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Team:Elan Vital South Korea/p results and conclusion
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<h1 class="title">Results and Conclusion</h1> | <h1 class="title">Results and Conclusion</h1> | ||
| + | <img class="wiki_img" src="https://static.igem.org/mediawiki/2014hs/2/29/Elan_vital_results_1.png" /> | ||
| + | <p class="listing">7 A, G, K, T: DNA of MRSA from patient 7 grown in ampicillin, gentamycin, kanamycin, and tetracycline, respectively.</p> | ||
| + | <p class="listing">8 A, G, K: DNA of MRSA from patient 8 grown in ampicillin, gentamycin, and kanamycin, respectively.</p> | ||
| + | <p class="listing">7 GA, KA, TA: DNA of E. coli grown in ampicillin, which were transformed with the DNA of MRSA from patient 7 grown in gentamycin, kanamycin, and tetracycline, respectively.</p> | ||
| + | <p class="listing">8 GK, KK: DNA of E. coli grown in kanamycin, which were transformed with the DNA of MRSA from patient 8 grown in gentamycin and kanamycin, respectively.</p> | ||
| + | <p class="listing">8 GG: DNA of E. coli grown in gentamycin, which were transformed with the DNA of MRSA from patient 8 grown in gentamycin.</p> | ||
| + | <p class="paragraph">The results show that wells 2-8 has about 300 base pairs, which means that most likely the type V primers were active in PCR, and the section of DNA between V-F and V-R with about 300 base pairs were multiplied in PCR of 7A, 7G, 7K, 7T, 8A, 8G, and 8K. This most likely means that 7A, 7G, 7K, 7T, 8A, 8G, and 8K all included the section of 300 base pairs that is between V-F and V-R. So, this 300 base pair long section of DNA has a possibility of coding for multidrug resistance. | ||
| + | The results also show that wells 9-11 has about 1000 and 1600 base pairs, which means that most likely the primers ccrAB-α3 and ccrAB-α4 were active in PCR, and the section of DNA between ccrAB-α3 and ccrAB-α4 with about 1000 base pairs and the section of DNA between ccrAB-α3 and ccrAB-α4 with about 1600 base pairs were multiplied in PCR of 7K, 8G, and 8K. This most likely means that 7K, 8G, and 8K all included the sections of 1000 and 1600 base pairs that is between ccrAB-α3 and ccrAB-α4. So, this 1000 base pair long section of DNA and the 1600 base pair long section of DNA has a possibility of coding for multidrug resistance.</p> | ||
| + | <p class="paragraph">The results show that wells 12-17 has about 150 base pairs, which means that most likely the primers MecA147 or the primers mecI were active in PCR, and the section of DNA between MecA147-F and MecA147-R or the section of DNA between mecI-F and mecI-R with about 150 base pairs were multiplied in PCR of 7GA, 7KA, 7TA, 8GK, 8GG, and 8KK. This most likely means that 7GA, 7KA, 7TA, 8GK, 8GG, and 8KK all included the section of 150 base pairs that is between MecA147-F and MecA147-R or the section of 150 base pairs between mecI-F and mecI-R. So, this 150 base pair long section of DNA has a possibility of coding for multidrug resistance.</p> | ||
<p class="paragraph">From the investigation, we could conclude that MRSA showed strong resistance to ampicillin, gentamycin, and kanamycin, and slight resistance to tetracycline. The transformed E. coli grew in high concentrations of ampicillin, gentamycin, and kanamycin, showing high resistance to those drugs. Also, the transformed E. coli grew in low concentrations of tetracycline, but died in high concentration of the drug, showing low resistance to tetracycline. This shows that the DNA from the MRSA that transformed the E. coli codes for multidrug resistance. Furthermore, we were able to get an idea of which of the DNA were involved in the multidrug resistance. By running PCR, we were able to amplify the DNA involved, and by analyzing this, we could come up with a better understanding of how the multidrug resistance works. An appropriate follow up on the project would be to research the sequence of the identified genes with the hopes of finding a possible drug that destroys even the most drug-resistant MRSA</p> | <p class="paragraph">From the investigation, we could conclude that MRSA showed strong resistance to ampicillin, gentamycin, and kanamycin, and slight resistance to tetracycline. The transformed E. coli grew in high concentrations of ampicillin, gentamycin, and kanamycin, showing high resistance to those drugs. Also, the transformed E. coli grew in low concentrations of tetracycline, but died in high concentration of the drug, showing low resistance to tetracycline. This shows that the DNA from the MRSA that transformed the E. coli codes for multidrug resistance. Furthermore, we were able to get an idea of which of the DNA were involved in the multidrug resistance. By running PCR, we were able to amplify the DNA involved, and by analyzing this, we could come up with a better understanding of how the multidrug resistance works. An appropriate follow up on the project would be to research the sequence of the identified genes with the hopes of finding a possible drug that destroys even the most drug-resistant MRSA</p> | ||
