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Further, the polymer used as a vehicle for drug delivery may induce vessel irritation, endothelial dysfunction, vessel hypersensitivity, and chronic inflammation at the stent site.
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This suggests that the addition of such growth factors may induce blood vessel ingrowth, which could be detrimental in any treatment, because it has been reported that this is also accompanied by nerve ingrowth [ 16].
Cells that do not coordinate angiogenic signaling may induce leaky vessels that temporarily increase blood flow (Nagy et al. 2012) until vessels collapse because of pressure loss resulting from excess permeability.
Of central importance is that many data have accumulated demonstrating that various inflammatory pathways lead to endothelial cell activation, which may induce complications such as vessel occlusion and tissue destruction in a predisposed host, and longstanding disease.
The presence of CMV in the vessel walls may induce smooth muscle cell proliferation and migration, increased uptake of oxidized low-density lipoprotein and expression of cytokines and chemokines as well as increased procoagulant activity by endothelial cells [16], [17], [25], [26].
For example, cancer cells that coordinate and regulate angiogenic signaling (for blood vessel growth) may induce greater blood flow to the tumor.
Exposed basement membranes may induce thrombus formation causing blood vessel congestion, blood flow reduction, and hypoxia resulting in necrosis and tumour cell death.
It is possible that intralysosomal accumulation of oxidized LDL within iron-rich lysosomes of vessel macrophages may induce foam cell formation and apoptotic cell death due to lysosomal destabilization, contributing to atherosclerosis (Li et al. 2001, 2006).
As shown in Figure 1, when non-diabetic mice of different genotypes were compared, ApoE−/− mice were found to express higher VCAM-1 levels than wt mice (p<0.05), suggesting that hyperlipidemia may induce VCAM-1 expression in retinal vessels.
Another histopathological investigation indicated that IVB may induce changes in immature, newly formed vessels, leading to endothelial apoptosis with vascular regression and inducing the normalization of premature vessels in PDR or NVG eyes [ 15].
It has been postulated that severe hypoxia may induce the formation of new tumour blood vessels necessary for further tumour growth (Folkman, 1995).
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