10 thoughts on “D1 – Laurel

  1. Will the research you carried out affect clinical trials of the type of chemotherapy you studied?

    1. Sadly no, the hope would be for the next drug discovery section to continue working with Erlotinib and Capecitabine. We were limited in that our specific vials did not show hits including the positive control of colchicine so further research needs to be completed on their additive effects.

  2. What other model organism could be used to conduct this research that could provide more accuracy in relation to human’s drug absorbance in terms to metabolism, etc…

    1. At this level of the research the drosophila are the best living model due to their cheapness and similarities. They are different as mentioned in metabolic manners, but to my knowledge they are a very near model as an invertebrate. To move to a more similar organism would require a lot more tests in drosophila and then other smaller animals.

  3. How would the larger concentration gradients be found, and how would it be made more uniform through out all the fly food?

    1. Firstly the food question, this is difficult to assess as the manner we added to the food was the same as other groups. Per Dr. Harvey when adding water with food coloring the color appears to disperse evenly through the vials. A main limit was that we did not know the exact number of larvae per vial nor did we quantify any larvae/pupal cases that fell off the walls or never left the food. For instance a colchicine vial of ours produced a positive survival rate, because of the 5 pupal cases on the wall only 2 were dead. However, there were more than 50 dead cases and larvae in the food – but it was not within the methods of the experiment to quantify these.

      In terms of larger gradients the first step would be a more accurate repeat before moving to a broad range of concentrations with the drugs separately and together to find the best dosing of each drug and the best when used in combination.

  4. What part of the methods would result in the positive control not showing a significant hit within your viles and would you be able to go back and revise to get a result without having to redo the whole experiment?

    1. Sadly no way without redoing, in the methods the amount of larvae added to the vials was simply estimated to be between 50-100 which is a very broad range and likely has significant differences between vials. We also did not quantify any larvae/pupal cases that fell off the walls or never left the food. For instance a colchicine vial of ours produced a positive survival rate, because of the 5 pupal cases on the wall only 2 were dead. However, there were more than 50 dead cases and larvae in the food – but it was not within the methods of the experiment to quantify these.

  5. If you interfere with DNA to induce breaks and perturb tyrosine kinases why aren’t there catastrophic consequences leading to death of larvae? Why wouldn’t there be a hit as your data shows?

    1. Our main theory and that supported by data is simply that we did receive hits, we just did not within the experimental design per the DD lab quantify any larvae that did not pupate on the walls of the vials. This could be due to killing a ton of them, not enough larvae in the vials and too many in the negative controls, or simply that the drugs did not get through the food well enough. Dr. Harvey has shown that it is not likely that it was drug distribution, given the other limitations re quantification of outcomes it seems likely that the lack of hits was related to the methods rather than the drugs and radiation. Namely the fact that our positive controls were drastically different from the class as a whole suggests this.

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