BME100 f2013:W1200 Group8 L2

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Lab Write-Up 1 | Lab Write-Up 2 | Lab Write-Up 3
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OUR TEAM

Name: Colby Mark
Name: Hayden McIver
Name: Drew Wills
Name: Madison Grayson
Name: Isai Valdez

LAB 2 WRITE-UP

Descriptive Statistics

Experiment 1
Humans: Averages: 0mg distributed- 3.83 pg/ml of inflammotin. Standard deviation of 1.52301018. Standard error of .4816181068.

         5mg distributed- 8.932 pg/ml of inflammotin. Standard deviation of 1.59393155. Standard error of .5040454132.
         10mg distributed- 61.622 pg/ml of inflammotin. Standard deviation of 30.1106939. Standard error of 9.521837465.
         15mg distributed- 657.941 pg/ml of inflammotin. Standard deviation of 212.942976. standard error of 67.33848159.

Experiment 2
Rats: Averages: 0mg distributed- 8.84360302 pg/ml of inflammotin. Standard deviation of 4.55455091. Standard error of 1.440275459.

         10mg distributed- 11.112 pg/ml of inflammotin. Standard deviation of 7.40288592. Standard error of 2.340998077. 


Results


Human and Rat graph data.PNG




Analysis

Humans The change in data was significant across all tests. The inflammatin levels increased exponentially once it reached a dose of 15mg, as shown in the graph below.

Final graph for humans.PNG.

Rats The change in inflammotin was not significant in rats when given 10mg doses of LPS.





Summary/Discussion

(Please discuss the results and statistical analysis from both experiments. State your conclusion.)

After preforming the ANOVA test for the data of 'Inflammatin Levels of Humans given LPS', we determined a P-value of 1.4E-16. Because the P-value is less than 0.05, it supported the claim that there was statistical significance supporting a difference in the inflammatin levels between one or more of the LPS doses. The T-Test P value between each LPS dose (0mg-5mg, 0mg-10mg, 0mg-15mg, 5mg-10mg, 5mg-15mg, 10mg-15mg) was less than the P-value of .0125 (P-Val of .05/4 groups). These P-values were 8.59E-7, 9.94E-6, 1.39E-8,3. 01E-5, 1.57E-8, 6.48E-8 respectively. Because our P-values were less than .0125, we concluded that there was statistical significance supporting a difference in inflammatin levels between ALL of the LPS doses. After the experiment was conducted, the levels of Inflammatin in the Humans was substantially higher after we hit the 15mg threshold. This is significant because the levels jump to a very high amount after an increase of only 5mg. Even though the standard deviation is higher, it still is much more effective than administering lesser amounts of LPS'.

  After preforming the ANOVA test for the data of 'Inflammatin Levels of Rats given LPS', we determined a P-Value of .867. This P-Value, unlike that of the Human data, was above the determining value of 0.05. Therefore, our Rat data does is not statistically significant and supports an alternate hypothesis that there is no difference between inflammatin levels for LPS doses of 0mg and 10mg. This then proves the claim that the LPS drug does not effect the rats in the same way as humans, in addition, it seems to affect the rats to a very minimal degree. Certainly not enough to provide evidence that it is effective with the rats at increasing inflammatin levels.