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1.
Figure 2

Figure 2. Liver lesions in alcohol-drinking P rats. From: ALCOHOL INDUCES LIVER NEOPLASIA IN A NOVEL ALCOHOL-PREFERRING RAT MODEL.

A) Top: macroscopically visible neoplastic nodule from a P rat consuming alcohol for 18 months (circled). Middle: three visible neoplastic nodules from a P rat consuming alcohol for 18 months (circled). Bottom: cross section of the corresponding liver nodule shown in the middle panel, both circled by the yellow dashed line. B) A distinctive liver nodule (2.96 × 2.04mm) visualized by high-resolution ultrasound in an alcohol-consuming P rat.

Michele T. Yip-Schneider, et al. Alcohol Clin Exp Res. ;35(12):2216-2225.
2.
Figure 6

Figure 6. Analysis of GSTp+ lesions in iP rat livers. From: ALCOHOL INDUCES LIVER NEOPLASIA IN A NOVEL ALCOHOL-PREFERRING RAT MODEL.

A) GSTp+ hepatic lesions/cm2 in iP rats drinking water or alcohol for 18 months (n=5 per group). p>0.05. B) Large (>15,000 µm2) GSTp+ lesions/cm2 in iP water-drinkers compared with alcohol–drinkers (n=5 per group). C) GSTp+ lesion area as a percent of the total liver area (n=3 for water, n=4 for alcohol). Results are expressed as mean ± SEM. *p< 0.05.

Michele T. Yip-Schneider, et al. Alcohol Clin Exp Res. ;35(12):2216-2225.
3.
Figure 3

Figure 3. Histological analysis of P rat hepatic lesions. From: ALCOHOL INDUCES LIVER NEOPLASIA IN A NOVEL ALCOHOL-PREFERRING RAT MODEL.

A) Representative H&E-stained liver sections from 3 P rats consuming alcohol for 18 months. Gross liver lesions are indicated (black arrowheads). B) Representative H&E-stained sections from water-(left) and alcohol-drinking (right) P rats, demonstrating a well-demarcated, expansile nodule (top) compressing adjacent non-tumoral liver parenchyma below (100X). Dotted line denotes margin of nodule. C) Representative neoplastic nodule (right side of dotted line) demonstrating lack of reticulin fibers. Normal reticulin staining is present in adjacent liver (arrows) (400X).

Michele T. Yip-Schneider, et al. Alcohol Clin Exp Res. ;35(12):2216-2225.
4.
Figure 5

Figure 5. Phosphorylated MAPK/ERK expression. From: ALCOHOL INDUCES LIVER NEOPLASIA IN A NOVEL ALCOHOL-PREFERRING RAT MODEL.

A) Percent phosphorylated MAPK/ERK (P-ERK) staining was determined in water- and alcohol-drinking P rat livers after 18 months (n=7–9 animals/group, 3 fields/slide counted). Data are expressed as mean ± SEM. *p < 0.05. Positive P-ERK staining (brown) of sinusoidal lining cells (selected cells shown circled) in representative liver sections from water- and alcohol-drinking P rats is shown below (400X). B) CD68 (top) and P-ERK (bottom) staining of consecutive serial slides from two different sections of a representative liver is shown (400X). CD68-positive cells are indicated by the red arrowheads. Selected P-ERK-positive cells are shown circled; the corresponding cells shown circled in the serial CD68 slide are not positively stained.

Michele T. Yip-Schneider, et al. Alcohol Clin Exp Res. ;35(12):2216-2225.
5.
Figure 1

Figure 1. iP and P rat models of alcohol preference. From: ALCOHOL INDUCES LIVER NEOPLASIA IN A NOVEL ALCOHOL-PREFERRING RAT MODEL.

A) Alcohol consumption was monitored weekly. Average alcohol consumed is expressed as mg/kg body weight (BW)/day. The mean ± SEM is shown for iP (n=5) and P (n=32) rats. * P < 0.0001. B) Blood alcohol content (mmol/liter) of P rats was determined after alcohol consumption for 6 (n=7), 12 (n=11) or 18 months (n=11). Results are expressed as the mean ± SEM. C) Weights of water- or alcohol-consuming P rats were monitored from 6 months of age until sacrifice (6, 12 or 18 months of alcohol consumption). Weights are shown as mean ± SEM. D) Liver:body weight ratios, expressed as mean percent ± SEM, were determined for P rats given free access to water or alcohol for 6, 12 and 18 months.

Michele T. Yip-Schneider, et al. Alcohol Clin Exp Res. ;35(12):2216-2225.
6.
Figure 4

Figure 4. Immunohistochemical analysis of P rat livers. From: ALCOHOL INDUCES LIVER NEOPLASIA IN A NOVEL ALCOHOL-PREFERRING RAT MODEL.

A) Representative liver sections from 3 P rats consuming alcohol for 18 months stained for GSTp. Gross liver lesions stained by GSTp (black arrowheads) correspond to those stained by H&E (Figure 3A). Higher magnification (200X) of GSTp+ lesion shown below. B) Number of GSTp+ foci/cm2 was determined in alcohol- and water-consuming P rats after 6, 12 and 18 months (n=6–14 animal/group). C) Cross-sectional diameter (µm) of GSTp+ lesions was measured in P rats after 6, 12 and 18 months (n=16–186 lesions/group). D) Number of Ki-67-positive cells was counted within GSTp+ lesions in P rats at 6- and 12-month time points (n=17–81 lesions/group). Data are expressed as mean ± SEM. *p < 0.05. Ki-67 staining in representative water- and alcohol-drinking P rat livers is shown below (400X).

Michele T. Yip-Schneider, et al. Alcohol Clin Exp Res. ;35(12):2216-2225.
7.

Figure 7. Hepatic alcohol metabolizing enzyme expression/activity and oxidative stress in P rats. From: ALCOHOL INDUCES LIVER NEOPLASIA IN A NOVEL ALCOHOL-PREFERRING RAT MODEL.

A) Representative Western blots demonstrating ADH, ALDH and CYP2E1 protein level in pooled liver tissue resected from water- and alcohol-drinking P rats (6, 12 and 18 months). Wistar rats (W, 6 months old, pooled from n=6) were run as a control. Similarly, 6-month old naive P rats (P, pooled from n=6) were run as control. Blots were probed with β-actin to confirm equal protein loading. Relative expression, corrected to β-actin, is shown below each lane. B) Expression of ADH, ALDH and CYP2E1 were quantified by performing densitometry following Western blot analysis of individual lysates from each water/alcohol group. Band intensities are expressed as mean ± SEM. *p< 0.05 vs. corresponding water group. C) CYP2E1 mRNA levels were determined by RT-PCR in pooled liver samples (n=6–8 per group). β-actin expression was used as a loading control. b.p.= ladder; N=negative control D) CYP2E1 activity was assessed as rate of p-nitrophenol hydroxylation to 4-nitrocatechol (n=6–8 per group). CYP2E1 activity is shown as mean ± SEM. *p< 0.05. E) Intrahepatic oxidative stress was measured using a thiobarbituric acid reactive substances (TBARS) assay (n=6–8 per group). Results are expressed as mean ± SEM. *p< 0.05.

Michele T. Yip-Schneider, et al. Alcohol Clin Exp Res. ;35(12):2216-2225.

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