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34 results on '"Miyagi, Kyoko"'

13. Comparison of two screening tests for HIV-Associated Neurocognitive Disorder suspected Japanese patients with respect to cART usage

Author

Kami-Onaga, Kaoru, primary, Tateyama, Masao, additional, Kinjo, Takeshi, additional, Parrott, Gretchen, additional, Tominaga, Daisuke, additional, Takahashi-Nakazato, Ai, additional, Nakamura, Hideta, additional, Tasato, Daisuke, additional, Miyagi, Kyoko, additional, Maeda, Saori, additional, Arae, Hirotaka, additional, Uehara, Hitoshi, additional, Miyagi, Kazuya, additional, Haranaga, Shusaku, additional, and Fujita, Jiro, additional

Published
2018
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14. FP052EFFECTIVENESS AND SAFETY OF TOLVAPTAN IN AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE PATIENTS WITH CKD STAGE G4: A RETROSPECTIVE MULTICENTER STUDY IN JAPAN

Author

Yamada, Kazunori, primary, Muramoto, Hiroaki, additional, Araki, Hideo, additional, Kakuchi, Yasushi, additional, Miyagi, Kyoko, additional, Kitajima, Susumu, additional, Tani, Yukiko, additional, Suzuki, Yasunori, additional, Onoe, Tamehito, additional, Muto, Hisao, additional, Hirata, Masayoshi, additional, Takeda, Masahiro, additional, Nomura, Hideki, additional, Miyazaki, Ryoichi, additional, and Kawano, Mitsuhiro, additional

Published
2018
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17. MP052THE USEFULNESS OF TOLVAPTAN IN PATIENTS WITH AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE WITH CHRONIC KIDNEY DISEASE STAGE G3 TO G4

Author

Yamada, Kazunori, primary, Muramoto, Hiroaki, additional, Araki, Hideo, additional, Kakuchi, Yasushi, additional, Miyagi, Kyoko, additional, Kitajima, Susumu, additional, Tani, Yukiko, additional, Onoe, Tamehito, additional, Hirata, Masayoshi, additional, Takeda, Masahiro, additional, Miyazaki, Ryoichi, additional, and Kawano, Mitsuhiro, additional

Published
2016
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19. Evaluation of the Lipid Concentrations after Switching from Antiretroviral Drug Tenofovir Disoproxil Fumarate/Emtricitabine to Abacavir Sulfate/Lamivudine in Virologically-suppressed Human Immunodeficiency Virus-infected Patients

Author

Arae, Hirotaka, primary, Tateyama, Masao, additional, Nakamura, Hideta, additional, Tasato, Daisuke, additional, Kami, Kaoru, additional, Miyagi, Kyoko, additional, Maeda, Saori, additional, Uehara, Hitoshi, additional, Moromi, Makiko, additional, Nakamura, Katsunori, additional, and Fujita, Jiro, additional

Published
2016
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21. A Pathogenic C Terminus-truncated Polycystin-2 Mutant Enhances Receptor-activated Ca2+ Entry via Association with TRPC3 and TRPC7

Author

Miyagi, Kyoko, primary, Kiyonaka, Shigeki, additional, Yamada, Kazunori, additional, Miki, Takafumi, additional, Mori, Emiko, additional, Kato, Kenta, additional, Numata, Tomohiro, additional, Sawaguchi, Yuichi, additional, Numaga, Takuro, additional, Kimura, Toru, additional, Kanai, Yoshikatsu, additional, Kawano, Mitsuhiro, additional, Wakamori, Minoru, additional, Nomura, Hideki, additional, Koni, Ichiro, additional, Yamagishi, Masakazu, additional, and Mori, Yasuo, additional

Published
2009
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31. A Pathogenic C Terminus-truncated Polycystin-2 Mutant Enhances Receptor-activated Ca2+ Entry via Association with TRPC3 and TRPC7.

