10 thoughts on “D5a – G Thompson

  1. you may have said this already but are the drugs run at the same concentration for the first test?

    1. For the first test they’re all at their pharmaceutical concentrations which is the concentration that they’re administered when used as chemotherapies. So they’re all ’10X’ but that concentration is different for each of them depending on their specific molecular weights and chemotherapeutic concentration.

  2. Hello Grace! I am wondering why you guys decided to use ampicillin as your positive control? What properties allowed it to be considered the positive control?

    1. Hi! Ampicillin is used as our positive control because it is known to inhibit the growth of Salmonella. It was discovered on accident by Flemming and is commonly used as a positive control to inhibit bacteria growth due to how drastically it inhibits the bacterial growth. Also, it is polar so it can dissolve in our DMSO which made it a useful control to use.

    1. Good question! Prior studies showed a decrease in phosphorylation of transmembrane protein receptors TRK, SCF, MuSK, Mer, Erb, and cRet when cells were exposed to sorafenib and imatinib. Because sorafenib and imatinib inhibited bacterial growth, it could then be inferred that those receptors or some combination of those receptors are present in S. Typhimurium. However, more testing would have to be done to solidify that inference.

  3. I really like the figures on your poster, one question is why did you guys use those for your positive and negative control and why did all of the dilutions show grow and what does that tell you about these compounds?

    1. Thanks! We used ampicillin as our positive control because it has been well studied and known to inhibit bacterial growth. We used DMSO as our negative control because we knew that it would have no effect on bacterial growth. Both of these controls dissolved in our bacteria/media mix so that was another reason they were useful.
      The lowest dilutions had the biggest absorbance, which is what we expected. The lowest absorbance meant that inhibition was greatest- so the most diluted having the tallest bars told us they did not inhibit the bacteria as well.

  4. My only question is what is the difference between imatinib and soraatanib, and how exactly do these things impact your results, this might have been explained in the presentation, I just lost where this was explained

    1. Hi! They both are competitive inhibitors of tyrosine kinase and inhibit that pathway by directly blocking the phosphorylation that is required to activate that pathway. Sorafenib inhibits the RAF/MEK/ERK receptors and imatinib inhibits KIT/Bcr‐Abl/α‐PDGFR/β‐PDGFR. So they both do the same thing and inhibit tryrosine kinase but they act on some different receptors to do this. This is useful for pharmaceutical purposes (especially chemotherapy) because if one of them stops eliciting a response in the patient, a different TKI can be administered to target a different receptor but cause the same physiological response in the patient.

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