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        Enhancement of the Curie Temperature due to the Coupling Between Fe Itinerant Electrons and Dy Localized Electrons in DyFe2Zn20

        Yosikazu Isikawa,Toshio Mizushima,Souta Miyamoto,Keigou Kumagai,Mako Nakahara,Hiroaki Okuyama,Takashi Tayama,Tomohiko Kuwai,Pascal Lejay 한국물리학회 2013 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.63 No.3

        The temperature dependences of the magnetization and the specific heat of the ferromagneticcompound DyFe2Zn20 have been measured in detail in various magnetic fields. We have observedanomalous magnetic behaviors, i.e., a strong anisotropy at 2 K, the disappearance of this anisotropyat temperatures between approximately 30 K and Tc, and an anomalous behavior of the specificheat in magnetic fields at temperatures near 20 K. These anomalous phenomena have been analyzedbased on the strong exchange interaction between the Fe itinerant electrons and the Dy localizedelectrons, as well as the crystalline electric field, the Zeeman energy, and an usual exchange interactionbetween two Dy atoms. The higher Tc of DyFe2Zn20 compared with that of DyRu2Zn20 iscaused by this exchange interaction between the Fe and the Dy atoms.

      • KCI등재후보

        Genetic Polymorphisms in Dopamine- and Serotonin-Related Genes and Treatment Responses to Risperidone and Perospirone

        Atsushi Tsutsumi,Tetsufumi Kanazawa,Hiroki Kikuyama,Gaku Okugawa,Hiroyuki Uenishi,Toshio Miyamoto,Naoki Matsumoto,Jun Koh,Kazuhiro Shinosaki,Toshifumi Kishimoto,Hiroshi Yoneda,Toshihiko Kinoshita 대한신경정신의학회 2009 PSYCHIATRY INVESTIGATION Vol.6 No.3

        We investigated the possible association between genetic polymorphisms in the dopamine receptor and serotonin transporter genes and the responses of schizophrenic patients treated with either risperidone or perospirone. The subjects comprised 27 patients with schizophrenia who were clinically evaluated both before and after treatment. The genotyping of the polymorphisms of the dopamine D2 receptor gene (DRD2) (rs1801028 and rs6277), the dopamine D4 receptor gene (DRD4) (120-bp tandem repeats and rs1800955), and serotonin transporter gene (5HTT)(variable number of tandem repeats; VNTR) were performed using the real-time polymerase chain reaction and sequencing. In DRD2 and 5HTT-VNTR, there were no significant correlations between clinical response and polymorphism in the case of risperidone, and for perospirone treatment it was impossible to analyze the clinical evaluation due to the absence of genotype information. On the other hand, in DRD4 there were significant correlations in the two-factor interaction effect on the Positive and Negative Syndrome Scale (PANSS) between the two drugs [120-bp tandem repeat, p=0.003; rs1800955, p=0.043]. Although the small sample represents a serious limitation, these results suggest that variants in DRD4 are a predictor of whether treatment will be more effective with risperidone or with perospirone in individual patients. We investigated the possible association between genetic polymorphisms in the dopamine receptor and serotonin transporter genes and the responses of schizophrenic patients treated with either risperidone or perospirone. The subjects comprised 27 patients with schizophrenia who were clinically evaluated both before and after treatment. The genotyping of the polymorphisms of the dopamine D2 receptor gene (DRD2) (rs1801028 and rs6277), the dopamine D4 receptor gene (DRD4) (120-bp tandem repeats and rs1800955), and serotonin transporter gene (5HTT)(variable number of tandem repeats; VNTR) were performed using the real-time polymerase chain reaction and sequencing. In DRD2 and 5HTT-VNTR, there were no significant correlations between clinical response and polymorphism in the case of risperidone, and for perospirone treatment it was impossible to analyze the clinical evaluation due to the absence of genotype information. On the other hand, in DRD4 there were significant correlations in the two-factor interaction effect on the Positive and Negative Syndrome Scale (PANSS) between the two drugs [120-bp tandem repeat, p=0.003; rs1800955, p=0.043]. Although the small sample represents a serious limitation, these results suggest that variants in DRD4 are a predictor of whether treatment will be more effective with risperidone or with perospirone in individual patients.

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        v-ATPase V<sub>0</sub> subunit d2–deficient mice exhibit impaired osteoclast fusion and increased bone formation

        Lee, Seoung-Hoon,Rho, Jaerang,Jeong, Daewon,Sul, Jai-Yoon,Kim, Taesoo,Kim, Nacksung,Kang, Ju-Seob,Miyamoto, Takeshi,Suda, Toshio,Lee, Sun-Kyeong,Pignolo, Robert J,Koczon-Jaremko, Boguslawa,Lorenzo, Jo Nature Publishing Group 2006 Nature medicine Vol.12 No.12

        Matrix-producing osteoblasts and bone-resorbing osteoclasts maintain bone homeostasis. Osteoclasts are multinucleated, giant cells of hematopoietic origin formed by the fusion of mononuclear pre-osteoclasts derived from myeloid cells. Fusion-mediated giant cell formation is critical for osteoclast maturation; without it, bone resorption is inefficient. To understand how osteoclasts differ from other myeloid lineage cells, we previously compared global mRNA expression patterns in these cells and identified genes of unknown function predominantly expressed in osteoclasts, one of which is the d2 isoform of vacuolar (H<SUP>+</SUP>) ATPase (v-ATPase) V<SUB>0</SUB> domain (Atp6v0d2). Here we show that inactivation of Atp6v0d2 in mice results in markedly increased bone mass due to defective osteoclasts and enhanced bone formation. Atp6v0d2 deficiency did not affect differentiation or the v-ATPase activity of osteoclasts. Rather, Atp6v0d2 was required for efficient pre-osteoclast fusion. Increased bone formation was probably due to osteoblast-extrinsic factors, as Atp6v02 was not expressed in osteoblasts and their differentiation ex vivo was not altered in the absence of Atp6v02. Our results identify Atp6v0d2 as a regulator of osteoclast fusion and bone formation, and provide genetic data showing that it is possible to simultaneously inhibit osteoclast maturation and stimulate bone formation by therapeutically targeting the function of a single gene.

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