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It has been hypothesized that statins exhibit early anti-inflammatory effects that may explain their benefit in acute manifestations of CVD (e.g., ACS).
It has also been hypothesized that statins may promote β-cell apoptosis, enhancing nitric oxide production by the endothelium [ 5].
It has been hypothesized that statins mediate their effects by increasing the expression in bone of the growth factor bone morphogenic protein-2 (BMP-2) which in turn leads to osteoblast differentiation and bone formation [ 2].
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Therefore, it was hypothesized that: H1.
It has also been hypothesized that lipophilic and hydrophilic statins have different effects on adiponectin and insulin resistance.
It has been hypothesized that reducing sunlight by only 1% should eliminate this problem.
Søyseth et al. hypothesized that statins might improve all-cause mortality in COPD because many COPD patients probably have unrecognized ischaemic heart disease [ 22].
In view of these previous studies, it is hypothesized that treatment with statin increases intracellular oxidative stress by disrupting the antioxidant defense system in certain transformed and cancer cells, particularly by inhibiting biosynthesis of isoprenoid antioxidants such as CoQ10 and dolichol.
Given the fact that most of the patients studied were taking aspirin, ACEI and a statin, it might be hypothesized that the impact of low glucose on fibrin clots is potent enough to be detectable despite some beneficial effects attributed to those medications.
It could be hypothesized that, in the lower blood pressure interval, as found in the ADVANCE trial, the statin preventive effect could override the impact of blood pressure lowering by antihypertensive drugs.
Thus, it may be hypothesized that.
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