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In cirrhotic livers, we observed positive staining in 13 of 29 (45%) samples.
In Parp-1-/ ES cells and livers, we observed that the majority of the altered genes were down-regulated.
By contrast, in nontreated livers, we observed a cloudy diffuse cytosolic fluorescence standing for cells with depolarized mitochondria and 1(d)).
In 11 of 18 cirrhotic livers, we observed clusters of hepatocytes overexpressing IGF-2, and a consistent decrease of hepatocellular M6P/IGF-2R-specific immunostaining in all of the examined cirrhotic liver specimens compared to normal liver indicating that these mechanisms play a role early in hepatocarcinogenesis prior to the appearance of dysplastic nodules.
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In liver, we observed an accumulation of polyamines (putrescine and spermidine), which could suggest an elevated metabolic state (Fig. 5).
For the liver, we observed an estimated effective half-life slightly exceeding the physical half-life for some patients.
In liver, we observed vacuolizations, a depletion of the glycogen content, an increased number of melanomacrophages, a disintegrated structure of hepatocytes, cellular hypertrophy, and irregularly shaped nuclei.
Accordingly, in the XpdTTD liver, we observed a dramatic down-regulation of genes involved in xenobiotic metabolism (Table S5).
In the liver, we observed 86.3% quantitation efficiency, and in the brain, we observed 41.7% quantitation efficiency for the phosphopeptides (Figure 3A).
In the fetal liver, we observed that the 3D conformation of the PAC3K and PACΔ3K transgenes is virtually identical to that observed for the PAC1B and PACΔ1B transgenes (data not shown).
The increased glycogen storage might explain the enlarged liver we observed in hypothyroid mice.
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