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Symptoms include sudden permanent blindness, but may occur more slowly over several days, weeks or months, [3] dilated pupils. Pupillary light reflexes are usually reduced but present; the slow phase mediated by melanopsin in retinal ganglion cells is retained.
Dogs are ten times more likely to be infected than humans. The disease in dogs can affect the eyes, brain, lungs, skin, or bones. [15] Histoplasmosis* is a fungal disease caused by Histoplasma capsulatum that affects both dogs and humans. The disease in dogs usually affects the lungs and small intestine. [16]
Collie eye anomaly (CEA) is a congenital, inherited, bilateral eye disease of dogs, which affects the retina, choroid, and sclera. It can be a mild disease or cause blindness. It can be a mild disease or cause blindness.
A medical triad is a group of three signs or symptoms, the result of injury to three organs, which characterise a specific medical condition. The appearance of all three signs conjoined together in another patient, points to that the patient has the same medical condition, or diagnosis.
Cherry eye is a disorder of the nictitating membrane (NM), also called the third eyelid, present in the eyes of dogs and cats. [1] Cherry eye is most often seen in young dogs under the age of two. [2] Common misnomers include adenitis, hyperplasia, adenoma of the gland of the third eyelid; however, cherry eye is not caused by hyperplasia ...
Progressive retinal atrophy (PRA) is a group of genetic diseases seen in certain breeds of dogs and, more rarely, cats. Similar to retinitis pigmentosa in humans, [1] it is characterized by the bilateral degeneration of the retina, causing progressive vision loss culminating in blindness.
Glaucoma in a dog. Canine glaucoma refers to a group of diseases in dogs that affect the optic nerve and involve a loss of retinal ganglion cells in a characteristic pattern. . An intraocular pressure greater than 22 mmHg (2.9 kPa) is a significant risk factor for the development of glauco
The cleavage model was first proposed in 1993 based on work done with Drosophila Notch and C. elegans lin-12, [16] [17] informed by the first oncogenic mutation affecting a human Notch gene. [18] Compelling evidence for this model was provided in 1998 by in vivo analysis in Drosophila by Gary Struhl [19] and in cell culture by Raphael Kopan. [20]