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Mouse lung tissues were fixed in 4% polyformaldehyde solution at 4°C overnight, and then embedded in paraffin.
We also thank Leslie Taylor for immunohistochemistry staining of mouse lung tissues and Sabrina Dalton for assisting in preparation of the manuscript.
Standard stereological sample preparation, sectioning, and imaging of mouse lung tissues were performed for semi-automated acquisition of mean linear intercept (Lm) data.
For mouse lung tissues, bacterial numbers were generated from 2 non-sequential lung lobe sections for every timepoint for five mice per treatment group.
Histopathology of neonatal mouse lung tissues at 24 h post-infection showed that PA14 (Figure 1E) caused a typical lobar pneumonia characterized by pulmonary consolidation and intra-alveolar hemorrhage with massive inflammatory infiltrates.
Besides tumour cells, mouse lung tissues also expressed higher mRNA expression levels for the mouse receptor.
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Fig. 2: SiNPs induce apoptosis and autophagosome accumulation in mouse lung tissue.
Detection of upregulated sialidases in bleomycin-treated mouse lung tissue lysates.
Previously, we reported that the expression of ACE2 protein was downregulated in H5N1-infected mouse lung tissue.
NETs formation was detected in mouse lung tissue after LPS administration but was not observed in phosphate-buffered saline (PBS) control mice.
In addition, on Western blots, compared to saline, bleomycin-treated mouse lung tissue lysates had significantly upregulated levels of NEU3 (Fig. 3e and f).
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