Vogt–Koyanagi–Harada disease at the University of Tokyo, in 1911. It was the much later article, published in 1929, that definitively associated Koyanagi with the disease. Harada's 1926 paper is recognized for its comprehensive description of what is now known as Vogt–Koyanagi–Harada disease. Vogt–Koyanagi–Harada disease Vogt–Koyanagi–Harada disease (VKH), also known as Vogt–Koyanagi–Harada syndrome, uveomeningitis syndrome and uveomeningoencephalitic syndrome, is a multisystem disease of presumed autoimmune cause, that affects pigmented tissues, which have melanin. The most significant manifestation is bilateral, diffuse uveitis, which affects the eye. VKH may variably also involve the inner ear with effects on hearing, the skin, and the meninges of
Neoteny in humans lower second and third molars. Populations with a history of dairy farming have evolved to be lactose tolerant in adulthood, whereas other populations generally lose the ability to break down lactose as they grow into adults. Down syndrome neotenizes the brain and body. The syndrome is characterized by decelerated maturation (neoteny), incomplete morphogenesis (vestigia) and atavisms. Neoteny in humans Neoteny in humans is the retention of juvenile features well into adulthood. This trend is greatly amplified in humans especially when compared to non-human primates. Adult humans more closely resemble the infants of gorillas and chimpanzees than the adults. Neotenic features