Osaka, Japan

Osaka Dental University is a private university in Hirakata, Osaka, Japan. The predecessor of the school was founded in 1911, and it was chartered as a university in 1947. There is a hospital associated with the university located near Temmabashi Station in Chūō-ku, Osaka. Wikipedia.

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Takeuchi H.,Osaka University | Takeuchi H.,Osaka Dental University | Furuta N.,Osaka University | Morisaki I.,Osaka Dental University | Amano A.,Osaka University
Cellular Microbiology | Year: 2011

Gingival epithelial cells function as an innate host defence system to prevent intrusion by periodontal bacteria. Nevertheless, Porphyromonas gingivalis, the most well-known periodontal pathogen, can enter gingival epithelial cells and pass through the epithelial barrier into deeper tissues. However, it is poorly understood how this pathogen exits from infected cells for further transcellular spreading. The present study was performed to elucidate the cellular machinery exploited by P.gingivalis to exit from immortalized human gingival epithelial cells. P.gingivalis was shown to be internalized with early endosomes positive for the FYVE domain of EEA1 and transferrin receptor, and about half of the intracellular bacteria were then sorted to lytic compartments, including autolysosomes and late endosomes/lysosomes, while a considerable number of the remaining organisms were sorted to Rab11- and RalA-positive recycling endosomes. Inhibition experiments revealed that bacterial exit was dependent on actin polymerization, lipid rafts and microtubule assembly. Dominant negative forms and RNAi knockdown of Rab11, RalA and exocyst complex subunits (Sec5, Sec6 and Exo84) significantly disturbed the exit of P.gingivalis. These results strongly suggest that the recycling pathway is exploited by intracellular P.gingivalis to exit from infected cells to neighbouring cells as a mechanism of cell-to-cell spreading. © 2011 Blackwell Publishing Ltd.

Imamura Y.,Matsumoto Dental University | Wang P.-L.,Osaka Dental University
Journal of Inflammation (United Kingdom) | Year: 2014

Background: Salivary histatins are bioactive peptides related to the innate immune system associated with antimicrobial activities. However, very little is known about the physiological and biological functions of histatins against host cells or their role in oral cell inflammation. Histatin 3 binds to heat shock cognate protein 70 (HSC70, a constitutively expressed heat shock protein (HSP)). It is unclear whether HSC70 is involved in the inflammatory response in oral cells. Injured oral cells release some intracellular proteins including HSC70. It is possible that released HSC70 induces toll-like receptor (TLR) activation, just as extracellular HSP70 (a stress inducible HSP) does, and that histatin 3 affects this process. Therefore, we tested the hypothesis that HSC70 activates TLR signaling and histatin 3 inhibits this activation and inflammatory cytokine production. Methods. A nuclear factor (NF)-κB-dependent luciferase reporter plasmid was transfected into HEK293 cells stably expressing TLR2 with coreceptor CD14 (293-TLR2/CD14 cells) or stably expressing TLR4 with CD14 and the accessory molecule MD2 (293-TLR4/MD2-CD14 cells). The cells were stimulated with HSC70 in the presence or absence of histatin 3, and examined using luciferase assays. We also stimulated human gingival fibroblasts (HGFs) with HSC70 with or without histatin 3. Then, we analyzed the levels of inflammatory cytokines (interleukin (IL)-6 and IL-8) in the culture media. Cell proteins were analyzed using enzyme-linked immunosorbent assay and Western blotting with antibodies of mitogen-activated protein kinases and NF-κB inhibitor IκB-α, respectively. Histatin 3-bound form of HSC70 was analyzed using limited V8 protease proteolysis. Results: HSC70 induced NF-κB activation in a dose-dependent manner in 293-TLR2/CD14 and 293-TLR4/MD2-CD14 cells, and histatin 3 inhibited this process and when histatin 3 binding to HSC70 was precluded by 15-deoxyspergualin, which augmented NF-κB-triggered activation. In HGFs, histatin 3 also inhibited HSC70-induced inflammatory cytokine production, extracellular signal-regulated protein kinase phosphorylation, and degradation of IκB-α. Moreover, HSC70 in the presence of histatin 3 was relatively resistant to digestion by V8 protease compared with HSC70 in the presence of control peptide. Conclusions: Histatin 3 may be an inhibitor of HSC70-triggered activation of TLR signaling and inflammatory cytokine production and may be involved in inflammation processes noted in oral cells. © 2014 Imamura and Wang; licensee BioMed Central Ltd.

