{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T21:39:30Z","timestamp":1757540370984},"reference-count":28,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2005,2,3]],"date-time":"2005-02-03T00:00:00Z","timestamp":1107388800000},"content-version":"vor","delay-in-days":10474,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Am. J. Anat."],"published-print":{"date-parts":[[1976,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Spina bifida occulta is one of the major effects of the recessive mutant \u201csnubnose\u201d (symbol <jats:italic>sno<\/jats:italic>). Linkage tests have located this mutant in chromosome 4. Defective spinal arch formation typically includes the lumbar and often the posterior thoracic and sacral vertebrae. There is great variation in detail, from nearly normal closure to a trough\u2010like spinal column. Causes of the variation are not understood. Severely affected specimens may also have defective anterior thoracic vertebrae and reduced size of the sacral vertebrae, with kyphosis. The tail is essentially normal. No external lesion or myelomeningocele has been found, but there have been some instances of paralysis of the hind limbs, possibly from injury. The spinal cord seems normal as a rule, and pigmentation is normal. Embryological study has not been attempted, but the condition seems to be primarily osteogenic in origin.<\/jats:p>","DOI":"10.1002\/aja.1001460205","type":"journal-article","created":{"date-parts":[[2005,2,26]],"date-time":"2005-02-26T13:50:04Z","timestamp":1109425804000},"page":"173-179","source":"Crossref","is-referenced-by-count":13,"title":["Genetic spina bifida occulta in the mouse"],"prefix":"10.1002","volume":"146","author":[{"given":"W. 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