The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Editor

Share

Personal info

View

Links

About

Terms

 

 
 
 
 

Dissociation of damage to spatial and luminance channels in early Leber's hereditary optic neuropathy manifested by the visual evoked potential.

Leber's hereditary optic neuropathy (LHON) is a maternally inherited disorder characterised by the acute or subacute loss of central vision, leading to severe optic atrophy. The occurrence of a demyelinating disease such as multiple sclerosis ( MS) has been reported mainly in females with the mitochondrial DNA 11778 mutation. They had a poor visual outcome. To investigate the damage to the optic nerve in an early stage of LHON as compared with optic neuritis (ON), including MS, we examined patients by testing their pattern visual evoked potential (PVEP) and flash VEP (FVEP). The mean amplitude and latency in the PVEP were reduced and delayed, respectively, in patients with LHON or ON. The mean amplitude in the FVEP was reduced in patients with LHON or ON, but the mean latency was not delayed in patients with LHON as compared with normal subjects or patients with ON. Luminance-related fibres may be less affected than are the spatial-vision-related fibres in patients with early LHON.[1]

References

  1. Dissociation of damage to spatial and luminance channels in early Leber's hereditary optic neuropathy manifested by the visual evoked potential. Mashima, Y., Imamura, Y., Oguchi, Y. Eye (London, England) (1997) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
 
WikiGenes - Universities