TL;DR: It is argued that, given the problems raised by genetic tests, a moratorium similar to that suggested by the Nuffield Council on Bioethics should be extended to all forms of insurance in which underwriting is based on medical risks.
Abstract: insurance. Finally, the use of genetic tests exacerbates the dilemma of underwriting described above as the tests increase the amount of information available regarding a person's risk of becoming ill. Because of these distinctions between monogenic and non-genetic tests a strong case can be made for forbidding the use oftests for monogenic conditions. Given the rapid technical advances in medical genetics, testing for a predisposition to many common disorders-such as heart disease, diabetes, and various forms of cancer-may soon be possible. For these diseases both genetic and environmental factors are usually implicated in the pathogenesis. As these diseases, like most diseases, are neither exclusively genetic nor exclusively environmental, tests for them cannot be readily distinguished from other medical tests. The blurring of the distinction between genetic and nongenetic medical conditions does not mean that the use of tests that provide genetic information about multifactorial conditions will be no more problematic than non-genetic medical tests. Typically, genetic tests, especially those for multifactorial conditions, provide less predictive information about the course of a disease than is commonly believed. Moreover, stigmatisation and discrimination will not disappear so long as genes are believed to play a dominant part in determining our lives. The Insurance Task Force of the Human Genome Project proposed a moratorium on the use of genetic tests in health insurance until a national health care programme was in place.3 We would argue that, given the problems raised by genetic tests, a moratorium similar to that suggested by the Nuffield Council on Bioethics should be extended to all forms of insurance in which underwriting is based on medical risks.4
TL;DR: It is demonstrated that extensive proliferation occurs in all three otolithic endorgans of the ears in a fish and that such proliferation continues for virtually the whole life of the animal.
Abstract: Bony fishes add sensory hair cells to the saccule and lagena of the ear for at least several years after hatching. However, it is not known whether hair cell proliferation occurs for the whole lifetime of an animal, whether proliferation occurs in all endorgans of the ear, or whether the rate of proliferation is the same in all of the endorgans. To obtain answers to these questions, the extent of postembryonic hair-cell proliferation was determined in the saccule, lagena, and utricle of the ear in the European hake, Merluccius merluccius, for fish ranging from 7 to 75 cm in total length (6 months to 9 years of age). Results demonstrated that hair-cell addition continued throughout this period in all three otic endorgans, although endorgan size was proportionally greatest in smaller animals. Of the three endorgans, cell addition was greatest in the saccule. Moreover, far more cells were added to the caudal end of the saccule than to the rostral end. Each saccule of the largest hake had over 900,000 hair cells. It is estimated that each saccule adds approximately 110,000 new hair cells each year (or 302 cells/day) over the life span of the fish studied. A significant number of small ciliary bundles, thought to represent newly proliferated hair cells, was found throughout each endorgan, and the number of such bundles declined as the rate of hair cell proliferation decreased. The results demonstrate that extensive proliferation occurs in all three otolithic endorgans of the ears in a fish and that such proliferation continues for virtually the whole life of the animal. The functional significance of this addition is not known.
TL;DR: It is demonstrated that the zebrafish, Danio rerio, contains a highly conserved gene, otop1, that is essential for otolith formation and the size and shape of the developing otolith.
TL;DR: It is suggested that each cycle of the BCV or ACS stimulus causes fluid displacement which deflects the short, stiff, hair bundles of type I receptors at the striola and so triggers the phase-locked neural response of primary otolithic afferents.
TL;DR: The results provide evidence for a functional vestibulo-oculomotor circuit in 72 hpf zebrafish larvae that relies upon sensory input from anterior/utricular otolith organs.
Abstract: Background
Vestibular reflexes coordinate movements or sensory input with changes in body or head position. Vestibular-evoked responses that involve the extraocular muscles include the vestibulo-ocular reflex (VOR), a compensatory eye movement to stabilize retinal images. Although an angular VOR attributable to semicircular canal stimulation was reported to be absent in free-swimming zebrafish larvae, recent studies reveal that vestibular-induced eye movements can be evoked in zebrafish larvae by both static tilts and dynamic rotations that tilt the head with respect to gravity.