BME100 s2014:W Group11 L2
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LAB 2 WRITE-UP
Inflammotin Experiment in Rats
With the goal of determining the minimum dose of lipopolysaccharide, an inflammotin inducing agent, required to increase production of the protein inflammotin, the drug was first administered to rats.
The average amount of the protein inflammotin produced in the control group of rats (rats given 0mg of LDS) was 10.516pg/ml. The average amount of inflammotin produced in rats given 10mg of LPS was 11.112pg/ml.
The standard deviation of inflammotin production for the control group of rats was 2.226pg/ml. The standard deviation for the group of rats given 10mg of LPS was 7.403pg/ml.
The standard error for inflammotin production in the control group of rats was 0.995pg/ml. The standard error for the group given 10mg of LPS was 3.311pg/ml.
Inflammotin Experiment in Humans
After testing on the rats, the experiment was conducted on human subjects with a wider variety of dosages.
The average amount of the protein inflammotin produced in the control group of humans (people given a placebo) was 3.834pg/ml. In the group given 5mg of LPS, the average amount of inflammotin produced was 8.932pg/ml. In the group given 10mg of LPS, the average amount of inflammotin produced was 61.622pg/ml. Finally, the average amount of inflammotin produced in the group given 15mg of LPS was 657.941pg/ml.
The standard deviation of inflammotin production for the control group of humans was 1.523pg/ml. The standard deviation for the group given 5mg of LPS was 1.594pg/ml. The standard deviation for the group given 10mg of LPS was 30.110pg/ml, and the standard deviation for the group given 15mg of LPS was 212.943pg/ml.
The standard error for inflammotin production in the control group of humans was 0.482pg/ml. The standard error for the group of humans given 5mg of LPS was 0.504pg/ml. The standard error for the group given 10mg of LPS was 9.522pg/ml, and the standard error for the group given 15mg of LPS was 67.338pg/ml.
A t-test was used to analyze the data collected from the rat experiment because it was necessary to investigate the differences between two groups of test subjects.
ANOVA testing was used to analyze the data from the human experimentation so as to investigate the differences between multiple groups of test subjects.
Based on the t-test, the p-value for the test conducted with rats was 0.867. Since this value is larger than 0.05, the results were found to be not statistically significant. The probability that the change in inflammotin levels between the two groups was not actually caused by the LPS is over than 5%.
For the human experiments, each test group was compared using ANOVA testing. For the Post-hoc tests, the corrected p-value to achieve significance, the Bonferroni correction, was found to be 0.0083. The t-test value for each comparison was considerably less than this value, meaning that the differences between the inflammotin production of each test group were statistically significant. There is less than 5% probability that the test results were caused by variables other than the dosage of LPS administered.
The purpose of this study was to determine the effects of different dosages of LPS on inflammotin production in elderly humans. In order to determine the lowest dosage for which inflammotin levels were affected, first rats were tested for inflammotin levels after the administration of 0mg and 10mg of LPS. Then human groups were tested for 0mg, 5mg, 10mg, and 15mg. The results of the first experiment showed no statistical significance in the difference in inflammotin production in rats based on the administration of LPS. This contrasts the high statistical significance in inflammotin production between each group of human test subjects. The results showed a significant increase in inflammotin production in humans after the administration of 5mg of LPS. Further experiments may be necessary in order to determine if an even lower dosage of LPS will have an effect on inflammotin production in elderly humans. This is half the dosage that prior experiments had shown to have an effect. Experimental results showed a high variability in individual production of inflammotin in rats regardless of the administration of LPS. This was also true in humans, but the larger sample size allowed for statistical significance. Were more rats tested, it is possible that the variance might have had less of an effect on the t-test. However, current test results show that rats may not be an adequate predictor of the effects of LPS in elderly humans.