</div> | </div> | ||
Revision as of 12:43, 17 June 2014
Results and Conclusion
7 A, G, K, T: DNA of MRSA from patient 7 grown in ampicillin, gentamycin, kanamycin, and tetracycline, respectively.
8 A, G, K: DNA of MRSA from patient 8 grown in ampicillin, gentamycin, and kanamycin, respectively.
7 GA, KA, TA: DNA of E. coli grown in ampicillin, which were transformed with the DNA of MRSA from patient 7 grown in gentamycin, kanamycin, and tetracycline, respectively.
8 GK, KK: DNA of E. coli grown in kanamycin, which were transformed with the DNA of MRSA from patient 8 grown in gentamycin and kanamycin, respectively.
8 GG: DNA of E. coli grown in gentamycin, which were transformed with the DNA of MRSA from patient 8 grown in gentamycin.
The results show that wells 2-8 has about 300 base pairs, which means that most likely the type V primers were active in PCR, and the section of DNA between V-F and V-R with about 300 base pairs were multiplied in PCR of 7A, 7G, 7K, 7T, 8A, 8G, and 8K. This most likely means that 7A, 7G, 7K, 7T, 8A, 8G, and 8K all included the section of 300 base pairs that is between V-F and V-R. So, this 300 base pair long section of DNA has a possibility of coding for multidrug resistance. The results also show that wells 9-11 has about 1000 and 1600 base pairs, which means that most likely the primers ccrAB-α3 and ccrAB-α4 were active in PCR, and the section of DNA between ccrAB-α3 and ccrAB-α4 with about 1000 base pairs and the section of DNA between ccrAB-α3 and ccrAB-α4 with about 1600 base pairs were multiplied in PCR of 7K, 8G, and 8K. This most likely means that 7K, 8G, and 8K all included the sections of 1000 and 1600 base pairs that is between ccrAB-α3 and ccrAB-α4. So, this 1000 base pair long section of DNA and the 1600 base pair long section of DNA has a possibility of coding for multidrug resistance.
The results show that wells 12-17 has about 150 base pairs, which means that most likely the primers MecA147 or the primers mecI were active in PCR, and the section of DNA between MecA147-F and MecA147-R or the section of DNA between mecI-F and mecI-R with about 150 base pairs were multiplied in PCR of 7GA, 7KA, 7TA, 8GK, 8GG, and 8KK. This most likely means that 7GA, 7KA, 7TA, 8GK, 8GG, and 8KK all included the section of 150 base pairs that is between MecA147-F and MecA147-R or the section of 150 base pairs between mecI-F and mecI-R. So, this 150 base pair long section of DNA has a possibility of coding for multidrug resistance.
From the investigation, we could conclude that MRSA showed strong resistance to ampicillin, gentamycin, and kanamycin, and slight resistance to tetracycline. The transformed E. coli grew in high concentrations of ampicillin, gentamycin, and kanamycin, showing high resistance to those drugs. Also, the transformed E. coli grew in low concentrations of tetracycline, but died in high concentration of the drug, showing low resistance to tetracycline. This shows that the DNA from the MRSA that transformed the E. coli codes for multidrug resistance. Furthermore, we were able to get an idea of which of the DNA were involved in the multidrug resistance. By running PCR, we were able to amplify the DNA involved, and by analyzing this, we could come up with a better understanding of how the multidrug resistance works. An appropriate follow up on the project would be to research the sequence of the identified genes with the hopes of finding a possible drug that destroys even the most drug-resistant MRSA