Nishiyama J.,Kanagawa University | Makita Y.,Osaka Dental University | Kihara N.,Kanagawa University
Organic Letters | Year: 2015

Secondary ammonium salts bearing a cyclopentyl terminal group rapidly formed pseudorotaxane with 1.5 equiv of DB24C8. Acylation of the pseudorotaxane with 50 equiv of benzoyl chloride in the presence of 50 equiv of triethylamine in toluene afforded rotaxane, the product of active transport, in 95% yield. The cyclopentyl group is small enough to allow rapid formation of pseudorotaxane, and bulky enough to facilitate the quantitative active transport by steric repulsion. (Chemical Equation Presented). © 2014 American Chemical Society.

Okada M.,Osaka Dental University | Furuzono T.,Kinki University
Science and Technology of Advanced Materials | Year: 2012

Hydroxylapatite (or hydroxyapatite, HAp) exhibits excellent biocompatibility with various kinds of cells and tissues, making it an ideal candidate for tissue engineering, orthopedic and dental applications. Nanosized materials offer improved performances compared with conventional materials due to their large surface-to-volume ratios. This review summarizes existing knowledge and recent progress in fabrication methods of nanosized (or nanostructured) HAp particles, as well as their recent applications in medical and dental fields. In section 1, we provide a brief overview of HAp and nanoparticles. In section 2, fabrication methods of HAp nanoparticles are described based on the particle formation mechanisms. Recent applications of HAp nanoparticles are summarized in section 3. The future perspectives in this active research area are given in section 4. © 2012 National Institute for Materials Science.

Ishizuka T.,Osaka Dental University | Yamatodani A.,Osaka University
Frontiers in Systems Neuroscience | Year: 2012

Feeding behavior is regulated by a complex interplay of many endogenous substances, such as peptides and neurotransmitters in the central nervous system. Histamine is a neurotransmitter which expresses an anorectic effect on food intake via histamine H 1 receptors. The histaminergic system exists downstream of leptin, a satiety factor secreted from white adipose tissue. Because direct stimulation of the histaminergic system by histamine H 3-inverse agonists or antagonists can normalize the obese phenotype in which animal models with exogenous leptin resistance, which resembles human obesity, the potential roles of histamine H 3 receptors as a therapeutic target now draw attention. Histaminergic activity is enhanced during feeding, and an oral somatic sensation is thought to affect histaminergic activity while blood glucose levels do not. In addition, gustatory information can modulate histaminergic activity by two mechanisms: by physiological excitation of the chorda tympani nerve, one of the taste nerves and by emotions elicited by taste perception, i.e., taste palatability. Particularly, aversive and hazardous taste stimuli tonically facilitate histaminergic activity, suggesting that the histaminergic system is involved in the response to harmful stimuli. Together with recent findings, it is postulated that the histaminergic system responds to both mechanical and chemical sensory input from the oral cavity during feeding and is exerted as a part of the danger response system. © 2012 Ishizuka and Yamatodani.

Periodontal disease as a biofilm infectious disease is considered. Periodontal disease-associated bacteria formed biofilm in periodontal pockets or on the surface of cementum. Planktonic bacteria from biofilm invade into periodontal tissues and lead to inflammation and destruction of tissues directly and indirectly by eliciting the host defense mechanism. Supragingival dental plaques (biofilm) are easily removed by professional mechanical tooth cleaning, while subgingival dental plaques and bacteria invading into periodontal tissues are difficult to remove. Therefore, the development of a method for periodontal disease based on the concept that regards periodontal disease as a biofilm infectious disease is needed. Hereby, I report the effect of antibiotics on an in vitro biofilm model of periodontal disease and the systemic administration of azithromycin for early-onset (aggressive) periodontitis like a treatment resistant periodontitis. © 2010 The Japanese Pharmacological Society.

