BME100 f2014:Group25 L2

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BME 100 Fall 2014 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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Brandon Dorr
Beniamin Drotar
Diana Tran
Angus Cheung
Srekar Krishna Nagishetty Ravi
Daniel Gentry


Descriptive Statistics

Table 1

  • No mode available for this data set

Human Raw Data Set

Table 2

Rat Raw Data Set

Table 3


Human Processed Data

Table 4

The ANOVA test showed that our data contained negligible amounts of variance and our measurements were precise. Furthermore, our t-test values were incredibly small. This disproves the null hypothesis and leads us to believe that there is a relationship between the dosage of LPS and levels of inflammotin in the body.

Table 5

Rat Processed Data

Table 6

The data collected from the rats that were given dosages of LPS showed no apparent relationship between how much of the protein they received and the levels of inflammotin in their body. Furthermore, the p-value from the t-test performed on the data supports the null hypothesis and suggests that there is not a relationship between how much LPS is given to the rats and the levels of inflammotin in the body afterwards.


Human ANOVA Analysis

  • The one-way ANOVA test was chosen to analyze the human data set due to the fact that there are more than two groups being compared and analyzed for variance.
    The one-way ANOVA test was used to analyze the statistical significance of the LPS dosage on Inflammotin levels in humans. Upon running the ANOVA, the test yielded a p-value of 1.4E-16. This number is exponentially smaller than 0.05, allowing us to firmly state that this experiment has a large margin of confidence that these results were not statistically influenced by chance or spontaneity. Furthermore, as shown in Table 2, the error bars do not coincide with one another, physically showing the significant differences between each dosage category (e.g. 0mg, 5mg, 10mg, 15mg). After running the one-way ANOVA, the Post-hoc test was performed, which is a series of t-tests for every possible dosage comparison. As shown in Table 5, every t-test had a t-test value high enough to show statistical significance between each category.

Rat 2-variable t-test

The 2-variable t-test used to analyze the data of the rat portion of the experiment yielded a p-value of 0.8674035. Since this calculated value is far greater than the established normal confidence factor of 0.05, there is no significance in Inflammotin levels between the 0 and 10 milligram dosages of LPS. This can be further witnessed in the above bar graph which show the overlap in standard deviation error bars. As a result, the null hypothesis must be accepted and thus, the alternative hypothesis rejected. The 2-variable t-test was chosen to serve as the statistical analysis tool to compare the Inflammotin level after different dosages of LPS were administered because this portion of the experiment only had two different groups. More specifically, the version of the t-test used was unpaired because the two groups of rats were taken to be from a total of ten rats so each group of five rats were unique. Had the experimenter decided to use a group of ten rats in two trials, a paired t-test would have been implemented instead.


With the Human Testing of LSP on Inflammotin levels, Inflammotin increased dramatically, over the increase of dosage, peaking with an almost 9 fold increase from 10 to 15 mg dose. As the p-value for the between group variance was 1.4*10^-16, the results for the Human tests were significant, and conclusive. The p-values between each dosage group for the Human tests were also significant, as the values were below 0.05, or the 5% likelihood that the results occurred strictly by chance. In humans the data was also very precise and had negligible amounts of variance; the t-test values were also small. There is enough evidence to be able to reject the null hypothesis and accept the alternate hypothesis establishing that a relationship exists between the independent (LSP) and dependent variables (Inflammotin levels) for humans. However contrary to the human tests, which were highly conclusive and showed a dramatic change of Inflammotin levels as the dosage of LSP is increased, the rat tests were far less conclusive. The p-value of the rat tests between the doses is 0.87, which indicates that the results are very likely to have come simply from pure chance, rather than an effect of LSP on Inflammotin levels. There is not enough evidence to be able to reject the null hypothesis and establish that a relationship between the independent (LSP) and dependent variables (Inflammotin levels) exists for rats.

The rat's base Inflammotin levels were around 10 pg/mL, while the human's base Inflammotin levels were around 4 pg/mL. The rat's Inflammotin levels did not seem to be affected by the drug, LSP; however no significant statements can be made about LSP's effect on Inflammotin levels in rats, as their Inflammotin values were not consistent in any way and the p-value is far larger than 0.05.