After today’s presentation

today’s presentation was fun though i was answer badly and unprofessionally because didn’t expect to have this kind of questions asked. but it’s a good experience at least to know what is the weakness when intends to present data to public or in thesis.

My project is largely based on one vascular triad hypothesis and because we knew that in Malaysian, the acute coronary syndrome (ACS) or in common term as “heart attack” is very common acute disease in Malaysia. In Sarawak General Hospital, each year the circulation problem remains second reason why people admitted to hospital, despite from pregnancy. It’s how dangerous and when it attack a person, the cure doesn’t really can cure. Patients will first taken medication to relieve their chest pain (mostly morphine) and will taken streptokinase to get rid the platelets from the coronary plaque. When the platelet sudden released after activation from a plaque rupture, it can block the artery and therefore the oxygenated blood flow can’t do its work. This we called as myocardial ischemia (deoxygenated blood supply) and leading to myocardial necrosis (heart muscle cell death), and once the heart is malfunction, the rest of the organ also in risk.

It becomes important to prevent such acute disease before it happens. Therefore we’ve the objective to look at the pathogenesis of how this disease occurs from both basic and clinical view.

In fact, during the presentation i was asked is there any study has been done in overseas? I would say Yes because similar studies has carried out everywhere, but we and they are target on different population. Different population different person has different genetic make-up, so it’s worthwhile to do this kind of study (though similar) in our population. Second thing, what this information be useful for clinical? Answer is from the basic science of view, = “find the root cause, prove it”, if we prove our hypothesis that expression patterns is varied among stable heart disease or ACS, we can draw a finding that by targeting on this marker level we can provide better diagnosis for ACS in healthcare or to prove that this marker is useful as golden cardiac marker? (Big picture objective).

Also, i was told that my presentation’s objective is not clear. In fact, i believe most judges they probably don’t realise there is regulating factors in central dogma affect how the protein is synthesised (the marker) when a disease occurs. Interestingly, i found association of inflammation and platelet activation (plaque rupture marker) at transcript level, but not at protein level. How we explain this? that’s long way to go, we should be objective with the current result at this moment.

By targeting on 4 markers can’t really describe the complex pathogenesis of ACS, the only way to see distinctive patterns would be better is to run a microarray.

Ok, just a sharing of overview of what i doing. The findings from this project just a validation if can compare to previous study, but it would be much interesting if i can find out why a young one, no risk factor of smoking, hypertension, high cholesterol, and no blockage of artery can have heart attack????