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According to our results, Phd2 haplodeficiency constitutively upregulates Tie2 in macrophages, thus triggering the accumulation of proarteriogenic macrophages and enhancing collateral maturation at baseline.
Previous animal studies have proven the feasibility of enhancing collateral function by delivery of angiogenic factors to the myocardium [ 1, 2, 22- 24].
Taken together, this evidence suggests a biological role for vitamin D in cardiovascular function and angiogenesis [ 36, 37], such as enhancing collateral development.
Furthermore it was shown that adenoviral transfection of PR39, a protein that enhances hypoxia-inducible factor-1 alpha- (HIF-1 alpha-) dependent gene expression by selectively inhibiting proteasome degradation of this transcription factor, improves blood flow and myocardial function in a pig model of chronic myocardial ischemia by enhancing collateral formation [ 7].
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For example, new service and delivery technologies, combined with significantly enhanced collateral standards, will practically eliminate the need for intraday credit in the tri-party repo market by the end of next year.
In murine ischemic models, bone marrow stromal cells have been shown to enhance collateral flow recovery and remodeling, thereby attenuating muscle atrophy [46].
Additionally, interaction of FGF5 with cardiomyocytes has been reported to stimulate angiogenesis, enhance collateral blood flow, and relieve stress-induced ischaemia.
As one mechanism of protection, KD025 improved cortical perfusion in a distal middle cerebral artery occlusion model, implicating enhanced collateral flow.
As a result, ONO-1301SR treatment enhanced collateral growth in relation to increased number of the capillaries, attenuated collagen fraction in the myocardial interstitium and reduced LV volume, indicating that this treatment reversed the LV remodelling.
Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen that induces increases in vascular permeability and angiogenesis, enhances collateral vessel formation, and increases the permeability of the microvasculature [ 38].
The fact that the number of BDA-labelled fibres not only increased in the ipsilateral dorsal funiculus (intact corticospinal tract) but also in the contralateral dorsal funiculus (injured corticospinal tract) implies that human NPCs may enhance collateral (cross midline) sprouting of the intact corticospinal tract into denervated regions of the spinal cord (Chen et al., 2002; Liu et al., 2008).
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