The effect of different concentrations of rocuronium bromide used for anesthesia induction during thyroid surgery on the intraoperative recurrent laryngeal nerve monitoring was evaluated. One hundred patients undergoing thyroid operation were randomized into five groups (20 patients per group). Patients in group I were operated and monitored without the use of rocuronium bromide. Patients in groups II-V were respectively injected with 0.5x, 1x, 1.5x, and 2x ED95 rocuronium bromide intravenously. The time from injecting the rocuronium bromide to the beginning of tube insertion was recorded, the conditions of tracheal intubation were evaluated, and the changes in blood pressure and pulse during the intubation process were monitored. Vagus nerve/recurrent laryngeal nerve evoked muscle potential was monitored using the NIM-Response3.0 nerve electromyography monitor. The amplitude of electromyography signal was recorded every 5 min during 30 min after successful tracheal intubation. The tracheal intubation success rate was 100% in all groups. Compared with group I, intubating condition scores (Cooper scores) in the patients of groups II-V were higher (P < 0.05). The stability of intraoperative neuromonitoring signal amplitude in groups I-III met the monitoring standards. The findings suggest that the use of 0.5x or 1x ED95 rocuronium bromide during the anesthesia induction can improve the tracheal tube conditions without affecting the intraoperative recurrent laryngeal nerve monitoring. The use of 1x ED95 rocuronium bromide induction was associated with the best results.

Abstract. Colorectal carcinoma (CRC) is a malignant solid tumor arising from the large intestine and is associated with an increasing incidence and poor prognosis. Further understanding of the molecular mechanisms underlying CRC may contribute to the development of novel effective therapeutic strategies. MicroRNAs (miRs), including miR-155, have been reported to be associated with the etiology and biology of CRC; however, the molecular mechanisms by which miR-155 affect CRC remain to be fully elucidated. The present study used a multidisciplinary approach, involving reverse transcription-quantitative polymerase chain reaction, northern blotting, MTT assay, cell cycle progression analysis, immunoblotting, and animal experiments, to determine the possible targets of miR-155 in CRC cells. miR-155 was found to be overexpressed in CRC tissue samples, compared with paired normal colon tissue samples. In addition, the inhibition of miR-155 induced a deceleration in CRC cell proliferation and inactivation of the Wnt/β-catenin signaling pathway. miR-155 suppression also reduced the growth of CRC xenografts in an animal model. HMG-box transcription factor 1 (HBP1) was identified as a novel target of miR-155, which mediated its effect on CRC via the Wnt/β-catenin pathway. Furthermore, patients with CRC exhibiting higher serum levels of miR-155 exhibited reduced survival rates. In conclusion, the present study demonstrated that miR-155 may contribute to the progression and growth of CRC by enhancing the Wnt/β-catenin pathway in an HBP1-associated mechanism. Therefore, miR-155 may be considered a promising therapeutic target for the treatment of CRC.

