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The prediction of resonance is very important with respect to the vessels stability in the early stages of design.
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Additional swimming pools, coupled with a number of slack tanks when in operational service, further reduce vessel stability.
Among the angiopoietins, angiopoietin-1 is involved in vessel stability, whereas angiopoietin-2 is involved in vessel sprouting.
Pericyte-endothelial cell (EC) interactions are critical to both vascular development and vessel stability.
To assess vessel stability we quantified Fibronectin 1 content and blood vessel diameter in blood vessels of tumors.
In ECs, TGF-β1 activation of ALK5 is growth inhibitory and is thought to mediate vessel stability [10].
We assessed vessel stability as determined by immunofluorescence staining against fibronectin (FN1) and SMA (smooth muscle actin, which identifies pericytes).
To assess vessel stability we quantified Fibronectin 1 content in blood vessels of controls, WT BM-VPC and mDll4GOF BM-VPC tumors.
Compared to the relatively subtle effects on the speed of retinal angiogenesis and endothelial cell proliferation, astrocyte VEGF deletion had more pronounced consequences on vessel stability.
Dll4 expressed by BM-VPC was able to regulate FN1 and ICAM2 (among other genes) expression on mature EC, suggesting it might modulate vessel stability and activation programs.
As already described in the context of the Dll4 overexpression mutant, Notch signalling activation by Dll4 on EC was able to regulate the expression of several components of the extracellular matrix including FN1 [28], suggesting it modulates vessel stability by controlling the expression of ECM components of the basement membrane.
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