BME100 s2014:T Group3 L2

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BME 100 Fall 2013 Home
Lab Write-Up 1 | Lab Write-Up 2 | Lab Write-Up 3
Lab Write-Up 4 | Lab Write-Up 5 | Lab Write-Up 6
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Name: Maria C Morrow
Name: Hannah V Spehar
Name: Kazhan Kader
Name: Jaquelyn L Corr
Name: Sayer Aldaady


Descriptive Statistics

Experiment 1
Experiment 1 was performed on rats. LPS treatment was administered to the rats in doses of 0 mg and 10 mg, with 5 subjects per treatment. An ELISA test was used to measure the presence of inflammatory protein, inflammotin. The average value of inflammotin in subjects who did not receive the treatment was 10.5pg/mL. Subjects who received a dose of 10 mg averaged 11.1pg/mL of infammotin. The standard deviations of the groups were 2.23 and 7.40, respectively. The standard error was 0.445 for the group who received the 0 mg treatment and 1.48 for the group who received the 10 mg treatment.

Experiment 2
Experiment 2 was performed on elderly people at a retirement center. LPS was administered in doses of 0 mg, 5 mg, 10 mg, and 15 mg, with 10 subjects per group. The average amount of the inflammotin in the group that did not receive the treatment was 3.83 pg/mL. The group that received a 5 mg treatment averaged 8.93 pg/mL. The average for the group who received 10 mg was 61.6 pg/mL. The 15 mg treatment group averaged 658 pg/mL of inflammotin. The standard deviations of the groups were 1.52, 1.59, 30.1, and 213 and the standard errors were 0.152, 0.159, 3.01, and 21.3, respectively.


Experiment 1

Experiment 2


Experiment 1
It was appropriate to use a t-test for the rat experiment because there was only one comparison being made. The results of the t-test produced a p-value of 0.867. This means that it is unlikely that there is a causation relationship between the LPS treatment and the level of inflammotin of the rats. If the experiment was to be performed again, the chances of getting different result is 86.7%. There was not a significant difference between the groups of data.

Experiment 2
The ANOVA was used for the human study because there were more than two comparisons being made. The results of the ANOVA confirmed that there was a significant difference between the groups of data. The Bonferroni Correction was performed to find if there was a significance between each group: 0 mg vs 5 mg, 0 mg vs 10 mg, 0 mg vs 15 mg, 5 mg vs 10 mg, 5 mg vs 15 mg, and 10 mg vs 15 mg. The p-values produced after running t-tests between each group were 8.60E-7, 9.94E-6, 1.39E-8, 3.01E-5, 1.57E-8, and 6.48E-8, respectively. This illustrates that there is a high likelihood of causation between dosage of LPS and presence of infammotin in elderly humans.


The first experiment was performed on rats. The t-test performed after the experiment demonstrated that there was no statistical difference between the two test groups of rats. The p-value produced from this test demonstrates a minimal likelihood that the increase in LPS was the reason for the levels of inflammotin in the rats. The second experiment showed the opposite. The ANOVA test performed on the elderly humans' data illustrated a significant difference in the treatment groups with various dosages of LPS. It was then possible to infer that there is a causal relationship between the increased dosage of LPS and the increased levels of inflammotin in elderly humans. When looking at both experiments together, it can be deduced that the LPS treatment is likely to be effective in human subjects but not rat subjects.