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In the present study, we evaluated the protective effects of amentoflavone (AMF) against high-fat (HF) diet-induced metabolic dysfunction and focused on the influence of AMF on adipogenic differentiation during 3T3-L1 adipocyte differentiation. For this purpose, male Wistar rats were fed a HF diet or a HF diet with AMF (10 or 50 mg/kg). We found that AMF protected against HF diet-induced metabolic dysfunction in a dose-dependent manner, as evidenced by a decrease in the fasting blood glucose levels, fasting insulin levels and the homeostatic model assessment-insulin resistance index (HOMA-IR), as well as by a decrease in the glucose level, as shown by the intraperitoneal glucose tolerance test and intraperitoneal insulin tolerance test. Moreover, the results revealed that AMF significantly inhibited the increase in body weight, the weight of perirenal adipose tissues and the serum triglyceride (TG) content of the rats fed the HF diet in a dose-dependent manner. AMF also inhibited the accumulation of oil droplets in differentiated 3T3-L1 adipocytes in a concentration-dependent manner. The incubation of the cells with AMF for 0–8, 0–2, 2–4, or 4–8 days markedly inhibited adipogenesis. During the early phase of the adipocyte differentiation of 3T3-L1 cells, AMF decreased CCAAT/enhancer-binding protein (C/EBP) β expression in a concentration-dependent manner, leading to the inhibition of mitotic clonal expansion (MCE). Moreover, our results demonstrated that AMF significantly increased reactive oxygen species (ROS) generation in the cells and the antioxidant, N-acetylcysteine (NAC), markedly attenuated the inhibitory effects of AMF on adipogenesis. AMF also inhibited the expression of peroxisome proliferator-activated receptor γ (PPARγ) and C/EBPα and the expression of downstream targets in a concentration-dependent manner. The overexpression of PPARγ and C/EBPα (by transfection with respective overexpression plasmids) attentuated the inhibitory effects of AMF on the formation of oil droplets. The inhibitory effects of AMF on adipocyte differentiation may contribute to its protective effects against HF diet-induced metabolic dysfunction. Overall, the data in our study provide novel insight into the mechanisms responsible for the protective effects of AMF against HF diet-induced metabolic dysfunction and those for its inhibitory effect on adipocyte differentiation.

Abstract. The present study aimed to assess whether different anesthesia methods (general anesthesia and general anesthesia combined with epidural block) were associated with tumor metastasis during the perioperative period and the possible molecular mechanisms of tumor metastasis. A rat hepatoma tumor xenograft model was constructed via the subcutaneous injection of Morris hepatoma 3924A cells into the upper axillary fossa. General anesthesia and general anesthesia combined with epidural block prior to hepatectomy were conducted on tumor-bearing rats. The average numbers of metastatic nodules on the lung surface were calculated in the different groups and the presence of abdominal lymph node metastases, rate of malignant ascites and abdominal wall-implanted nodules were recorded. Blood samples were collected from the orbits of rats immediately prior to surgery and at 2, 7 and 30 days following surgery. Plasma levels of interferon-γ, transforming growth factor-α and vascular endothelial growth factor (VEGF) were measured. Finally, the expression of phosphorylated signal transducer and activator of transcription-3 and phosphorylated VEGF were measured by western blot analysis. The results of this analysis demonstrated that tumor metastasis was greatly suppressed when the rats underwent general anesthesia combined with epidural block prior to hepatectomy, compared with general anesthesia alone. The results of cytokine quantification and western blot analysis revealed that the anti-metastatic effect of general anesthesia combined with epidural block may have been mediated by inhibition of STAT3 and the relevant cytokines.

This study aimed to explore effects of Sevoflurane on ischemia-reperfusion (I/R) injury after total knee arthroplasty (TKA). To explore potential molecular mechanism, Ras related dexamethasone induced 1 (RASD1), a Protein kinase A (PKA) activator, frequently associated with various models of I/R injury, was also investigated. In vivo mouse models with I/R injury after TKA and in vitro cell models with I/R injury were induced. Contents of creatinine kinase (CK), lactic dehydrogenase (LDH), superoxide dismutase (SOD), and malondialdehyde (MDA), serum levels of inflammatory factors, expression of PKA pathway-related genes and cell proliferation and apoptosis were measured. RASD1 was altered and PKA pathway was inhibited in mice and cells to elucidate the involvement of RASD1 and PKA pathway in Sevoflurane treatment on I/R injury. RASD1 was upregulated in I/R injury after TKA. Sevoflurane treatment or silencing RASD1 reduced RASD1 expression, CK, LDH and MDA contents, inflammation, apoptosis, but increased proliferation, SOD content, cAMP expression, and extents of PKA and cAMP responsive element binding protein (CREB) phosphorylation in skeletal muscle cells of I/R injury. Additionally, PKA pathway activation potentiated the therapeutic effect of Sevoflurane on I/R injury after TKA. Altogether, Sevoflurane treatment confines I/R injury after TKA via RASD1-mediated PKA pathway activation.

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