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Kitakyushu, Japan

Kyushu Dental University is a public university in Kitakyushu, Fukuoka, Japan. The predecessor of the school was founded in 1914, and it was chartered as a university in 1949. Wikipedia.


Hyperon-nucleons interactions constructed by two frameworks, the Kyoto-Niigata SU6 quark model and the chiral effective field theory, are compared by investigating equivalent interactions in a low-momentum space and, in addition, by calculating hyperon single-particle potentials in the lowest-order Brueckner theory in symmetric nuclear matter. Two descriptions are shown to give similar matrix elements in most channels after renormalizing high momentum components. Although the range of the ΛN interaction is different in two potentials, the Λ single-particle potential in nuclear matter is very similar. The Σ-nucleus and Ξ-nucleus potentials are also found to be similar. These predictions are to be confronted with forthcoming experimental data. © 2010 The American Physical Society. Source


Takahama U.,Kyushu Dental College | Hirota S.,Kyushu Womens University
Journal of Agricultural and Food Chemistry | Year: 2011

During the digestion of starch in foods, starch is mixed with bile in the duodenum. Because fatty acids and some kinds of polyphenols could bind to starch, it was postulated that bile salts might also bind to starch. The purpose of this paper is to study the effects of bile and bile salts on starch/iodine complex formation and pancreatin-induced starch digestion. Bile suppressed starch/iodine complex formation and inhibited pancreatin-induced starch digestion slightly in control buckwheat starch, but did so significantly in buckwheat starch from which fatty acids and polyphenols had been extracted. Such significant suppression and inhibition by bile were also observed in a reagent soluble starch. The effects of cholate and taurocholate on the starch/iodine complex formation and the pancreatin-induced starch digestion were essentially the same as those of bile. Bile, cholate, and taurocholate suppressed amylose/iodine complex formation more significantly than amylopectin/iodine complex formation and inhibited pancreatin-induced amylose digestion more effectively than the digestion of amylopectin. It is concluded from the results that bile salts could bind to starch, especially amylose, the helical structures of which were not occupied by other molecules such as fatty acids and polyphenols, and that the binding resulted in the inhibition of starch digestion by pancreatin. The conclusion suggests that the function of bile salts can be discussed from the point of not only lipid digestion but also starch digestion. © 2011 American Chemical Society. Source


Takahama U.,Kyushu Dental College | Hirota S.,Kyushu Womens University
Journal of Agricultural and Food Chemistry | Year: 2012

The food additive sulfite is mixed with saliva, which contains nitrite, in the oral cavity, and the mixture is mixed with gastric juice in the stomach. In the stomach, salivary nitrite can be transformed to nitric oxide (NO). In this study, the effects of sulfite on nitrite-dependent NO production were investigated using acidified saliva (pH 2.6) and acidic buffer solutions (pH 2.0). Sulfite enhanced NO production in acidified saliva and acidic buffer solutions, and the enhancement increased with the increase in sulfite concentration from 0 to 0.1 mM, whereas suppressed NO production and the suppression increased as the concentration was increased over 0.2 mM. The enhancement was due to the increase in reaction rate between nitrous acid and nitrososulfonate (ONSO 3 -) that was formed by the reaction of nitrous acid with hydrogen sulfite, and the suppression was due to the increase in hydrogen sulfite-dependent consumption rate of ONSO 3 -. A salivary component SCN - (1 mM) enhanced and suppressed NO production induced by 1 mM nitrite when sulfite concentrations were lower and higher than 1 mM, respectively. ONSO 3 - formed from hydrogen sulfite and nitrosyl thiocyanate (ONSCN), which was produced by the reaction of nitrous acid with SCN -, seemed to contribute to the enhancement and suppression. NO production induced by nitrite/ascorbic acid systems was suppressed by sulfite, and the suppressive effects were decreased by SCN -, whereas sulfite-induced suppression of NO production in nitrite/rutin systems was increased by SCN -. During reactions of nitrite with sulfite in the presence and absence of SCN -, oxygen was taken up. The oxygen uptake is discussed to be due to autoxidation of NO and radical chain reactions initiated by hydrogen sulfite radicals. The results of the present study suggest that sulfite can enhance and suppress nitrite-dependent NO production. It is discussed that radicals including hydrogen sulfite radicals can be formed through the reactions of nitrite and sulfite in the stomach. © 2012 American Chemical Society. Source


