ObjectivePostoperative delirium (POD) is a serious complication in elderly patients undergoing cardiac surgery. This study was aimed at investigating the effect of perioperative administration of dexmedetomidine for general anesthesia maintenance on occurrence and duration of POD in elderly patients after cardiac surgery.MethodsOne hundred and sixty-four patients were enrolled after cardiac surgery between June 2009 and December 2016. Patients were assigned by a computer-generated randomization sequence in a 1:1 ratio to receive dexmedetomidine general anesthesia maintenance or propofol general anesthesia maintenance. POD was assessed every day with confusion assessment method for intensive care units (ICU) during the first 5 postoperative days.ResultsThere was no significance in incidence of POD between the dexmedetomidine group and the propofol group (P=0.0758). In patients treated with dexmedetomidine, the median onset time of delirium was delayed (second day vs first day) and the duration of delirium reduced (2 days vs 3 days) when compared with propofol-treated patients. The dexmedetomidine-treated patients also displayed a lower VAS score and less opiate analgesic consumption. No difference was observed in respect to other postoperative outcomes.ConclusionFor elderly patients, perioperative administration of dexmedetomidine reduced incidence, delayed onset and shortened duration of POD after cardiac surgery.

At the request of the authors, the Editor and Publisher of Clinical Interventions in Aging wish to retract the published article. Following publication, concerns were raised that the reported study did not match with details of the associated study that had been registered in the Chinese Clinical Trial Registry under registration number, ChiCTR-IOR-17014122.The authors responded to our queries and explained that they failed to complete registration of the study to the Chinese Clinical Trial Registry before starting their clinical research. Their request to retrospectively register the study prior to publication was declined by the Chinese Clinical Trial Registry because the trial had already been completed for three years. To comply with journal requirements the authors provided the clinical registration number (ChiCTR-IOR -17014122) from an unrelated dexmedetomidine study by members of their own research group. The owners of the study associated with registration number, ChiCTR-IOR-17014122, were unaware this number had been used in the publication of another study.The authors contacted the journal to request that the article be retracted and put this error in judgement down to inexperience and wish to apologise for any confusion that was caused.Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction.The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as "Retracted".

Background: Non-compressive disc herniation is induced by an inflammatory response from the nucleus pulposus tissue and nerve roots. Lipoxins (LXs) are important endogenous anti-inflammatory mediators in the body, helping to inhibit neutrophil recruitment and stimulate autophagy in monocytes and macrophages. Here, we investigated the molecular mechanisms underlying the effects of exogenous lipoxin administration on rats with non-compressive disc herniation. Method: A non-compressive disc herniation model was established in rats. Fifty rats were randomly divided into: sham group, model group, PI3K inhibitor (LY294002) group, lipoxin A4 group (LXA4), and PI3K inhibitor and lipoxin A4 group (LY294002 + LXA4). Similar groupings were established for rat spinal neurons. Changes in the mechanical pain threshold and thermal pain threshold were monitored at different times. The expression of proinflammatory and anti-inflammatory mediators was assessed by ELISA, while immunohistochemistry was employed to measure the expression levels of NLRP3 and p-JNK1. The expression levels of autophagy-related proteins were measured by western blot.

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