The mushroom, Pleurocybella porrigens, is widely consumed in Japan; however, in autumn 2004, acute encephalopathy due to ingestion of the mushroom in a large group of patients was reported in Japan. We have continued working on the mushroom to clarify the mechanisms underlying the acute encephalopathy that occurred due to its consumption. The data collected to date have shown that three compounds, pleurocybelline (PC), a Pleurocybella porrigens lectin (PPL), and pleurocybellaziridine (PA), in the mushroom are potentially responsible for the onset of the disease; PC that exhibit lethal activity in mice and PPL formed a complex, and the complex of the two components exhibited proteolytic activity and disrupted the blood-brain barrier. Although PA was not isolated directly from the mushroom, the existence of this compound in the mushroom was predicted. The compound was chemically synthesized and its endogeneity in the mushroom was demonstrated. Furthermore, PA exhibited toxicity to oligodendrocytes.

The recent industrial growth has made our lives more comfortable; however, it has led to an increase in the concentration of harmful compounds, such as carbon monoxide, volatile organic compounds (e.g., toluene), and phenolic compounds (e.g., phenol and cresol), in the environment. Catalytic oxidation using environmental catalysts is an important method for the removal of harmful compounds. To date, novel environmental catalysts have been developed from unique concepts based on solid-state ionics. In particular, the oxygen supply ability of a promoter can supply active oxygen from inside the lattice to the catalytically active site. Our catalysts exhibited high activity for the oxidation of harmful chemicals under moderate conditions in both the gaseous and liquid phases compared to conventional catalysts. This short review article describes our concepts of material design and our novel catalysts (ceria–zirconia (CeO₂–ZrO₂), apatite-type lanthanum silicate (La₁₀Si₆O₂₇), and lanthanum oxyfluoride (LaOF) based catalysts).

Inflammation is a host defense response to various invading stimuli, but an excessive and persistent inflammatory response can cause tissue injury, which can lead to irreversible organ damage and dysfunction. Excessive inflammatory responses are believed to link to most human diseases. A specific type of leukocyte infiltration into invaded tissues is required for inflammation. Historically, the underlying molecular mechanisms of this process during inflammation were an enigma, compromising research in the fields of inflammation, immunology, and pathology. However, the pioneering discovery of chemotactic cytokines (chemokines), monocyte-derived neutrophil chemotactic factor (MDNCF; interleukin [IL]-8, CXCL8) and monocyte chemotactic and activating factor (MCAF; monocyte chemotactic factor 1 [MCP-1], CCL2) in the late 1980s finally enabled us to address this issue. In this review, we provide a historical overview of chemokine research over the last 35 years.