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The %ID/g activity in the livers of group II animals is 42% of that in the group I animals at 3 hours post-injection, and 56% of that in the group I animals at 24 hours post-injection.
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At first, by using a well-established intravenous infection model [35], we compared tissue burdens in kidneys and livers of groups of infected mice.
The present results were confirmed by absence of histopathological changes in livers of groups (2) and (4) in comparison with liver of control group.
The liver of group I showed normal hepatic parenchyma with no evidence of hepatocellular necrosis or inflammatory reaction (Fig. 4a).
The liver of group IV showed nearly similar picture to those demonstrated in the control one (Fig. 4h).
Meanwhile, the liver of group II revealed various histopathological alterations characterized by focal area of hepatocellular necrosis infiltrated by mononuclear cells (Fig. 4b) and polyploidy hepatocytes represented by hepatic cytokaryomegaly, binucleated hepatocytes associated with activation of Kupffer cells and sporadic cell necrosis (Fig. 4c) as well as apoptosis (Fig. 4d).
Sections from liver of group (4) which were sacrificed 15 dpc showed normal hepatic tissue.
The histologic injury scores in the liver of group 4 were significantly lower than those of group 3 (P < 0.05).
Gross examination of chicks liver of group B showed slight enlargement from the 1st week, whereas that of kidney from the 3rd week.
Mean log10 of bacterial growth in the liver of group A and of group B on sacrifice was 3.47 and 1.32, respectively (P = 0.043); and in the right kidney was 5.78 and 1.94, respectively (P = 0.004).
Fig. 3 Morphological change and histological pathologic qualitative evaluation for the livers of experimental group and controlled group.
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