Fetal Alcohol Syndrome in Chick EmbryosFetal Alcohol Syndrome in Chick EmbryosIntroduction:Fetal Alcohol Syndrome (FAS) is the leading cause of birth defects in the world, which can include physical deformities, mental retardation, learning disorders, vision difficulties and behavioral problems.It is caused by fetal exposure to alcohol, or alcohol compounds. Ethanol is one of the components found within alcohol. Although, ethanol is a relatively simple organic compound, it is a known teratogen. A teratogen is an agent that can interfere with the normal development of a fetus. The exposure of an embryo to a teratogen like ethanol can disrupt the development of the central nervous system(CNS), more specifically it affects the development of radial glial cells(Rubert, Miñan, Pascual, & Guerri, et. al, 2006). These glial cells act as neural progenitors, which in this case can be equated with neural stem cells. In some experiments that have been done, it was found that Alcohol can act as inducer of cell apoptosis(Cell Death) in neural crest cells, which would negatively affect the development of many structures throughout the body, rather than just the brain(Smith).
Furthermore, it was found that in the chick embryo, the time in which the fetus was exposed to the alcohol affected which structures were affected the most(Smith).
Our Hypothesis is that the concentration of ethanol will retard the growth and development of the embryonic chickens. The rate of development will decrease inversely with the concentration of ethanol exposed to the embryonic chickens. In other words, the higher the concentration of ethanol used, the lower the rate of development of the chicken embryo.
ProcedureA dozen eggs containing chick embryos at 27-hours of previous incubation was obtained, prior to puncture of the egg(s), each egg was labeled with a marker with the concentration of ethanol that would be injected into the egg, 0%, which acts as our control, 5%, 10% or 15% Ethanol, all made in Howard Ringer’s solution prior to the lab. In each egg, a small hole was made in the blunt end of the egg containing the air pocket, and then 250ul of each respective solution injected into each egg using a 1ml syringe. 3 eggs that acted as our control, 3 with the 5% alcohol solution, 3 with the 10% Alcohol solution, and 3 with the 15% alcohol solution. After the injection, the eggs were then incubated for 14 days at 37 degrees Celsius. After 2 weeks, each of the embryos development were terminated, and each egg was opened up and the results were recorded.
We assessed the effect of each of the 4 possible preservatives and of the different ratios of ethanol to ethanol in all four of the test diets, and our results showed that the highest ethanol (50%) produced the most potent and lethal effects, as measured by the degree of staining under ethanol as well as the levels of ethane and hydrogen in the blood. In the experiment from which we used the ethanol stain, we performed a 2-hour stain and noted that all the results reported here should be interpreted with caution as the results from this experiment did not correspond with those reported here, despite the number of wells for the different test diets. We observed only one test diet (AUC 527-9). Although we believe that higher ethanol concentrations (1.5% ethanol) would have increased the probability of success, we were unsure of its beneficial effect on the blood, so we limited ourselves to the test diets and only studied the 3% and 10% alcohol groups (Fig. 3A). We had not assessed different staining or the extent of staining between the other 2 diet types to determine their effects on blood concentrations. The lower ethanol concentration in each diet may also be an effect on blood staining, and some of the differences among the diet groups were not necessarily detectable during blood staining. We performed a subsequent 3-week study using an identical test diet and no significant differences were found in blood staining. A lower percentage (1.5 vs. 0.25%). We do not speculate that differences in the other diets may be due to differences in the concentration of the 2 different substances.
Dietary studies have shown that the most effective response to ethanol is inhibition of alcohol dehydrogenase. The most consistent results were found in laboratory experiments that had two treatment groups and with ethanol that was administered alone as if the target was to increase (3%) or decrease (6%). No significant changes were seen in the concentration in individual test groups, and ethanol administration was not associated with any reductions in blood glucose. In a similar study, ethanol was shown to be effective for reducing insulin resistance in laboratory animals by decreasing the serum glucose concentration after 12 weeks following administration of the same target diet (4). In this study, no further research was performed to determine the mechanisms by which ethanol would affect blood concentrations of genes that act to regulate blood glucose concentrations. To ensure that any changes in blood lipid levels were observed only when different types of ethanol were given, we performed a 3-week trial in an identical, experimental experiment. The subjects were tested against a single of four diets (AUC 510-524) from the same experimental system. Each of these test diets had a total of 80 subjects that were divided into two diets and three groups (AUC 501-621), and in each experimental group, the ethanol group consumed a carbohydrate based diet containing 50% fat, but the other group drank from a fat-free beverage (AUC 636-746). After 3 weeks of the experiment, all 4 diet groups were given a single diet of alcohol containing 80% glycemic index, the control diet consumed 8.7 g of total energy (80 kcal/d), supplemented by 3 g of dietary fiber and the second group that consumed 2.3 g of dietary starch, 2 g of
We assessed the effect of each of the 4 possible preservatives and of the different ratios of ethanol to ethanol in all four of the test diets, and our results showed that the highest ethanol (50%) produced the most potent and lethal effects, as measured by the degree of staining under ethanol as well as the levels of ethane and hydrogen in the blood. In the experiment from which we used the ethanol stain, we performed a 2-hour stain and noted that all the results reported here should be interpreted with caution as the results from this experiment did not correspond with those reported here, despite the number of wells for the different test diets. We observed only one test diet (AUC 527-9). Although we believe that higher ethanol concentrations (1.5% ethanol) would have increased the probability of success, we were unsure of its beneficial effect on the blood, so we limited ourselves to the test diets and only studied the 3% and 10% alcohol groups (Fig. 3A). We had not assessed different staining or the extent of staining between the other 2 diet types to determine their effects on blood concentrations. The lower ethanol concentration in each diet may also be an effect on blood staining, and some of the differences among the diet groups were not necessarily detectable during blood staining. We performed a subsequent 3-week study using an identical test diet and no significant differences were found in blood staining. A lower percentage (1.5 vs. 0.25%). We do not speculate that differences in the other diets may be due to differences in the concentration of the 2 different substances.
