Infected mice showed typical signs of dengue infection, including fever, rash, weight loss and thrombocytopenia.
Nalp3+/+ mice showed typical vascular occlusion with parasitized erythrocytes as well as lymphomonocytic infiltrates and microvascular destruction including pathological endothelial cells (Figure 7d (i)).
Histopathology of the brains of ncsiRNA treated mice showed typical features of viral encephalitis, such as meningeal vessels with perivascular cuffing of lymphocytes (Fig 9a) and focus of gliosis & demyelination in cortex (Fig 9b).
When the mice were given antibodies that prevented transthyretin from interacting with the β-amyloid protein, the mice showed typical brain cell death.
Histological examination of the colons from prolapsed CD4cre:PP4f/f mice showed typical signs of colitis, such as submucosa thickening, epithelial hyperplasia, loss of goblet cells, and mononuclear cell infiltration.
Prior to death, CD2-Smad7 mice showed typical EAE with progressive ascending paralysis but no clinical signs of an exaggerated systemic inflammatory response.
The SPAK CCT domain knock-in mice showed typical features of Gitelman Syndrome with mild hypokalaemia, hypomagnesaemia, hypocalciuria and displayed salt wasting on switching to a low-Na diet.
In the histological analysis, the affected joints of Lck-Cre/ IFT20+/+ mice and CD4-Cre/IFT20+/+ mice showed typical features of arthritis, characterized by synovial hyperplasia and perivascular infiltration of inflammatory cells.
Histological analysis of the ankle, metatarsophalangeal, and interphalangeal joints of 1-MT-treated and vehicle-treated mice showed typical arthritis characterized by extensive leukocyte infiltration, synovial proliferation, pannus formation, and erosions.
The critical role of AHR in pHAH toxicity has been demonstrated by AHR knockout studies in which AHR knockout mice do not show typical dioxin-induced toxicity compared with their AHR-expressing littermates (Fernandez-Salguero et al. 1996).
