Intravenous versus Volatile Anesthetic Effects on Postoperative Cognition in Elderly Patients Undergoing Laparoscopic Abdominal Surgery.

BACKGROUND: Delayed neurocognitive recovery after surgery is associated with poor outcome. Most surgeries require general anesthesia, of which sevoflurane and propofol are the most commonly used inhalational and intravenous anesthetics. The authors tested the primary hypothesis that patients with laparoscopic abdominal surgery under propofol-based anesthesia have a lower incidence of delayed neurocognitive recovery than patients under sevoflurane-based anesthesia. A second hypothesis is that there were blood biomarkers for predicting delayed neurocognitive recovery to occur. METHODS: A randomized, double-blind, parallel, controlled study was performed at four hospitals in China. Elderly patients (60 yr and older) undergoing laparoscopic abdominal surgery that was likely longer than 2 h were randomized to a propofol- or sevoflurane-based regimen to maintain general anesthesia. A minimum of 221 patients was planned for each group to detect a one-third decrease in delayed neurocognitive recovery incidence in propofol group compared with sevoflurane group. The primary outcome was delayed neurocognitive recovery incidence 5 to 7 days after surgery. RESULTS: A total of 544 patients were enrolled, with 272 patients in each group. Of these patients, 226 in the propofol group and 221 in the sevoflurane group completed the needed neuropsychological tests for diagnosing delayed neurocognitive recovery, and 46 (20.8%) in the sevoflurane group and 38 (16.8%) in the propofol group met the criteria for delayed neurocognitive recovery (odds ratio, 0.77; 95% CI, 0.48 to 1.24; P = 0.279). A high blood interleukin-6 concentration at 1 h after skin incision was associated with an increased likelihood of delayed neurocognitive recovery (odds ratio, 1.04; 95% CI, 1.01 to 1.07; P = 0.007). Adverse event incidences were similar in both groups. CONCLUSIONS: Anesthetic choice between propofol and sevoflurane did not appear to affect the incidence of delayed neurocognitive recovery 5 to 7 days after laparoscopic abdominal surgery. A high blood interleukin-6 concentration after surgical incision may be an independent risk factor for delayed neurocognitive recovery.

[Corrigendum] Propofol­induced HOXA11­AS promotes proliferation, migration and invasion, but inhibits apoptosis in hepatocellular carcinoma cells by targeting miR­4458.

Following the publication of the above article, an interested reader drew to the authors' attention that the western blots for the PCNA and cyclin D1 bands appeared to be strikingly similar. The authors were able to re­examine their original data, and recognize how the error was made with respect to the compilation of this figure (they were also able to demonstrate to the Editorial Office how the error occurred). The revised version of Fig. 3, now incorporating the correct data for the PCNA bands in Fig. 3A, is shown on the next page. The authors can confirm that the errors associated with this figure did not have a significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 46: 1135­1145, 2020; DOI: 10.3892/ijmm.2020.4667].

The Role of TAMs in Tumor Microenvironment and New Research Progress.

Tumor-associated macrophages (TAMs) are an important part of tumor microenvironment (TME) and play a key role in TME, participating in the process of tumor occurrence, growth, invasion, and metastasis. Among them, metastasis to tumor tissue is the key step of malignant development of tumor. In this paper, the latest progress in the role of TAMs in the formation of tumor microenvironment is summarized. It is particularly noteworthy that cell and animal experiments show that TAMs can provide a favorable microenvironment for the occurrence and development of tumors. At the same time, clinical pathological experiments show that the accumulation of TAMs in tumor is related to poor clinical efficacy. Finally, this paper discusses the feasibility of TAMs-targeted therapy as a new indirect cancer therapy. This paper provides a theoretical basis for finding a potentially effective macrophage-targeted tumor therapy.

Propofol­induced HOXA11­AS promotes proliferation, migration and invasion, but inhibits apoptosis in hepatocellular carcinoma cells by targeting miR­4458.

Propofol is a commonly used drug for the induction and maintenance of anesthesia. Previous studies have reported that propofol is involved in the progression of numerous human cancer types, including hepatocellular carcinoma (HCC). However, the underlying molecular mechanisms in HCC are yet to be elucidated. The present study aimed to investigate the potential mechanism of propofol in HCC development. MTT assay, flow cytometry analysis and Transwell assays were conducted to examine cell proliferation, apoptosis, migration and invasion, respectively. Western blotting was also performed to determine the protein expression levels of Bcl­2 and cleaved­caspase 3. An in vivo experiment was performed to assess the effect of propofol on tumor growth. Moreover, reverse transcription­quantitative PCR was conducted to measure the mRNA expression levels of HOMEOBOX A11 (HOXA11) antisense RNA (HOXA11­AS) and microRNA (miR)­4458. Dual­luciferase reporter and RNA pull­down assays were performed to evaluate the target relationship between HOXA11­AS and miR­4458. It was demonstrated that propofol inhibited HCC cell proliferation, migration and invasion, and promoted cell apoptosis in vitro. Furthermore, propofol could suppress tumor growth in vivo. Propofol suppressed the expression of HOXA11­AS in HCC cells, while HOXA11­AS overexpression reversed the inhibitory effect of propofol treatment on cell progression in HCC. In addition, miR­4458 was identified as a target of HOXA11­AS, and miR­4458 inhibition reversed the effect of HOXA11­AS knockdown on HCC cell progression. The results also indicated that propofol promoted the expression of miR­4458, while HOXA11­AS restored this effect in HCC. Thus, it was suggested that propofol suppressed cell progression by modulating the HOXA11­AS/miR­4458 axis in HCC.

NEAT1 aggravates sepsis-induced acute kidney injury by sponging miR-22-3p.

BACKGROUND AND AIM: Acute kidney injury (AKI) is a common complication of sepsis. Long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) plays a vital role in various diseases, including AKI. This study aimed to investigate the function and mechanism of NEAT1 in sepsis-induced AKI. MATERIALS AND METHODS: A septic AKI model was established by treating HK-2 cells with lipopolysaccharide (LPS). The levels of NEAT1 and miR-22-3p were measured by quantitative real-time PCR. Cell apoptosis was assessed by flow cytometry. The levels of apoptosis-related protein and autophagy-related factors were examined by the western blot assay. An enzyme-linked immunosorbent assay was used to calculate the contents of inflammatory factors. The interaction between NEAT1 and miR-22-3p was validated by dual-luciferase reporter assay, RNA immunoprecipitation assay, and RNA pull-down assay. The levels of nuclear factor (NF)-κB pathway-related proteins were evaluated by the western blot assay. RESULTS: NEAT1 was upregulated, while miR-22-3p was downregulated in patients with sepsis and in LPS-stimulated HK-2 cells. LPS treatment triggered cell apoptosis, autophagy, and inflammatory response in HK-2 cells. NEAT1 knockdown attenuated LPS-induced cell injury. NEAT1 modulated LPS-triggered cell injury by targeting miR-22-3p. Furthermore, NEAT1 regulated the NF-κB pathway by modulating miR-22-3p. CONCLUSION: Depletion of NEAT1 alleviated sepsis-induced AKI via regulating the miR-22-3p/NF-κB pathway.