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Next, RNA was isolated from aortic arches of p55−/−LDLR−/− and control mice and expression levels of the macrophage marker CD-68 were determined.
LiCl was injected into mice, and expression of PLD was investigated in several tissues using anti-PLD antibody which recognizes both PLD1 and PLD2.
The PI3K pathway is activated after allergen challenge in sensitized mice and expression of a dominant-negative PI3K subunit or use of PI3K inhibitors ameliorate the inflammatory response to allergen [4], [5], [6].
Significantly (p≤0.01) elevated mRNA transcripts for both CXCL1 and CXCL2 were observed throughout infection compared to sham-infected control mice, and expression was independent of viral load (Figure 1B).
Previous studies using DC expressing firefly luciferase as a reporter gene indicate that DC selectively traffic to the spleen and pancreatic lymph node of NOD mice and expression of luciferase in these tissues suggests the numbers of DC peak in these tissues between day 1 and day 3 and then wane significantly by day 8 post-injection [6].
AP was induced by repetitive intraperitoneal injections of cerulein, an analog of the secretagogue cholecystokinin, to wild type mice and expression of TCPTP was determined.
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Dr. Laurence Quilliam (Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA) kindly provided the FLAG-tagged mouse AND-34 expression vector.
Clonal cell lines expressing transgenes were inoculated into SCID mice and the expression of the transgene was controlled by tetracycline administered ad libitum in the drinking water.
Cold-induced expression of Dio2 and Cidea was also attenuated in iWAT in the COX2 KO mice and PGC1α expression also tended to be attenuated (Figure 5B).
STRA13 KO mice express lower levels of Rae-1 transcripts than the control mice and their expression is not circadian [10].
Furthermore, DNA repair was delayed in splenocytes of hPARP-1 mice, and gene expression of pro-inflammatory cytokines was dysregulated.
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