BME100 f2014:Group26 L2

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Ambike Bhraguvanshi
Timothy Chen
Andrew Polson
Rachel Ponstein
Rebecca Schiavone
Jiaqi Wu


Descriptive Statistics

Human Study
Inflammotin Mean-
0 mg: 3.834 pg/ml
5 mg: 8.932 pg/ml
10 mg: 61.622 pg/ml
15 mg: 657.941 pg/ml

Inflammotin Variability-

Standard Deviation-
0 mg: 1.523 pg/ml
5 mg: 1.594 pg/ml
10 mg: 30.111 pg/ml
15 mg: 212.943 pg/ml

Standard Error-
0 mg: 0.4816 pg/ml
5 mg: 0.5040 pg/ml
10 mg: 9.5218 pg/ml
15 mg: 67.3385 pg/ml

Rat Study
Inflammotin Mean-
0 mg: 10.516 pg/ml
10 mg: 11.112 pg/ml

Inflammotin Variability-

Standard Deviation-
0 mg: 2.226 pg/ml
10 mg: 7.403 pg/ml

Standard Error-
0 mg: 0.9953 pg/ml
10 mg: 3.3107 pg/ml


Human Study

Rat Study

Inferential Statistics

Human Study
One-Way ANOVA Results-

Because there were four groups for the dosage of lipopolysaccharide in the human study, ANOVA testing was done to demonstrate and display the significance of differences between the groups.

ANOVA Post-Hoc Tests-

Rat Study
t-Test Value- 0.8674035

t-Testing was used to compare the means of the two groups; as there were two groups for the dosage of lipopolysaccharide in the rat study, the t-Test was chosen. The independent t-Test was used to find whether there was a statistically significant difference between the two unrelated groups of 0 mg and 10 mg of the LPS.

The ANOVA Post-Hoc values conclude that all the results for 0 mg, 5 mg, 10 mg, and 15 mg doses of Inflammotin are significant. However, the t-Test value for the rat study is above 0.05, meaning that the results are not significant. Based on the significant ANOVA Post-Hoc values, lipopolysaccharide doses raise the Inflammotin levels in the elderly. However, the insignificant t-Test value from the rat study shows that the dosages of lipopolysacharide do not increase the Inflammotin levels in rats.

Summary and Discussion

Human Study
The results of the human study demonstrate a strong positive relationship between LPS and Inflammotin levels. As the dosage of the lipopolysaccharide increases, the Inflammotin level increases as well. The 0 mg, 5 mg, and 10 mg dosages exhibit a gradual increase in the level of Inflammotin, while the 15 mg dosage shows a tremendous increase in Inflammotin levels compared to the 10 mg dosage. The results also showed a considerably high standard deviation in the 10 mg and 15 mg dosages, which can be attributed to how there were only 10 subjects tested for each dosage. This limitation could be resolved by testing more subjects for each dosage; confidence in results increases as the number of subjects tested increases. The t-Test value determined through the one-way ANOVA test was 1.4E-16, which is substantially smaller than 0.05, meaning that there is a statistically significant difference among the lipopolysaccharide dosages. Furthermore, the Bonferroni Correction post-hoc tests demonstrated that there is a significant difference between all of the comparisons of the lipopolysaccharide dosages, as all of the t-Test values were lower than the adjusted p-value of 0.0083. Overall, it is reasonable to say that lipopolysaccharide has a statistically significant effect on Inflammotin levels in humans, as shown through the t-Test value calculated from the one-way ANOVA test and the comparisons made in the post-hoc tests. Therefore, it is also justifiable to say that lipopolysaccharide is an effective treatment in increasing Inflammotin protein levels in the elderly.

Rat Study
The t-Test value for the average amount of Inflammotin the rats produced was above 0.05, meaning it did not significantly affect the rats' production of Inflammotin. However, the Inflammotin levels in the rats was varied, and the standard deviation of data was very large when they were given a 10 mg dose. However, since there were only 10 subjects in the testing group, there was much room for error and/or deviation in data. These results go against Kristen's hypothesis (that LPS treatment increases Inflammotin protein levels in rats), as there was actually no relationship between lipopolysaccharide and Inflammotin levels in the rats.

Linking the Two
While the dosages of lipopolysaccharide given to the rats did not significantly affect the production of Inflammotin, those given to humans were significant to the production of Inflammotin, or rather, there is a giant leap in the production of Inflammotin in humans between the 10 mg and 15 mg dosages. Thus, perhaps for the rat tests, the samples given were not a large enough dose to affect anything. If the rats were given 15 mg samples, there could be a significant change in the p-value and t-Test values and thus a statistically significant effect of the lipopolysaccharide on Inflammotin levels in rats. However, we definitely know that there is this giant gap in the production of Inflammotin between the 10 mg and 15 mg groups in humans. This could be investigated in the rats by using additional dosages.

The rat study exhibits how in-vivo testing in this case would not be beneficial in demonstrating the effects of lipopolysaccharide on Inflammotin levels. Because there is a lack of similitude in the results of the rat study and human study, concluding from the results of the rat study (lipopolysaccharide has no effect on Inflammotin levels) would be problematic. However, the rat study itself is limited in that only two dosages of the lipopolysaccharide were tested in comparison to the four different levels tested for humans. Including more dosages for the rat study would allow for a more expansive perspective on the effect of lipopolysaccharide on Inflammotin levels in rats and how this effect relates to humans to be attained.