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Results: 4

1.
Figure 1

Figure 1. From: Cardiac and gastrointestinal liabilities caused by deficiency in the immune modulatory enzyme indoleamine 2,3-dioxygenase.

Calcification of the cardiac endometrium in IDO deficient BALB/c mice. Representative illustrations of gross pathology (left panels) and representative histology (right panels) are shown of calcification of the cardiac endometrium proximal to the right ventricle which were observed in female animals with a ∼30% penetrance. RV, right ventricle.

Mee Young Chang, et al. Cancer Biol Ther. 2011 December 15;12(12):1050-1058.
2.
Figure 3

Figure 3. From: Cardiac and gastrointestinal liabilities caused by deficiency in the immune modulatory enzyme indoleamine 2,3-dioxygenase.

IDO deficiency accentuates hyperlipidemia in a mouse model of atherosclerosis driven by high fat diet. Blood serum samples were analyzed from WT, LDLR-/- or IDO-/-LDLR-/- mice on the C57BL6/J strain background. A representative illustration of hyperlipidemia present in mice fed a high fat diet is shown. Quantification of serum lipids demonstrated a significant increase in serum triglycerides in IDO-/-LDLR-/- mice fed an atherogenic diet (p < 0.02). No significant differences in levels of serum cholesterol were observed. Total mice tested in each group was IDO-/- (n = 10), IDO-/-LDLR-/- (n = 10), LDLR-/- (n = 9).

Mee Young Chang, et al. Cancer Biol Ther. 2011 December 15;12(12):1050-1058.
3.
Figure 4

Figure 4. From: Cardiac and gastrointestinal liabilities caused by deficiency in the immune modulatory enzyme indoleamine 2,3-dioxygenase.

IDO deficiency accentuates the effects of inflammatory insults that promote colon carcinogenenesis. (A) Colitis induction. Colons from WT and IDO-/- mice treated 3 d with 3% DSS in drinking water were fixed in paraffin and processed for H&E staining. Representative examples scored for no colitis, mild colitis and severe colitis are shown at original magnifications of 10× (middle) or 20× (bottom). (B) Colon carcinogenesis. WT and IDO-/- mice were treated once i.p. with 20 mg/kg DMH and then 7 d 2% DSS in drinking water followed by normal drinking water to an endpoint of 18 wks. Colons were harvested from euthanized mice, fixed in paraffin and processed for H&E staining. Representative images of gross pathology in WT or IDO-/- mice (top panels) illustrate observations of macroscopic tumors (arrows) or prolapsed rectums (arrowheads). Representative images of histopathology in IDO-/- mice (bottom panels) illustrate observations of (a) no tumor, (b) mucosal invasion, (c) submucosal invasion and (d) muscular invasion. Original magnifications are 4× (top), 10× (middle), 20× (bottom).

Mee Young Chang, et al. Cancer Biol Ther. 2011 December 15;12(12):1050-1058.
4.
Figure 2

Figure 2. From: Cardiac and gastrointestinal liabilities caused by deficiency in the immune modulatory enzyme indoleamine 2,3-dioxygenase.

Acute pancreatitis induced by complete Freund's adjuvant in IDO deficient mice. (A) Gross pathology. Freshly dissected pancreata are shown to illustrate the marked increase in organ size produced in mice 28 d after treatment with CFA + peptide (untreated WT n = 5, untreated IDO-/- n = 4, CFA + Peptide treated WT n = 5, CFA + Peptide treated IDO-/- n = 5) (see Material and Methods). (B) Pancreas histology. Representative samples are shown to illustrate pancreatitis that developed after treated with CFA or CFA + Peptide in WT and IDO-/- mice. Lower magnification images are presented in the upper row and boxed areas are magnified in the lower row. Areas indicated by arrows show normal acinar regions of pancreatic tissue. Scale bar = 100 µM. (CFA treated WT n = 5, CFA treated IDO-/- n = 5, CFA + Peptide treated WT n = 5, CFA + Peptide treated IDO-/- n = 5). (C) Insulin expression. Pancreatic tissue sections were stained with H&E for histology or processed for immunohistochemical expression of insulin in islet β-cells. Brown staining demonstrates the presence of insulin containing β-cells in these tissues. Scale bar = 100 µM.

Mee Young Chang, et al. Cancer Biol Ther. 2011 December 15;12(12):1050-1058.

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