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These results are also useful to those interested in improving the mechanical properties of this class of materials since we demonstrate that a material with "perfect" laminae and "perfect bonding" is substantially stronger than the experimental material.
On the other hand, statistically correcting for individual to examine annual patterns might inappropriately shape the global relationships among immune indices since we demonstrate that these relationships varied from individual to individual.
On the one hand, statistically correcting for month revealed among individual patterns that appear to be well-supported since we demonstrate that relationships among immune indices were consistent from one month to the next.
Since we demonstrate that PAD2 is expressed in mammary tissue, we next sought to define which cell types express PAD2 during the different phases of the canine estrous cycle.
In this study we confirm these in vitro finding since we demonstrate 1) co-localization of CXCR4 and MIF in the urothelium, both in saline treated rats and after CYP treatment; 2) CXCR4-MIF areociations are present in saline-treated bladder and increase after CYP treatment.
Since we demonstrate that the presence of IL-17A is important for protection from LVS (Figure 10), but the IL-17A-secreting γδ T cells are non-essential (Figure 7), it could be speculated that other cellular sources of IL-17A, such as Th17 -cells (Figure 5), produce sufficient amounts of IL-17A to resolve the low-dose infection.
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Since we demonstrated that several caseinolytic proteases are secreted by H. pylori independently of functional T4SS, it is likely that other secretion systems exist.
Moreover our studies provide additional mechanistic insights, since we demonstrated that NOD2 selectively interacted with NLRP3 and NLRP12, but not with NLRP2, NLRP7, NLRP10, or NRLP11.
Since we demonstrated by various assays (EMSA, gene reporter assays, and immunofluorescence assays) that 20(OH)D3 inhibits NF-κB activity, we next examined the underlying mechanism responsible for this activity.
Since we demonstrated that Ang II activates quiescent cells and upregulates key transcription factors necessary for myoblast proliferation (i.e. Myf5, cyclin D1), we tested whether Ang II possessed the ability to induce quiescent cells to proliferate.
Additionally, since we demonstrated that the basement-membrane-codifying pro-collagen Col4a1 mRNA was down-regulated with aging (Figure 5A), we then analyzed the organization of the basement membrane by TEM in young and aged prostates.
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