Objective To investigate whether there has any difference of gastric and small bowel transit time and completion rates between two capsule endoscopes with different size and weight. Methods Clinical data of patients who had undergone OMOM or MiroCam (smaller and lighter than OMOM) capsule endoscopy were retrospectively studied. Comparison of gastric and small bowel transit time and completion rates were made between the two kinds of capsule endoscopy. Results 1, 448 patients (628 in OMOM group and 820 in MiroCam group) were finally includ-ed. In patients with Crohn's disease or suspected Crohn's disease, gastric transit time of OMOM was significantly longer than that of MiroCam [(53.4 ± 52.6) minutes vs (41.1 ± 47.9) minutes, = 0.022]. In patients with gastroin-testinal bleeding, gastric transit time in OMOM was significantly shorter than that in MiroCam [(42.1 ± 44.8) minutes vs (62.0 ± 78.6) minutes, = 0.016). No significant difference in small bowel transit time or completion rate was found. Conclusions We conclude that the differences of gastric transit time, small bowel transit time and completion rates between the two kinds of capsule endoscopy with different size and weight are not significantly. Whereas, in patients with Crohn's disease or suspected Crohn's disease, gastric transit time of smaller and lighter capsule en-doscopy is shorter in patients with gastrointestinal bleeding, but longer of gastric transit time in smaller and lighter capsule endoscopy.

Background::Hyperglycemia frequently induces apoptosis in endothelial cells and ultimately contributes to microvascular dysfunction in patients with diabetes mellitus (DM). Previous research reported that the expression of integrins as well as their ligands was elevated in the diseased vessels of DM patients. However, the association between integrins and hyperglycemia-induced cell death is still unclear. This research was designed to investigate the role played by integrin subunit β5 (ITGB5) in hyperglycemia-induced endothelial cell apoptosis.Methods::We used leptin receptor knockout (Lepr-KO) ( db/ db) mice as spontaneous diabetes animal model. Selective deletion of ITGB5 in endothelial cell was achieved by injecting vascular targeted adeno-associated virus via tail vein. Besides, we also applied small interfering RNA in vitro to study the mechanism of ITGB5 in regulating high glucose-induced cell apoptosis. Results::ITGB5 and its ligand, fibronectin, were both upregulated after exposure to high glucose in vivo and in vitro. ITGB5 knockdown alleviated hyperglycemia-induced vascular endothelial cell apoptosis and microvascular rarefaction in vivo. In vitro analysis revealed that knockdown of either ITGB5 or fibronectin ameliorated high glucose-induced apoptosis in human umbilical vascular endothelial cells (HUVECs). In addition, knockdown of ITGB5 inhibited fibronectin-induced HUVEC apoptosis, which indicated that the fibronectin-ITGB5 interaction participated in high glucose-induced endothelial cell apoptosis. By using RNA-sequencing technology and bioinformatic analysis, we identified Forkhead Box Protein O1 (FoxO1) as an important downstream target regulated by ITGB5. Moreover, we demonstrated that the excessive macroautophagy induced by high glucose can contribute to HUVEC apoptosis, which was regulated by the ITGB5-FoxO1 axis. Conclusion::The study revealed that high glucose-induced endothelial cell apoptosis was positively regulated by ITGB5, which suggested that ITGB5 could potentially be used to predict and treat DM-related vascular complications.