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1.
Fig 3

Fig 3. From: Despite antiatherogenic metabolic characteristics, SCD1-deficient mice have increased inflammation and atherosclerosis.

Skin of Ldlr/ mice lacking SCD1. Levels of ICAM-1 mRNA (a) and protein (b). n = 5–6 mice per group. (c) Dermatitis in Scd1−/− Ldlr−/− mice but not Scd1+/+Ldlr−/− mice (Scd1ab-J, p = 0.016; Scd1ab-2J, p = 0.023). n = 28–35 mice per group.

Marcia L.E. MacDonald, et al. Arterioscler Thromb Vasc Biol. ;29(3):341-347.
2.
Fig 4

Fig 4. From: Despite antiatherogenic metabolic characteristics, SCD1-deficient mice have increased inflammation and atherosclerosis.

Inflammation in Ldlr−/− mice lacking SCD1. Plasma IL-6 (a), sICAM-1 (b), IL-1β (c), IL-12p70 (d), MCP-1 (e), and RANTES (f) levels were determined in mice fed a western diet. n = 8–12 mice per group.

Marcia L.E. MacDonald, et al. Arterioscler Thromb Vasc Biol. ;29(3):341-347.
3.
Fig 1

Fig 1. From: Despite antiatherogenic metabolic characteristics, SCD1-deficient mice have increased inflammation and atherosclerosis.

Lesion area in Ldlr−/− mice lacking SCD1. (a) Lesions in aortic roots of Scd1+/+Ldlr−/− (left) and Scd1−/− Ldlr−/− (right) mice carrying the Scd1ab-J allele were stained with oil red O to detect accumulation of lipids and photographed. (b) Quantitation of atherosclerotic lesion area in the aortic root. n = 6–11 mice per group.

Marcia L.E. MacDonald, et al. Arterioscler Thromb Vasc Biol. ;29(3):341-347.
4.
Fig 5

Fig 5. From: Despite antiatherogenic metabolic characteristics, SCD1-deficient mice have increased inflammation and atherosclerosis.

HDL phenotype in Ldlr−/− mice lacking SCD1. (a) Relative amount of liver mRNAs. n = 12 mice per group. Plasma SAA (b), apoA-I (c), and apoA-II (d). Relative units (RU). n = 6–12 mice per group. (e) Serum PON1 activity. n = 3 mice per group.

Marcia L.E. MacDonald, et al. Arterioscler Thromb Vasc Biol. ;29(3):341-347.
5.
Fig 6

Fig 6. From: Despite antiatherogenic metabolic characteristics, SCD1-deficient mice have increased inflammation and atherosclerosis.

Macrophages from mice lacking SCD1. (a) LPS-induced mRNAs in thioglycollate-elicted peritoneal macrophages. Lesion area (b) and representative sections (c) of Ldlr−/− mice reconstituted with Scd1+/+ and Scd1/ bone marrow and fed a western diet for 6 weeks. n = 12 mice per group. (d) Cholesterol efflux assays from bone-marrow macrophages from Scd1+/+ and Scd1/ transplanted mice. n = 4 mice per group.

Marcia L.E. MacDonald, et al. Arterioscler Thromb Vasc Biol. ;29(3):341-347.
6.
Fig 2

Fig 2. From: Despite antiatherogenic metabolic characteristics, SCD1-deficient mice have increased inflammation and atherosclerosis.

Lesion morphology Ldlr−/− mice lacking SCD1. (a,b) Necrotic cores (absence of purple/black nuclei, NC) and extracellular cholesterol clefts (needle-shaped lucencies; C) were observed with Movat pentachrome staining. The absence of yellow stain indicates the lack of significant collagen deposition. (c), Semi-quantitative assessment of lesion severity. n = 16–22 mice per group.

Marcia L.E. MacDonald, et al. Arterioscler Thromb Vasc Biol. ;29(3):341-347.

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