1. Volume 120, Issue 2, Pages 506-511 (February 2001)
Gallbladder muscle dysfunction in patients with chronic acalculous disease 
Joseph Amaral, Zuo-Liang Xiao, Qian Chen, Peirong Yu, Piero Biancani, Jose Behar 
Gastroenterology 
Volume 120, Issue 2, Pages (February 2001)
DOI: /gast
Copyright © 2001 American Gastroenterological Association Terms and Conditions

2. Fig. 1
Dose-response studies with CCK-8 in intact muscle cells of gallbladders with PS (○) and AGD (●). The contractions in response to CCK-8 were significantly reduced at all doses in muscle cells of gallbladders with AGD compared with those with PS. Values are means ± SE of 3 experiments. *P < 0.001, ANOVA.
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

3. Fig. 2
(A) Dose-response studies with GTPγS in muscle cells of gallbladders with PS (●), ChS (▵), and AGD (■). Cells were permeabilized with saponin to allow diffusion of GTPγS into the cytosol. GTPγS-induced contraction was significantly reduced at all doses in muscle cells from gallbladders with AGD compared with those from PS and ChS. Values are means ± SE of 3 experiments. *P < 0.001, ANOVA. (B) Effect of AlF4 on intact muscle cells of gallbladders with PS (●), ChS (▵), and AGD (■). AlF4-induced contraction was significantly reduced at all doses in muscle cells of gallbladders with AGD compared with those from PS and ChS. Values are means ± SE of 3 experiments. *P < 0.01, ANOVA.
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

4. Fig. 3
Dose-response studies with second messenger DAG in intact muscle cells of gallbladders with PS (○) and AGD (●). The contractile responses to DAG were significantly reduced at all doses in muscle cells of gallbladders with AGD compared with those from PS. Values are means ± SE of 3 experiments. *P < 0.001, ANOVA.
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

5. Fig. 4
(A) Stimulation of [35S]GTPγS binding with 1 mmol/L CCK-8 in muscle membranes of gallbladders with PS (2) and AGD (■). CCK-8 caused a significant increase in [35S]GTPγS binding to Gαi-3, but not to Gαi-1,2, Gαq-11, Gαs. The stimulation of GTPγS binding to Gαi-3 induced by CCK-8 was not significantly different in these 2 groups. Data are expressed as percentage increase over basal level (without stimulation); values are means ± SE of 3 experiments. (B) Stimulation of [35S]GTPγS binding with 1 mmol/L VIP in muscle membranes of gallbladders with PS (2) and AGD (■). VIP caused a significant increase in [35S]GTPγS binding to Gαs, but not to Gαi-1,2, Gαq-11, Gαi-3. The stimulation of GTPγS binding to Gαs induced by VIP was not significantly different in these 2 groups. Data are expressed as percentage increase over basal level (without stimulation); values are means ± SE of 3 experiments.
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

6. Fig. 5
CCK receptor binding study in muscle membranes of gallbladders with AGD (■), PS (○), and ChS (▵). Membranes were incubated for 90 minutes at 25°C with 50 pmol/L 125I–CCK-8 plus the indicated concentrations of unlabeled CCK-8. Results are expressed as a percentage of the value measured with the radiolabeled ligand alone (maximum binding). In each experiment, each value was measured in triplicate; results are means from 4 separate experiments.
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions