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Biomedical subjects

Eric S Storey

Publications and source records attributed to Eric S Storey.

6 recordsLinked to original sources
PubMed2004

Lacrimostimulants and lacrimomimetics.

A thorough understanding of tear film physiology and the clinical manifestations of tear film abnormalities enables the veterinarian to diagnose and treat quantitative (decreased aqueous layer) and qualitative (decreased mucin or lipid layers) tear film abnormalities accurately and to monitor the responses to lacrimostimulatory and lacrimomimetic therapy. This article reviews the embryology,anatomy, and physiology of the lacrimal glands; glands of the nictitating membrane; goblet cells; and tarsal glands as well as the pathophysiology of tear film deficiencies. We also review lacrimo-stimulants, including cyclosporine, tacrolimus, sirolimus, pilocar-pine, and lacrimomimetics (tear film replacements).

Adjuvants, Immunologic↗
PubMed2002

Survival of equine herpesvirus-4, feline herpesvirus-1, and feline calicivirus in multidose ophthalmic solutions.

OBJECTIVE: To determine survival over time of infectious equine herpesvirus-4, feline herpesvirus-1, and feline calicivirus in three commercially available and commonly used ophthalmic solutions (eyewash, fluorescein, and proparacaine HCl). SAMPLE POPULATION: Viruses used in this study were originally isolated from eyes of animals referred to the University of Illinois. Equine herpesvirus-4 was propagated in MDBK cells and feline herpesvirus-1 and feline calicivirus in CRFK cells. PROCEDURE: After separately inoculating a designated solution with a specific titer of an individual virus, solutions were incubated per manufacturer's recommendations, either at 4 degrees C or 25 degrees C. Virus titers within solutions were subsequently measured at 1, 8, and 24 h and 3, 5 and 7 days post inoculation using either plaque or TCID50 assays. RESULTS: Equine herpesvirus-4, feline herpesvirus-1, and feline calicivirus were present in eyewash for 7 days, 5 days, and 7 days, respectively. Eyewash did not decrease survival time of any virus when compared to controls. Equine herpesvirus-4 and feline herpesvirus-1, both enveloped viruses, were not recovered at any time > or = 1 h post inoculation in fluorescein. Feline calicivirus, a nonenveloped virus, was present in fluorescein for 7 days. Equine herpesvirus-4 and feline herpesvirus-1 did not remain infectious in proparacaine at any time > or = 1 h post inoculation, but feline calicivirus was recovered at up to 24 h post inoculation. CONCLUSIONS: Equine herpesvirus-4, feline herpesvirus-1, and feline calicivirus may be readily transmissible via the eyewash solution used in this study. Risk of iatrogenic transmission of the three viruses used in this study was significantly reduced in both fluorescein and proparacaine solutions. Feline calicivirus, the only nonenveloped virus evaluated, remained viable longer in both fluorescein and proparacaine solutions.

Animals↗
PubMedDate not supplied

Inherited retinal dysplasia and persistent hyperplastic primary vitreous in Miniature Schnauzer dogs.

The objectives of this study were to define the clinical syndrome of retinal dysplasia and persistent primary vitreous in Miniature Schnauzer dogs and determine the etiology. We examined 106 Miniature Schnauzers using a biomicroscope and indirect ophthalmoscope. The anterior and posterior segments of affected dogs were photographed. Four enucleated eyes were examined using routine light microscopy and scanning electron microscopy. A pedigree was constructed and related dogs were test-bred to define the mode of inheritance of this syndrome. Congenital retinal dysplasia was confirmed in 24 of 106 related Miniature Schnauzer dogs. Physical and postmortem examinations revealed that congenital abnormalities were limited to the eyes. Biomicroscopic, indirect ophthalmoscopic, and neuro-ophthalmic examinations confirmed that some of these dogs were blind secondary to bilateral retinal dysplasia and detachment (nonattachment) (n = 13), and the remainder had generalized retinal dysplasia (n = 11). Fifteen of these dogs were also diagnosed with unilateral (n = 9) or bilateral (n = 6) persistent hyperplastic primary vitreous. Nutritional, infectious, or toxic etiologies were not evident on physical, postmortem, light microscopic, or transmitting and scanning electron microscopic examination of four affected Miniature Schnauzers. We examined the pedigree and determined that an autosomal recessive mode of inheritance was most likely. Three test-bred litters including those from affected parents, carrier and affected parents, and carrier parents confirmed this mode of inheritance. This study confirms that retinal dysplasia and persistent hyperplastic primary vitreous is a congenital abnormality that is inherited as an autosomal recessive condition in Miniature Schnauzers.

Animals↗
PubMedDate not supplied

Multifocal chorioretinal lesions in Borzoi dogs.

OBJECTIVES: To identify the prevalence of Borzoi chorioretinopathy in western Canada, characterize lesions with fluorescein angiography, determine if lesions were progressive, clarify the association of progressive retinal atrophy and investigate the etiology. MATERIALS AND METHODS: Serial ophthalmic examination, fundus photography, electroretinography, and fluorescein angiography were used to evaluate Borzoi dogs with lesions of Borzoi chorioretinopathy. Pedigree analysis and test breeding of two affected dogs were completed to determine the heritability of Borzoi chorioretinopathy. RESULTS: One hundred three Borzoi dogs were examined between 1998 and 2003. Focal, peripheral, tapetal, hyper-reflective and pigmented areas consistent with focal retinal degeneration and RPE pigmentation were identified in 12 dogs between 7 months and 7 years of age. Seven males and five female dogs were affected. Ophthalmoscopy and fundus photography over 5 years revealed individual lesions that did not progress or coalesce in 12 affected dogs. Electroretinography of affected and normal Borzoi dogs confirmed that retinal function was similar in normal and affected dogs up to 7 years of age. Fluorescein angiography was performed in three affected dogs and confirmed intact blood-ocular barriers, focal retinal pigment epithelium hypertrophy, and focal absence of choroiocapillaris corresponding to chronic, focal lesions. Pedigree analysis precluded simple dominant, X-linked dominant, or X-linked recessive inheritance. One male dog from the test-bred litter developed bilateral lesions at 14 months of age. Simple recessive, polygenetic, and acquired etiologies of these lesions cannot be ruled out at this time. CONCLUSIONS: Borzoi chorioretinopathy is an acquired condition that initially manifests as focal retinal edema and loss of choriocapillaris and tapetum. With time the retina degenerates becoming hyper-reflective and with RPE hyper-pigmentation and clumping within the borders of the tapetal lesions. Choriocapillaris remains hypofluorescent on fluorescein angiography. Progressive retinal atrophy was excluded as an etiology of multifocal chorioretinopathy in Borzois dogs. This condition is not inherited by simple autosomal dominant or sex-linked modes of inheritance.

Abnormalities, Multiple↗