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Purpose : This study aims to investigate the status of delirium intervention in adult intensive care unit (ICU) patients and the perception of this delirium by medical staff.Methods : This retrospective study involves 185 patients, whereas, a descriptive survey is conducted with 197 medical staff members.Results : The delirium group includes 100 patients (54.1%). The incidence of delirium is 64.9% in the medical ICU, 65.9% in the surgical ICU, 42.4% in the neuro ICU, and 46.5% in the cardiac ICU. The percentages of delirium prevention intervention differs between the two groups: 65.0% in the delirium group and 95.3% in the non-delirium group. The medical staff recognize that delirium is a common problem in the ICU (100.0%) and requires active medical intervention (98.5%).Conclusion : The length of stay at the ICU is longer in the delirium group than in the non-delirium group. It is necessary to standardize delirium prevention and treatment protocols to be equally applicable to all ICU patients.

Background Intestinal epithelium is essential for maintaining normal intestinal homeostasis; its breakdown leads to chronic inflammatory pathologies, such as inflammatory bowel diseases (IBDs). Although high concentrations of S100A9 protein and interleukin-6 (IL-6) are found in patients with IBD, the expression mechanism of S100A9 in colonic epithelial cells (CECs) remains elusive. We investigated the role of IL-6 in S100A9 expression in CECs using a colitis model. Methods IL-6 and S100A9 expression, signal transducer and activator of transcription 3 (STAT3) phosphorylation, and infiltration of immune cells were analyzed in mice with dextran sulfate sodium (DSS)-induced colitis. The effects of soluble gp130-Fc protein (sgp130Fc) and S100A9 small interfering (si) RNA (si-S100A9) on DSS-induced colitis were evaluated. The molecular mechanism of S100A9 expression was investigated in an IL-6-treated Caco-2 cell line using chromatin immunoprecipitation assays. Results IL-6 concentrations increased significantly in the colon tissues of DSS-treated mice. sgp130Fc or si-S100A9 administration to DSS-treated mice reduced granulocyte infiltration in CECs and induced the down-regulation of S100A9 and colitis disease activity. Treatment with STAT3 inhibitors upon IL-6 stimulation in the Caco-2 cell line demonstrated that IL-6 mediated S100A9 expression through STAT3 activation. Moreover, we found that phospho-STAT3 binds directly to the S100A9 promoter. S100A9 may recruit immune cells into inflamed colon tissues. Conclusions Elevated S100A9 expression in CECs mediated by an IL-6/STAT3 signaling cascade may play an important role in the development of colitis.