Iron(III) ingested as a food component or supplement for iron deficiencies can react with salivary SCN - to produce Fe(SCN) 2+ and can be reduced to iron(II) by ascorbic acid in the stomach. Iron(II) generated in the stomach can react with salivary nitrite and SCN - to produce nitric oxide (NO) and FeSCN +, respectively. The purpose of this investigation is to make clear the reactions among nitrite, SCN -, iron ions, and ascorbic acid under conditions simulating the mixture of saliva and gastric juice. Iron(II)-dependent reduction of nitrite to NO was enhanced by SCN - in acidic buffer solutions, and the oxidation product of iron(II) reacted with SCN - to produce Fe(SCN) 2+. Almost all of the NO produced was autoxidized to N 2O 3 under aerobic conditions. Iron(II)-dependent production of NO was also observed in acidified saliva. Under anaerobic conditions, NO transformed Fe(SCN) 2+ and FeSCN + to Fe(SCN)NO + in acidic buffer solutions. Fe(SCN)NO + was also formed under aerobic conditions when excess ascorbic acid was added to iron(II)/nitrite/SCN - systems in acidic buffer solutions and acidified saliva. The Fe(SCN)NO + formed was transformed to Fe(SCN) 2+ and iron(III) at pH 2.0 and pH 7.4, respectively, by O 2. Salivary glycoproteins could complex with iron(III) in the stomach preventing the formation of Fe(SCN) 2+. Ascorbic acid reduced iron(III) to iron(II) to react with nitrite and SCN - as described above. The above results suggest (i) that iron(II) can have toxic effects on the stomach through the formation of reactive nitrogen oxide species from NO when supplemented without ascorbic acid and through the formation of both reactive nitrogen oxide species and Fe(SCN)NO + when supplemented with ascorbic acid, and (ii) that the toxic effects of iron(III) seemed to be smaller than and similar to those of iron(II) when supplemented without and with ascorbic acid, respectively. Possible mechanisms that cause oxidative stress on the stomach through Fe(SCN)NO + are discussed. © 2011 American Chemical Society. Source


Masuda W.,Kyushu Dental College | Betzenhauser M.J.,Columbia University | Yule D.I.,University of Rochester
Journal of Biological Chemistry | Year: 2010

Ca2+ release through inositol 1,4,5-trisphosphate receptors (InsP3R) can be modulated by numerous factors, including input from other signal transduction cascades. These events shape the spatio-temporal characteristics of the Ca2+ signal and provide fidelity essential for the appropriate activation of effectors. In this study, we investigate the regulation of Ca2+ release via InsP3R following activation of cyclic nucleotide-dependent kinases in the presence and absence of expression of a binding partner InsP3R-associated cGMP kinase substrate (IRAG). cGMP-dependent kinase (PKG) phosphorylation of only the S2+ InsP3R-1 subtype resulted in enhanced Ca2+ release in the absence of IRAG expression. In contrast, IRAG bound to each InsP3R subtype, and phosphorylation of IRAG by PKG attenuated Ca2+ release through all InsP3R subtypes. Surprisingly, simply the expression of IRAG attenuated phosphorylation and inhibited the enhanced Ca2+ release through InsP3R-1 following cAMP-dependent protein kinase (PKA) activation. In contrast, IRAG expression did not influence the PKA-enhanced activity of the InsP3R-2. Phosphorylation of IRAG resulted in reduced Ca2+ release through all InsP3R subtypes during concurrent activation of PKA and PKG, indicating that IRAG modulation is dominant under these conditions. These studies yield mechanistic insight into how cells with various complements of proteins integrate and prioritize signals from ubiquitous signaling pathways. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc. Source

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