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.

NUP37, a positive regulator of YAP/TEAD signaling, promotes the progression of hepatocellular carcinoma.

Activation of YAP/TEAD signaling is very common in the progression of HCC (Hepatocellular carcinoma). Nuclear pore complex (NPC) regulates the shuttling of proteins between cytoplasm and nucleus. Nuclear accumulation of YAP protein has been observed in the majority of HCC tissues. However, whether NPC could regulate the YAP/TEAD signaling remains unknown. In this study, it was found NUP37, the component of NPC, significantly up-regulated in HCC clinical samples and mouse model. Over-expression of NUP37 promoted the growth, migration and invasion of HCC cells, while knocking down the expression of NUP37 inhibited the growth, migration, invasion and metastasis of HCC cells and improved the survival of the mouse model. NUP37 interacted with YAP and activated YAP/TEAD signaling by enhancing the interaction between YAP and TEAD. Taken together, these data demonstrated the oncogenic roles of NUP37 in the progression of HCC and suggested that NUP37 might be a promising therapeutic target.

PKMYT1 promoted the growth and motility of hepatocellular carcinoma cells by activating beta-catenin/TCF signaling.

Over-activation of beta-catenin/TCF signaling has been frequently observed in hepatocellular carcinoma (HCC). Better understanding the molecular mechanism for the aberrant activation of beta-catenin/TCF signaling would provide novel insights into the treatment of this malignancy. In this study, we have shown that the expression of PKMYT1 was up-regulated in HCC. PKMYT1 positively regulated the growth, migration, colony formation, metastasis and epithelia mesenchymal transition (EMT) of HCC cells. Mechanically, PKMTY1 activated the beta-catenin/TCF signaling by binding and inactivating GSK3beta. Taken together, our study demonstrated the oncogenic activity of PKMYT1 in the progression of HCC and suggested that PKMYT1 might be a therapeutic target.

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.

Sevoflurane affects evoked electromyography monitoring in cerebral palsy.

BACKGROUND: To explore the effect of sevoflurane inhalation anesthesia on evoked electromyography monitoring of spinal nerve root in children associated with cerebral palsy. METHODOLOGY: Children with cerebral palsy (n=40) were selected and further divided into 1MAC (minimum alveolar concentration) sevoflurane group and 2MAC sevoflurane group. Following the induction of anesthesia, Nicolet Endeavor-CR16 channel electrophysiological monitor was used to implement three times of successive electrical stimulation with interval of 5 sec at 3.50 mA. RESULTS: Our results suggested a statistical significance of amplitude retention ratio and latency in the sevoflurane inhalation time (P<0.01), with an interaction effect between the sevoflurane inhalation time and concentration for amplitude retention ratio (P<0.01), while there is no interaction effect between the sevoflurane inhalation time and concentration for latency (P>0.05). Compared to 1MAC sevoflurane group, the amplitude retention ratio of 2MAC sevoflurane group decreased remarkably (P<0.01) and the latency of 2MAC sevoflurane group extended at T3 and T4 (P<0.05 or P<0.01). CONCLUSIONS: In evoked electromyography monitoring of spinal nerve root in children with cerebral palsy, with the increasing of concentration and duration of sevoflurane inhalation, evoked electromyogram retention ratio reduces gradually, latency extends and the retention ratio has more changes than the latency.