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This model has been accepted as an in vitro simplified model of dermal aging.
Gleevec treatment has also been shown to reduce the synthesis of ECM proteins in a model of dermal fibrosis [ 26].
However, the profibrotic potential of Ang II has not been evaluated in any model of dermal fibrosis.
This model of dermal degeneration due to MMP interactions with interstitial collagens may be implicated for down-stream effects of other external stimuli such as ultraviolet radiation.
A further model is the bleomycin-induced model of dermal fibrosis, in which bleomycin has been found to increase expression of ECM proteins, potentially via the mediation of TGF-β and CTGF/CCN2 [ 21].
Reports also suggest that TG2 is downregulated in endothelial cells undergoing capillary morphogenesis, while Greenberg and colleagues demonstrated that TG2 was pro-angiogenic after finding that its addition to a window flap model of dermal wounding promoted angiogenesis.
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For this reason, first, a computation-based approach for in silico modeling of dermal cell proliferation and differentiation was developed.
The studies also involve the use of models of dermal inflammation in rats and rabbits and the mouse air pouch model.
Exposure intensity models developed and validated for the cohort study (Burstyn et al. 2003) were used in modeling exposures in the case control study; additional models of dermal exposure were developed on the basis of newly available measurements and observations.
Similarly, BAY 41-2272 restablishedblished fibrosis in modified mouse models of dermal fibrosis [ 34] and PDE5 inhibition reduced myofibroblast numbers and total size of preformed TGF β1-induced Peyronie's disease-like plaques in rats [ 117].
In the 3D model ablation of "dermal" perlecan had no deleterious effect on BM deposition or epithelial morphology, when using fibroblasts from perlecan-null embryos [ 105] with normal HaCaT cells [ 32].
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