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Tumour angiogenesis relies on an intricate interplay between tumour cells, endothelial cells, and surrounding mesenchymal cells (pericytes in microvessels and vascular smooth-muscle cells in large vessels) to activate endothelial cell proliferation, to recruit migrating endothelial cells and pericytes, and to form new vessels through vascular remodelling and maturation (Hamada et al, 2005).
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We have proposed that breast tumour cells that secrete nucleoside diphosphate kinase (NDPK) promote their intravasation and extravasation from blood vessels by generating nucleotides to activate P2Y receptors on endothelium.
Based on recent data in various in vitro and in vivo experimental systems [ 49, 50] we hypothesize that this phenomenon is, to a significant degree, due to the fact that aged blood vessels lose their ability to activate Nrf2, and thereby they are unable to mount proper antioxidant defenses, leading to an increased oxidative-nitrosative stress, and hyperactivation of downstream damage pathways.
In aging vessels, increased production of ROS fails to activate Nrf2, resulting in increased blood vessel sensitivity to the deleterious effects of ROS [ 48].
This result is assumed to be due to the fact that the study's treatment aimed to activate ICG in the vessels after systemic venous injection, rather than for topical PDT.
Finally, exosome-like vesicles released from adipose tissue were shown to activate macrophages at the vessel wall that can secrete IL-6 and TNF-α in a TLR4/TRIF-dependent way, mediating insulin resistance [ 39] (Fig. 1).
Inflammation is also known to activate endothelial cells and promote vessel branching.
Now undergoing clinical trials, the hood works by sending electromagnetic impulses to the brain to activate the formation of new blood vessels.
Additionally, the SNS activates (or continues to activate) the smooth muscle surrounding peripheral blood vessels, causing vasoconstriction and decreased peripheral blood flow.
Fibrin-based matrices appear to activate angiogenic signaling in ASCs while P-fibrin matrices are uniquely able to also drive a vessel-like ASC phenotype.
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