Oxidative stress leads to many kinds of diseases. Currently, urinary 8-hydroxydeoxyguanosine (8-OHdG) is widely measured as an oxidative stress biomarker. There is a specific advantage if saliva can be used as the sample to measure the oxidative stress biomarker, because saliva is much easier to collect than urine. In this study, we investigated the measurement of 8-hydroxyguanine (8-OHGua) as an oxidative stress marker in saliva, by a column switching HPLC system equipped with an electrochemical detector (HPLC-ECD). The 8-OHGua in saliva could be detected as a single peak by HPLC-ECD. The average level of 8-OHGua in saliva was 3.80 ng/mL in ordinary, non-smoking subjects. The salivary 8-OHGua levels of smokers were significantly higher than those of non-smokers. Salivary 8-OHGua may be a useful noninvasive and promising oxidative stress biomarker.

In endothelial cells (ECs), Ca²⁺-activated K⁺channels KCa2.3 and KCa3.1 play a crucial role in the regulation of arterial tone via producing NO and endothelium-derived hyperpolarizing factors. Since a rise in intracellular Ca²⁺levels and activation of p300 histone acetyltransferase are early EC responses to laminar shear stress (LS) for the transcriptional activation of genes, we examined the role of Ca²⁺/calmodulin-dependent kinase kinase (CaMKK), the most upstream element of a Ca²⁺/calmodulin-kinase cascade, and p300 in LS-dependent regulation of KCa2.3 and KCa3.1 in ECs. Exposure to LS (15 dyn/cm²) for 24 h markedly increased KCa2.3 and KCa3.1 mRNA expression in cultured human coronary artery ECs (3.2 ± 0.4 and 45 ± 10 fold increase, respectively; P < 0.05 vs. static condition; n = 8–30), whereas oscillatory shear (OS; ± 5 dyn/cm²× 1 Hz) moderately increased KCa3.1 but did not affect KCa2.3. Expression of KCa2.1 and KCa2.2 was suppressed under both LS and OS conditions, whereas KCa1.1 was slightly elevated in LS and unchanged in OS. Inhibition of CaMKK attenuated LS-induced increases in the expression and channel activity of KCa2.3 and KCa3.1, and in phosphorylation of Akt (Ser473) and p300 (Ser1834). Inhibition of Akt abolished the upregulation of these channels by diminishing p300 phosphorylation. Consistently, disruption of the interaction of p300 with transcription factors eliminated the induction of these channels. Thus a CaMKK/Akt/p300 cascade plays an important role in LS-dependent induction of KCa2.3 and KCa3.1 expression, thereby regulating EC function and adaptation to hemodynamic changes.

Using umami can help reduce excessive salt intake, which contributes to cardiovascular disease. Differences in salt-exposed environment at birth and preference for the salty taste might affect the sense of taste. Focusing on these two differences, we investigated the effect of monosodium L-glutamate (MSG) on the saltiness and palatability of low-salt solutions. Japanese participants (64 men, 497 women, aged 19–86 years) tasted 0.3%, 0.6%, and 0.9% NaCl solutions with or without 0.3% MSG to evaluate saltiness and palatability. They were also asked about their birthplace, personal salty preference, and family salty preference. Adding MSG enhanced saltiness, especially in the 0.3% NaCl solution, while the effect was attenuated in the 0.6% and 0.9% NaCl solutions. Palatability was rated higher with MSG than without MSG for each NaCl solution, with a peak value for the 0.3% NaCl solution with MSG. There was no difference in the effect of umami ingredients on palatability between the average salt intake by the regional block at birth and salty preference (all p > 0.05). Thus, adding an appropriate amount of umami ingredients can facilitate salt reduction in diet while maintaining palatability regardless of the salt-exposed environment in early childhood or salty preference.

BackgroundKawasaki disease is suspected to be triggered by previous infection. The prevention measures for COVID-19 have reportedly reduced transmission of certain infectious diseases. Under these circumstances, the prevention measures for COVID-19 may reduce the incidence of Kawasaki disease.MethodWe conducted a retrospective study using registration datasets of patients with Kawasaki disease who were diagnosed in all 11 in-patient pediatric facilities in Yamanashi prefecture. The eligible cases were 595 cases that were diagnosed before the COVID-19 pandemic (from January 2015 to February 2020) and 38 cases that were diagnosed during the COVID-19 pandemic (from March to November 2020). Incidence of several infectious disease were evaluated using data from the Infectious Disease Weekly Report conducted by the National Institute of Infectious Diseases.ResultsEpidemics of various infectious diseases generally remained at low levels during the first nine months (March to November 2020) of the COVID-19 pandemic. Moreover, the incidence of COVID-19 was 50–80 times lower than the incidence in European countries and the United States. The total number of 38 cases with Kawasaki disease for the nine months during the COVID-19 pandemic was 46.3% (-3.5 standard deviation (SD)) of the average (82.0 (SD, 12.7)) for the corresponding nine months of the previous five years. None of the 38 cases was determined to be triggered by COVID-19 based on their medical histories and negative results of severe acute respiratory syndrome coronavirus 2 testing at admission.ConclusionThese observations provide a new epidemiological evidence for the notion that Kawasaki disease is triggered by major infectious diseases in children.