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Biomedical subjects

K C Barnett

Publications and source records attributed to K C Barnett.

At least 19 recordsLinked to original sources
PubMed1999

An immunohistochemical study of an autosomal dominant feline rod/cone dysplasia (Rdy cats).

An autosomal dominant, early onset feline model of rod/cone dysplasia has been described. The clinical features, light and electron microscopy, and the electrophysiology were documented. We have now examined in more detail the histopathological and immunohistochemical changes during the early phase of the disease using antibodies against opsin, synaptophysin, glial fibrillary acidic protein (GFAP) and an epithelial marker (MNF118). We have also demonstrated programmed cell death by a modified TUNEL (Terminal deoxynucleotidyl transferase, Uridine triphosphate, Nick End Labelling) technique. In the Rdy cats, there was significant photoreceptor degeneration between 5 and 17 weeks of age. The TUNEL-labeled cell and pyknotic cell counts in the outer nuclear layer peaked at around 9 weeks of age. Accumulation of opsin in the entire outer nuclear layer of the retina was noted with opsin-immunolabeled rod neurite sprouting. There was a reduction in synaptophysin immunoreactivity in the outer plexiform layer. The Muller cells were activated and expressed GFAP. No significant change of immunolabeling of MNF118 was found. These findings closely parallel those seen in human RP.

Animals↗
PubMed1999

Repeated injections of a ciliary neurotrophic factor analogue leading to long-term photoreceptor survival in hereditary retinal degeneration.

PURPOSE: To determine whether ciliary neurotrophic factor (CNTF) or brain-derived neurotrophic factor (BDNF) treatment leads to long-term photoreceptor survival in hereditary retinal degeneration. METHODS: An autosomal dominant feline model of rod-cone dystrophy was used throughout the study with two normal animals. In the first experiment, intravitreal injections of a human CNTF analogue (Axokine; Regeneron Pharmaceuticals, Tarrytown, NY) were administered to one eye of each animal (n = 10) beginning on postnatal day 10 and were repeated every 4 weeks. Clinical and histopathologic examinations were performed at 5.5, 9.5, and 13.5 weeks. In the second experiment, animals (n = 17) were randomly assigned to receive intravitreal injections of either Axokine (at half the initial dose), human BDNF, or the vehicle for Axokine to one eye at 5.5 weeks. The same therapy was repeated every 4 weeks in each group. Clinical and histopathologic examinations were performed at 9.5, 13.5, and 17.5 weeks. Photoreceptor survival was assessed by cell counting. Apoptotic cells were identified by morphology and a modified TdT-dUTP terminal nick-end labeling (TUNEL) technique. In the third experiment, two normal animals were treated with Axokine as in the first experiment. Glial fibrillary acidic protein ((GFAP) immunohistochemistry was performed to assess glial cell reaction. RESULTS: In the first two experiments, Axokine significantly prolonged photoreceptor survival (P < 0.01) and reduced the presence of apoptotic cells (P < 0.05) and TUNEL-positive cells (P < 0.05). In the second experiment, results in the the BDNF- and sham-injected eyes were not significantly different from those in the untreated eyes. Minimal posterior subcapsular cataract and mild retinal folds were found in all Axokine-treated eyes in both dystrophic and normal animals. These complications were milder in the second experiment when injections were started later and at a reduced dose. GFAP immunolabeling was also increased in all Axokine-treated eyes. CONCLUSIONS: Axokine, but not BDNF, delays photoreceptor loss in this hereditary retinal degeneration. Repeated injections maintain the protective effect.

Animals↗
PubMed1998

Lacrimal pseudotumour in a young bull terrier.

An inflammatory mass arising from the lower lacrimal canaliculus of unknown cause is reported in a dog. A 10-month-old Staffordshire bull terrier was presented with a history of epiphora and a red mass protruding from the left lower lacrimal punctum. The tissue was removed and histopathological examination of the lesion revealed a mass of highly vascularised granulation tissue with areas of epithelial ulceration and multiple stromal haemorrhages. Fibrosis and collagen deposition were evident as was a cellular infiltrate composed primarily of neutrophils and plasma cells. Regrowth necessitated further attempts at complete excision before a permanent cure was achieved.

Animals↗
PubMed1996

Canine conjunctival papilloma: a review of five cases.

Five cases of unilateral bulbar conjunctival papillomata are reported in five different breeds of dog. The dogs ranged from six to nine years of age, four were female and one was male. In all but one case the mass was an incidental finding. The morphology and histopathology are described. The authors have been unable to find any details or descriptions of this type of papilloma in the veterinary literature.

Animals↗
PubMed1995

Treatment of keratoconjunctivitis sicca in dogs with cyclosporine ophthalmic ointment: a European clinical field trial.

