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As confirmed by morphometric analysis of the label distribution patterns, our results show that about 80% of labeled fibrinogen and prothrombin, but only 25% of labeled platelets and FXa, accumulated into features of >3100 pixels (Fig. 6C).
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Rapid analysis of the labeled primer extension products (mutant or wild type) was obtained by capillary electrophoresis using denaturing sieving matrix and laser-induced fluorescence detection.
Kinetic analysis of the labeling reaction between MINC protein and IC-L peptide revealed pseudo first-order rate constants kobs of (5.0±0.7 ×10−5 s−1 and (3.8±0.6 ×10−5 s−1 in the absence and presence of TCEP, respectively (Figure 2C).
Like HA and α1AT (Figs. 2 and Fig. 3E, respectively), analysis of the labeled NHK after a 10 min chase revealed the same electrophoretic mobility in cells expressing normal (Fig. 3A, lane 1) and elevated levels of Malectin (lane 4), consistent with unperturbed N-glycosylation of nascent polypeptides.
For analysis of the labeled amino acids, plasma was deproteinized using sulfosalisylic acid.
PBS was used as mobile phase for analysis of the labeling efficiency.
Morphometric analysis of the labeled neurons demonstrated that TLCd neurons were significantly smaller (Fig. 10b).
For M1 and M2, quantitative analysis of the labeling in the occipital and temporal cortex was carried out (Table 2).
The total BrdU-positive cell number could be automatically calculated for the complete crypt or, alternatively, compartmental analysis of the labelling pattern within the crypt could be obtained.
A detailed analysis of the labeled target candidates led to the identification of proteins involved in cell death and survival, stress response, transport and lipid metabolism.
FACS analysis of the labeled cancer cells revealed that CD24+ cells fuels the cancer process by giving rise to the CD24− cells that comprise the tumor bulk.
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