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In the optically cleared mouse lung, we observed branching major blood vessels in transplanted mouse lung (Fig. S7A).
Using lentiviral delivery of Sox2 specifically to the mouse lung, we tested the ability of Sox2 to promote tumorigenesis in multiple tumor suppressor backgrounds.
To confirm the results obtained with RT-PCR and determine the distribution of miRNA expression in the inflamed mouse lung, we examined the expression of miRNA-223 using in situ hybridisation since this was the only miRNA that was significantly up-regulated at all time points.
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To further examine whether Ponatinib could inhibit the growth of micro-metastases of breast cancer in mouse lungs, we injected LM2 cells into the tail veins of nude mice and waited for 4 days to let the form of micro-metastases in the lungs (Padua et al., 2008).
In our studies in isolated and ventilated perfused mouse lungs, we investigated the expression of three commonly used housekeeping genes β2 microglobulin (B2m), ribosomal protein L 32 (Rpl32) and hypoxhantine phosphoribosyl transferase I (Hprt1), and in addition also of tyrosine kinase 2 (Tyk2).
Based on this mesenchymal expression in the developing mouse lungs we hypothesized that EPHA3 might function during the pseudoglandular stage of lung development.
To assess whether the increased replication seen in M1 cells in vitro was due to an increased ability to inhibit INF production (as previously shown in mouse lungs), we also measured IFN-β induction of infected cell supernatants using mouse IFN-β ELISA.
On the background of approximately 1 2×106 AT2 cells within the mouse lung [21] we conclude that in both founder lines only a very limited number of AT2 cells serve as tumor initiating cells.
Using total RNA from E18.5 mouse lung tissue, we performed 5' RLM-RACE in order to identify the Fgf-10 transcription start site.
In order to investigate the association of transcriptional and post-transcriptional regulating activities in the mouse lung development, we define the significant triple relations among miRNAs, TFs and mRNAs as circuits.
We recently reported that 5-week exposure to environmentally relevant levels (10 and 100 ppb) of As in drinking water significantly altered components of the innate immune response in mouse lung, which we hypothesize is an important contributor to the increased risk of lung disease in exposed human populations.
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