BME100 f2013:W1200 Group11 L2

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Contents

OUR TEAM

Name: Nitish Peela
Name: Nitish Peela
Name: Shayan Naeini
Name: Shayan Naeini
Name: Meera Doshi
Name: Meera Doshi
Name: Nathan Dacasin
Name: Nathan Dacasin
Name: Angelina Ledesma
Name: Angelina Ledesma

LAB 2 WRITE-UP

Descriptive Statistics

Experiment 1

Image:Human study chart.png

Experiment 2

Image:rat study chart.png


Results

Human Study


Image:adkjd.png


This bar graph shows that as the LPS dosage increases, the amount of inflammotin in the human body also increases. The stars on the graph represent that it is statistically significant. The lines above the bars on the graph represents the standard deviation in the study.


Rat Study

Image:Lena.png

This bar graph shows that there is no real correlation between LPS dosage and the amount of inflammotin in rats. The lack of a star represents that the graph is not statistically significant. The lines above the bars on the graph represents the standard deviation in the study.

Analysis

Human Study
Bonferroni Image:bonferoni1211.png

We ran six t-tests and preformed a Bonferroni correction to determine the significance of the human data. The Bonferroni correction gave us a p-value of 0.0125. Since all of our p-values were below 0.0125, our results fell within the 95% confidence interval. Therefore our results were significant.
Image:dalskjdas.png

We also ran an ANOVA test because there were more than two groups being compared. Based on our results from the ANOVA test we got a p-value of 1.4E-16. Since this p-value is below 0.05 the data is significant.

Rat Study
Image:ldk2e.png

We ran a t-test to determine the significance of rat data. Our t-test gave us a value of 0.867. Since this p-value is above the 0.05 then the data is not signifcant because it doesn't fall within the 95% confidence interval.

Summary/Discussion

In the first experiment (the effect of lipopolysaccharide on amount of Inflammotin in humans), we ran a t-test and discovered a p-value of 0.0125. This p-value is less than the alpha value of 0.05 and consequently, our results are statistically significant. Even the groups that were given a lower concentration of lipopolysaccharide (5 mg) were substantially affected by it. The experimental group that was given 5 mg of lipopolysaccharide had almost three times the amount of Inflammotin that the control group did. This means that we are 98.75% confident that there is a strong, positive correlation between the amount of lipopolysaccharide given to the subject and the amount of Inflammotin in their bloodstreams. We can conclude that there is a relationship between increased dosage of lipopolysaccharide and the amount of Inflammotin in their bloodstreams.

In the second experiment (the effect of lipopolysaccharide on the amount of Inflammotin in rats), we ran a t-test and discovered a p-value of 0.867. This p-value is greater than the alpha value of 0.05 and consequently, our results are not statistically significant. This means that we are only 13.3% confident that there is a correlation between the lipopolysaccharide dosage and the amount of Inflammotin found in the rats' bloodstreams. Although a 10mg dosage of lipopolysaccharide did increase the average of the amount of Inflammotin by approximately 0.6 pg/ml, our confidence level is too low for our data to hold any weight. Since our confidence level is so low, our results are inconclusive and the relationship between the dosage of lipopolysaccharide and the amount of Inflammotin in rats can not be determined.


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