T Gorman

Publications and source records attributed to N T Gorman.

At least 19 recordsLinked to original sources
PubMed1989

Natural cytotoxicity in the dog: description of two new allogeneic tumour targets.

Three canine tumour cells were studied for their susceptibility to cytotoxicity by allogeneic canine natural killer (NK) cells: a lymphoma line, 3132 of B cell origin, and two adherent cell lines emanating from the same non-lymphoid tumour isolate, one (A72F) with a fibroblast morphology and one (A72E) with an epithelioid appearance. Both 3132 and A72E have preliminary evidence of retrovirus infection. Unstimulated canine peripheral blood mononuclear cells, used as the source of NK cells, were able to mediate significant lysis of 3132 and A72F cells at effector cell:target cell ratios of under 50:1, although an 18 h incubation was necessary for maximum cytotoxicity. NK activity against the 3132 tumour cells proved to be variable both within a group of dogs as well as on different occasions utilising the same individual donor. The epithelioid form of the A72 tumour cell line, A72E, had gained a marked resistance to NK lysis, although like the 3132 cells, there is preliminary evidence of persistent retrovirus infection in this cell line. Interestingly the A72F cells were as successful as homologous 3132 cells in the cold target inhibition of labelled 3132 cytotoxicity, while A72E did not. This latter result could indicate that not only do A72F and 3132 share NK determinants recognised by the same NK receptor, but the A72E line has lost this important recognition determinant.

Animals↗
PubMed1987

Myeloproliferative disease in the dog and cat: clinical presentations, diagnosis and treatment.

The myeloproliferative diseases may present with a variety of clinical signs including regenerative or non-regenerative anaemias, bleeding diatheses, septicaemia or fever of unknown origin. These signs will raise suspicions of myeloproliferative disease but such disease may also be an incidental finding on routine haematological examination. In either case a bone marrow biopsy will be required for confirmation. Investigation for other causes of anaemia, haemostatic dysfunction or other causes of white cell abnormalities is important in animals where the peripheral blood and bone marrow findings are equivocal or atypical of myeloproliferative disease. Treatment of acute myeloproliferative diseases is presently impractical in veterinary medicine. Therapy of the chronic myeloproliferative diseases depends upon the suppression of the proliferation of the affected clones together with attention to the secondary effects of the disease and to the adverse effects of therapy.

Animals↗
PubMed1987

Von Willebrand's disease in dogs in the United Kingdom.

An assay for the measurement of von Willebrand factor antigen has been established. In a period of 18 months, 13 dogs have been identified as suffering from von Willebrand's disease. The affected animals had levels of von Willebrand factor antigen which ranged from undetectable to 43 per cent of normal. Factor VIII levels were also reduced. Haemorrhagic episodes were usually associated with trauma or surgery, and often required transfusion with fresh blood or plasma to arrest haemorrhage.

Animals↗
PubMed1987

Myeloproliferative disease in the dog and cat: definition, aetiology and classification.

The term myeloproliferative disease may be applied to all the non-lymphoid dysplastic and neoplastic conditions arising from the haematopoietic stem cell or its progeny. Thus the chronic and acute myeloid leukaemias, thrombocythaemia, megakaryocytic myelosis, myelofibrosis, the myelodysplastic syndromes and some cases of aplastic anaemia may be viewed as variants of a single disease process. This view is useful in explaining the common occurrence of mixed forms of disease or interconversions between the myeloproliferative diseases. This variability is a consequence of the development of all the haematopoietic lineages from a single class of haematopoietic stem cell by progressive differentiation. The aetiology of the myeloproliferative diseases in the domestic animals is uncertain but feline leukaemia virus infection has been implicated in the cat. These conditions may be classified as aplastic anaemia, as preleukaemic dysplastic conditions with variable cytopenias and morphological abnormalities of blood cells, as smouldering leukaemias, or as leukaemias with a frankly leukaemic blood or bone marrow.

Animals↗
PubMed1986

Chemotherapy of synovial cell sarcoma in a dog.

A synovial cell sarcoma of the tarsus in a 6-year-old dog was treated with doxorubicin HCl and cyclophosphamide. The tumor regressed after treatment. There was no recurrence 3 years after initiation of treatment. Previously, synovial cell sarcoma has not been reported to be responsive to chemotherapeutic agents, and the treatment of choice has been amputation.

Animals↗
PubMed1985

Sulfadiazine-induced allergy in six Doberman pinschers.

Treatment with sulfadiazine-trimethoprim caused serious, but reversible, allergic drug reactions in 6 Doberman Pinschers 10 to 21 days after the first drug exposure and/or within 1 hour to 10 days after reexposure. Nonseptic polyarthritis was found in all dogs. Glomerulonephropathy, focal retinitis, polymyositis, skin rash, fever, anemia, leukopenia, and thrombocytopenia were found in some dogs. These clinical abnormalities were typical of an immune-mediated vasculitis and mimicked other immune-mediated disorders. In a drug challenge study, 1 dog was given sulfadiazine and trimethoprim separately. Administration of trimethoprim alone did not result in any abnormalities; however, exposure to sulfadiazine caused recurrence of the polyarthritis, glomerulonephropathy, and focal retinitis within 5 days, suggesting that sulfadiazine likely was the offending agent in all cases. In addition, during the sulfadiazine reexposure, marked complement activation was documented at the time clinical signs were apparent, supporting the suggestion that sulfadiazine caused an immune complex disease (type-III hypersensitivity reaction). Since all dogs were of the same breed, a genetic predisposition of some Doberman Pinschers to react adversely to sulfadiazine was suspected.

Animals↗
PubMed1984

Uterine defense mechanisms in the mare: Serum opsonins affecting phagocytosis of Streptococcus zooepidemicus by equine neutrophils.

The addition of serum to uterine secretions was shown to opsonize Streptococcus zooepidemicus and significantly enhance bacterial phagocytosis by equine neutrophils. Treatment of serum by heat inactivation at 56 degrees C, EDTA treatment, and C3 consumption reduced phagocytosis and therefore demonstrated that the process was complement-dependent. The amount of C3 present in uterine secretions was measured in a series of 14 mares infected with Streptococcus zooepidemicus . Ten of the 14 mares had detectable amounts of C3; however, the C3 had been cleaved and rendered nonfunctional. The importance of these findings in relationship to chronic uterine infections in the mare is discussed.

Journal Article↗
PubMed1984

Activation of the alternative complement pathway by lymphoblasts isolated from canine thymic lymphomas.

The ability of lymphocytes isolated from cases of canine thymic lymphomas to activate the alternative complement pathway has been studied. In a series of 14 thymic lymphomas 5 were found to activate the alternative pathway. This ability to activate was not abrograted by trypsinisation of the cells. It was found that normal canine thymic lymphocytes did not activate the alternative pathway.

Animals↗