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Risk Factors for Delirium after Spine Surgery: An Age-Matched Analysis
Tadao Morino,Masayuki Hino,Shintaro Yamaoka,Hiroshi Misaki,Tadanori Ogata,Hiroshi Imai,Hiromasa Miura 대한척추외과학회 2018 Asian Spine Journal Vol.12 No.4
Study Design: A retrospective cohort study. Purpose: To investigate the risk factors for postoperative delirium after spine surgery, excluding older age, which has already been established as a strong risk factor. Overview of Literature: More than 30 risk factors have been reported for delirium after spine surgery, making it challenging to identify which factors should be prioritized. We hypothesized that risk factors could not be prioritized to date because the factor of older age is very strong and influenced other factors. To eliminate the influence of older age, we performed an age-matched group comparison analysis for the investigation of other risk factors. Methods: This study involved 532 patients who underwent spine surgery. Two patients of the same age without delirium (delirium negative group) were matched to each patient with delirium (delirium positive group). Differences in suspected risk factors for postoperative delirium between the two groups identified from previous reports were analyzed using univariate analysis. Multivariate analysis was performed for factors that showed a significant difference between the two groups in the univariate analysis. Results: Fifty-nine (11.1%) of 532 patients developed postoperative delirium after spine surgery. Large amounts of intraoperative bleeding, low preoperative concentration of serum Na, high postoperative (day after surgery) serum level of C-reactive protein, low hematocrit level, low concentration of albumin, and high body temperature were detected as significant risk factors in the univariate analysis. Large amounts of intraoperative bleeding remained a risk factor for postoperative delirium in the multivariate analysis. Conclusions: We should pay attention to and take precautions against the occurrence of postoperative delirium after spine surgery in patients of older age or those who experience severe intraoperative bleeding.
Persistent activation of Nrf2 through p62 in hepatocellular carcinoma cells
Inami, Yoshihiro,Waguri, Satoshi,Sakamoto, Ayako,Kouno, Tsuguka,Nakada, Kazuto,Hino, Okio,Watanabe, Sumio,Ando, Jin,Iwadate, Manabu,Yamamoto, Masayuki,Lee, Myung-Shik,Tanaka, Keiji,Komatsu, Masaaki The Rockefeller University Press 2011 The Journal of cell biology Vol.193 No.2
<P>Suppression of autophagy is always accompanied by marked accumulation of p62, a selective autophagy substrate. Because p62 interacts with the Nrf2-binding site on Keap1, which is a Cullin 3–based ubiquitin ligase adapter protein, autophagy deficiency causes competitive inhibition of the Nrf2–Keap1 interaction, resulting in stabilization of Nrf2 followed by transcriptional activation of Nrf2 target genes. Herein, we show that liver-specific autophagy-deficient mice harbor adenomas linked to both the formation of p62- and Keap1-positive cellular aggregates and induction of Nrf2 targets. Importantly, similar aggregates were identified in more than 25% of human hepatocellular carcinomas (HCC), and induction of Nrf2 target genes was recognized in most of these tumors. Gene targeting of <I>p62</I> in an HCC cell line markedly abrogates the anchorage-independent growth, whereas forced expression of p62, but not a Keap1 interaction-defective mutant, resulted in recovery of the growth defect. These results indicate the involvement of persistent activation of Nrf2 through the accumulation of p62 in hepatoma development.</P>