Application of the Left Lateral Decubitus Position in Laparoscopic Right Posterior Lobectomy.

OBJECTIVE: To investigate the value of the left lateral decubitus position in laparoscopic right posterior lobe tumor resection. PATIENTS AND METHODS: The clinical data of patients who underwent laparoscopic right posterior lobectomy from January 2020 to March 2023 were retrospectively collected and divided into group A (left lateral decubitus position group, n=30) and group B (conventional position group, n=35) according to different body positions. Intraoperative and postoperative data were collected and compared between the 2 groups. RESULTS: The operation time (210.43±57.56 vs. 281.97±65.89, t =5.887, P <0.05), hilar occlusion time (23.97±14.25 vs. 35.79±12.62, t =4.791, P <0.05), intraoperative blood loss (162.14±72.61 vs. 239.65±113.56, t =5.713, P <0.05), postoperative feeding time (1.13±0.36 vs. 1.57±0.67, t =3.681, P <0.05), postoperative visual analog scale score (5.16±0.89 vs. 7.42±1.31, t =3.721, P <0.05), postoperative abdominal drainage tube indwelling time (4.58±1.34 vs. 5.42±1.52, t =4.553, P <0.05), incidence rate of complications (43.33% vs. 82.86%, χ 2 =11.075, P <0.05) in group A were lower than those in group B ( P <0.05). Symptoms/side effects (32.42±3.42 vs. 27.44±3.31, t =4.331, P <0.05), and there were significant differences in social function (33.55±2.56 vs. 29.31±3.32, t =4.863, P <0.05). CONCLUSION: For right posterior lobe tumors of the liver, the left lateral decubitus position has many advantages in laparoscopic right posterior lobectomy, such as a wide field of view, simple steps, a short operation time, less bleeding, and a high postoperative quality of life. It is an effective treatment for right posterior lobe tumors of the liver and is worthy of being widely popularized.

Propofol Prevents Hippocampal Neuronal Loss and Memory Impairment in Cerebral Ischemia Injury Through Promoting PTEN Degradation.

Neuroprotective effect of propofol against cerebral ischemia injury was widely investigated. However, its mechanisms remain unclear. Phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway is supposed as a cell survival pathway, and phosphatase and tensin homolog deleted on chromosome ten (PTEN) is a negative regulator of AKT phosphorylation. Whether PTEN was involved in the protective effect of propofol against cerebral ischemia injury was not elucidated. In this study, the function of PTEN in the acute phase of cerebral ischemia injury was investigated. Our data showed that propofol promoted the PTEN degradation in the acute phase of cerebral ischemia injury and concurrently activated AKT phosphorylation. The increase of ubiquitinated PTEN caused by cerebral ischemia injury were degraded in propofol-pretreated rats. Moreover, we evidenced that proteasome activity was stimulated in propofol-treated rats. These data pointed that PTEN degradation was facilitated in the acute phase after propofol treatment possibly through activating ubiquitin-proteasome system. Therefore, we applied PTEN inhibitor-bpV before cerebral ischemia injury. Like propofol, bpV pretreatment also mitigated cerebral ischemia injury-induced cell loss in CA1 region and memory impairment. Taken together, our data suggest that PTEN degradation is neuroprotective against cerebral ischemia injury and propofol facilitates PTEN degradation to prevent hippocampal neuronal loss and memory deficit in cerebral ischemia injury.