Titlebook: Retinal Degenerative Diseases and Experimental Therapy; Joe G. Hollyfield,Robert E. Anderson,Matthew M. La Book 1999 Springer Science+Busi

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CRALBP and Inherited Retinal Degenerationblishing that the arRP modification was responsible for a loss of protein function. In addition, we present progress in the development of CRALBP knockout mice for studying . functions and therapeutic approaches to retinal degenerations related to CRALBP.

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Autosomal Dominant Macular Degeneration Localized to Chromosome 6q by Linkage Analysisterval on chromosome 6q11–13 and excludes the loci for North Carolina Macular Dystrophy and Progressive Bifocal Chorioretinal Atrophy. Three other retinalJ.macular dystrophies map to overlapping intervals and could be allelic forms of the same gene or from a cluster of genes causing retinal/macular degeneration.

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um on Retinal Degeneration as a satellite meeting of the International Congress of Eye Research. The timing and varying location of these meetings provides an important assembly for investigators from throughout the world to convene for presentation of their new findings on the causes and potential

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Loss of Cone and Reduction in Rod ERG Responses in the Guanylyl Cyclase-E (GC-E) Deficient Mouseable cone ERG in mice >8 wks. An early loss of cones or a failure of cones to develop was confirmed by histological analysis. The maximum rod photoresponse amplitude (.) was 70% lower than normal at 3–5 wks despite a normal histological appearance of rods. Recovery from activation, as assessed by a

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Leber’s Congenital Amaurosisetinal findings appeared. None of the 9 reexamined patients showed a normal fundus. Nystagmus and strabismus were principal presenting symptoms. Eleven patients presented with the oculodigital sign, three of them were enophthalmic, and 12 patients showed roving eye movements. Patients with additiona

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