• Tuberculosis and Respiratory Diseases
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• v.73 no.5
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• pp.258-265
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• 2012

Background: Vitamin D can translocate a vitamin D receptor (VDR) from the nucleus to the cell membranes. The meaning of this translocation is not elucidated in terms of a role in pathogenesis of chronic obstructive pulmonary disease (COPD) till now. VDR deficient mice are prone to develop emphysema, suggesting that abnormal function of VDR might influence a generation of COPD. The blood levels of vitamin D have known to be well correlated with that of lung function in patients with COPD, and smoking is the most important risk factor in development of COPD. This study was performed to investigate whether cigarette smoke extracts (CSE) can inhibit the translocation of VDR and whether mitogen activated protein kinases (MAPKs) are involved in this inhibition. Methods: Human alveolar basal epithelial cell line (A549) was used in this study. 1,25-$(OH_2)D_3$ and/or MAPKs inhibitors and antioxidants were pre-incubated before stimulation with 10% CSE, and then nucleus and microsomal proteins were extracted for a Western blot of VDR. Results: Five minutes treatment of 1,25-(OH2)D3 induced translocation of VDR from nucleus to microsomes by a dose-dependent manner. CSE inhibited 1,25-$(OH_2)D_3$-induced translocation of VDR in both concentrations of 10% and 20%. All MAPKs inhibitors did not suppress the inhibitory effects of CSE on the 1,25-$(OH_2)D_3$-induced translocation of VDR. Quercetin suppressed the inhibitory effects of CSE on the 1,25-$(OH_2)D_3$-induced translocation of VDR, but not in n-acetylcysteine. Conclusion: CSE has an ability to inhibit vitamin D-induced VDR translocation, but MAPKs are not involved in this inhibition.

• Clinical and Experimental Pediatrics
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• v.54 no.7
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• pp.298-303
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• 2011

Purpose: To evaluate the clinical characteristics of vitamin D deficiency and its association with iron deficiency anemia (IDA). Methods: A total of 171 children aged less than two years underwent 25-hydroxyvitamin $D_3$ tests between January 2007 and July 2009. The study was classified into two groups: normal and vitamin D insufficiency, by their vitamin 25-hydroxyvitamin $D_3$ levels. Results: In total, 120 children were in the normal group (mean age, body weight and heights $12.5{\pm}7.0$, $9.3{\pm}0.9$ kg and $76.8{\pm}1.1$ cm), and 51 children in the vitamin D insufficiency group ($9.9{\pm}5.4$ months, $9.0{\pm}0.9$ kg and $75.1{\pm}0.9$ cm). Vitamin D insufficiency was most commonly diagnosed in the spring (44%). The proportion of complete breast-feeding was higher in the insufficiency (92%), and 25.5% of the children in the deficient group also experienced IDA compared that 12% of normal group. Ten children in the insufficiency group experienced bony changes. Six children received calcitriol medication in the normal group, in whom the mean vitamin 25-hydroxyvitamin $D_3$ level increased from $39.6{\pm}14.6$ ng/mL (pre-medication) to $41.8{\pm}17.2$ ng/mL (post-medication), and 13 in the insufficiency group, in whom the mean vitamin 25-hydroxyvitamin $D_3$ increased from $20.7{\pm}7.0$ ng/mL to a mean post-treatment level of $43.7{\pm}23.8$ ng/mL. Conclusion: This study demonstrated that approximately 30% of children aged ${\leq}2$ years experienced vitamin D insufficiency associated with subclinical rickets. Many children also experienced concurrent IDA. Guidelines for vitamin D supplement in such children must therefore be established.

• Journal of Periodontal and Implant Science
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• v.48 no.1
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• pp.34-46
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• 2018

Purpose: The purpose of this study was to evaluate the effects of 1,25-dihydroxyvitamin $D_3$ on the proliferation, differentiation, and matrix mineralization of MC3T3-E1 osteoblast-like cells in vitro. Methods: MC3T3-E1 osteoblastic cells and 1,25-dihydroxyvitamin $D_3$ were prepared. Cytotoxic effects and osteogenic differentiation were evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, alkaline phosphatase (ALP) activity assay, ALP staining, alizarin red S staining, and reverse transcription-polymerase chain reaction (RT-PCR) for osteogenic differentiation markers such as ALP, collagen type I (Col-I), osteocalcin (OCN), vitamin D receptor (VDR), and glyceraldehyde 3-phosphate dehydrogenase. Results: The MTT assay showed that 1,25-dihydroxyvitamin $D_3$ did not inhibit cell growth and that the rate of cell proliferation was higher than in the positive control group at all concentrations. ALP activity was also higher than in the positive control group at low concentrations of 1,25-dihydroxyvitamin $D_3$ ($10^{-10}$, $10^{-12}$, and $10^{-14}M$). RT-PCR showed that the gene expression levels of ALP, Col-I, OCN, and vitamin D receptor (VDR) were higher at a low concentration of 1,25-dihydroxyvitamin $D_3$ ($10^{-12}M$). Alizarin red S staining after treatment with 1,25-dihydroxyvitamin $D_3$ ($10^{-12}M$) showed no significant differences in the overall degree of calcification. In contrast to the positive control group, formation of bone nodules was induced in the early stages of cell differentiation. Conclusions: We suggest that 1,25-dihydroxyvitamin $D_3$ positively affects cell differentiation and matrix mineralization. Therefore, it may function as a stimulating factor in osteoblastic bone formation and can be used as an additive in bone regeneration treatment.