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Sham-treated mice showed multiple granulomas in both lung and liver tissues, characterized by dominant epithelioid cells (indicated by green arrows in Fig. 5) at centre with surrounding lymphocytes, neutrophil and monocytes in peribronchial and perivascular areas (lung) and peri-central vein areas of the hepatic lobules (liver).
While numerically not elevated in the CNS at 12 months, the PD-1-deficient CD8+ cells of PLPwt/PD-1-/ mice showed multiple clonal T-cell expansions, as opposed to PD-1-expressing CD8+ cells of normal wild type mice which do not show any repertoire perturbations.
Terminally-ill mice showed multiple symptoms including lack of food-intake, difficulty in standing, walking and breathing, visible abnormal growth at localized body parts, dramatic loss of body weight, ulcerated skin infections that did not respond to antibiotic treatment, and bleeding from the mouth, vagina, and/or anus, etc.
The intestinal mucosa in irinotecan-treated mice showed multiple features of damage that were quite distinct from the mucosa of TKO mice: i) loss of crypts (Fig. 10B), ii) increased apoptosis in the crypts (Fig. 10 (D,E,F)), iii) lack of premature enterocytic differentiation in the crypts (Fig. 10G), iv) loss of villus goblet cells (Fig. 10H), and v) increase in acute inflammatory cells (Fig. 10I).
In addition, Pb+LPS-treated mice showed multiple profoundly necrotic areas in the liver.
In addition, after addition of isoproterenol, all the RyR2 S/S mice showed multiple ventricular ectopic beats.
Similar(52)
Igf1 knockout mice show multiple defects including reduced myelination and loss of striatal neurons [ 3].
Bcl11b-deficient mice show multiple defects at the bell stage and have abnormal incisors and molars [ 142].
The deletion of Mist1 blocks normal mucous neck cell redifferentiation into zymogenic chief cells as all basal zymogen-secreting cells in Mist1-/ mice show multiple structural defects [ 21].
Tbx22 null mice show multiple craniofacial defects that include submucous or overt CP, choanal atresia, reduced vomer and ankyloglossia, which are all consistent with its known expression pattern (12, 18, 19).
Ltbp1 hypomorphs show facial dysmorphia [ 19] and Ltbp1L loss leads to embryonic lethality due to heart malformation [ 20], Ltbp2 loss-of-function mutations cause glaucoma in humans and lens defects in mice [ 21], Ltbp3 loss-of-function mutation results in severe bone malformation [ 3, 22, 23] and Ltbp4S-null mice show multiple organ defects [ 4, 9, 10].
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