Postoperative cognitive dysfunction (POCD) is serious disorder in the central nervous system common in aged patients after anesthesia. Although its clinical symptoms are well recognized, however, the molecular etiology of the POCD remains unrevealed. Similarly, neither gold standard molecular diagnosis nor effective treatment is available for POCD until the present. Therefore, we aimed to explore the molecular mechanism of this disorder through investigating lncRNAs and mRNAs associated with POCD human patients and investigate their underlying regulatory pathways. In this study, we recruited 200 patients requiring hip or knee replacement surgery. Their neurological functions were assessed at two time points, 1 day before the surgery and 30 days post-surgery. In parallel, serum samples were collected from the participants to analyze lncRNAs and mRNAs differential expression profile between POCD and non-POCD patients using microarray analysis. To further investigate the role differentially expressed mRNA and lncRNAs, Gene Ontology (GO), pathway analyses on mRNAs and lncRNA-mRNA interaction network were performed. As a result, 68 lncRNAs and 115 mRNAs were dysregulated in the POCD group compared to non-POCD group. Among them, the top 10 upregulated lncRNAs and 10 downregulated lncRNAs were listed for enrichment analysis. Interestingly, we found that these lncRNA and mRNA are involved in biological process, molecular function, and cellular component in addition to various signaling pathways, suggesting that the pathogenesis of POCD involves lncRNAs and mRNAs differential expression. Consequently, the genetic dysregulation between the non-POCD and POCD patients participates in the occurrence and development of POCD, and could be served as diagnostic biomarkers and drug targets for POCD treatment.

Even after successful hip arthroplasty, elderly patients who have undergone this procedure remain subject to cognitive decline and may collectively develop postoperative cognitive dysfunction (POCD). However, no consensus exists as to the risk factors resulting in a higher likelihood that a patient may present with this complication, and the aetiology of POCD is not well understood. We conducted a systematic review of papers concerning the influence of POCD‐related risk factors in patients undergoing hip arthroplasty but limited the literature search to papers in English. A systematic and electronic search for manuscripts in the PubMed database was performed in order to identify all studies in which the risk factors for POCD were investigated. Articles were also obtained from the authors' files. Keywords for the search were postoperative cognitive dysfunction/change/impairment/decline/deficit, elderly/older/aged patients, and hip arthroplasty/replacement surgery. The evidence published to date suggests that POCD is a multifactorial disease, which includes an individual patient's characteristics, surgery, type of anaesthesia, and pain levels. All of these factors can increase the risk of POCD incidence. There are a number of factors that appear to influence the risk of early cognitive dysfunction after hip arthroplasty. Nevertheless, the specific mechanism and explicit risk factors associated with this cognitive dysfunction are not completely understood. Hip arthroplasty has made it possible for older patients to find relief from pain and improve their function, whereas it also increases the risk for suffering POCD that may affect these patients' quality of life and increase their mortality. Therefore, it is worthwhile investigating the mechanism of POCD in future studies in order to prevent and treat this condition.

Summary Introduction Myocardial ischemia/reperfusion injury (myocardial I/R injury) has a high disability rate and mortality. Novel treatments for myocardial I/R injury are necessary. Aim In order to explore the protective effect of hydromorphine on myocardial I/R injury, we illuminate the underlying mechanism of the protective effect. Results Hydromorphine significantly reduced myocardial infarct size (IFN/AAR), CKMB (Creatine Kinase MB) and TN‐T (Troponin T) release, and improved cardiac function compared with I/R group. However, these advantageous effects were partly suppressed in the presence of hydromorphine. Myocardial I/R injury significantly decreased the phosphorylation of Akt and eNOS, and down‐regulated total nitric oxide and nitrotyrosine content, while these inhibitory effects were partly abolished by hydromorphine. Conversely, the activated effects of hydromorphine on the phosphorylation of Akt and eNOS, and NO release were totally reversed by LY294002, which, used individually, show the same influence on reperfusion injury. Conclusions These findings suggest that hydromorphine postconditioning may protect isolated rat heart against reperfusion injury via activating P13K/Akt/eNOS signaling.

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