Assessment of urine partial oxygen pressure to predict postoperative acute kidney injury in major surgical patients

　Urine partial oxygen pressure (PuO2) was monitored in postoperative intensive care unit (ICU) patients to verify if an earlier diagnosis of acute kidney injury (AKI) is possible. Fifty-nine patients who were admitted to the ICU after surgery for at least 48 hours at Kawasaki Medical Center between January 2019 and June 2020 were assessed for AKI using the Kidney Disease: Improving Global Outcome (KDIGO) criteria. The AKI group had 15 patients while the non-AKI group had 44 cases. The PuO2 of each group showed no significant difference. Arterial partial oxygen pressure (PaO2) was measured concurrently with PuO2. When the ratio of PuO2 to PaO2 (PuO2 / PaO2) from each group was compared, the AKI group had a significantly higher ratio just 2 hours after admission to the ICU. Reduced oxygen consumption in the renal medulla may be a possible cause of AKI in those patients. Thus, measuring the PuO2 / PaO2 ratio in postoperative patients 2 hours after ICU admission could be useful to predict AKI earlier than is currently done

Dieu, tu n'es jamais aussi beau que sur une face humaine

Katsuya Araki, Naoto Yagi, Yuka Ikemoto, Hisashi Yagi, Chi-Jing Choong, Hideki Hayakawa, Goichi Beck, Hisae Sumi, Harutoshi Fujimura, Taro Moriwaki, Yoshitaka Nagai, Yuji Goto & Hideki Mochizuki "Synchrotron FTIR micro-spectroscopy for structural analysis of Lewy bodies in the brain of Parkinson’s disease patients", Scientific Reports, volume 5, Article number: 17625, Springer Nature, 201

A potential protective effect of 5-aminolevulinic acid against anticancer drug-induced damage to intestinal mucosa

　An effective anti-cancer chemotherapy regimen can cause adverse events such as antineoplastic drug-induced oxidative stress in tissues. When hemeoxygenase-1 (HO1) is induced in tissues under oxidative stress, a tissue protective effect is observed. The non-proteinogenic amino acid 5-aminolevulinic acid (5-ALA) induces HO-1 in normal tissue and is hypothesized to provide an intestinal epithelial protective effect against drug-induced gastrointestinal mucosal disorders such as diarrhea and stomatitis. To validate this hypothesis, we introduced organoid culture from mouse intestinal epithelium. Using this organoid culture system, SN-38, the active metabolite of the antineoplastic drug irinotecan which is known to induce gastrointestinal mucosal disorders, was administered with and without 5-ALA to investigate the cytotoxic and protective effects of HO-1 suppression and expression. In normal intestinal epithelial cells, HO-1 induction by 5-ALA was observed. HO-1 expression was suppressed by the administration of SN-38 in the absence of 5-ALA, but was maintained by the co-administration of 5-ALA. In the mouse intestinal organoids, the same administration of 5-ALA induced HO-1 expression. When SN-38 was administered to the organoids, a cell death signal was expressed with an oxidative stress response, but the co-administration of 5-ALA induced HO-1 expression and cell death was decreased. The induction of HO-1 expression by 5-ALA administration suppresses intestinal epithelial cell death mediated by oxidative stress caused by antineoplastic drugs and is a potential new intestinal epithelial protective therapy against drug-induced gastrointestinal mucosal injury