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- Klassen, Henry, et al.
(författare)
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Neural precursors isolated from the developing cat brain show retinal integration following transplantation to the retina of the dystrophic cat
- 2007
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Ingår i: Veterinary Ophthalmology. - : Wiley. - 1463-5216 .- 1463-5224. ; 10:4, s. 245-253
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Tidskriftsartikel (refereegranskat)abstract
- The cat has served as an important nonrodent research model for neurophysiology and retinal degenerative disease processes, yet very little is known about feline neural precursor cells. To culture these cells and evaluate marker expression, brains were dissected from 45-day-old fetuses, enzymatically dissociated, and grown in the presence of EGF, bFGF and PDGF. Expanded cells widely expressed nestin, Sox2, Ki-67, fusin (CXCR4) and vimentin, while subpopulations expressed A2B5, GFAP, or beta-III tubulin. Precursors prelabeled with BrdU and/or transduced with a recombinant lentivirus that expresses GFP were transplanted subretinally in five dystrophic Abyssinian cats. Two to 4 weeks following surgery, histology showed survival of grafted cells in three of the animals. Labeled cells were found in the neuroretina and RPE layer, as well as in the vitreous and the vicinity of Bruch's membrane. There was no evidence of an immunologic response in any of the eyes. Neural precursor cells can therefore be cultured from the developing cat brain and survive as allografts for up to 4 weeks without immune suppression. The feasibility of deriving and transplanting feline neural precursor cells, combined with the availability of the dystrophic Abyssinian cat, provide a new feline model system for the study of retinal repair.
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| 2. |
- Hertil, Eva, et al.
(författare)
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A slowly progressive retinopathy in the Shetland Sheepdog
- 2011
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Ingår i: Veterinary Ophthalmology. - : Wiley. - 1463-5216 .- 1463-5224. ; 14, s. 227-238
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Tidskriftsartikel (refereegranskat)abstract
- Conclusion Slowly progressive retinopathy is a generalized rod-cone degeneration that on ophthalmoscopy looks similar to early stages of progressive retinal atrophy. The ophthalmoscopic findings are slowly progressive without tapetal hyper-reflectivity. Visual impairment is not obvious and the electroretinogram is more subtly altered than in progressive retinal atrophy. The etiology remains unclear. SPR is not caused by the prcd-mutation.
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| 3. |
- Hertil, Eva, et al.
(författare)
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Retinal degeneration in nine Swedish Jämthund dogs
- 2010
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Ingår i: Veterinary Ophthalmology. - : Wiley. - 1463-5216 .- 1463-5224. ; 13, s. 110-116
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Tidskriftsartikel (refereegranskat)abstract
- The Jamthund is the fourth most common breed in Sweden with approximately 1600 pups registered each year. Although it has been known that some adult dogs go blind, so they cannot hunt, the Jamthund dog has historically not been screened for hereditary eye diseases. This report describes nine Swedish Jamthund dogs with retinal degeneration. These dogs represent all Jamthund dogs diagnosed with progressive retinal atrophy (PRA) by the Swedish Eye Panel and registered with the Swedish Kennel Club from January 1998 to September 2008. The dogs were examined with indirect opthalmoscopy and slitlamp biomicroscopy. Additionally, electroretinograms (ERGs) following ECVO guidelines were performed in two dogs (one affected and one normal) and the eyes from three affected dogs were examined by light-microscopy postmortem. Typical findings were bilateral symmetric generalized retinal degeneration with tapetal hyper-reflectivity, attenuation of blood vessels and pigment clumping in the nontapetal fundus. These retinal findings progressed with time in two dogs after re-examination. Visual impairment, especially under dim light conditions, was observed in the affected dogs. ERG from one affected dog showed profoundly reduced rod responses, whereas cone responses were better preserved. Microscopic changes in the eyes from three dogs were characterized by a severe diffuse predominantly outer retinal degeneration and atrophy. Re-sequencing of the prcd-gene for eight of the nine investigated dogs revealed that none of the individuals carried disease allele that has been associated with prcd-PRA in other breeds. In conclusion, ophthalmoscopic, electroretinographic, and light-microscopic alterations observed in nine Jamthund dogs were compatible with PRA. The prcd mutation was excluded as a cause of this retinopathy.
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| 4. |
- Karlsson, Anna-Carin, et al.
(författare)
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The Dominant white mutation in the PMEL17 gene does not cause visual impairment in chickens
- 2009
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Ingår i: Veterinary Ophthalmology. - : Wiley. - 1463-5216 .- 1463-5224. ; 12:5, s. 292-298
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To examine whether the Dominant white mutation (causing a hypopigmented phenotype in chicken) affects the visual ability and gives rise to ocular abnormalities in chickens (Gallus gallus). PROCEDURE: Chickens homozygous for either the Dominant white mutation or the wild-type alleles were tested in a visual contrast behavioral test and subjected to histological and ophthalmologic examination. RESULTS: There were no differences between the genotypes in the visual contrast behavioral test, and there were no abnormal structures among the Dominant white chickens in the ophthalmic examination. The histological sections from the Dominant white chickens did not differ from the wild-type chicken in structure, photoreceptor density, or RPE pigmentation. CONCLUSIONS: The results indicate that the Dominant white mutation in PMEL17 does not seem to affect the visual ability or eye structures in chickens.
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| 5. |
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| 6. |
- Narfström, Kristina, et al.
(författare)
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Neuronal ceroid lipofuscinosis : Clinical and morphologic findings in nine affected Polish Owczarek Nizinny (PON) dogs
- 2007
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Ingår i: Veterinary Ophthalmology. - : Wiley. - 1463-5216 .- 1463-5224. ; 10:2, s. 111-120
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Tidskriftsartikel (refereegranskat)abstract
- Objective: The aim of this study was to characterize the clinical and morphologic features of neuronal ceroid lipofuscinosis (NCL) in the Polish Owczarek Nizinny (PON) breed of dog. Animals: Nine Swedish PON dogs of both sexes were included in the study. Procedure: All dogs underwent a detailed clinical evaluation, with emphasis on ophthalmic exams. Histopathology and electron microscopy were performed on the eyes, brain and various internal organs. Immunohistochemical staining for detection of sphingolipid activator proteins (SAPs) and mitochondrial ATP synthase (SCMAS) was performed on the eyes and brain. Results: The dogs showed behavioral abnormalities, motor disturbances and visual impairment or blindness. Pupillary responses were abnormal while fundus changes varied from normal to severe retinal atrophy. Electroretinography (ERG) showed variable changes, from slight alterations in the process of dark adaptation to severely reduced or nonrecordable ERG a- and b-wave amplitudes. Histopathology revealed intracytoplasmic storage bodies within neurons of the brain and in retinal cells, especially the retinal pigment epithelium (RPE). Round to oval granular type of inclusion bodies, known as granular osmiophilic dense deposits (GRODS), were found in neuronal cells in the brain and in the retina. Immunohistochemistry identified the storage material in the brain and retina as consisting of SAPs. Conclusion: The presently described NCL disease in PON dogs shows similarities to previously recorded cases in the Miniature Schnauzer. The closest human equivalent to this disease is infantile NCL (CLN1), in which the major stored proteins are SAPs and the ultrastructure of the inclusion bodies of neuronal cells is granular. © 2007 American College of Veterinary Ophthalmologists.
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