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About Ardyen

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  • Birthday 08/30/1988

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  • Location
    India, Somewhere in
  • College Major/Degree
  • Favorite Area of Science
    Physics, Astronomy, Medicine
  1. I like a debate as well! I did read similar views a while ago(I will read the paper's you've quoted sometime today), but I don't think they have been incorporated into mainstream clinical/medical literature. Part of the reason for that may be that, if we acknowledge that vascular/hemodynamic fators (yes, the sheer stress and non-laminar blood flow causes the initial damage to vascular endothelium, and hence increased leukocyte adherence) are a significant etiology, then atherosclerosis will then have to be considered Idiopathic, rather than related to measurable biochemical parameters. And
  2. Unless you know something I don't, Its still caused by lipoproteins/LDL/Cholesterol. I quote abstract texts from Harrison's Principles of internal medicine. 17th edition. Pages 1501-1505: "The early lesions most often seem to arise from focal increases in the content of lipoproteins within regions of the intima......." "Lipoproteins sequestered from plasma anti-oxidants in the extracellular space of the intima, become particularly susceptible to oxidative modificatins, giving rise to hydroperoxides......" which is essentially ageing. I don't think we need to debate on the molec
  3. 1.It is used to measure both. 2.Yes it measures both (De and re-polarization). Thats essential because for you to know how fast the muscle is going to respond the next time to the same action potential, you need to know the potential(at the highest point) of depolarization. 3.Spikes represent the highest action potential of that muscle, and consequently higher muscle function. 4.That the muscle is depolarizing and repolarizing quckly. i.e its twitching, or physiologically in clonus. I'd just wanted to ask, Where did you perform this on? A cadaver? Or some lower organisms like a frog?
  4. I'd like to add something here. The mechanism of thrombus formation is essentially the same(through the cytokines and other inflammatory mediators), though the stimulating insult may vary. Every infection dosen't cause a thormbus. Atherosclerosis is something that happens innately, and its related to ageing and LDL/cholesterol levels. It makes certain arteries(cornary and the cerebral) more prone to occlusion, but it itself doesn't cause thrombosis as previously suggested. I know someone's then gonna say that thrombi in infective endocarditis, are essentially from plaqes, which are a
  5. Hi! I'm Ardyen and I'm a medical graduate(just completed!) from India. And I'm interesed in anything under the sun!!(maybe beyond it as well).
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