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VSMC identity was initially confirmed by α-smooth muscle actin staining.
CD123+ (high endothelial venules), and smooth muscle actin staining patterns are depicted in Figure 1 D and E respectively.
Furthermore, smooth muscle actin staining (Fig 3C) revealed thin, straight vessels in treated tumors when compared to numerous, wide, tortuous blood vessels from tumors of untreated mice.
Myocytes were identified by smooth muscle actin staining after one week in culture (Figure 6C), and were also observed to comprise approximately 30% ±10% of derivatives.
As shown by reductions in smooth muscle actin staining around the glands [67], the microinvasive lesions appear to emanate from these morphologically transformed cribriform, or partially cribriform lesions (Figure 6 7).
Interestingly, in most of the Cribriform-PIN/CIS lesions, there was a maintenance of at least some basal cells, which were identified by staining for Keratin 5 (Figure 4B) and p63 (not shown), despite the often near complete loss of smooth muscle actin staining (Figures 6B and 6D).
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Nuclei stained in blue and α-smooth muscle actin stained in red-brown, identifying α- smooth muscle actin expressing cells.
Myofibroblasts were present in α-smooth muscle actin stained sections in significantly increased numbers post injury.
The samples were used for hematoxylin and eosin staining, Masson staining, and smooth muscle actin immunohistochemistry staining.
However, abrogation of Apc significantly inhibited both proximal airway and vasculature smooth muscle cell differentiation, as detected by α-smooth muscle actin (SMA) staining in Fig. 7a.
The lack of smooth muscle actin (SMA) staining provided further evidence that MCF7 cells did not differentiate into myoepithelial cells in these conditions (data not shown).
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