Postoperative delirium (POD) is an acute cognitive dysfunction that is mainly characterized by memory impairment and disturbances in consciousness. POD can prolong the hospital stay and increase the 1-month mortality rate of patients. The overall incidence of POD is approximately 23%, and its prevalence can go up to 50% in high-risk surgeries. Neuroinflammation is an important pathogenic mechanism of POD that mediates microglial activation and leads to synaptic remodeling. Neuroinflammation, as an indispensable pathogenesis of POD, can occur due to a variety of factors, including aseptic inflammation caused by surgery, effects of anesthetic drugs, disruption of the blood-brain barrier, and epigenetics. Understanding these factors and avoiding the occurrence of risk factors may help prevent POD in time. This review provides a brief overview of POD and neuroinflammation and summarizes various factors affecting POD development mediated by neuroinflammation, which may serve as future targets for the prevention and treatment of POD.
Accumulating evidence indicates that long non-coding RNAs (lncRNAs) may serve essential roles during tumorigenesis of colorectal cancer (CRC). The lncRNA ZFPM2-AS1 was observed to be involved in the progression of numerous types of cancer, such as lung adenocarcinoma and cervical cancer. The aim of the present study was to investigate the expression levels and function of ZFPM2-AS1 in CRC. Expression levels of ZFPM2-AS1 in tissue and CRC cells were measured by reverse transcription-quantitative PCR. Furthermore, cell proliferation and Transwell assays were conducted to investigate the functional role of ZFPM2-AS1 in vitro. In addition, bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation assay and western blotting were performed to explore the possible underlying mechanism. The expression levels of ZFPM2-AS1 were significantly upregulated in tissue samples from patients with CRC and CRC cell lines compared with normal tissue and normal human colorectal mucosa cell line. Notably, the upregulation of ZFPM2-AS1 was significantly associated with tumor size, histological differentiation, lymph node metastasis and TNM stage. In addition, ZFPM2-AS1 knockdown significantly inhibited cell proliferation, migration and invasion compared with the control group in vitro. Moreover, it was found that ZFPM2-AS1 positively regulated tripartite motif containing 24 (TRIM24) expression by sponging miR-137. In conclusion, the present study indicated that ZFPM2-AS1 may serve as an oncogene in CRC by regulating the miR-137/TRIM24 axis.
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