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Hindsight bias (HB) is the tendency to retrospectively exaggerate one's foresight knowledge about the outcome of an event. Cognitive processes influenced by newly obtained outcome information are used to explain the HB phenomenon, but the neural correlates remain unknown. This study investigated HB in the context of election results using a memory design and functional magnetic resonance imaging for the first time. Participants were asked to predict and recall the percentage of votes obtained by (pairs of) candidates before and after an election. The results revealed that 88% of participants showed HB by recalling that their predictions were closer to the actual outcomes than they really were; and participants had HB for 38% of the events. The HB effect was associated with activation in the medial superior frontal gyrus and bilateral inferior frontal gyrus (IFG), which have been implicated in updating an old belief due to new information and is similar to the process of reconstruction bias. Furthermore, participants with a greater HB effect showed greater activation of the left IFG. In conclusion, we successfully observed the HB phenomenon in election results, and our imaging results suggested that the HB phenomenon might involve reconstruction bias. [ABSTRACT FROM AUTHOR]

Background: Large gap healing is a difficult issue in the recovery of peripheral nerve injury. The present study provides in vivo trials of silicone rubber chambers filled with collagen containing IFN-γ or IL-4 to bridge a 15 mm sciatic nerve defect in rats. Fillings of NGF and normal saline were used as the positive and negative controls. Neuronal electrophysiology, neuronal connectivity, macrophage infiltration, location and expression levels of calcitonin gene-related peptide and histology of the regenerated nerves were evaluated. Results: At the end of 6 weeks, animals from the groups of NGF and IL-4 had dramatic higher rates of successful regeneration (100 and 80%) across the wide gap as compared to the groups of IFN-γ and saline controls (30 and 40%). In addition, the NGF group had significantly higher NCV and shorter latency compared to IFN-γ group (P < 0.05). The IL-4 group recruited significantly more macrophages in the nerves as compared to the saline controls and the NGF-treated animals (P < 0.05). Conclusions: The current study demonstrated that NGF and IL-4 show potential growth-promoting capability for peripheral nerve regeneration. These fillings in the bridging conduits may modulate local inflammatory conditions affecting recovery of the nerves. [ABSTRACT FROM AUTHOR]

Liver disorders are a major health concern. Saikosaponin-d (SSd) is an effective active ingredient extracted from Bupleurum falcatum, a traditional Chinese medicinal plant, with anti-inflammatory and antioxidant properties. However, its hepatoprotective properties and underlying mechanisms are unknown. We investigated the effects and underlying mechanisms of SSd treatment for thioacetamide (TAA)-induced liver injury and high-fat-diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) in male C57BL/6 mice. The SSd group showed significantly higher food intake, body weight, and hepatic antioxidative enzymes (catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD)) and lower hepatic cyclooxygenase-2 (COX-2), serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and fibroblast growth factor-21 (FGF21) compared with controls, as well as reduced expression of inflammation-related genes (nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS)) messenger RNA (mRNA). In NAFLD mice, SSd reduced serum ALT, AST, triglycerides, fatty acid–binding protein 4 (FABP4) and sterol regulatory element–binding protein 1 (SREBP1) mRNA, and endoplasmic reticulum (ER)-stress-related proteins (phosphorylated eukaryotic initiation factor 2α subunit (p-eIF2α), activating transcription factor 4 (ATF4), and C/EBP homologous protein (CHOP). SSd has a hepatoprotective effect in liver injury by suppressing inflammatory responses and acting as an antioxidant. [ABSTRACT FROM AUTHOR]

Abstract: Hydrolysis of sodium borohydride (NaBH4) is a promising method for on-board hydrogen supply to polymer electrolyte membrane fuel cells (PEMFC). This article presents an attempt to design a novel solid-state NaBH4 composite, which is made up of NaBH4 powder, Co2+/IR-120 catalyst and silicone rubber, for hydrogen generator. The silicone rubber can act as a stabilizer in the solid-state NaBH4 composite because of its surface hydrophobicity leading to reduced diffusion rate of water into the composite. The solid-state NaBH4 composite can produce hydrogen stably near 25mLmin−1 for at least 2h without employment of any mechanical control system. Using the hydrogen generated from the solid-state NaBH4 composite, a 2W PEMFC stack is successfully operated to power a cellular phone. [Copyright &y& Elsevier]

Abstract: An original study of an immobilized iron oxide catalyst (SiG1) with one hydroxylation intermediate of phenol (catechol) in the reductive dissolution process was performed. Also, SiG1 was applied as the catalyst for the oxidation of phenol and catechol in the presence of hydrogen peroxide. The SiG1 used in this study reacted more efficiently with catechol than the other iron oxides. Only the hydroxylation intermediates of phenol (i.e. catechol and 1,4-hydroquinone) were able to reductively dissolve SiG1. However, there are no interactions between SiG1 and phenol. The reductive dissolution of SiG1 not only occurred at acidic solution but also occurred at alkali solution in the presence of catechol. Furthermore, the solution of pH 5 was found to be a critical condition in which the interactions of SiG1 and catechol were weak in the presence or absence of H2O2. The yields of Fe2+ from SiG1 in the presence of catechol were limited by the equilibrium of reduction and the oxidation rate of iron(III, II) species. A kinetic model was applied to obtain the estimated maximum concentration of Fe2+ produced by SiG1 and estimated proportional constant in the presence of catechol at different pH conditions by using a trial and error method. Catechol induced the reductive dissolution of SiG1 and then promoted its own oxidation along with that of phenol in the presence of hydrogen peroxide. [Copyright &y& Elsevier]

Liver disorders have been recognized as one major health concern. Fucoidan, a sulfated polysaccharide extracted from the brown seaweed Fucus serratus, has previously been reported as an anti-inflammatory and antioxidant. However, the discovery and validation of its hepatoprotective properties and elucidation of its mechanisms of action are still unknown. The objective of the current study was to investigate the effect and possible modes of action of a treatment of fucoidan against thioacetamide (TAA)-induced liver injury in male C57BL/6 mice by serum biochemical and histological analyses. The mouse model for liver damage was developed by the administration of TAA thrice a week for six weeks. The mice with TAA-induced liver injury were orally administered fucoidan once a day for 42 days. The treated mice showed significantly higher body weights; food intakes; hepatic antioxidative enzymes (catalase, glutathione peroxidase (GPx), and superoxide dismutase (SOD)); and a lower serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and C-reactive protein (CRP) levels. Additionally, a reduced hepatic IL-6 level and a decreased expression of inflammatory-related genes, such as cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) mRNA was observed. These results demonstrated that fucoidan had a hepatoprotective effect on liver injury through the suppression of the inflammatory responses and acting as an antioxidant. In addition, here, we validated the use of fucoidan against liver disorders with supporting molecular data. [ABSTRACT FROM AUTHOR]