Hepatocellular carcinoma (HCC) is one of the most common malignancies with a rising incidence around the world. MicroRNAs (miRNAs) have been reported to play essential roles in the progression of HCC. However, the precise mechanism of miR-3662 in the HCC process remains poorly understood. This study was aimed to determine the regulatory network of miR-3662 and hexokinase 2 (HK2) in HCC. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect miR-3662 expression. Cell proliferation and invasion were measured by Cell Counting Kit-8 (CCK-8) assay and Transwell assay, respectively. Glucose consumption and lactate production assays were used to detect glucose metabolism activity in HCC cells. The potential binding sites between miR-3662 and HK2 were predicted by TargetScan online software and the relationship between miR-3662 and HK2 was verified by luciferase report assay. The protein expression of HK2 was measured by western blot analysis. A xenograft tumor model was established to confirm the role of miR-3662 and HK2 in vivo. miR-3662 expression was downregulated in HCC tissues and cells, and it was reduced in hypoxia-induced HCC cells in a time-dependent manner. Overexpression of miR-3662 or knockdown of HK2 inhibited cell proliferation, invasion, and glucose metabolism in HCC cells, which could be reversed by upregulating HK2. Besides, HK2 was a direct target of miR-3662 in HCC cells, and hypoxia upregulated the expression of HK2. In addition, the upregulation of HK2 could abolish miR-3662 overexpression-induced inhibitory effects on tumor growth and glucose metabolism in vivo.

-MicroRNAs (miRNAs) are widely known as critical regulators in isoflurane-induced neurotoxicity during the development of brain. Moreover, isoflurane could aggravate cognitive impairment in diabetic rats. The present study was designed to investigate the role and mechanism of miR-140-5p on isoflurane-induced neurotoxicity in diabetic rats. Firstly, a diabetic rat model was established by injection of streptozotocin (STZ) and identified by Morris water maze test. The result indicated that isoflurane treatment exacerbated STZ-induced cognitive impairment, as demonstrated by increase of the latency to the platform and decrease of the proportion of time spent in the target quadrant. Secondly, miR-140-5p was up-regulated in diabetic rats treated with isoflurane. Functional assays revealed that knockdown of miR-140-5p attenuated neurotoxicity in diabetic rats, which was shown by a decrease of the latency to the platform and an increase of the proportion of time spent in the target quadrant. Mechanistically, we demonstrated that miR-140-5p directly bonded to SNX12 (sorting nexin 12). At last, the neuroprotective effect of miR-140-5p knockdown against isoflurane-aggravated neurotoxicity in diabetic rats was dependent on up-regulation of SNX12 and inhibition of cell apoptosis. In summary, these meaningful results demonstrated the mitigation of miR-140-5p knockdown against isoflurane-aggravated neurotoxicity in diabetic rats via SNX12, suggesting a novel target for neuroprotection in diabetes under isoflurane treatment.

Coronavirus disease 2019 (COVID-19) outbreaks have occurred in many countries around the world. The numbers of confirmed cases and deaths continue to increase. It is increasingly likely that COVID-19 patients will require emergency surgeries in the operating room (OR). As COVID-19 can easily be transmitted to healthcare workers and other patients during surgery, it is important to establish a set of infection prevent and control management strategy to prevent COVID-19 from spreading in the OR. Based on our experience in COVID-19 prevention and control in the OR, we introduce this COVID-19 prevention and control management strategy for preventing COVID-19 from spreading in the OR. This management strategy includes a number of COVID-19 prevention and control procedures including (I) conduct COVID-19 knowledge training at the early stage of outbreak, (II) formulate the surgery arrangement procedures and suspend the elective surgery if the patient confirmed to COVID-19, (III) divide an isolated OR area for COVID-19 surgery, (IV) preoperative preparation procedures, (V) procedures for wearing and removing personal protective equipment, (VI) anesthesia management, intraoperative management, (VII) post-operative disposable waste management and disinfection. This management strategy has worked very effectively since the outbreak of COVID-19 in Wuhan at the end of 2019. We have performed emergency surgeries on several COVID-19 confirmed patient and dozens of COVID-19 suspected patients under this COVID-19 prevention and control management strategy, and have achieved an excellent result of zero COVID-19 infection in the OR.

Objectives: MicroRNAs (miRNAs) are widely known as critical regulators in isoflurane-induced neurotoxicity during the development of brain. Isoflurane could aggravate cognitive impairment in diabetic rats. The present study was designed to explore the role and mechanism of miR-140-5p on isoflurane-induced neurotoxicity in diabetic rats. Methods: Diabetic rats model was established by injection of streptozotocin (STZ) and identified by Morris water maze test. Expression of miR-140-5p in diabetic rats under isoflurane treatment was evaluated via qRT-PCR (quantitative real-time polymerase chain reaction). Latency to platform and time spent in the target quadrant were calculated to detect the effect of miR-140-5p on neurotoxicity. The potential target for miR-140-5p was validated via dual luciferase activity assay. Results: Morris water maze test indicated that isoflurane treatment exacerbated STZ-induced cognitive impairment, as demonstrated by increase of latency to platform and decrease of time spent in the target quadrant. MiR-140-5p was up-regulated in diabetic rats under isoflurane treatment. Moreover, knockdown of miR-140-5p attenuated neurotoxicity in diabetic rats. Mechanistically, we found that miR-140-5p could directly bind to SNX12 (sorting nexin 12). The neuroprotective effect of miR-140-5p against isoflurane-aggravated neurotoxicity in diabetic rats dependent on up-regulation of SNX12 and inhibition of cell apoptosis. Conclusions: Knockdown of miR-140-5p relieved isoflurane-aggravated neurotoxicity in diabetic rats through targeting SNX12, suggesting a novel target for neuroprotection in diabetes under isoflurane treatment.

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