Sentence examples for mouse joints during from inspiring English sources

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Again, although IL-1β levels were elevated in mouse joints during CIA, IL-1F8 levels were not.

This study describes genome-wide gene activity taking place in mouse joints during three major phases of autoimmune arthritis: initiation, acute inflammation, and chronic inflammation.

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Many proinflammatory cytokines were reduced in IL-18 gene-knockout mouse joint homogenates during ZIA, including macrophage inflammatory protein-3α (MIP-3α/CCL20), vascular endothelial cell growth factor (VEGF), and IL-17.

Therefore, Shh specifically becomes necessary for normal limb development at or just distal to the stylopod/zeugopod junction (elbow/knee joints) during mouse limb development.

First, TLR4-/ mice produce minimal amounts of IL-12p35 in their joints during antibody-induced arthritis compared with WT mice.

Meanwhile, the administration of recombinant IL-1β, IL-12 or IFN-γ to TLR4-/ mice reduced TGF-β transcript levels in the joints during antibody-induced arthritis, indicating that these pro-inflammatory cytokines inhibit joint TGF-β production.

Furthermore, injection of recombinant IL-12 into TLR4-/ mice enhanced the production of IFN-γ and IL-1β in the joints during antibody-induced arthritis, whereas recombinant IFN-γ and IL-1β did not enhance IL-12p35 production.

For example, by placing reflective markers at leg joints, Leblond et al. measured angular variations of leg joints during walking in a treadmill of wild-type and spinalized mice allowing a complete reconstruction of the step cycle [ 9].

As shown in Figure 6, all mice showed detectable levels in joint homogenates of all cytokines tested; however, ZIA IL-18 gene-knockout mice showed significant reductions in IL-17 (a), VEGF (b), and MIP-3α/CCL20 (c) compared with ZIA Wt mice, indicating that expression of IL-18 can initiate proinflammatory cytokine release in joints during acute arthritis.

They can bleed spontaneously in their joints during stressful moments.

To show whether T-cell accumulation in the joints during the development of CIA depends on the CXCR4/SDF-1 sysTem, T cells from Cxcr4 flox/flox/ Lck-Cre mice and Cxcr4 +/+/ Lck-Cre mice were labeled with radioisotopes and injected into IIC/CFA-immunized mice, and T-cell migration into joints was analyzed.

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