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R6/1 mice displayed marked alterations in all social behaviors which were mainly observed in males.
AnxA1+/+ mice displayed marked synovitis accompanied by pannus formation and cartilage destruction (figure 3B, left panels).
The db/AD mice displayed marked cognitive impairment in the Morris Water Maze, compared to either db/db or APP ΔNL x PS1 P264L mice.
Although the NK1R−/− mice displayed marked anxiety-like behaviour, guanfacine did not affect the behaviour of either genotype in the EPM.
As a matter of fact, CD151-deficient mice displayed marked, although not quantified, albuminuria and survived for at least 5 months.
MCD-fed mice displayed marked suppression of mRNA encoding acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) compared to MCS controls, as has been reported previously [ 8] (Fig. 5d).
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On the other hand, both LDL receptor-deficient (LDLR-/) and particularly apolipoprotein E-deficient (ApoE-/) mice display marked atherosclerosis [ 28, 29] but ApoE-/ mice develop lower diet-induced obesity, less profound insulin resistance and adipose tissue inflammation when fed a high-fat diet [ 30- 32].
Laminin β2-deficient mice also displayed marked proteinuria, but the mice did not grow normally and died prematurely [ 33].
TLR8 deficient mice (B6.TLR8−/−) and particularly double TLR8/9-deficient mice (B6.TLR8/9−/−) displayed marked induction of TLR7, which was associated with more severe disease.
Mice fed with an HFD for 24 weeks displayed marked symptoms of hepatic fatty infiltration compared to ND-fed mice, but long-term dietary quercetin supplementation significantly alleviated these symptoms.
Abdominal aortic transplants from donor mice deficient in HS-GAG (Ndst1−/−) or the chemokine CCR2 receptor (Ccr2−/−) displayed marked reductions in plaque growth while HS GAG or CCR2 deficiency in the recipient mouse had minimal effects.
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