The results are reported of a six-week clinical trial of the efficacy of 0.2 per cent cyclosporine ophthalmic ointment for the treatment of chronic idiopathic keratoconjunctivitis sicca in dogs in the United Kingdom, Germany and France. The 87 dogs were referral cases with a history of chronic unresponsive keratoconjunctivitis sicca of which the aetiology was unknown, and they had to meet stringent criteria before being included in the trial. The clinical response to the therapy was monitored after seven, 21 and 42 days and the results for the right and left eyes were analysed separately. There was a statistically significant increase in lacrimal secretion throughout the study, with most of the increase occurring during the first week of treatment. The percentage of eyes with improved lacrimal secretion was higher in the dogs with initial Schirmer tear test values > or = 2 mm/min than in those with initial values of 0 or 1 mm/min. The observed steady improvement in conjunctival health was not always correlated with an improvement in lacrimal secretion. The incidence of blepharospasm, other signs of discomfort and corneal oedema decreased significantly during the study. No improvement in corneal vascularisation or pigmentation was observed during the six-week trial. Overall, 76 per cent of the left eyes and 87 per cent of the right eyes were considered to have improved at the end of the treatment period. No serious adverse reactions were observed and only mild irritation was noticed by the owners immediately after the application of the ointment. This irritation resulted in the recording of an adverse reaction at the scheduled observations in only three cases.

Animals↗
PubMed1995

Investigation of the role of opsin gene polymorphism in generalized progressive retinal atrophies in dogs.

The generalized progressive retinal atrophies (gPRAs) form a group of retinal degenerations of pedigree dogs and cats, which have a variety of genetic origins (mostly unknown). We have examined the opsin gene for polymorphisms in several breeds of pedigree dog suffering from distinct forms of gPRA, by methods including single-strand conformation polymorphism analysis, microsatellite analysis and direct sequencing. The breeds examined included the Tibetan terrier, the miniature schnauzer, the Irish setter, the miniature poodle, the Labrador retriever and the English cocker spaniel, as well as individuals from breeds in which PRA has not been described and of mixed breed. Individuals from each of the named breeds suffering from PRA were compared with clinically normal dogs. Two polymorphisms were found. One, segregating within the Tibetan terrier population, but not seen in other breeds, was a synonymous transition at nucleotide position 780 in exon 3. Inheritance of this polymorphism suggests that opsin is unlikely to contain mutations causative of gPRA in this breed. The other polymorphism occurred between all miniature schnauzers examined and dogs of other breeds. It consisted of a single base insertion in intron 2. No polymorphisms in the opsin sequence were detected in any other breed. DNA sequencing allowed rigorous exclusion of mutations in opsin as a cause of gPRA in miniature poodles, English cocker spaniels or Labrador retrievers.

Animals↗
PubMed1995

Incidence of the gene mutation causal for rod-cone dysplasia type 1 in Irish setters in the UK.

A survey to establish the UK prevalence of the gene mutation causing the rod-cone dysplasia type one (rcd1) form of generalised progressive retinal atrophy (gPRA) in Irish setters was carried out. The dogs were selected by members of two Irish setter breed societies to provide examples from most of the main breeding lines in the UK. A total of 210 Irish setters were tested and one bitch was found to be a carrier of the rcd1 mutation. These results show that although a confirmed case of rcd1 has not been reported in Irish setters in the UK for over a decade the gene is still present in the gene pool.

Animals↗
PubMed1989

Suspected Aleutian disease in a wild otter (Lutra lutra).

Clinical and pathological observations of a naturally occurring disease in a British wild otter (Lutra lutra) are reported. Systemic lymphoreticular proliferative changes with plasmacytosis, glomerulonephritis, arteritis and biliary hyperplasia closely resembled the pathological changes in Aleutian disease of mink (Mustela vison). Feral mink provided a possible source of infection.

Adrenal Glands↗
PubMed1988

Progressive retinal atrophy in Tibetan terriers.

Progressive retinal atrophy was studied in 17 Tibetan Terriers. The diagnosis was made on the basis of clinical signs of the disease, retinal histopathologic findings, or both. Affected dogs were the progeny of matings of affected or ophthalmoscopically normal dogs. Results of the mating supported a simple autosomal recessive mode of inheritance. The disease initially could be diagnosed by findings of night blindness and ophthalmoscopic signs of tapetal hyperreflectivity in affected dogs that were approximately 1 year old. Electroretinograms recorded from affected dogs, compared with those of clinically normal dogs of the same age, did not reveal appreciable abnormalities until affected dogs were 10 months old, at which time a reduction in the amplitude of the b wave was seen in response to a Ganzfeld white-light stimulus. The peak times of the response were unaffected. With progression of the disease, the electroretinographic b-wave amplitude was gradually reduced, and the electroretinographic response was extinguished in affected dogs by the time they were 30 months old. Early in the disease, rod and cone functions were affected equally, with more rapid loss of rod function developing only later in the disease. Fluorescein angiography of affected dogs did not reveal abnormalities earlier than could be detected by ophthalmoscopy. Despite the electroretinographic findings, histopathologic findings included patchy disorientation and disorganization of the outer segments of rods and cones in affected dogs as young as 9 weeks. With progression of the disease, rods were lost at a faster rate than cones, and atrophy of the inner retinal layer was observed.

Animals↗