Pyrroloquinoline quinone (PQQ) is contained in fruits and vegetables and in human breast milk. It has been reported that PQQ has high reactivity and changes to an imidazole structure (imidazole pyrroloquinoline) by a reaction with an amino acid at a high ratio in nature. A comparative study was conducted to clarify physiological effects including neuroprotective effects, growth-promoting effect, antioxidative effects and a stimulatory effect on mitochondriogensis of PQQ and imidazole pyrroloquinoline (IPQ) using a human neuroblastoma cell line and a hepatocellular carcinoma cell line. We also compared the expression levels of human cytochrome c oxidase subunit IV isoform I (COX4/1), which is an index of the amount of mitochondria in the cells that had been exposed to PQQ, PQQH 2 and IPQ. The results of the comparison showed that IPQ had almost the same biological activities as those of PQQ except for anti-oxidative activity. It was also shown that PQQ and IPQ improve the memory learning ability of aged mice and that BioPQQ® improves brain function in the language field in humans.

Background The purpose of this study was to clarify the practical clinical treatment for acute carbon monoxide (CO) poisoning in Japan and to investigate the efficacy of hyperbaric oxygen (HBO2) therapy in preventing delayed neurological sequelae (DNS) in the acute phase of CO poisoning. Methods We conducted a multicenter, prospective, observational study of acute CO poisoning in Japan. Patients with acute CO poisoning were enrolled and their treatment details were recorded. The primary endpoint was the onset of DNS within 2 months of CO exposure. Factors associated with DNS were assessed with logistic regression analysis. Results A total of 311 patients from 57 institutions were registered and 255 were analyzed: 171 received HBO2 therapy (HBO2 group) and 84 did not (normobaric oxygen [NBO2] group). HBO2 therapy was performed zero, once, twice, or three times within the first 24 h in 1.8%, 55.9%, 30.9%, and 11.3% of the HBO2 group, respectively. The treatment pressure in the first HBO2 session was 2.8 ATA (47.9% of the HBO2 group), 2.0 ATA (41.8%), 2.5 ATA (7.9%), or another pressure (2.4%). The incidence of DNS was 13/171 (7.6%) in the HBO2 group and 3/84 (3.6%) in the NBO2 group (P = 0.212). The number of HBO2 sessions in the first 24 h was one of the factors associated with the incidence of DNS (odds ratio, 2.082; 95% confidence interval, 1.101–3.937; P = 0.024). Conclusions The practical clinical treatment for acute CO poisoning, including HBO2 therapy, varied among the institutions participating in Japan. HBO2 therapy with inconsistent protocols showed no advantage over NBO2 therapy in preventing DNS. Multiple HBO2 sessions was associated with the incidence of DNS.

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Lecithin-cholesterol acyltransferase (LCAT) plays a significant role in the progression from premature to mature high-density lipoprotein (HDL) in circulation. Consequently, primary or secondary LCAT deletion or reduction naturally results in low serum HDL cholesterol levels. Recently, rare cases of acquired HDL deficiency with LCAT autoantibodies have been reported, mainly from Japan, where LCAT autoantibodies of immunoglobulin G (IgG) caused the HDL deficiency. Here to our knowledge, we report for the first time two cases of acquired HDL deficiency caused by IgG4 linked LCAT autoantibodies with or without a high serum IgG4 level. Furthermore, these cases can extend to a new concept of "IgG4 autoimmune disease" from the viewpoint of verifying the serum autoantibody and/or renal histopathology.