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12 thoughts on “D16 – Schaal”
I was wondering what other errors besides incorrect pipetting technique could have impacted your data.
In our experiments we were testing with Salmonella Typhimurium which is a live bacterium. When working with a live bacterium there are going to be aspects that we as researchers cannot always control. This can lead to slight differences in data from trial to trial which is why it is important to do as many trials as possible and then average them.
Would you ever be able to test directly on the Salmonella Typhi without it being already in humans?
I do not know the exact answer to this question because it is slightly out of the scope of this class. However, what is unique about our research is Salmonella Typhi is structurally identical to Salmonella Typhimurium so when a compound is effective against Salmonella Typhimurium it is reasonable to conclude that this compound will also be effective against Salmonella Typhi. Another notable feature of Salmonella Typhimurium is that it causes typhoid fever in mice which is important because when testing in mice the results will show how the compound treats symptoms of typhoid fever.
You mentioned that there were some errors in your experiment. What would you have done to avoid or rectify any of the errors that occurred your trials?
I think the best way for my group to rectify these errors would be to do more trials. The more data the better. Then, we can average are data and get a value that is closer to the “truer” value.
How was your hypothesis supported on antibiotic resistance?
We determined this through statistics. Our negative control was DMSO, and in order for a compound to be considered a statistical hit (or an effective antibiotic) the absorbance value of the compound needed to be outside +/- 2 standard deviations of the average absorbance values of DMSO. For our experiments we used the compiled class data on DMSO to increase accuracy and reliability of our results.
What about mytomycin being a chemotheraputic drug suggests that it has capacities to inhibit or kill bacteria?
There have been multiple studies done on mitomycin that show that it can use the same mechanisms it uses to kill cancer to kill pathogens. The sources in the references section of my poster describe these studies in more detail.
I enjoyed your presentation! Do you think the mitomycin interacts with the bacteria in a similar way to cancers when its used as a chemotherapeutic? Does it damage and kill them with the same mechanism of action?
It is reasonable to infer that the mechanisms of action are the same. There have already been studies done to support this; I invite you to check them out in the references section of my poster. Determining the exact mechanism of action mitomycin uses could be a next step in our research.