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Universlty of Manitoba, ln Partîal Fulfiìlment - MSpace at the ...

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t25<br />

7. Dlscusst0N<br />

1'/i th progressive control <strong>of</strong> infectious diseasesi congenitar defects<br />

have become an inportant cause <strong>of</strong> ¡nfant mortal ity and morbidity. Open<br />

defects <strong>of</strong> <strong>the</strong> central nervous system form a signifrcant proportion <strong>of</strong><br />

<strong>the</strong> major malform<strong>at</strong>ions. Anencephaly ls uniformly f<strong>at</strong>al, but <strong>the</strong> effect<br />

<strong>of</strong> spina bifîda varles ¡¡îth <strong>the</strong> exrent and level <strong>of</strong> <strong>the</strong> cord lesion (Barson,<br />

1970).<br />

<strong>ln</strong> an êttempt to <strong>ln</strong>vestlg<strong>at</strong>e <strong>the</strong> embryogenesis <strong>of</strong> anencephaly and<br />

sp<strong>ln</strong>a bifida, ên exper¡mental method has been developed for produc<strong>ln</strong>g<br />

open defects <strong>of</strong> <strong>the</strong> brain and sp<strong>ln</strong>al cord in <strong>the</strong> chlck embryo, by a simple<br />

physlcal procedure.<br />

The dlscussion ls llmlted to cons¡der<strong>at</strong>ion <strong>of</strong> <strong>the</strong> malform<strong>at</strong>ions<br />

obtained by thls technlc - open neural lesions, skeletal defects <strong>of</strong> <strong>the</strong><br />

vertebra¡ column, and a range <strong>of</strong> associ<strong>at</strong>ed non-neural malform<strong>at</strong>ions.<br />

Anterîor spina bifida and neuro-enteric connectlons, hydrocephalus and<br />

<strong>the</strong> Arnotd-chlari nalform<strong>at</strong>ion, syringomyelia and myelocystocele were not<br />

diagnosed in <strong>the</strong> experimental enbryos, and so êre not consîdered in this<br />

d i scuss íon.<br />

A wlde renge <strong>of</strong> neural malform<strong>at</strong>íons has been produced in domestic<br />

and fabor<strong>at</strong>gly animals by a plethora <strong>of</strong> agents - vitamin and míneral<br />

deflciences, stêrv<strong>at</strong>¡on, hypervítaminosis A, ionizing radî<strong>at</strong>ions, infections,<br />

hypoxla, hypo<strong>the</strong>rmia, hyper<strong>the</strong>rrnía, and many drugs, dyes, hormones and<br />

chemîcal n<strong>at</strong>eriêls (Kalter, l!68; Shepard, 1976; persaud, 1977).<br />

0pen neural defects have been produced in <strong>the</strong> chick embryo by x-rays,<br />

ultraviolet light, ultrasound, víruses, hypoxla, hypercarbía, and a variety<br />

<strong>of</strong> drugs, hornones and chemicals (see Section 2.3.2 for references).

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