“It is the weight, not numbers of experiments that is to be regarded”1. As Sir Isaac Newton, one of the most influential scientists in history, states – the design of an experiment is very important. Therefore, aspiring scientists must learn about many different types of techniques and its applications. Over the past six weeks, students were exposed to six experts discussing different fields of research but their studies contained many overlapping qualities. Some common topics discussed were using animals to model mental illnesses, paths to drug discovery in oncology, and the role of inflammation in mental illness etiology. Firstly, the use of animals to model mental illness was presented by Dr. José Nobrega in lecture two and Dr. Ali Salahpour
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For example, he presented a study using mice to exhibit prodromal syndrome by causing lesions in the hippocampus2,3 – an area of the brain Dr. Andreazza also connected to schizophrenia and bipolar disorder4,5 – and treating them with antioxidants2,3. These researchers noticed that mice with lesions and no treatment had higher levels of DNA oxidation in parvalbumin interneurons which uses the neurotransmitter glutamate2,3. This suggests that schizophrenia is linked to DNA oxidation – possibly by mitochondrial dysfunction4,5 – within neurons leading to irregular glutamate levels2,3. The hypothesis that glutamate may be linked to mental illness was also suggested by Dr. Salahpour6. His field of study focuses on merging two major hypotheses of schizophrenia manifestation – increased dopamine levels and hypoactive N-methyl-D-aspartate (NMDA) glutamate receptors – using genetically altered mice6-8. These mice were genetically created to have low levels of NMDA and exhibited schizophrenic symptoms6. However, some stopped when given dopamine receptor …show more content…
Mattieu Schapira in lecture five and Dr. Brent Williams in lecture six discussed two different ways to discover lifesaving drugs for hematological malignancies. Dr. Schapira spoke about histone tail modification, specifically lysine acetylation and methylation, to control gene expression9. For example, in many hematological malignancies the MYC, a prominent oncogene, enhancer has been translocated with the IgH super-enhancer causing overexpression of MYC and then cancer9. Bromodomain protein 4 (BRD4) – which reads acetylated lysines – can read the IgH enhancer and regulate MYC but when inhibited, MYC expression falls to non-cancerous levels9,10. Dr. Williams took a different approach when researching a treatment for hematological malignancies, specifically acute myeloid lymphoma (AML)11. His scientific career led to immunotherapies like the phase I clinical trial at Princess Margret Cancer Centre that’s investigating cancerous natural killer (NK) cells to kill other cancer cells more effectively11. Cancerous NK cells extracted from a 1992 Non-Hodgkin’s lymphoma patient are more cytotoxic than normal NK cells thus, after irradiation to prevent cell proliferation, it can be given to AML patients – called NK-9211,12. I found this very interesting as it seems counterintuitive to give cancer patients cancerous cells but in the phase 1 trials have demonstrated promising results11. Overall, Dr. Schapira and Dr. Williams chose different mechanisms – epigenetics and
For example, he presented a study using mice to exhibit prodromal syndrome by causing lesions in the hippocampus2,3 – an area of the brain Dr. Andreazza also connected to schizophrenia and bipolar disorder4,5 – and treating them with antioxidants2,3. These researchers noticed that mice with lesions and no treatment had higher levels of DNA oxidation in parvalbumin interneurons which uses the neurotransmitter glutamate2,3. This suggests that schizophrenia is linked to DNA oxidation – possibly by mitochondrial dysfunction4,5 – within neurons leading to irregular glutamate levels2,3. The hypothesis that glutamate may be linked to mental illness was also suggested by Dr. Salahpour6. His field of study focuses on merging two major hypotheses of schizophrenia manifestation – increased dopamine levels and hypoactive N-methyl-D-aspartate (NMDA) glutamate receptors – using genetically altered mice6-8. These mice were genetically created to have low levels of NMDA and exhibited schizophrenic symptoms6. However, some stopped when given dopamine receptor …show more content…
Mattieu Schapira in lecture five and Dr. Brent Williams in lecture six discussed two different ways to discover lifesaving drugs for hematological malignancies. Dr. Schapira spoke about histone tail modification, specifically lysine acetylation and methylation, to control gene expression9. For example, in many hematological malignancies the MYC, a prominent oncogene, enhancer has been translocated with the IgH super-enhancer causing overexpression of MYC and then cancer9. Bromodomain protein 4 (BRD4) – which reads acetylated lysines – can read the IgH enhancer and regulate MYC but when inhibited, MYC expression falls to non-cancerous levels9,10. Dr. Williams took a different approach when researching a treatment for hematological malignancies, specifically acute myeloid lymphoma (AML)11. His scientific career led to immunotherapies like the phase I clinical trial at Princess Margret Cancer Centre that’s investigating cancerous natural killer (NK) cells to kill other cancer cells more effectively11. Cancerous NK cells extracted from a 1992 Non-Hodgkin’s lymphoma patient are more cytotoxic than normal NK cells thus, after irradiation to prevent cell proliferation, it can be given to AML patients – called NK-9211,12. I found this very interesting as it seems counterintuitive to give cancer patients cancerous cells but in the phase 1 trials have demonstrated promising results11. Overall, Dr. Schapira and Dr. Williams chose different mechanisms – epigenetics and