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Interestingly, the core of the infarct manifested markedly increased uptake, exemplified by a brighter staining (yellow arrow), as compared to the more peripheral regions (red arrowheads).
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We performed immunostaining on NK cells, and observed a bright staining when cells were incubated with CX3CR1 Ab.
Interestingly, the discrete brighter staining in bipolar and ganglion cells was also positioned in an apical orientation with respect to the nucleus.
However a bright stain was evident in the proximal region of the ventral axonems.
At this peak of expression, a much brighter staining was assigned to ACTH-producing cells (Figure S1A, arrows).
The general pattern of results found in each series was very similar, showing very weak staining in the controls (A), slightly brighter staining in the I/R (B) and I/R+IPC (C) groups, and much stronger staining in the IPC group (D).
The intensity of HER2 staining of CTCs from patients with BC observed on the FITC channel of the CellSearch® system was a continuous variable ranging from absent to very weak, weak, intermediate, bright and very bright staining.
Both HPSE-low and HPSE-high cells exhibited bright staining on the cell surface, often in patches (Fig. 1).
Low staining intensity indicates normal fiber diameter, and bright staining intensity correlates with increased fiber diameter.
We again saw bright staining for PD-1 on cells in the follicles, while weak staining for PD-1 could be seen between follicles.
While almost no HA306-318 peptide was detectable when the loading was carried out in the absence of the dipeptide-MLE, the addition of the catalyst resulted in a bright surface staining that colocalized with the HLA-DR1-GFP fusion protein.
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