Background: Hepatic iron overload is often seen in alcoholic liver disease (ALD). We previously reported that the expression of 4-hydroxy-2-nonenal-protein adducts, which is a lipid peroxidative product and can be used as a marker of radical-mediated cellular damage, was increased in iron-overloaded hepatocytes with ALD. However, the mechanism of hepatic iron overload in ALD has not been clarified. In this study, to elucidate the mechanism of hepatic iron overload in ALD, we immunohistochemically investigated the expression of transferrin receptor (TfR), which mainly acts for cellular iron uptake.Methods: Hepatic tissues were obtained from 31 patients with ALD and 5 normal livers by percutaneous needle biopsy under laparoscopy or ultrasound guidance. Chemical detection of hepatic iron accumulation was performed by Perls' Prussian blue stain. Immunohistochemical detection of TfR expression was done using human monoclonal anti-TfR antibody (TR104) according to the avidin-biotin complex method with alkaline phosphatase.Results: Excess iron accumulation was found in 22 hepatic tissues with ALD but not in any normal hepatic tissues. TfR expression was increased in hepatocytes of 18 hepatic tissues with ALD but was not detected in any normal hepatic tissues. The mean duration of abstinence of patients who demonstrated positive TfR expression in hepatocytes was significantly shorter than that of patients who demonstrated negative TfR expression (positive: 14 days; negative: 30 days). However, total ethanol consumption, daily ethanol intake, and serum aspartate aminotransferase and ␥-glutamyl transpeptidase values on admission were not significantly correlated with TfR expression in hepatocytes.Conclusions: The up-regulation of TfR expression in hepatocytes is implicated in hepatic iron overload in ALD, and habitual alcohol drinking is an important factor for the induction of TfR expression.
Postoperative delirium (POD) represents a disturbance in attention, awareness, and cognition that develops over the postoperative period. The prevalence of POD after coronary artery bypass grafting (CABG) is reported from 37 to 52% 1,2) . Because POD increases postoperative complications and prolongs intensive care unit and hospital stay 3) , patient's outcomes could have been worse. Some medicines were reported to reduce the incidence of POD. Ramelteon, as a melatonin receptor agonist, regulates the sleep cycle and improves subjective sleep quality of patients with chronic insomnia 4) . Ramelteon also is reported to reduce the occurrence of delirium in patients admitted to the intensive care unit (ICU) 5) .Recently, Suvorexant, as a new type of sleep medication as an orexin receptor antagonist, is noted for subjective measures of sleep onset and maintenance 6) . The orexin neuropeptide signal system supports wakefulness, but Suvorexant inhibits the bind-ing of orexin neuropeptides to receptors and suppresses the wake drives. Recently, a few studies reported the effect of Suvorexant for delirium [7][8][9] .The purposes of this study were to investigate the availability of Suvorexant for POD after CABG and to evaluate the effect of Suvorexant for the operative outcome.
II. Patients and methods
Thisretrospective study was approved by the institutional review board of Soka municipal hospital. Cardiac surgery has started since February 2013 in our institution. In a total of 175 consecutive patients who underwent elective CABG from February 2013 to May 2019. We investigated the patients weaned ventilator support at the first postoperative day (under 24 hours after operation), excluded patients with a mental disorder, sleep disorder and dementia patient. And the patients with emergency operations were excluded. Because benzodiazepine could induce POD, patients with benzodiazepine sedative-hypnotic agent for insomnia after CABG were excluded, too. So, 138 patients (29 women, mean age 69.7 ± 3.4 years) were intended.Induction and maintenance of operative anesthesia were similar for all patients and consisted of weight-related doses of fentanyl, midazolam, and pancuronium bromide.
We report that spice, vegetable and fruit extracts inhibit 12-0-tetradecanoylphorbol-13-acetate (TPA)-induced ear oedema in mice. About 100 methanol extracts obtained from spices, vegetables and fruits were assayed and their inhibition ratios calculated. In general, the spice extracts were more effective inhibitors than vegetable and fruit extracts. The methanol extracts of hop, stevia, cinnamon, turmeric, mate, mint, New Zealand spinach, watercress, tomato and seedling of radish markedly inhibited the inflammatory activity induced by TPA in mice. Two active compounds, humulone and lupeol3-palmitate were separated from hop and stevia, respectively.
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