[Case study of early detection and intervention of infectious disease outbreaks in an institution using Nursery School Absenteeism Surveillance Systems (NSASSy) of the Public Health Center].

Objectives Detecting outbreaks early and then activating countermeasures based on such information is extremely important for infection control at childcare facilities. The Sumida ward began operating the Nursery School Absenteeism Surveillance System (NSASSy) in August 2013, and has since conducted real-time monitoring at nursery schools. The Public Health Center can detect outbreaks early and support appropriate intervention.

A high-sensitive and non-radioisotopic fluorescence dye method for evaluating bacterial adhesion to denture materials.

Oral bacteria adhered to dental material surfaces are known to cause various oral diseases. This study aimed to develop a highsensitive and non-radioisotopic fluorescence dye method for quantification of oral bacteria (Streptococcus, Actinomyces and Veillonella) adhered to denture material surfaces. The amount of adhered bacteria was estimated from the fluorescence intensity derived from resazurin, which is reduced by bacterial metabolic reactions.

High-dose glucocorticoid treatment induces rapid loss of trabecular bone mineral density and lean body mass.

A recent large-scale study revealed that glucocorticoid treatment increased fracture risk, which occurred at a far smaller dose and by a shorter duration than previously thought. To study the underlying mechanism for the increased risk of fracture, we studied the early changes in bone mineral density (BMD) and body composition by dual energy X-ray absorptiometry (DXA) after initiating high-dose glucocorticoid treatment. High-dose glucocorticoid treatment was arbitrarily defined as daily doses of >or=40 mg of a predonisolone equivalent.

Complementary antagonistic actions between C-type natriuretic peptide and the MAPK pathway through FGFR-3 in ATDC5 cells.

We previously reported that C-type natriuretic peptide (CNP) stimulates endochondral ossification and corrects the reduction in body length of achondroplasia model mouse with constitutive active fibroblast growth factor receptor 3 (FGFR-3). In order to examine the interaction between CNP and FGFR-3, we studied intracellular signaling by using ATDC5 cells, a mouse chondrogenic cell line, and found that FGF2 and FGF18 markedly reduced CNP-dependent intracellular cGMP production, and that these effects were attenuated by MAPK inhibitors. Western blot analysis demonstrated that the level of GC-B, a particulate guanylyl cyclase specific for CNP, was not changed by treatment with FGFs.

Distributions and chemical forms of arsenic after intravenous administration of dimethylarsinic and monomethylarsonic acids to rats.

The observed toxicity of arsenic is highly dependent on animal species and differences in metabolism. Rats are one of the most tolerant species, and the metabolic pathway is quite different in some aspects from those of other mammals. The distinct metabolic pathway including the preferential accumulation in red blood cells (RBCs) has been explained, whereby allowing an effective use of rats as an animal model for the arsenic metabolism.

Dimethylthioarsenicals as arsenic metabolites and their chemical preparations.

Two unidentified arsenic metabolites were detected in the liver of rats on a gel filtration column by HPLC inductively coupled argon plasma mass spectrometry after an injection of dimethylarsinic (DMA(V)), dimethylarsinous (DMA(III)), monomethylarsonic (MMA(V)), or monomethylarsonous (MMA(III)) acid. The same arsenicals were also produced in vitro by incubation of DMA(III) in the liver supernatant but not by DMA(V). The two arsenic metabolites eluted at the same retention times as those of the two arsenicals prepared by reaction of DMA(V) with either thiosulfate plus disulfite or hydrogen sulfide or sodium sulfide plus sulfuric acid.

Stimulation of cAMP production and cyclooxygenase-2 by prostaglandin E(2) and selective prostaglandin receptor agonists in murine osteoblastic cells.

Prostaglandins (PGs), particularly PGE(2), can stimulate bone resorption and formation and auto-amplify their effects by inducing cyclooxygenase (COX)-2. We examined the role of different PG receptors in stimulating cAMP production and COX-2 expression in murine calvarial osteoblasts. Cells were obtained from PGE(2) receptor (EP2R and EP4R) wild-type and knockout (KO) mice and from mice transgenic for the COX-2 promoter fused to a luciferase reporter.

Bone morphogenetic protein 2 induces cyclo-oxygenase 2 in osteoblasts via a Cbfal binding site: role in effects of bone morphogenetic protein 2 in vitro and in vivo.

We tested the hypothesis that induction of cyclo-oxygenase (COX) 2 mediates some effects of bone morphogenetic protein (BMP) 2 on bone. BMP-2 induced COX-2 mRNA and prostaglandin (PG) production in cultured osteoblasts. BMP-2 increased luciferase activity in calvarial osteoblasts from mice transgenic for a COX-2 promoter-luciferase reporter construct (Pluc) and in MC3T3-E1 cells transfected with Pluc.

Thyroid hormones promote chondrocyte differentiation in mouse ATDC5 cells and stimulate endochondral ossification in fetal mouse tibias through iodothyronine deiodinases in the growth plate.

Thyroid hormones (THs), 3,3',5-triiodo-L-thyronine (T3) and L-thyroxine (T4), are important for the normal development of the growth plate (GP); congenital TH deficiency leads to severe dwarfism. In mouse chondrogenic cell line, ATDC5, T3 enhanced differentiation and increased Alizarin red staining, but did not affect Alcian blue staining. In organ-cultured mouse tibias, THs stimulated the cartilage growth, especially in the hypertrophic zone.

A novel interaction between thyroid hormones and 1,25(OH)(2)D(3) in osteoclast formation.

Thyroid hormones enhance osteoclast formation and their excess is an important cause of secondary osteoporosis. 3,5,3' -Triiodo-L-thyronine (T3) induced the mRNA expression of receptor activator of nuclear factor-kappa B ligand (RANKL), which is a key molecule in osteoclast formation, in primary osteoblastic cells (POB). This effect was amplified in the copresence of 1 alpha,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)).