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National parks and national historic sites of Canada in Quebec
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Ultrafast fiber laser and amplifier systems for precision applications (Invited Paper) [5460-31]
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국내 항인지질항체 증후군 환자 실태분석
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팥빙수의 전설 : 이지은 그림책
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Müller^ Hans. Die Eisenbahnen im Gebiet der Oberweser (Book Review)
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2023년 한국교육학회 연차학술대회 한국교원교육학회 분과세션 신진예비학자 및 현장교원 논문경진대회 자료집
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- 저자 : Hideki Sudo (검색결과 5 건)
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Sudo, Toshiki,Ito, Hideki,Kimura, Yukio Taylor Francis 2003 Platelets Vol.14 No.6
<P>Vasodilator-stimulated phosphoprotein (VASP) is a regulator of actin dynamics in platelets and a common substrate of both cAMP- and cGMP-dependent protein kinases (PKA and PKG). Elevations of the cAMP and cGMP concentration have been shown to inhibit platelet aggregation. Intracellular levels of cAMP and cGMP are regulated by the synthesizing system of adenylate cyclases, and hydrolysis by cyclic nucleotide phosphodiesterases (PDEs). The present study examined the effect of the anti-platelet drug, cilostazol, which inhibits PDE3 activity, on VASP phosphorylation in platelets. VASP phosphorylation was examined by immunoblotting with an anti-VASP antibody, M4, and an anti-phospho-VASP antibody, 16C2. Cilostazol phosphorylated VASP at both Ser 157 and Ser 239 in a concentration-dependent manner, but EHNA (PDE2 inhibitor), dipyridamole and zaprinast (PDE5 inhibitors) did not. Forskolin (adenylate cyclase activator) and sodium nitroprusside (SNP, NO donor) resulted in the VASP phosphorylation, with increase in the cAMP and cGMP level, respectively. Cilostazol increased cAMP, but not cGMP levels, in platelets. EHNA, zaprinast and dipyridamole, had no effect on cAMP and cGMP levels. The PKA/PKG inhibitor, H-89, inhibited VASP phosphorylation by cilostazol. These results demonstrated that cilostazol phosphorylates VASP through the PDE3 inhibition, increase of cAMP level, and PKA activation in platelets.</P>
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Low-Temperature FTIR Spectroscopy of Bacteriorhodopsin and Phoborhodopsin
Kandori, Hideki,Furutani, Yuji,Shimono, Kazumi,Iwamoto, Masayuki,Sudo, Yuki,Shichida, Yoshinori,Kamo, Naoki Korean Society of Photoscience 2002 Journal of Photosciences Vol.9 No.2
Archaeal rhodopsins possess retinal molecule as their chromophores, and their light-energy and light-signal conversions are triggered by all-trans to 13-cis isomerization of the retinal chromophore. Relaxation through structural changes of protein then leads to functional processes, proton pump in bacteriorhodopsin (bR) and transducer activation in phoborhodopsin (pR). It is known that sensory rhodopsins can pump protons in the absence of their transducers. Thus, there should be common and specific features in their protein structural changes for function. In this paper, our r ecent studies on pR from Natronobacterium pharaonis (ppR) by means of low-temperature Fourier-transform infrared (FTIR) spectroscopy are compared with those of bR. In particular, protein structural changes upon retinal photoisomerization are studied. Comparative investigation of ppR and bR revealed the similar structures of the polyene chain of the chromophore and water-containing hydrogen-bonding network, whereas the structural changes upon photoisomerization were more extended in ppR than in bR. Extended protein structural changes were clearly shown by the assignment of the C=O stretch of Asnl05. FTIR studies of a ppR mutant with the same retinal binding site as in bR revealed that the Schiff base region is important to determine their colors.
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Effect of Asp193 on Proton Affinity of the Schiff Base in pharaonis phoborhodopsin
Iwamoto, Masayuki,Furutani, Yuji,Sudo, Yuki,Shimono, Kazumi,Kandori, Hideki,Kamo, Naoki Korean Society of Photoscience 2002 Journal of Photosciences Vol.9 No.2
Spectroscopic titration of D 193N and D 193E mutants of pharaonis phoborhodopsin (ppR) were performed to evaluate the pK$_{a}$ of the Schiff base Asp 193 corresponds to Glu204 of bacteriorhodopsin (bR). The pK$_{a}$ of the Schiff base (SBH$^{+}$) of D193N was 10.1~10.0 (at XH$^{+}$) and 11.4~11.6 (at X) depending on the protonation state of a certain residue (designated by X) and independent on CI$^{[-10]}$ , while those of the wild-type and D193E were> 12. pK$_{a}$ of XH$^{+}$ were; 11.8~11.2 at the state of SB, 10.5 at SBH$^{+}$ state in the presence of CI$^{[-10]}$ , and 9.6 at SBH$^{+}$ without CI$^{[-10]}$ These imply the presence of a long-range interaction in the extracellular channel.r channel.
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Akira Iwata,Kuniyoshi Abumi,Masahiko Takahata,Hideki Sudo,Katsuhisa Yamada,Tsutomu Endo,Norimasa Iwasaki 대한척추외과학회 2019 Asian Spine Journal Vol.13 No.2
Study Design: Retrospective case-control study, level 4. Purpose: To clarify the risk factors for late subaxial lesion after occipitocervical (O-C) reconstruction. We examined cases requiring fusion-segment-extended (FE) reconstruction in addition to/after O-C reconstruction. Overview of Literature: Patients with rheumatoid arthritis (RA) frequently require O-C reconstruction surgery for cranio-cervical lesions. Acceptable outcomes are achieved via indirect decompression using cervical pedicle screws and occipital plate–rod systems. However, late subaxial lesions may develop occasionally following O-C reconstruction. Methods: O-C reconstruction using cervical pedicle screws and occipital plate–rod systems was performed between 1994 and 2007 in 113 patients with RA. Occipito-atlanto-axial (O-C2) reconstruction was performed for 89 patients, and occipito-subaxial cervical (O-under C2) reconstruction was performed for 24 patients. We reviewed the cases of patients requiring FE reconstruction (fusion extended group, FEG) and 26 consecutive patients who did not require FE reconstruction after a follow-up of >5 years (non-fusion extended group, NEG) as controls. Results: FE reconstructions were performed for nine patients at an average of 45 months (range, 24–180 months) after O-C reconstruction. Of the 89 patients, three (3%) underwent FE reconstruction in cases of O-C2 reconstruction. Of the 24 patients, five (21%) underwent FE reconstruction in cases of O-under C2 reconstruction (p =0.003, Fisher exact test). Age, sex, RA type, and neurological impairment stage were not significantly different between FEG and NEG. O-under C2 reconstruction, larger correction angle (4° per number of unfixed segment), and O-C7 angle change after O-C reconstruction were the risk factors for late subaxial lesions on radiographic assessment. Conclusions: Overcorrection of angle at fusion segments requiring O-C7 angle change was a risk factor for late subaxial lesion in patients with RA with fragile bones and joints. Correction should be limited, considering the residual mobility of the cervical unfixed segments.
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