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To test monocyte migration in vivo, we used an RA ST SCID mouse chimera model.
On the other hand, the RA synovial/SCID mouse chimera model is not quite the same with the CIA model in pathogenesis or/and manifestations.
The synovial endothelium targeting peptide (SyETP) CKSTHDRLC has been identified previously and was shown to preferentially localise to synovial xenografts in the human/severe combined immunodeficient (SCID) mouse chimera model of rheumatoid arthritis (RA).
Nakano et al. [ 47] have shown that, in RA synovial/SCID mouse chimera model, a selective D2-like receptor antagonist haloperidol significantly induces accumulation of IL-6+ and IL-17+ T cells with exacerbated cartilage destruction.
Dissimilarly, in RA synovial/SCID mouse chimera model, a selective D1-like receptor antagonist SCH-23390 alleviates both accumulation of IL-6+ and IL-17+ T cells and cartilage destruction [ 47], suggesting an involvement of D1-like receptors in RA disease.
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The direct relationship between tumor-derived CXCL-8 and tumorigenesis was demonstrated in in vivo model of human tumorigenesis (i.e., human NSCLC/SCID mouse chimera) [ 76].
Fate tracing bone marrow derived monocytes was performed using a mouse chimera as previously described.
Human synovium-severe combined immunodeficiency (SCID) mouse chimeras were treated with TSP2-transfected fibroblasts deposited into the peritoneum.
*These new "chimera" models are hodge-podged from old toy parts initially created by other people.
Mouse chimeras were generated by C57BL/6 host blastocyst injection of mutant embryonic stem cell clones, and the chimeras obtained were bred with C57BL/6 mice to generate heterozygous Cthrc1 mice.
That is, the pattern observed in mouse chimeras is also seen in rat chimeras in a given tissue.
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