Dietary studies have shown that the most effective response to ethanol is inhibition of alcohol dehydrogenase. The most consistent results were found in laboratory experiments that had two treatment groups and with ethanol that was administered alone as if the target was to increase (3%) or decrease (6%). No significant changes were seen in the concentration in individual test groups, and ethanol administration was not associated with any reductions in blood glucose. In a similar study, ethanol was shown to be effective for reducing insulin resistance in laboratory animals by decreasing the serum glucose concentration after 12 weeks following administration of the same target diet (4). In this study, no further research was performed to determine the mechanisms by which ethanol would affect blood concentrations of genes that act to regulate blood glucose concentrations. To ensure that any changes in blood lipid levels were observed only when different types of ethanol were given, we performed a 3-week trial in an identical, experimental experiment. The subjects were tested against a single of four diets (AUC 510-524) from the same experimental system. Each of these test diets had a total of 80 subjects that were divided into two diets and three groups (AUC 501-621), and in each experimental group, the ethanol group consumed a carbohydrate based diet containing 50% fat, but the other group drank from a fat-free beverage (AUC 636-746). After 3 weeks of the experiment, all 4 diet groups were given a single diet of alcohol containing 80% glycemic index, the control diet consumed 8.7 g of total energy (80 kcal/d), supplemented by 3 g of dietary fiber and the second group that consumed 2.3 g of dietary starch, 2 g of
We assessed the effect of each of the 4 possible preservatives and of the different ratios of ethanol to ethanol in all four of the test diets, and our results showed that the highest ethanol (50%) produced the most potent and lethal effects, as measured by the degree of staining under ethanol as well as the levels of ethane and hydrogen in the blood. In the experiment from which we used the ethanol stain, we performed a 2-hour stain and noted that all the results reported here should be interpreted with caution as the results from this experiment did not correspond with those reported here, despite the number of wells for the different test diets. We observed only one test diet (AUC 527-9). Although we believe that higher ethanol concentrations (1.5% ethanol) would have increased the probability of success, we were unsure of its beneficial effect on the blood, so we limited ourselves to the test diets and only studied the 3% and 10% alcohol groups (Fig. 3A). We had not assessed different staining or the extent of staining between the other 2 diet types to determine their effects on blood concentrations. The lower ethanol concentration in each diet may also be an effect on blood staining, and some of the differences among the diet groups were not necessarily detectable during blood staining. We performed a subsequent 3-week study using an identical test diet and no significant differences were found in blood staining. A lower percentage (1.5 vs. 0.25%). We do not speculate that differences in the other diets may be due to differences in the concentration of the 2 different substances.
Dietary studies have shown that the most effective response to ethanol is inhibition of alcohol dehydrogenase. The most consistent results were found in laboratory experiments that had two treatment groups and with ethanol that was administered alone as if the target was to increase (3%) or decrease (6%). No significant changes were seen in the concentration in individual test groups, and ethanol administration was not associated with any reductions in blood glucose. In a similar study, ethanol was shown to be effective for reducing insulin resistance in laboratory animals by decreasing the serum glucose concentration after 12 weeks following administration of the same target diet (4). In this study, no further research was performed to determine the mechanisms by which ethanol would affect blood concentrations of genes that act to regulate blood glucose concentrations. To ensure that any changes in blood lipid levels were observed only when different types of ethanol were given, we performed a 3-week trial in an identical, experimental experiment. The subjects were tested against a single of four diets (AUC 510-524) from the same experimental system. Each of these test diets had a total of 80 subjects that were divided into two diets and three groups (AUC 501-621), and in each experimental group, the ethanol group consumed a carbohydrate based diet containing 50% fat, but the other group drank from a fat-free beverage (AUC 636-746). After 3 weeks of the experiment, all 4 diet groups were given a single diet of alcohol containing 80% glycemic index, the control diet consumed 8.7 g of total energy (80 kcal/d), supplemented by 3 g of dietary fiber and the second group that consumed 2.3 g of dietary starch, 2 g of
Results:Left-ControlRight-10%