BME100 f2014:Group13 L2
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OUR TEAMLAB 2 WRITE-UPDescriptive StatisticsExperiment 1 Experiment 2
ResultsExperiment 1
The above graph shows the averages of the Inflammotin produced by the four test groups, as well as the standard deviations for the groups.
AnalysisExperiment 1
Summary/DiscussionFrom the data from the two tests, we concluded that increased dosages of Lipopolysaccharide was linked to an increased production in Inflammotin. However, this increased production of Inflammotin was only found in the human test subjects, while the rat test subjects did not show a significant increase in the production of Inflammotin, with the p-value for the Anova: single factor test for the human test group being 1.4E-16 and the rat test group t-test value being 0. 87. In addition, the standard deviation and error for the data of the rat test subjects was high, decreasing any confidence in a correlation between the Lipopolysaccharide and the Inflammotin in rats. The difference in results between the two tests can probably be attributed to a difference in anatomy between the rats and the humans, with the humans having the proteins necessary for the processing of Lipopolysaccharide, where as the rats lack this protein and thus can not process the the Lipopolysaccharide. Despite the differences in the tests, the evidence provided by the tests involving human patients was conclusive enough to show that the dosage of Lipopolysaccharide was linked to the production of Inflammotin. This can be seen in the graphs of the average production values of Inflammotin in humans, with the amount of Inflammotin produced increasing exponentially as dosages of Lipopolysaccharide was increased. The data also showed reasonable standard deviation and error, helping to boost confidence in the claim that the Lipopolysaccharide and Inflammotin are linked. |