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1 Conclusions: Transforming growth factor-beta and famotidine accelerate ulcer healing delayed by indomethacin.
2 There was no difference in the mRNA expression of transforming growth factor-beta1.
3 Nov overexpression did not activate Notch or transforming growth factor beta signaling.
4 Transforming growth factors-beta are potent regulators of cellular proliferation, differentiation and morphogenesis.
5 Neutralizing antibodies against transforming growth factor-β inhibited myofibroblast formation induced by M2 macrophages.
6 However, no changes in tumor necrosis factor-a or transforming growth factor-β expression were observed.
7 Inhibitory cytokines, especially transforming growth factor-beta, are important in homeostasis of normal human melanocytes.
8 The transforming growth factor-beta family and fibroblast growth factors interact with extracellular matrix proteins.
9 Transforming growth factor-beta 1 prevented the induction of both enzymes.
10 Monoclonal antibody against transforming growth factor-β1 restored the T cells proliferation inhibited by DPSCs.
11 Enhancement of bone ingrowth with transforming growth factor-beta was evaluated in a canine model.
12 RAS involvement in NSF is unclear compared to transforming growth factor beta and Smad.
13 Transforming growth factor-beta-induced secretion of collagens was inhibited by nintedanib.
14 In this case it was transforming growth factor beta-3.
15 Transforming growth factor-beta was associated with an increase in epithelial and granulation tissue cell proliferation.
16 These manifestations reflect excessive signaling of transforming growth factor beta (TGF-β).
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