Sawai H.,Osaka Dental University
Leukemia Research | Year: 2014

Caspase-independent programmed necrotic cell death (necroptosis) has recently been described. Previously described models of necroptosis required 16. h or more of induction, which made the interpretation of findings somewhat difficult. In human monocytic leukemia cell line U937 necroptosis could be induced within 6. h by combination of TNF and Z-VAD-fmk. Here we show that the reduction in intracellular ATP levels may not be the sole determinant of necroptosis, and that necroptosis is associated with the loss of mitochondrial membrane potential, but not the activation of Bak/Bax or calcineurin. © 2014 Elsevier Ltd.

Sawai H.,Osaka Dental University | Domae N.,Osaka Dental University
Biochemical and Biophysical Research Communications | Year: 2011

Apoptotic cell death eventually results in secondary necrotic cell death, whereas caspase-independent primary necrotic cell death has been reported and its mechanism involving RIP1 and RIP3 has been recently elucidated. Dual staining with fluorescent Annexin V and propidium iodide (PI) has been used to discriminate apoptotic and necrotic cell death, in which Annexin V-positive/PI-negative staining is regarded as apoptosis and PI-positive staining as necrosis. Here we demonstrate that primary necrotic cells unexpectedly show Annexin V-positive/PI-negative staining before they become PI-positive, and that primary necrotic and apoptotic Annexin V-positive/PI-negative cells can be discriminated by necrostatin-1, an inhibitor of primary necrosis by inhibition of RIP1. © 2011 Elsevier Inc.

Sawai H.,Osaka Dental University
Biochemical and Biophysical Research Communications | Year: 2013

TNF has been reported to induce caspase-independent necroptosis in the presence of Z-VAD-fmk, a pan-caspase inhibitor. We examined whether necroptosis was induced by caspase inhibitors other than Z-VAD-fmk. TNF-induced necroptosis was detected in the presence of Z-DEVD-fmk, which is commonly used as a caspase-3-specific inhibitor, but not in the presence of Z-Asp-CH2-DCB, which was reported to be a pan-caspase inhibitor. TNF-induced caspase-3 activity was completely inhibited by Z-VAD-fmk, Z-DEVD-fmk, or Z-Asp-CH2-DCB. Although TNF-induced proteolytic activation of procaspase-3 was completely prevented by Z-VAD-fmk or Z-DEVD-fmk, the partial proteolysis of procaspase-3 was induced in the presence of Z-Asp-CH2-DCB. Furthermore, although TNF-induced proteolytic activation of procaspase-8 was completely inhibited by Z-VAD-fmk or Z-DEVD-fmk, the partial proteolysis of procaspase-8 to the p43/41 intermediate and p18 active fragment was detected in the presence of Z-Asp-CH2-DCB. The cleavage of RIP1, which plays a crucial role in TNF-induced necroptosis and is cleaved by caspase-8, was completely inhibited by Z-VAD-fmk or Z-DEVD-fmk, whereas the partial degradation of RIP1 was detected in the presence of Z-Asp-CH2-DCB. These results suggest that the partial activation of caspase-8 in the presence of Z-Asp-CH2-DCB may suppress TNF-induced necroptosis via the cleavage of RIP1, and also suggest that Z-Asp-CH2-DCB, but not Z-DEVD-fmk, may be used as a caspase-3-specific inhibitor in cells. © 2013 Elsevier Inc.

To compare the effects of 60 Gy/10 fractions (twice a day) with those of 54 Gy/9 fractions in high-dose-rate interstitial brachytherapy (HDR-ISBT) for early tongue cancer, we performed a matched-pair analysis of patients with early tongue cancer (T1-2N0M0), who were treated with 60 or 54 Gy of radiation between 1996 and 2004. Seventeen patients treated with 54 Gy and 34 matched-pair patients treated with 60 Gy were extracted and analyzed. Local recurrence occurred in two patients in the 54-Gy arm and five patients in the 60-Gy arm. The 2-year local control rates were 88% for both the 54-Gy arm and 60-Gy arm (not significant). The 2-year overall survival rates were 88% in the 60-Gy arm and 82% in the 54-Gy arm. Two-year actuarial complication-free rates were 91% in the 60-Gy arm and 83% in the 54-Gy arm (not significant), respectively. There was no significant association between the total dose and local control rate and late complications. The outcome of 54 Gy/ 9 fractions was similar to that of 60 Gy/ 10 fractions in patients with early tongue cancer.

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