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Biomedical subjects

N J Millichamp

Publications and source records attributed to N J Millichamp.

27 records · Page 2Linked to original sources
PubMed1986

Retinal function in rats and guinea-pigs reared on diets low in essential fatty acids and supplemented with linoleic or linolenic acids.

Rats were reared into a third generation on diets deficient in essential fatty acids supplemented with linoleic acid (18:2 n-6) or linolenic acid (18:3 n-3) with the object of depleting the retina of n-6 or n-3 fatty acids. In the rats fed 18:2 n-6 the percentage by weight of 22:6 n-3 in retinal fatty acids fell from 22.5 to 8.5% in first-generation animals but then remained unchanged in second and third generations. There was no difference in b-wave amplitudes of the electroretinogram between the rats fed 18:2 n-6 and those fed 18:3 n-3. In guinea-pigs fed purified diets low in 18:3 n-3 the percentage by weight of 22:6 n-3 in retinas fell from 8 to less than 0.5% by the third generation. However, there were no statistical differences in the b-wave amplitudes between these animals and those reared on a commercial diet. It is concluded that if n-3 fatty acids are involved in retinal function their role is too subtle to be detected by standard electroretinographic techniques.

Aging↗
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↗
PubMedDate not supplied

Early diagnosis of familial nephropathy in English cocker spaniels.

Two litters of English cocker spaniels (ECSs) produced by familial nephropathy (FN) carriers were evaluated to characterize the early features of this disease. Three puppies developed FN. Proteinuria, which began when these puppies were five-to-eight months old, was the first abnormality detected. Proteinuria persisted while each puppy's growth rate slowed, and renal function gradually deteriorated. The interval from onset of proteinuria to development of azotemia was two-to-nine months. Characteristic glomerular capillary basement membrane (GCBM) lesions were seen with transmission electron microscopy (TEM) of renal biopsy specimens obtained during this interval. Ultrastructural GCBM lesions progressed substantially during the interval from biopsy to necropsy. However, routine light microscopic findings did not allow definitive diagnosis of FN in either biopsy or necropsy specimens. Detection of FN can be accomplished by screening at-risk ECSs for proteinuria. Renal biopsies are required to confirm the diagnosis in dogs for which proteinuria cannot be explained otherwise. Percutaneous needle biopsy specimens sufficient for TEM must be used to examine the GCBM to make a definitive diagnosis.

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