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Background The aim of this study was to investigate the effects of different minimally invasive surgical procedures on intestinal mucosal barrier function. Methods In this study, 76 patients who underwent minimally invasive gastric cancer surgery were selected, and peripheral blood was collected to test the levels of serum plasma d-lactic acid, diamine oxidase, and bacterial endotoxin before and 1 and 3 days after surgery. These markers were compared at different time points before and after surgery to understand the recovery of the intestinal mucosal barrier function in patients after surgery. Results On the first postoperative day, the change in serum d-lactic acid relative to the preoperative levels was significantly (P < 0.05) lower in the laparoscopic surgery group (4.05 [−0.195, 6.917 mmol/L]) than in the robot-assisted surgery group (7.56 [5.190, 12.145 mmol/L]). Both the serum d-lactic acid and bacterial endotoxin levels were significantly higher on the first postoperative day compared with preoperative levels, and although they showed a gradual decrease by the third day, they remained significantly higher than the preoperative levels (P < 0.05). The Student-Newman-Keuls method for pairwise comparison of the measurements at each time point demonstrated that the differences in d-lactic acid and bacterial endotoxin levels between the preoperative sample and the sample collected on the third postoperative day were statistically significant (P < 0.05). Conclusions Compared with the laparoscopic surgery group, the robotic surgery group showed larger changes in the postoperative serum d-lactic acid level, suggesting that the robotic surgery resulted in greater damage to the barrier function of the intestinal mucosa. The serum d-lactic acid and bacterial endotoxin levels were significantly higher in postoperative patients and showed a trend to gradually decrease, suggesting that the intestinal mucosal barrier function of patients after minimally invasive gastric cancer surgery is damaged and then gradually recovers.
Background The aim of this study was to investigate the effects of different minimally invasive surgical procedures on intestinal mucosal barrier function. Methods In this study, 76 patients who underwent minimally invasive gastric cancer surgery were selected, and peripheral blood was collected to test the levels of serum plasma d-lactic acid, diamine oxidase, and bacterial endotoxin before and 1 and 3 days after surgery. These markers were compared at different time points before and after surgery to understand the recovery of the intestinal mucosal barrier function in patients after surgery. Results On the first postoperative day, the change in serum d-lactic acid relative to the preoperative levels was significantly (P < 0.05) lower in the laparoscopic surgery group (4.05 [−0.195, 6.917 mmol/L]) than in the robot-assisted surgery group (7.56 [5.190, 12.145 mmol/L]). Both the serum d-lactic acid and bacterial endotoxin levels were significantly higher on the first postoperative day compared with preoperative levels, and although they showed a gradual decrease by the third day, they remained significantly higher than the preoperative levels (P < 0.05). The Student-Newman-Keuls method for pairwise comparison of the measurements at each time point demonstrated that the differences in d-lactic acid and bacterial endotoxin levels between the preoperative sample and the sample collected on the third postoperative day were statistically significant (P < 0.05). Conclusions Compared with the laparoscopic surgery group, the robotic surgery group showed larger changes in the postoperative serum d-lactic acid level, suggesting that the robotic surgery resulted in greater damage to the barrier function of the intestinal mucosa. The serum d-lactic acid and bacterial endotoxin levels were significantly higher in postoperative patients and showed a trend to gradually decrease, suggesting that the intestinal mucosal barrier function of patients after minimally invasive gastric cancer surgery is damaged and then gradually recovers.
Traumatic brain injury (TBI) is a prevalent disease that poses a significant threat to global public health. Digestive dysfunction, as a common complication, is of particular importance to understand its pathogenesis, diagnostic criteria, and relevant treatment strategies. TBI can affect digestive function through inflammatory immune responses, the enteric nervous system, and hormonal levels. Furthermore, TBI can also impact neurologic recovery through bidirectional communication along the brain-gut axis. Therefore, this article aims to summarize the underlying mechanisms and further explore individualized feeding strategies, therapeutic approaches, long-term prognosis for TBI patients, as well as recent advancements in related technologies. Further understanding of the pathogenesis of digestive system dysfunction after TBI on the basis of the interaction of gut-brain axis is conducive to more future therapies to treat TBI and improve the long-term prognosis of patients through improving digestive function, and achieve good clinical efficacy.
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