# BME100 f2015:Group5 1030amL2

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# OUR TEAM

 Name: Mary Cauley Name: Andrew Soich Name: Doug Brown Name: Alexandra Davis Name: Taylor Barda Name: Steven Stamm

# LAB 2 WRITE-UP

## Descriptive Statistics

Experiment 1

Given data for rat test subjects.

Calculated averages, standard errors,T-test values, and counts for rat test subjects.

The first experiment utilized a small sample size of 10 rats versus the 40 people that took part in the second experiment. Half of the rats were given a placebo, or sugar injection, while the other half were given 10 mg of LPS treatment. ELISAs were run on each of the 10 rats to determine their Inflammotin protein levels. The lowest recorded Inflammotin level was 3.55 pg/mL; the highest, 22.34 pg/mL. This meant that the rats had a minute range of 18.79 pg/mL of Inflammotin. Further calculations showed that the average Inflammotin level in the rats that received a placebo was 10.516 pg/mL while the rats that received a dosage of 10 mg of LPS had a slightly higher average of 11.112 pg/mL. Standard errors for the placebo rats and the 10 mg rats were .995296 and 7.40288, respectively.

Experiment 2

Given data for human test subjects.

Calculated averages, standard errors,T-test values, and counts for human test subjects.

The second experiment was done on elderly people at the retirement center. There were 40 patients separated into 4 groups of 10. One of the groups received a placebo, or 0 mg of the LPS treatment. The other three groups received 5 mg, 10 mg, and 15 mg of the LPS treatment. ELISAs were performed on each of the 40 subjects to determine their Inflammotin protein levels. The results showed that the lowest level was 1.01 pg/mL of Inflammotin (in a patient that received a placebo) while the highest level was 934.23 pg/mL of Inflammotin (in a patient who received a 15 mg dose of LPS). This shows that the human data sample had a range of 933.22 pg/mL compared to the mere 18.79 pg/mL range of the rats involved in the test. Further calculations showed that the average Inflammotin level was 3.834 pg/mL for those that received a placebo, 8.932 pg/mL for those that received a dose of 5 mg, 61.622 pg/mL for those that received a dose of 10 mg, and 657.941 pg/mL for those that received a 15 mg dose of LPS. Standard errors for 0 mg, 5 mg, 10 mg, and 15 mg of LPS were 1.2341, 1.26251, 5.48742, and 14.5926, respectively.

## Results

Experiment 1

Visual results for rat test subjects.

After graphing the ELISA results for the Inflammotin protein levels in the 10 rats, two things were made obvious. Visually, the LPS treatment appears to have no significant effect on Inflammotin levels in the general rat population. However, the standard error bars for the 10 mg dosages are much larger than those of the placebo dosages. The LPS treatment appeared to have affected a select few rats both negatively and positively in regards to Inflammotin levels. The effect of the LPS treatment is not consistent and not reasonably applicable to large rat population.

Experiment 2

Visual results for human test subjects.

Post-hoc results for human test subjects.

After graphing the ELISA results for the Inflammotin protein levels in the 40 elderly people, it can be seen that the LPS treatment appears to have an exponentially positive effect on the increase in Inflammotin levels. The standard error bars were relatively minute in comparison to what was seen in the five rats given a 10 mg dosage. The bar graph shows that the treatment has negligible effect until a 15 mg dosage was administered. Based on the t-test value to corrected p-value comparison, the recorded data is significant.

## Analysis

Experiment 1
The results of experiment 1 show a slight increase in the average of Inflammotin levels in the the test subjects when the dosage of LPS was increased from 0 mg to 10 mg. However, it is imperative to note that the increase to 10 mg was also accompanied by a sharp increase in error in the data. This evident in the much larger error bar in the graph.

Experiment 2

The results of experiment 2 show that the effectiveness of the drug was very similar between the 5 mg dose and the 10 mg dose. There was an increase on this interval however it was not nearly as large as the increase of effectiveness that occurred from 10 mg to 15 mg. Not only was there a spike in effectiveness but it occurred without a serious increase in room for error.

## Summary/Discussion

In conclusion, the LPS treatments had a much greater and significant effect on the human subjects than the rats. There was little average effect on the Inflammotin levels in the rats, with only a few outliers existing where the LPS treatment either drastically affected the protein levels positively or negatively. However, the human subjects were greatly affected by the treatments. The greater the dosage, the greater the Inflammotin protein levels. Looking at the representative bar graph of the various dosages, averages, and standard errors, it can be seen that there appears to be exponential curve that can be fitted to the bars. If more tests of incrementally higher dosages were to be run, it can be inferred that the Inflammotin levels would keep increasing at an exponential rate until the system reaches the body's capacity for producing the protein. Whilst running the calculations, our data showed that we were 99% positive that our data was not skewed by random error and actually significant.