BME100 s2016:Group10 W1030AM L2

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BME 100 Spring 2016 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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Curtis McLoud
Gavin Steeber
Jade Nelson
Jordan Todd
Ekta Patel
Joe Schreiber


Descriptive Statistics

Experiment 1 (rats)
The average Inflammotin protein levels for the group of rats that were prescribed with 0mg lipopolysaccharide (LPS) was 10.52 pg/mL. The group of rats given 10mg of LPS had an average of 11.11 pg/mL.

The standard deviation within the group of rats given 0mg dosage was 2.23 pg/mL. The 10mg dosage rats had a standard deviation of 7.403 pg/mL.

The standard error for the 0mg dosage group of rats was .9952 pg/mL. The group of rats given the dosage of 10mg had a standard error of 3.31 pg/mL.

Experiment 2 (humans)

The mean Inflammotin protein levels differ based on varying doses. For the 0mg dosage, the average Inflammotin level is 3.834 pg/mL. For the 5mg dosage, the average Inflammotin level is 8.932 pg/mL. For the 10mg dosage, the average Inflammotin level is 61.622 pg/mL. For the 15mg dosage, the the average Inflammotin level is 657.941 pg/mL.

The standard deviation also differs based on dosages. The 0mg dosage yielded a 1.523 pg/mL standard deviation, the 5mg dosage yielded a 1.594 pg/mL standard deviation, the 10mg dosage yielded a 61.622 pg/mL standard deviation, and finally, the 15mg dosage yielded a 212.943 pg/mL standard deviation.

The standard error similarly differs based on dosages. The standard error for 0mg is 0.482 pg/mL, the standard error for 5mg is 0.504 pg/mL, the standard error for 10mg is 9.521 pg/mL, and the standard error for 15mg is 67.338 pg/mL.

Overall, the averages, standard deviations, and standard errors, all increase as the dosages increase.


Experiment 1 (rats)
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Experiment 2 (humans)
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Experiment 1 (rats)
In the rat experiment, the average level of Inflammotin between the two doses of 0mg and 10mg was not extremely different; the rats that were given 10mg of lipopolysaccharide (LPS) actually experienced a higher level of Inflammotin than the rats that received no dosage. Due to the data that was recorded from each trial, the standard deviation was significantly higher in the trial in which the rats were given 10mg of LPS than the trial with 0mg of LPS. However, regardless of this, because standard error is based upon the standard deviation, both t-test p-values for the 10mg trial and the 0mg trial were found to be higher than the p-value of 0.05, and therefore, both tests were deemed to be statistically insignificant.

Experiment 2 (humans)
In the human experiment, the levels of Inflammotin were found to rise significantly with the increase in the level of lipopolysaccharide (LPS) that the patients were given. For example, the patients that were given 0mg of LPS had an average of 3.834 pg/ml of Inflammotin, whereas the patients being given the dosage of 15mg of LPS had an average of 657.941 pg/ml of Inflammotin. Due to the drastic differences in the amount of Inflammotin found in the human patients depending on the dosage, the standard deviation differed greatly as well, with the differences ranging from 1.523 to 212.943 with the doses of 0mg of LPS and 15mg of LPS respectively; the same broad range was also found with the standard errors on each trial because the standard error is based off of the standard deviation. However, the p-values that were established from the ANOVA tests between the comparisons of the trials were all found to be statistically significant.


The claim that LPS increases the levels of inflammotin in the human subjects is valid because the result was statistically significant. This cannot be said for the rat trials, because the rat study was not statistically significant. The rat group was statistically insignificant, because the change in inflammotin was too small to be directly attributed to the LPS. This resulted in a p value greater than 0.05. The possible reasons for the difference in statistical significance could be in the size of the trial, since the human study had a larger pool of samples. Another potential reason for this is LPS has a profound biological impact on humans, but not as much on rats.

It is difficult to identify why LPS increased inflammotin levels in humans, but not statistically significant in rats. Differences in anatomy, physical structures, and chemical signals can all play a role. There is also the ability that the data obtained many have been inaccurate because of experimental errors. Based on the analysis however, it is safe to say that there needs to be more experiments and trials run, before a precise conclusion can be made.