During this internship program, working with Professor Gu and doctor Rachel has being an incredible experience which inspired me to investigate deeply and thoroughly into my subject, as they are great teachers and role-models who provided me with immense support towards my project. Meanwhile my fellow mates also gave support towards the direction of my work. Further, this program has not only empowered my ability to understand ostentatious and profession material, enriching my own comprehension towards writing a research proposal, yet has also more importantly lead me to a deeper grasp of the chronic obstructive pulmonary disease, a disease involved within the gradual deterioration of lung function. COPD is personal to my family, as my grandpa is a patient tormented by this obstructive disease. Therefore, it is always being my goal to investigate inside this chronic lung disease, and discover a treatment cure that will remedy my grandfather and the other 300 million people worldwide suffering from COPD. This program has inevitably enabled me to take the first step towards this goal, further establishing my own determination towards creating a cure for COPD. For instance: I have specifically investigated inside the epigenetic factors of COPD, how differential DNA methylation correlates to the development of this disease. My project focuses on three aspects of disease state, existing remedy and possibly remedies and research direction in the future.
Throughout this internship program, I have gained a foundational knowledge towards the association between differential methylation and chronic obstructive pulmonary disease in aspect of disease state. This is evident, when I discovered an inevitable relationship between differential DNA methylation and the pathogenesis of COPD, specifically, how hyper-methylation in specific genes of HIPK2, CAV1, ANGPT1 and more, causes DNA aberrations and the unregulated growth of cells, which correlate towards the disease states of COPD. This is shown as aberrant DNA will destabilise the cells and causes dysfunction towards certain areas of the pulmonary system, while the chronic obstructive pulmonary disease is also the combined effect of emphysema and bronchitis, emphysema is involved in alveoli expansion due to damaging of alveoli walls, and bronchitis is mainly the inflammation small airways, both are predominately due to unregulated cell growth partially under differential methylation. Further, the disease is caused mainly by external factors of smoking and the inhalation of other noxious gases, as the stimulus of gases can induce differential DNA methylation within the lungs therefore promoting the unregulated growth of cells. Meanwhile, in an internal and genetic context, an inheritable genetic condition known as alpha-1 antitrypsin deficiency can also cause COPD, under the mutation and hyper-methylation inside the SERPINA1 gene and the low antitrypsin level within blood, which together causes the unregulated white blood cells to attack the fragile wall of the alveolus, causing emphysema. Meanwhile antitrypsin is a type of protein produced by the liver. These factors show in which the disease state of COPD is closely associated towards differential methylation.
I have discovered that current treatment of COPD involves the uses of, bronchodilators, inhaled steroid, phosphodiesterase, oxygen therapy and bullectomy. Bronchodilators, inhaled steroid and phosphodiesterase are all inhaled medicines, that reduce inflammation inside the small airways, while inhaled steroid and phosphodiesterase have a more intensive treatment effect than Bronchodilators. Further, oxygen therapy is the induction of pure oxygen inside the lungs which compromises for the limited oxygen supply in blood due to the crippled functions of the alveolus. Bullectomy is a surgical method which removes small air-spaces known as bullas from the lungs, specifically, bullas are formed when the damaged alveolus burst under the stress of expansion, releasing air inside the lungs. Meanwhile, this project also discovered a possible relationship between differential methylation and treatment medicine. For instance, a level of DNA demethylase may be present inside bronchodilators, inhaled steroids and phosphodiesterase, to suppress the differential methylation patterns inside the disease states, specifically, the aberrant DNA methylation is a reversible process, and therefore by de-methylating and re-expression certain anti-inflammatory genes, the inflammation can be receded further under the body’s own defence mechanism. Though, this relationship is not proved by supporting evidence, as the specific components of medicine is hindered away from public. Current treatments of COPD are only by means to slow disease progression, and therefore cannot completely cure the disease.
The foundational knowledge of this disease therefore stimulated my own creativity in developing a treatment for COPD, with specificities towards aberrant DNA methylation. This is evident when I proposed epi-drugs as a possible treatment medicine towards COPD, as the targeting of epigenetic factors can effectively suppress certain disease states. Epi-drugs are substances involving various inhibitors of demethylase and more, according to their responding disease, specifically, inhibitors are responsible for controlling the unregulated growth of cells. Epi-drugs are mainly directed towards cancer treatment, though the finding from this experiment suggests in which epi-drugs can also create a measurable effect on COPD. This is shown, in the context of differential methylation, where epi-drugs containing DNA demethylase can disrupt the aberrant activity of DNA methyltransferase, therefore fixing mismatches of hyper-methylation, hypo-methylation and more inside epigenome. This signified its possible treatment effect on COPD, as the chronic obstructive pulmonary disease involves many differential methylation inside its disease state. For instance, DNA methylation inhibitors of Decitabine, 5-Azacitidine and Antisense oligonucleotides, are used in epi-drugs to allow the re-expression of previously silenced genes. Though, the change in DNA methylation pattern is not enough to completely suppress a disease state, therefore epi-drugs also focus to inhibit the aberrant histone methylation inside a disease. These findings therefore proposed a possible research direction that may lead to a cured for this chronic lung disease.
This program has also improved my reading and scientific writing skills, enhancing my understanding towards professional articles. This is shown during the research stages of my project, where I visited many professional reports regarding the relationship between differential methylation and COPD, which gave many practices to my reading and understanding skills. Further, during my reading, I researched many scientific terminologies in the articles which I did not understand in the first place. This enabled me with rudimentary knowledge to understand future article relating to this subject. Meanwhile, I also took notes during reading, which practiced my ability to retain information when viewing text. My research within my subject also exposed me to a variety of language use and writing styles in biology, specifically, the articles are written by different people in their own distinctive language styling and techniques. For instance: certain materials are written mostly in passive language, while others may be written predominantly with active language. This exposure towards different styles inevitably enhanced my understanding and writing skills, as I am given the opportunity to learn from other people’s expression, in improving my own scientific writing. In particular, the articles are often very succinct and clear in their language use, which is an important characteristic to learn from in improving my own writing skills in science, as clarity sometimes enable people to understand better.
Overall, within this program I have gained important knowledge towards the relationship between differential methylation and COPD which is separate into three aspect of disease states, current medicine and suggested direction of future treatment development. Meanwhile, I have also enhanced my reading and expressional ability. It is of my greatest thank you and appreciation towards professor Gu, Doctor Rachel and my peers for their support within this program, for their advices and suggestion which helped to structure my work. Ultimately, I am very grateful of this internship opportunity, as it not taught me to be a more diligent student, but also supported my determination and goal to become a doctor. I am definitely looking forward to future involvement within this program. Greatest thank you again to all.