Author

Miyagi, Kyoko, Kiyonaka, Shigeki, Yamada, Kazunori, Miki, Takafumi, Mori, Emiko, Kato, Kenta, Numata, Tomohiro, Sawaguchi, Yuichi, Numaga, Takuro, Kimura, Toru, Kanai, Yoshikatsu, Kawano, Mitsuhiro, Wakamori, Minoru, Nomura, Hideki, Koni, Ichiro, Yamagishi, Masakazu, and Mori, Yasuo

Subjects
*GENETIC mutation, *POLYCYSTIC kidney disease, *GLUTAMIC acid, *ENDOPLASMIC reticulum, *CELL membranes, *CELL growth
Abstract

Mutations in PKD2 gene result in autosomal dominant polycystic kidney disease (ADPKD). PKD2 encodes polycystin-2 (TRPP2), which is a homologue of transient receptor potential (TRP) cation channel proteins. Here we identify a novel PKD2 mutation that generates a C-terminal tail-truncated TRPP2 mutant 697fsX with a frameshift resulting in an aberrant 17-amino acid addition after glutamic acid residue 697 from a family showing mild ADPKD symptoms. When recombinantly expressed in HEK293 cells, wild-type (WT) TRPP2 localized at the endoplasmic reticulum (ER) membrane significantly enhanced Ca2+ release from the ER upon muscarinic acetylcholine receptor (mAChR) stimulation. In contrast, 697fsX, which showed a predominant plasma membrane localization characteristic of TRPP2 mutants with C terminus deletion, prominently increased mAChR-activated Ca2+ influx in cells expressing TRPC3 or TRPC7. Coimmunoprecipitation, pulldown assay, and cross-linking experiments revealed a physical association between 697fsX and TRPC3 or TRPC7. 697fsX but not WT TRPP2 elicited a depolarizing shift of reversal potentials and an enhancement of single-channel conductance indicative of altered ion-permeating pore properties of mAChR-activated currents. Importantly, in kidney epithelial LLC-PK1 cells the recombinant 679fsX construct was codistributed with native TRPC3 proteins at the apical membrane area, but the WT construct was distributed in the basolateral membrane and adjacent intracellular areas. Our results suggest that heteromeric cation channels comprised of the TRPP2 mutant and the TRPC3 or TRPC7 protein induce enhanced receptor-activated Ca2+ influx that may lead to dysregulated cell growth in ADPKD. [ABSTRACT FROM AUTHOR]

Published
2009
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34. Effect of ACEgene polymorphism on age at renal death in polycystic kidney disease in Japan

Author

Konoshita, Tadashi, Miyagi, Kyoko, Onoe, Tamehito, Katano, Kenichi, Mutoh, Hisao, Nomura, Hideki, Koni, Ichiro, Miyamori, Isamu, and Mabuchi, Hiroshi

Abstract

Polycystic kidney disease (PKD) is one of the most common genetic disorders and a major cause of renal death or end-stage renal disease (ESRD) requiring regular hemodialysis. The responsible genes recently have been cloned; however, genetic factors influencing the rate of progression to ESRD in patients with PKD have yet to be defined. Several studies have shown increased activity of the renin-angiotensin system (RAS) in patients with PKD. In addition, genetic polymorphisms of the RAS have been associated with the development of cardiovascular diseases. Therefore, these polymorphisms are good candidates for disease-modifying genetic factors or markers in PKD. In two previous reports of white subjects with a cumulative survival analysis, it was suggested that patients with PKD1homozygous for the deletion allele of the angiotensin-converting enzyme (ACE) gene are at increased risk for early renal death. To confirm this hypothesis in Japanese subjects, 103 individuals with PKD were genotyped for several components of the RAS, ie, ACEinsertion/deletion (I/D) polymorphism, angiotensinogen (AGT) M235T, and angiotensin II type 1 receptor (AT1) A1166C. Seventy-six of the 103 patients (73.8%) reached ESRD at an average age of 52.1 ± 11.3 years. The frequencies of each genotype of the genes were similar to those expected from Hardy-Weinberg equilibrium. There was a tendency to an excess of patients homozygous for the D allele in patients with ESRD (DD in patients with ESRD, 11.8%; DD in patients without ESRD, 3.7%; chi-square, 1.505; P= 0.22). Cumulative renal survival was significantly less in those with the DD genotype compared with ID/II genotypes. Estimated mean renal survival was 46.4 years (95% confidence interval, 39.5 to 53.3) in subjects with the DD genotype and 57.2 years (95% confidence interval, 54.2 to 60.2) in IDAI genotypes (chi-square, 7.76; P= 0.0053). There was no association between age at onset of ESRD and either M235T or Al 166C polymorphism. These findings suggest that Japanese patients with PKD homozygous for the D allele of the ACEgene are at increased risk for developing ESRD at an early age.

Published
2001
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