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34 In summary, unlike in clinical studies, and, although transient biological changes can be detected, disc trauma without loss of nucleus tissue or nucleus herniation and without endplate impairment so far has not shown to promote disc degeneration in biological models

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A splicing mutation has been held responsible for Japanese acatalasemia I where a substitution of a guanine residue with adenine residue at position 5 of intron 4 disturbed the splicing pattern of the RNA product producing a defective protein [137]

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