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Bradley M. Patten

Bradley Merrill Patten ( -1971) was an American embryologist, Western Reserve University, School of Medicine. Cleveland, Ohio.

Bradley Merrill Patten, the distinguished embryologist, is retiring from active service as Professor of Anatomy and Chairman of the Department of Anatomy in the Medical School, University of Michigan.

The son of a professor of zoology at Dartmouth College, he entered upon his own academic career with characteristic single-mindedness graduating from Dartmouth Phi Beta Kappa in 1911, and from Harvard Graduate School in 1914.


References

Patten BM. The Early Embryology of the Chick. (1920) Philadelphia: P. Blakiston's Son and Co.

Patten BM. Developmental defects at the foramen ovale. (1938) Am J Pathol. 14(2):135-162. PMID 19970381

Human Embryology. Ed. 2. Bradley M. Patten, Ph.D. New York, The Blakiston Company, 1953.

Patten BM. Embryology of the Pig. (1951) The Blakiston Company, Toronto.

The closure of the foramen oval (1931) | JAMA Review of - Embryology of the Pig | Open Library

In memoriam: Bradley M. Patten. Dev. Biol.: 1971, 26(4);659 PMID 4944077

BRADLEY M. PATTEN. Med Bull (Ann Arbor): 1958, 24(12);500-1 PMID 13625453


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Embryological stages in the development of spina bifida and myelosclzisis

This 1946 paper presented by Patten at the 1946 Meeting of the American Association of Anatomists.

Bradley M. PATTEN, Department of Anatomy, University of Michigan.

Three recently acquired human embryos show progressive stages in the development of spina bifida and myeloschisis. The youngest (8 mm) exhibits a broad opening of the neural tube in the sacral region. Measurements of the sections show the bulk of the spinal cord is startlingly greater ill the region of the defect than just above or below it. Similarly in the second embryo (49 mm) there is marked overgrowth of the cord with the additional factor of local cord duplication toward one end of the defect. The third specimen (160 mm) is beginning to show degenerative changes in the open cord and clubbing of the feet. The youngest embryo indicates the cord defect is primary because it has been established well before the primordia of the neural arches have begun to take shape. Conditions presented by these specimens strongly suggest that the open neural tube is the result of local overgrowth which interfered with closure, rather than the result of a “developmental arrest” which left the tube unclosed. The importance of this possibility lies in its implications as to causation. Because of the emphasis which has been placed on the developmental arrest concept, search for causes of congenital defects has been largely directed toward conditions which might inhibit growth. If anomalies are caused also by local overgrowth, we must scrutinize causative factors of different types.



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