Effect of thoracic paravertebral nerve block on the early postoperative rehabilitation in patients undergoing thoracoscopic radical lung cancer surgery.

OBJECTIVE: To evaluate the effect of thoracic paravertebral nerve block on early postoperative rehabilitation in patients undergoing radical thoracoscopic surgery for lung cancer. METHODS: Ninety patients scheduled for elective video-assisted thoracoscopic lobectomy of lung cancer were divided into 2 groups: the general anesthesia group (GA group, n = 45) and the TPVB group (TP group, n = 45). The primary outcome was the decline rate of the 6-min walking test (6MWT); the second outcomes were as follows: absolute value and the completion rate of 6MWT, postoperative analgesia deficiency and pain scores, oxycodone consumption, sleep quality, the incidence of postoperative pulmonary complications, and the hospital stay. RESULTS: Compared with the GA group, the TP group had a lower decline rate of the 6MWT on POD1 and POD2. The walking distance on POD1 and POD2 in the TP group was significantly longer than that in the GA group; the completion rate at POD1 in the TP group was higher than that in the GA group. The pain scores and oxycodone consumption at POD1 in the TP group were lower than the GA group. The sleep quality in the TP group was higher than the GA group. CONCLUSIONS: TPVB can significantly improve postoperative rehabilitation in patients undergoing thoracoscopic radical lung cancer surgery, which is helpful for promoting the early recovery of patients. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR1900026213. Registered 26 Sept. 2019, http://www.chictr.org.cn/showproj.aspx?proj=43733 .

LncRNA MALAT1 protects cardiomyocytes from isoproterenol-induced apoptosis through sponging miR-558 to enhance ULK1-mediated protective autophagy.

Investigating the molecular mechanisms of myocardial infarction (MI) and subsequent heart failure have gained considerable attention worldwide. Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been previously demonstrated to regulate the proliferation and metastasis of several tumors. However, little is known about the effects of MALAT1 in MI and in regulating the cell date after MI. In our study, first, it was shown that the expression levels of MALAT1 were increased in the MI samples compared with normal tissues using quantitative reverse-transcription polymerase chain reaction. Then, MALAT1 knockdown could significantly decrease the cell viability and increase the apoptotic rates in isoproterenol (ISO)-treated H9C2 cells. In addition, we screened the possible target and found that miR-558 is its direct target using dual luciferase reporter assay, indicating that MALAT1 functioned as decoys sponging miR-558. Transfection of miR-558 mimic decreased the cell viability and enhanced the apoptosis. Furthermore, we revealed that miR-558 could downregulate ULK1 expression and suppressed ISO-induced protective autophagy. Activation of MALAT1/miR-558/ULK1 pathway protected H9C2 cells from ISO-induced mitochondria-dependent apoptosis. Finally, we used MALAT1-knockout mice to further demonstrated that MALAT1 protected cardiomyocytes from apoptosis and partially improved the cardiac functions upon ISO treatment. In conclusion, we elucidated that lncRNA MALAT1 protected cardiomyocytes from ISO-induced apoptosis by sponging miR-558 thus promoting ULK1-dependent autophagy. Targeting lncRNA MALAT1 might become a potential strategy in protecting cardiomyocytes during MI.