This increase in survival of Nlrp3−/− mice was associated with a decrease in the number of tumor-associated MDSC.
Increased susceptibility of aged mice was associated with decreased TLR1, TLR6, and TLR9 mRNA expression and diminished IL1β mRNA expression.
The improvement in glycemic control in sitagliptin-treated mice was associated with a significant increase in glucose-dependent insulin secretion in both perfused pancreas and isolated islets.
The disruption in the organization of actin cytoskeleton of these Tg mice was associated with the inhibition of the activation of Cdc42 and down regulation of cofilin phosphorylation.
Deficiency of alpha CGRP (αCGRP knockout mice) was associated with enhanced inflammatory responses in the hippocampus and hypothalamus and reduced the survival rate compared to wild-type mice in septic shock condition [103].
Free cholesterol-induced NASH in mice was associated with decreased levels of docosahexaenoic acid-containing plasmalogens and impaired expression of PPARα, a critical transcriptional regulator of fatty acid oxidation.
In contrast, loss of IFN-signaling in stat1−/− mice was associated with more rapid disease progression.
However, systemic SFRP2-adenovirus treatment in Tgfbr2fspKO mice was associated with morbidity.
This data further suggested that the upregulation of these miRNAs in lupus mice was associated with the lupus development.
In one previous report a maternal duplication of the Peg3-region in mice was associated with neonatal lethality [14].
Accordingly, overexpression of HO-1 in the HO-1Tg mice was associated with strongly increased angiogenesis (Fig. 6B).
