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By histologic analysis, infected mice exhibited extensive remodeling characterized by significant pleural thickening with collagen deposition (blue stain) at 7 days compared to saline-treated controls (Fig. 2d).

Liver sections from DIO mice exhibited extensive intracellular vacuolization and significant lipid accumulation in both perivenular and periportal areas (Figure 6D).

In conclusion, polyps from Apcmin/+ mice exhibited extensive, aberrant DNA methylation.

The resulting mice exhibited extensive neuronal degeneration, apoptosis, reactive gliosis, and premature lethality.

Repeatedly caerulein treated mice exhibited extensive chronic pancreatitis as seen in Figure  2B, including multi-focal patterns of acinar loss, stromal fibrosis, and inflammatory cell infiltration.

Our findings indicated that Apcmin/+ mice exhibited extensive aberrant DNA methylation that affected certain signaling pathways, such as the EMT and Wnt/β-catenin pathways.

Second, Dutch/Iowa mutant Aβ peptides have highly vasculotropic nature and Tg-SwDI mice exhibit extensive microvascular amyloid deposition.

Affected mice exhibit extensive spongiform degeneration of the central nervous system (CNS) and substantial loss of peripheral neurons from sensory and sympathetic ganglia.

Aged 3xTg-AD mice exhibit extensive Aβ and tau pathology, and cognitive dysfunction, mimicking the hallmark pathologies of AD (Supporting Information Fig. S1A).

Sesn2−/− mice also exhibited extensive aggravation of ER stress, either upon Tm treatment- (Fig. 3a,b and Supplementary Fig. 4e g), HFD- (Fig. 3c f and Supplementary Fig. 4h,i) or Lepob mutation-induced obesity (Fig. 3g i and Supplementary Fig. 4j).

These mice also exhibited extensive reduction in many ECM genes expressed in the skeletal system together with reduced trabecularity and minerality in the calvarial and axial skeleton, features consistent with the skeletal pathology found in HGPS.