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To obtain transcriptome information from bacteria colonizing the murine GI tract, we initiated the murine model utilizing the P. aeruginosa PAK strain.
An in vivo murine model utilizing Ba/F3-JAK2V617F ascitumorsmors was developed as a FACS-based surrogate system with ready access to tumor cells for use in understanding the correlation between pharmacodynamics and PK of JAK2 inhibition.
We used a murine model utilizing the CT26 colon cancer cell line to analyze primary and memory tumor-specific T-cell responses induced by an attenuated actin A and internalin B deleted immunodominant tumor-associated antigen expressing strain of Listeria monocytogenes for the treatment of metastatic colorectal cancer.
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In addition, interventions in multiple murine models utilizing several of these pathways, either by blocking co-stimulatory receptors or by engaging inhibitory receptors, have profound therapeutic effects.
To test this, we utilized an in vitro model utilizing murine cell lines in order to exclude the possibility of involvement of other cell types.
An inflammatory response associated with severe sepsis may be harmful, whereas the inflammatory response is necessary to clear infection, as demonstrated in an elegant murine cecal ligation and puncture model utilizing variable caliber of puncture.
Such a situation is more common for humans [ 6], and thus, the murine head punch model utilized in our study is more relevant for human studies.
A number of murine models are utilized to study IPF and other human forms of pulmonary fibrosis in order to investigate disease progression and potential therapy.
In a study in the murine collagen-induced arthritis (CIA) model, utilized extensively to evaluate novel forms of therapy for rheumatoid arthritis (RA), DBA/1 mice were injected intraperitoneally with fibroblasts expressing IFN-β, resulting in continuous IFN-β delivery in vivo, before or after the onset of CIA [ 11].
An inbred murine model (BALB/c) was utilized to assess the protective effect of the immunomodulator methyl inosine 5′-monophosphate (MIMP) against infection with influenza A/PR/8/34 (H1N1) virus.
Our model utilized monthly discontinuation rates.
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