No abstract

SARS‐CoV‐2, a novel emerging coronavirus, has caused severe disease (COVID‐19), and rapidly spread worldwide since the beginning of 2020. SARS‐CoV‐2 mainly spreads by coughing, sneezing, droplet inhalation, and contact. SARS‐CoV‐2 has been detected in saliva samples, making saliva a potential transmission route for COVID‐19. The participants in dental practice confront a particular risk of SARS‐CoV‐2 infection due to close contact with the patients and potential exposure to saliva‐contaminated droplets and aerosols generated during dental procedures. In addition, saliva‐contaminated surfaces could lead to potential cross‐infection. Hence, the control of saliva‐related transmission in the dental clinic is critical, particularly in the epidemic period of COVID‐19. Based on our experience of the COVID‐19 epidemic, some protective measures that can help reduce the risk of saliva‐related transmission are suggested, in order to avoid the potential spread of SARS‐CoV‐2 among patients, visitors, and dental practitioners.

Urinary metabolites excreted after oral caffeine were quantified in a healthy sample (n = 68) from the Toronto population by HPLC analyses. The profile of metabolites, assessed by examining particular metabolite ratios, was found to differ widely among subjects. Ratios denoting cytochrome P-450-dependent activities were shown to be interethnically variable between oriental and Caucasian groups, whereas those indicative of xanthine oxidase activity exhibited neither significant interindividual variation nor an ethnic difference. It was also shown that a ratio providing an index of polymorphic N-acetyltransferase activity holds promise as a simple marker for acetylator status in man.

The NFAT family of transcription factors are key regulators of inducible gene expression in the immune system. We examined the function of two NFAT proteins after naïve T helper (T(H)) cell activation. We found that naïve T(H) precursors that are doubly deficient in NFATc2 and NFATc3 intrinsically differentiate into TH(2)-secreting cells, even in the absence of interleukin 4 (IL-4) production. We also found that lack of NFATc2 and NFATc3 obviates the necessity for engagement of CD28 on naïve cells and controls the time required to reach the first cell division upon activation. These results demonstrate a key role for NFATc2 and NFATc3 in modulating T cell receptor responsiveness and regulating subsequent cell division and T(H)2 differentiation.