Postoperative cognitive dysfunction (POCD) is a subtle disorder of thought processes, which may influence isolated domains of cognition and has a significant impact on patient health. The reported incidence of POCD varies enormously due to lack of formal criteria for the assessment and diagnosis of POCD. The significant risk factors of developing POCD mainly include larger and more invasive operations, duration of anesthesia, advanced age, history of alcohol abuse, use of anticholinergic medications, and other factors. The release of cytokines due to the systemic stress response caused by anesthesia and surgical procedures might induce the changes of brain function and be involved in the development of postoperative cognitive dysfunction. The strategies for management of POCD should be a multimodal approach involving close cooperation between the anesthesiologist, surgeon, geriatricians, and family members to promote early rehabilitation and avoid loss of independence in these patients.

Long non‐coding RNAs (lncRNAs) have been validated to play important role in multiple cancers, including non‐small cell lung cancer (NSCLC). In present study, our team investigate the biologic role of SNHG15 in the NSCLC tumorigenesis. LncRNA SNHG15 was significantly upregulated in NSCLC tissue samples and cells, and its overexpression was associated with poor prognosis of NSCLC patients. In vitro, loss‐of‐functional cellular experiments showed that SNHG15 silencing significantly inhibited the proliferation, promoted the apoptosis, and induced the cycle arrest at G0//G1 phase. In vivo, xenograft assay showed that SNHG15 silencing suppressed tumor growth of NSCLC cells. Besides, SNHG15 silencing decreased CDK14 protein expression both in vivo and vitro. Bioinformatics tools and luciferase reporter assay confirmed that miR‐486 both targeted the 3′‐UTR of SNHG15 and CDK14 and was negatively correlated with their expression levels. In summary, our study conclude that the ectopic overexpression of SNHG15 contribute to the NSCLC tumorigenesis by regulating CDK14 protein via sponging miR‐486, providing a novel insight for NSCLC pathogenesis and potential therapeutic strategy for NSCLC patients.

Acute lung injury is characterized by an increase of inflammatory reaction and severe lung edema. Even if there have been great advances in the identification of genes and signaling pathways involved in acute lung injury, the fundamental mechanisms of initiation and propagation of acute lung injury have not been understood completely. A growing amount of evidence indicates that microRNAs (miRNAs) are involved in various human diseases. However, the expression profile and function of miRNAs in acute lung injury have not been investigated. Here, using real-time polymerase chain reaction analysis, we show that a collection of miRNAs is dynamically regulated in lipopolysaccharide (LPS)-induced mouse acute lung injury. Among them, miR-199a and miR-16 are the most significantly down-regulated miRNAs. To study the role of miR-199a and miR-16 in acute lung injury, an over-expression of miR-199a or miR-16 assay was performed in LPS-treated A549 cells, and then the expression of inflammatory factors was analyzed. Over-expression of miR-199a could not alter the expression level of interleukin (IL)-6 and tumor necrosis factor-alpha (TNFα), while up-regulation of miR-16 could significantly down-regulate IL-6 and TNFα expression level. Using bioinformatic analysis, we show that a 3' untranslational region (UTR) of IL-6 and TNFα contains the binding sites of miR-16. Accordingly, over-expression of miR-16 could significantly suppress the luciferase activity of reporter fusion with the binding sites of TNFα in its 3'UTR region, suggesting that miR-16 played its role in LPS-induced lung inflammation by a direct manner. In this study, we show for the first time that miRNAs are dynamically regulated and play an important function in LPS-induced lung injury.

Introducing the PSS listening condition efficiently reveals both the brain substrates underlying schizophrenia-related speech-recognition deficits against informational masking and the schizophrenia-related neural compensatory strategy for impaired SPL functions.