Effect of reflux esophagitis on sleep fragmentation and stage transitions.

<p>(A) Number of stage bouts in the 12-h light period. (B) Number of stage counts in the 12-h light period. (C) Duration of each sleep stage in the 12-h light period. (D) Stage transitions during the 12-h light period. NREM, non-rapid eye movement; REM, rapid eye movement. (E) Relative average EEG power density of NREM sleep between 10:00 a.m. and 12:00 a.m. The horizontal bars indicate statistical difference (p<0.05) between control and reflux esophagitis group. N = 8. Data are mean ± SEM. White bars represented control rats and black bars represented reflux esophagitis rats. *p<0.05 versus control. **p<0.01 versus control.</p

Effect of reflux esophagitis on sleep.

<p>(A) Typical EEG, EMG, and LOC of control and reflux esophagitis. (B) Effect of reflux esophagitis on the amount of each stage during the 12-h light period and 12-h dark period. (C) Time course analysis of each stage during a whole day. N = 8. Data are mean ± SEM. White bars and circles represented control rats. Black bars and circles represented reflux esophagitis rats. *p<0.05 versus control. **p<0.01 versus control. EEG, electroencephalograph; EMG, electromyography; LOC, locomotor; NREM, nonrapid eye movement; REM, rapid eye movement.</p

Effects of omeprazole on gastric acid secretion in rats.

<p>Data were mean ± SEM. * p<0.01 versus control.</p><p>Effects of omeprazole on gastric acid secretion in rats.</p

Induction of rat acid reflux esophagitis, macroscopic, and histological findings.

<p>(A) A scheme of a rat reflux esophagitis model. (B) Macroscopic appearance of a normal esophagus. (C) Histology of the normal esophagus revealed thin epithelium with few inflammatory cells. (D) Macroscopic appearance of reflux esophagitis showed several erosions and ulcers at the middle and lower esophagus. (E) Mucosal thickening with basal cell hyperplasia and marked inflammatory cell infiltration were observed in reflux esophagitis. (Hematoxylin-eosin staining, original magnification ×200).</p

Effect of proton pump inhibitor on sleep disturbances in rats with reflux esophagitis.

<p>(A) Typical polygraphic recordings of the on-PPI group and the post-PPI group. (B) Amount of each stage for the 3 groups (pre-PPI group, on-PPI group, and post-PPI group) in the 12-h light period. (C) Number of NREM sleep bouts for the 3 groups in the 12-h light period. (D) Duration of each stage for the 3 groups in the 12-h light period. (E) Stage transitions for the 3 groups during the 12-h light period. N = 7. Data are mean ± SEM. *p<0.05 versus before PPI group. **p<0.01 versus before PPI group.</p

Baseline characteristics of patients.

<p>ARB, angiotensin II receptor blocker; IQR, interquartile range.</p><p>Baseline characteristics of patients.</p

Effect of TLR2 deficiency on intestinal ischemia/reperfusion injury.

<p>Wild-type (WT) mice and TLR2 knockout (KO) mice were subjected to 45 min of ischemia followed by 60 min of reperfusion. After removal of the small intestine, intestinal injuries were assessed by using the histological grading system, measuring the luminal hemoglobin concentration, and counting apoptotic epithelial cells with an antibody against ssDNA. (A) Histological findings of intestinal ischemia/reperfusion (I/R) injury in WT (a) and TLR2 KO (b) mice. Compared to WT mice (a), TLR2 KO mice exhibited less severe intestinal injury induced by 45 min of ischemia followed by 60 min of reperfusion (b). (B) Comparison of the histology grading scores between WT and TLR2 KO mice that were subjected to I/R injury. Each column represents the mean ± SD. N = 8. *<i>P</i><0.01 vs WT mice with sham operation, #<i>P</i><0.05 vs WT mice subjected to I/R injury. (C) Comparison of luminal hemoglobin concentrations between WT and TLR2 KO mice that were subjected to I/R injury. Each column represents the mean ± SD. N = 6–8. *<i>P</i><0.01 vs WT mice with sham operation, #<i>P</i><0.01 vs WT mice subjected to I/R injury. (D) Immunohistochemical staining of ssDNA in intestinal mucosa. I/R resulted in induction of apoptosis of epithelial cells labeled with an antibody against the ssDNA of injured mucosa in WT mice (a), and TLR2 deficiency prevented I/R-induced apoptosis of the small intestinal epithelial cells (b). (E) Comparison of apoptotic indices between WT and TLR2 KO mice that were subjected to I/R injury. Each column represents the mean ± SD. N = 8. *<i>P</i><0.01 vs WT mice with sham operation, #<i>P</i><0.01 vs WT mice subjected to I/R injury.</p

Expression of TLR2 during the development of the intestinal ischemia-reperfusion injury.

<p>Wild-type mice were subjected to 45 min of ischemia followed by 60 min of reperfusion. After removal of the small intestine, expression of TLR2 was examined by real-time RT-PCR and immunohistochemical staining. (A) Effect of the ischemia/reperfusion (I/R) treatment on intestinal TLR2 mRNA. Each column represents the mean ± SD. N = 6. *<i>P</i><0.01 vs mice with sham operation. (B, C) Immunohistochemical staining for TLR2. TLR2 proteins were expressed in epithelial cells, inflammatory cells (arrow heads), and endothelial cells (arrows) in the injured small intestine.</p

Changes in the severity of small intestinal mucosal breaks from baseline to posttreatment.

<p>Results were analyzed by McNemar test.</p

Changes in the levels of hemoglobin and albumin after treatment with placebo or rebamipide.

<p>Results are expressed as medians and interquartile ranges (IQRs)</p><p>Changes in the levels of hemoglobin and albumin after treatment with placebo or rebamipide.</p