1. Differentiation and proliferation in Barrett's esophagus and the effects of acid suppression 
Rodica Ouatu–Lascar, Rebecca C. Fitzgerald, George Triadafilopoulos 
Gastroenterology 
Volume 117, Issue 2, Pages (August 1999)
DOI: /gast

2. 1
Fig. 1. Box plots showing ambulatory 24-hour esophageal pH-monitoring characteristics (DeMeester scores) of the 2 groups. The lines at the top, bottom, and middle of the box correspond to the 75th, 25th, and 50th percentiles (median), respectively. The whiskers at the top and the bottom of the box extend from the 90th and 10th percentile, respectively. Open circles represent outliers. Despite being asymptomatic, group B has inadequate intraesophageal acid suppression with a median DeMeester score of 32.
Gastroenterology  , DOI: ( /gast )

3. 2
Fig. 2. Example of PCNA immunohistochemistry depicting dense brown nuclear staining of the BE glandular cells in biopsy specimens from a representative patient from group A (A) before and (B) after 6 months of therapy that had normalized the intraesophageal pH profile.
Gastroenterology  , DOI: ( /gast )

4. 3
Fig. 3. Cell proliferation as determined by PCNA expression in the 2 groups at baseline and after 6 months of therapy. On the y-axis, PCNA score represents percent of cells staining positive (see Patients and Methods). (A) Data on group A (normal intraesophageal pH profile); (B) data on group B (pathological intraesophageal pH profile). For each box plot, lines at the top, bottom, and middle of the box correspond to the 75th, 25th, and 50th percentile (median), respectively. The whiskers at the top and the bottom of the box extend from the 90th and 10th percentile, respectively. Open circles represent outliers. At 6 months, there is a significant decrease in PCNA expression in group A (normal intraesophageal pH profile on lansoprazole therapy; P < 0.001) and no change in group B (persistently abnormal intraesophageal pH profile despite lansoprazole therapy).
Gastroenterology  , DOI: ( /gast )

5. 4
Fig. 4. Example of villin immunoblot from a representative patient, comparing villin expression in mucosal biopsy lysates from normal esophagus (N, squamous epithelium), BE (B1, baseline; B2, 6 months), and duodenum (D, columnar epithelium). None of the squamous esophageal samples (negative control) and all duodenal samples (positive control) expressed villin (Mr = 95 kilodaltons).
Gastroenterology  , DOI: ( /gast )

6. 5
Fig. 5. Cell differentiation as determined by villin immunoblotting in the 2 groups at baseline and after 6 months of therapy. On the y-axis, villin score represents densitometry units over duodenum, used as internal standard for each patient (see Patients and Methods). (A) Data on group A (normal intraesophageal pH profile); (B) data on group B (pathological intraesophageal pH profile). For each box plot, the lines at the top, bottom, and middle of the box correspond to the 75th, 25th, and 50th percentile (median), respectively. The whiskers at the top and the bottom of the box extend from the 90th and 10th percentile, respectively. Open circles represent outliers. At 6 months, there is a significant increase in villin expression in group A (normal intraesophageal pH profile on lansoprazole therapy; P < 0.001) and no change in group B (persistently abnormal intraesophageal pH profile despite lansoprazole therapy).
Gastroenterology  , DOI: ( /gast )

7. 6
Fig. 6. Relationship between villin, a marker of intestinal differentiation, and PCNA, a marker of proliferation, in 42 BE patients at baseline examination. In these samples, there is a strong negative correlation (r = −0.79) between villin expression by immunoblotting and PCNA immunohistochemistry (P < 0.001).
Gastroenterology  , DOI: ( /gast )

8. 7
Fig. 7. Relationship between (A) villin, a marker of intestinal differentiation, and (B) PCNA, a marker of proliferation in 14 of 60 BE patients who had evidence of dysplasia. In these samples, there is no correlation (r = −0.18) between villin expression and dysplasia (top), but there is a strong positive correlation (r = 0.76) between PCNA expression by immunohistochemistry and degrees of dysplasia (bottom; P < 0.001).
Gastroenterology  , DOI: ( /gast )