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Acute chest pain is a commonly encountered symptom in hospital medical/surgical units; however, almost half of nurses in their second year of clinical experience in our facility have reported struggling to care for acute chest pain patients. We developed, implemented, and examined the effectiveness of a simulation-based, mastery learning clinical nursing educational program to improve self-efficacy and performance in caring for patients with acute chest pain.The study adopted a single-site, single-cohort design using simulation-based performance assessment and self-efficacy surveys on a convenience sample of 37 second-year clinical nurse participants in multi-stage hybrid mastery learning educational intervention using asynchronous e-learning, and hands-on simulation training and assessment with feedback on caring for chest pain patients. Performance assessments and self-efficacy surveys were administered pre-, post-, and 5 months post-intervention.Clinical performance on the post- and 5 months follow-up assessments were significantly higher than those for the pre-test (P .0001). The self-efficacy scores for the post- and the 5 months follow-up assessments were significantly higher than the pre-course scores (P .0001). Participants' self-efficacy perceptions were positively correlated with their performances at 5 months post-intervention.Performance and self-efficacy of novice nurses in caring for acute chest pain patients improved significantly with the multi-stage hybrid mastery learning educational intervention, with improvements retained 5 months post-intervention. The results suggest the applicability of simulation-based mastery learning in a clinical setting for novice nurses to attain specific skills, and raise their self-perception of competence to care for patients in acute settings.

Background and Aims: Many investigations have demonstrated that cell injuries caused by generation of reactive oxygen species (ROS) is a common mechanism of various hepatic disorders. Recently, we have demonstrated that epimorphin, originally cloned as a mesenchymal protein, protects cultured intestinal epithelial cells from ROS. We therefore examine whether epimorphin protects primary cultured hepatocytes from ROS-induced cell injury. Methods: We explored the cell viability and the intracellular ROS levels of purified murine hepatocytes after exposure to 0.5 mM H2O2 with or without pretreatment of epimorphin. Then, we observed mitochondrial permeability transition (MPT) and depolarization using confocal microscopy to make clear the mechanism that epimorphin inhibited cell injuries after exposure to H2O2. In addition, to clarify the signaling pathways related to cell survival, we carried out Western blotting analysis with phosphorylated stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) polyclonal antibody to evaluate the inhibition of JNK by epimorphin. Finally, we evaluated the cell viability in hepatocytes administered JNK inhibitor. Results: Epimorphin protected primary cultured hepatocytes from H2O2-induced cell injuries independent of intracellular ROS levels. Epimorphin also inhibited onset of MPT, depolarization of the mitochondrial membrane potential, and eventually cell killing. The cell protective function of epimorphin after exposure to H2O2 was not dependent on Akt signaling but on JNK signaling. Conclusion: Epimorphin can protect hepatocytes from MPT-dependent cell injury induced by ROS. Since hepatic disorders could be caused by MPT-dependent cell injuries with excessive ROS, epimorphin might open a new therapeutic avenue for hepatic disorders.

Non-alcoholic steatohepatitis (NASH) is a term used to describe a spectrum of conditions characterized by histological findings of hepatic macrovesicular steatosis with inflammation in individuals who consume little or no alcohol. The NASH patients progress to liver cirrhosis and even hepatocellular carcinoma (HCC). Hepatocyte-specific phosphatase and tensin homolog (PTEN)-deficient mice (PTEN-deficient mice), which the authors had generated previously, showed massive hepatomegaly and steatohepatitis with triglyceride accumulation followed by liver fibrosis and HCC, a phenotype similar to human NASH. Therefore, it was shown that PTEN deficiency in hepatocytes could induce hepatic steatosis, inflammation, fibrosis and tumors and that PTEN-deficient mice were a useful animal model for not only the understanding of the pathogenesis of NASH but also the development of treatment for NASH.

Background and Aim: A 70-kDa heat shock protein (stress-inducible HSP70, HSP72) has been reported to be a cytoprotectant in a variety of organs. It has been reported that HSP72 protected non-cirrhotic rats against endotoxemia. However, its cytoprotective effect against endotoxemia in cirrhotic rats has not yet been studied. In this study, we investigated the cytoprotective effect of HSP72 on lipopolysaccharide (LPS)-induced liver injury in carbon tetrachloride (CCl4)-induced cirrhotic rats. Methods: Liver cirrhosis was produced by an 8-week intraperitoneal injection of CCl4 in male Sprague–Dawley rats. Expression of HSP72 was investigated using western blot analysis. Cirrhotic rats were given an intraperitoneal injection of LPS (10 mg/kg) with or without hyperthermia (42.5°C, 15 min) preconditioning. Liver injury was assessed biochemically (aspartate transaminase, alanine transaminase, bilirubin, lactate dehydrogenase, creatinine) and histologically. The plasma tumor necrosis factor (TNF)-α level was determined. Results: Hyperthermia preconditioning induced a 4-fold increase in HSP72 in the cirrhotic rat liver. Pre-induction of HSP72 prevented LPS-induced liver injury, as evaluated using serum biochemical parameters and histology with reduced TNF-α response. Conclusion: These findings suggest that pre-induction of HSP72 may provide therapeutic strategies for Gram-negative sepsis-induced liver injury in liver cirrhosis.

To design superconducting microwave receivers, the surface resistance of the superconducting thin film must be considered. Therefore, a highly accurate technique for measuring the surface resistance of superconducting thin films should be established. In this paper, we propose a probe-coupled microstrip line resonator as a technique for measuring the surface resistance of superconducting thin films. In the resonator technique, the surface resistance is calculated from Qu, the unloaded Q, of the resonator. Since the microstrip line resonator searches for an accurate surface resistance of the superconducting thin film, establishing a technique that accurately determines the Qu of the resonator is crucial. We measure the Qu values of resonators fabricated from metal and superconducting thin film by a probe-coupled microstrip line resonator and describe the accuracy of Qu measurement by the probe-coupled micro-strip line resonator and the repeatability of the surface resistance measurement of a superconducting thin film. © 2003 Wiley Periodicals, Inc. Electron Comm Jpn Pt 2, 86(4): 27–35, 2003; Published online in Wiley InterScience (www.interscience. wiley.com). DOI 10.1002/ecjb.10035

The laparoscopic appearance of the liver surface in patients with primary sclerosing cholangitis (PSC) has not been fully delineated. We examined 5 patients with PSC and reviewed 35 previously reported cases. Intense white markings in a mesh-like pattern were characteristic of PSC. The findings varied depending on the histologic stage and affected site. Red patches which have also been seen in primary biliary cirrhosis (PBC), green patches indicating cholestasis, and dilatation of the terminal bile ducts were also observed. The red patches were wider than those in PBC. The white markings were less well defined in the red patches than in other areas. The severity of the fibrosis and histologic damage was judged to be mild at the red sites. The green patches were caused by localized cholestasis. This indicated that PSC unevenly affects the liver. Severe obstruction may be present between the interlobular bile ducts and the septal bile ducts in anicteric stages. (Dig Endosc 1999; 10: 37–41)