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Model 1 Null model.
LRT = Likelihood ratio test statistic for ω + = 1 (null) versus ω + unrestricted (alternative).
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Expression of a fc177 cDNA in dec-1 null mutants was sufficient to restore spaces within the endochorion layer.
The frequency of erosions after large wounds was greater (88 +/− 8%) in the C57BL6 mice compared to BALB/c (60 +/− 2%), and sdc-1 null mice (32 +/− 5%).
By using homozygous monocyte chemoattractant protein (MCP -1 null MCP -1we inulltigated the role of this key imiceoregulatory cytokine in mediating Vwe-investigatedoinflammathey roleofses.
The frequency of CESCD 4 weeks after the large wounds was significantly greater in the C57BL6 mice than in the BALB/c or sdc-1 null mice.
Studies using oshkt2 1 null mutants demonstrated that OsHKT2 1 (or OsHKT1) takes up Na+ under K+-starvation conditions [57].
Treatment with the MMP inhibitor doxycycline (DOX), significantly corrected the increased intimal hyperplasia response in Cav-1 null mice (Cav-1 null+DOX = 1975±620, Cav-1 null-DOX = 3627±1121 µm2 p<0.001, Figure 5A) while media area was not affected (Cav-1 null+DOX = 9217±1189 Cav-1 null-DOX = 9449±2815 µm2 p = 0.5, Figure 5B).
Intima-media ratio also significantly reduced compared to untreated Cav-1 null mice (Cav-1 null+DOX = 0.21±0.06 Cav-1-DOX = 0.38±0.09 p<0.001, Figure 5C).
MMP inhibition in Cav-1 null mice resulted in a significant attenuation of the increased intimal formation in Cav-1 null mice.
To confirm the intermediate role of IFN, we examined IFNAR-1 null mice.
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