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		Many of the structures affected by FAS stem from neural crest cells (NCC), a group of cells derived from the dorsal neuroectoderm during embryogenesis (Gilbert, 1997). Cartwright and Smith (1995) observed increased aberrant cell death of NCC after ethanol exposure in chicks. Sulik et al. (1988) also observed increased cell death after exposure to ethanol in mammalian models. The cranial neural crest, which leads to the formation of the entire facial skeleton, is an especially sensitive target of ethanol-induced apoptosis (Ahlgren et al., 2002). These research teams suggest that this increased NCC death may be responsible for FAS phenotypes. More recent research has explored the molecular causes of FAS. Expression of msx2, a homeobox gene, is an integral factor of the development of craniofacial structure and the developing brain. Expression of msx2 was found to decrease in mice exposed to alcohol (Rifas et al., 1997). The misexpression of this gene corresponds to the affected FAS phenotypic areas seen in previous research (Rifas et al., 1997). Blader and Strähle (1998) found phenotypic disturbances to be the result of misexpression of several ventral brain markers, including shh, axl, and nk2.2. Cell death is observed in the premigratory and migratory neural crest cells, similar to an observation made after blocking Sonic hedgehog (Shh) signaling (Ahlgren et al., 2002). Ahlgren and colleagues demonstrated that ethanol exposure results in a loss of Shh and transcripts in the Shh signaling pathway, and that ethanol-induced cranial NCC apoptosis and associated growth defects can be salvaged by application of Shh. Teratogens can also have different effects on the developing embryo depending on the magnitude and time of dose. Trunk NCC are precursors for the peripheral nervous system, ganglia, and glial cells. They are determined relatively late in migration, and thus are multipotent and can compensate for some cell death. Alcohol does not seem to affect these cells and their future structures to the same degree as the cranial NCC (Smith, 1997). It has been found in chick embryos that alcohol causes apoptosis of craniofacial cells only if treatment was administered before the emigration of NCC from the neurectoderm, at approximately 18 to 36 hours of development (Smith, 1997). Since the fate of these cells are determined at emigration, compensation for lost cells cannot occur in the same manner as the trunk NCC and deformities are observed (Bronner-Fraser and Fraser, 1991; Smith, 1997). Cell death induced by alcohol may not occur until 46-48 hours of development (Smith, 1997). To observe areas of apoptosis, Fallon and Saunders (1968) first reported the method of using the vital dye Neutral Red, and this method has been published in recent works to reveal the extent of cell death in tissues (Garcia-Martinez et al., 1993; Kim and Mirkes, 2003). Based on this knowledge, our experiment investigates the phenotypic responses of FAS at different treatment doses and times in the chick model. Apoptosis in response to ethanol treatment is visualized using Neutral Red staining techniques.