The formation of nanoscale precursors on the surface of dicalcium phosphate dihydrate (DCPD) is an important step in various methods; however, this process requires an unstable solution. Herein, we propose a simple method for the deposition of nanoscale fluorapatite (FAp) particles on the surface of DCPD particles using a weakly acidic, aqueous solution containing only calcium, phosphate, and fluoride ions (C-P-F solution). Repeated immersion in the same solution increases the amount of FAp deposition and almost no delay time is observed. Experimental results indicate that approximately 10 wt.% of FAp on the DCPD surface is optimal to enhance its reactivity with fluoride ions. Our results demonstrate an optimum FAp deposition amount on DCPD particles for improved reactivity with fluoride ions, and we achieved an improved surface of the DCPD particle for fluoride immobilization in wastewater and soil environments.

Background Phototherapy with narrow‐band ultraviolet B (narrow‐band UVB) is clinically effective treatment for atopic dermatitis. In the present study, we examined the effects of intranasal irradiation with narrow‐band UVB on nasal symptom, upregulation of histamine H1 receptor (H1R) gene expression and induction of DNA damage in the nasal mucosa of allergic rhinitis (AR) model rat. Methods AR model rats were intranasally irradiated with 310 nm of narrow‐band UVB. Nasal mucosal levels of H1R mRNA were measured using real‐time quantitative reverse transcriptase (RT)‐PCR. DNA damage was evaluated using cyclobutane pyrimidine dimer (CPD) immunostaining. Results In toluene 2,4‐diisocyanate (TDI)‐sensitized rats, TDI provoked sneezes and H1R gene expression in the nasal mucosa. Intranasal pre‐irradiation with 310 nm narrow‐band UVB at doses of 600 and 1400, but not 200 mJ/cm2 significantly inhibited the number of sneezes and upregulation of H1R gene expression provoked by TDI. CPD‐positive cells appeared in the nasal mucosa after intranasal narrow‐band UVB irradiation at a dose of 1400, but not 200 and 600 mJ/cm2. The suppression of TDI‐provoked sneezes and upregulation of H1R gene expression lasted 24 hours, but not 48 hours, after narrow‐band UVB irradiation with a dose of 600 mJ/cm2. Conclusions Intranasal pre‐irradiation with narrow‐band UVB dose‐dependently inhibited sneezes and upregulation of H1R gene expression of the nasal mucosa in AR model rats, suggesting that the inhibition of nasal upregulation of H1R gene expression suppressed nasal symptom. The suppression after narrow‐band UVB irradiation at a dose of 600 mJ/cm2 was reversible without induction of DNA damage. These findings indicated that low‐dose narrow‐band UVB phototherapy could be effectively and safely used for AR treatment in a clinical setting. Level of Evidence NA.

As the expression level of a disease-sensitive gene is correlated with the symptom severity, suppression of its gene expression should be good therapeutics. We demonstrated that histamine H 1 receptor (H1R) gene is an allergic rhinitis (AR)-sensitive gene. We isolated maackiain (MCN) from Kujin that suppresses H1R gene up-regulation. We also showed that MCN bound to Hsp90 and disrupts the interaction between PKCδ and Hsp90, suggesting MCN modulates steroid signaling. Western blot analysis showed that MCN completely inhibited ERK phosphorylation although the inhibition of PKC dphosphorylation was partial, suggesting that MCN suppresses H1R gene expression by the additional mechanism. MCN enhanced dexamethasone-activated GRE promoter activity. MCN also enhanced dexamethasone-induced gene up-regulation for dual-specificity phosphatase 1 (DUSP1), that dephosphorylizes ERK. On the other hand, dexamethasone suppressed H1R gene up-regulation. These findings suggest that MCN suppresses H1R gene expression through not only the disruption of interaction between PKCδ and Hsp90 but also the activation of ERK dephosphorylation by the enhancement of dexamethasone-induced DUSP1 gene expression.