The evolution of man: a popular exposition of the principal points of human ontogney phylogeny / From the German of Ernst Haeckel.

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The evolution of man: a popular exposition of the principal points of human ontogeny and phylogeny. From the German of Ernst Haeckel.

2

The evolution of man: a popular exposition of the principal points of human ontogeny and phylogeny. From the German of Ernst Haeckel.

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1.1 Lloyd Gaines: The Man, The Mission, & The Mystery

When great Civil Rights pioneers are discussed, the name Lloyd Gaines deserves to be mentioned. A man of humble beginnings, Gaines had dreams and goals for which he was willing to overcome outdated legal, social and educational systems do not only better himself but make a stand for his fellow man. The story of Lloyd Gaines is one of struggle, hope, success and injury. It is a life and legacy to be recognized, admired and celebrated.

Exhibit: Lloyd Gaines: The Man, The Mission & The Mystery

This Exhibit is on display at Inman E. Page Library Room 317 and online at Blue Tiger Commons: http://bluetigercommons.lincolnu.edu/lgaines_exhibit/

Disease sequence from mutant rhodopsin allele to rod and cone photoreceptor degeneration in man

Mutations in the gene encoding rhodopsin, the visual pigment in rod photoreceptors, lead to retinal degeneration in species from Drosophila to man. The pathogenic sequence from rod cell-specific mutation to degeneration of rods and cones remains unclear. To understand the disease process in man, we studied heterozygotes with 18 different rhodopsin gene mutations by using noninvasive tests of rod and cone function and retinal histopathology. Two classes of disease expression were found, and there was allele-specificity. Class A mutants lead to severely abnormal rod function across the retina early in life; topography of residual cone function parallels cone cell density. Class B mutants are compatible with normal rods in adult life in some retinal regions or throughout the retina, and there is a slow stereotypical disease sequence. Disease manifests as a loss of rod photoreceptor outer segments, not singly but in microscopic patches that coalesce into larger irregular areas of degeneration. Cone outer segment function remains normal until >75% of rod outer segments are lost. The topography of cone loss coincides with that of rod loss. Most class B mutants show an inferior-nasal to superior-temporal retinal gradient of disease vulnerability associated with visual cycle abnormalities. Class A mutant alleles behave as if cytotoxic; class B mutants can be relatively innocuous and epigenetic factors may play a major role in the retinal degeneration.