This table lists the averages, standard deviation, number of rats per group, and standard error of the data along with data results.
this data was collected from two groups of ordinary rats.

Experiment 2

This is the table of the Averages, Standard Deviations, Number of Patients per Group, and Standard Error of the data.
The data was collected from a subject pool with an average age of 68.

Results

Experiment 1

The graph above shows the averages of Inflammotin pproduced by the two seperate rat test groups, the standard deviation, as well as the p-value collected from a t-test.

The table above shows the Inflammotin levels, as well as the dosage given to each group.

Experiment 2

The above graph shows the averages of the Inflammotin produced by the four test groups, as well as the standard deviations for the groups.

The above table shows the results of the Anova: Single Factor Test for the data collected from the four test groups. Attention should be brought to the P-Value in the second table, as it is the value that shows the correlation between the dosage and the production of Inflammotin in the test groups is significant.

Analysis

Experiment 1
We used the T-test, because we only had two groups to work with. We concluded that there is no statistical difference between the 10 mg, and 0 mg dosage , for the p-value is .85 >.05.There was a small deviation between both groups however the error value was so high in the 10 mg rat group that the deviation is negligible. LPS did not have a major effect on the rat groups and there was a large variation in the data collected from the 10mg group.

Experiment 2
After running the Anova: Single Factor test on the data collected from the four groups, we received a P-Value of 1.4E-16, meaning that there was a significant correlation between the increased dosage Lipopolysaccharide and increased production of Inflammotin in the blood. This can also be seen in the graph of the average production of the protein, as the group that was given the highest dosage of LPS, 15 mg, produced around ten times more Inflammotin than the next highest group, which received 10 mg of the LPS. From the data portrayed in the graph, we can conclude that the drug does have a significant effect on the production of Inflammotin, with the data from the Anova: Single Factor test backing the claim up.

Summary/Discussion

From 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.