Ardyen

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 the normal LDL/cholesterol levels causing fatty streaks in some individuals, may well be related to their inherent responses(What's normal for most, may not be normal for a small subset, like Blood Pressure, Leukocyte count...etc). I think that the current clinical view is that its multifactorial, and that we have established a major portion of what we presume to be the etiological factors, and reluctant to add the others without conclusive proof, because that would then make the current stress on lowering lipid levels(with statins, modified diets, finding ways to decrease oxidative stress and ruling genetic/familal causes for isolated hyperlipidemias) , pretty much redundant. Also with epidemiological evidences for the older beliefs as with the Framingham Heart Study (one of the classical longitudial studies, I'm sure you'd have heard of it: http://en.wikipedia.org/wiki/Framingham_Heart_Study, and many such in the late 80's to 90's) I think the medical community will find it hard to disregard these factors. Maybe, just maybe a few decades later, we'd come to think of our current views as pretty outdated:-p.

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 molecular mechanisms or specific pathological processes in the formation or re-organizatinon of a plaque, because the inciting factors remain the same: Higher Lipoprotein levels and oxidants. NO other etiological cause: bacterial/infective, genetic, or immune mediated disorder has been PROVED to cause it, though there are a number of hypotheses for the same. And if you read my entire post, I said that atherosclerosis PREDISPOSED to formation of a thrombus. A thrombus is formed on a plaque when it ruptures. But it doesn't arise from within the plaque or the original cellular/endothelial defect/mass.It dosen't have to always form when a plaque ruptures as well. Procoagulant factors in blood come in contact with exposed plaque collagen, can cause thrombosis. Rupture of an atherosclerotic plaque causes predisposition to thrombsis. Normal plaques DO NOT cause thrombosis. They occlude the lumen, so that an emboli may get lodged here and subsequently cause infarction. So Plaques predispose to thrombosis when they rupture, which is NOT a normal outcome of re-organization of an atherosclerotic lesion.

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?

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 result of inflammation itself, but we'll take it as a one off. (What actually happens is that the palque acts as a platform of sort for the bacteria to develop and produce blood clots). I guess a part of the answer to this question must be through sepsis. This is when the bacteria overwhelm the humoral immunity, which was lacking in that individual for a large number of reasons(the cell mediated immunity is still intact but overworked as well), and start multiplying rapidly. One of the manifestations of this is that toxins are released at a higher rate than in an uncontrolled infection and this is what predisposes to microthrombi in capillary circulation. Also some bacteria possess Hemagglutination receptors, and they cause clotting in vitro( i'm not sure whether its in vivo as well). So, lets say someone has uncontrolled pneumonia, and if untreated can cause microthromi in pulmonary circulation apart form the pathological process of consolidation. And Scilearner, you're right in the opening post that inflammation itself causes more tissue harm than the bacteria themselves. But in the long-term outcome is going to be much adverse, maybe death. So, you could consider it as some sort of collateral damage!!

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).