start-ver=1.4 cd-journal=joma no-vol=409 cd-vols= no-issue=2 article-no= start-page=247 end-page=252 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20110603 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Mechanical stretch increases CCN2/CTGF expression in anterior cruciate ligament-derived cells en-subtitle= kn-subtitle= en-abstract= kn-abstract=Anterior cruciate ligament (ACL)-to-bone interface serves to minimize the stress concentrations that would arise between two different tissues. Mechanical stretch plays an important role in maintaining cell-specific features by inducing CCN family 2/connective tissue growth factor (CCN2/CTGF). We previously reported that cyclic tensile strain (CTS) stimulates alpha 1(I) collagen (COL1A1) expression in human ACL-derived cells. However, the biological function and stress-related response of CCN2/CTGF were still unclear in ACL fibroblasts. In the present study, CCN2/CTGF was observed in ACL-to-bone interface, but was not in the midsubstance region by immunohistochemical analyses. CTS treatments induced higher increase of CCN2/CTGF expression and secretion in interface cells compared with midsubstance cells. COL1A1 expression was not influenced by CCN2/CTGF treatment in interface cells despite CCN2/CTGF stimulated COL1A1 expression in midsubstance cells. However, CCN2/CTGF stimulated the proliferation of interface cells. Our results suggest that distinct biological function of stretch-induced CCN2/CTGF might regulate region-specific phenotypes of ACL-derived cells. en-copyright= kn-copyright= en-aut-name=MiyakeYoshiaki en-aut-sei=Miyake en-aut-mei=Yoshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=FurumatsuTakayuki en-aut-sei=Furumatsu en-aut-mei=Takayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KubotaSatoshi en-aut-sei=Kubota en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KawataKazumi en-aut-sei=Kawata en-aut-mei=Kazumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=OzakiToshifumi en-aut-sei=Ozaki en-aut-mei=Toshifumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TakigawaMasaharu en-aut-sei=Takigawa en-aut-mei=Masaharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences en-keyword=CCN2/CTGF kn-keyword=CCN2/CTGF en-keyword=Anterior cruciate ligament kn-keyword=Anterior cruciate ligament en-keyword=Cyclic tensile strain kn-keyword=Cyclic tensile strain en-keyword=Collagen kn-keyword=Collagen en-keyword=Ligament-to-bone interface kn-keyword=Ligament-to-bone interface END start-ver=1.4 cd-journal=joma no-vol=409 cd-vols= no-issue=4 article-no= start-page=663 end-page=668 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20110617 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Plural assay systems derived from different cell lines and hepatitis C virus strains are required for the objective evaluation of anti-hepatitis C virus reagents en-subtitle= kn-subtitle= en-abstract= kn-abstract=Persistent hepatitis C virus (HCV) infection causes chronic liver diseases and is a global health problem. HuH-7 hepatoma-derived cells are widely used as the only cell-based HCV replication system for HCV research, including drug assays. Recently, using different hepatoma Li23-derived cells, we developed an HCV drug assay system (ORL8), in which the genome-length HCV RNA (O strain of genotype 1b) encoding renilla luciferase replicates efficiently. In this study, using the HuH-7-derived OR6 assay system that we developed previously and the ORL8 assay system, we evaluated 26 anti-HCV reagents, which other groups had reported as anti-HCV candidates using HuH-7-derived assay systems other than ORB. The results revealed that more than half of the reagents showed different anti-HCV activities from those in the previous studies, and that anti-HCV activities evaluated by the ORB and ORL8 assays were also frequently different. In further evaluation using the HuH-7-derived AH1R assay system, which was developed using the AH1 strain of genotype 1b, several reagents showed different anti-HCV activities in comparison with those evaluated by the OR6 and ORL8 assays. These results suggest that the different activities of anti-HCV reagents are caused by the differences in cell lines or HCV strains used for the development of assay systems. Therefore, we conclude that plural HCV assay systems developed using different cell lines or HCV strains are required for the objective evaluation of anti-HCV reagents. en-copyright= kn-copyright= en-aut-name=UedaYouki en-aut-sei=Ueda en-aut-mei=Youki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MoriKyoko en-aut-sei=Mori en-aut-mei=Kyoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AriumiYasuo en-aut-sei=Ariumi en-aut-mei=Yasuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences en-keyword=HCV kn-keyword=HCV en-keyword=HCV RNA replication system kn-keyword=HCV RNA replication system en-keyword=Li23 cells kn-keyword=Li23 cells en-keyword=Reporter assay for anti-HCV reagents kn-keyword=Reporter assay for anti-HCV reagents END start-ver=1.4 cd-journal=joma no-vol=402 cd-vols= no-issue=2 article-no= start-page=329 end-page=334 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=20101112 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Combined use of bFGF and GDF-5 enhances the healing of medial collateral ligament injury en-subtitle= kn-subtitle= en-abstract= kn-abstract=Basic fibroblast growth factor (bFGF) and growth and differentiation factor (GDF)-5 stimulate the healing of medial collateral ligament (MCL) injury. However, the effect of isolated and combined use of bFGF/GDF-5 remains still unclear. We investigated cellular proliferation and migration responding to bFGF/GDF-5 using rabbit MCL fibroblasts. Rabbit MCL injury was treated by bFGF and/or GDF-5 with peptide hydrogels. Gene expression and deposition of collagens in healing tissues were evaluated. bFGF/GDF-5 treatment additively enhanced cell proliferation and migration. bFGF/GDF-5 hydrogels stimulated Col1a1 expression without increasing Col3a1 expression. Combined use of bFGF/GDF-5 stimulated type I collagen deposition and the reorganization of fiber alignment, and induced better morphology of fibroblasts in healing MCLs. Our study indicates that combined use of bFGF/GDF-5 might enhance MCL healing by increasing proliferation and migration of MCL fibroblasts, and by regulating collagen synthesis and connective fiber alignment. en-copyright= kn-copyright= en-aut-name=SaigaKenta en-aut-sei=Saiga en-aut-mei=Kenta kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=FurumatsuTakayuki en-aut-sei=Furumatsu en-aut-mei=Takayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YoshidaAki en-aut-sei=Yoshida en-aut-mei=Aki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MasudaShin en-aut-sei=Masuda en-aut-mei=Shin kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakihiraShota en-aut-sei=Takihira en-aut-mei=Shota kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=AbeNobuhiro en-aut-sei=Abe en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OzakiToshifumi en-aut-sei=Ozaki en-aut-mei=Toshifumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Intelligent Orthopaedic System Development, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences en-keyword=Medial collateral ligament kn-keyword=Medial collateral ligament en-keyword=bFGF kn-keyword=bFGF en-keyword=GDF-5 kn-keyword=GDF-5 en-keyword=Hydrogel scaffold kn-keyword=Hydrogel scaffold en-keyword=Ligament healing kn-keyword=Ligament healing END start-ver=1.4 cd-journal=joma no-vol=391 cd-vols= no-issue=1 article-no= start-page=1142 end-page=1147 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=20100101 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Anterior cruciate ligament-derived cells have high chondrogenic potential en-subtitle= kn-subtitle= en-abstract= kn-abstract=Anterior cruciate ligament (ACL)-derived cells have a character different from medial collateral ligament (MCL)-derived cells. However, the critical difference between ACL and MCL is still unclear in their healing potential and cellular response. The objective of this study was to investigate the mesenchymal differentiation property of each ligament-derived cell. Both ligament-derived cells differentiated into adipogenic, osteogenic, and chondrogenic lineages. In chondrogenesis, ACL-derived cells had the higher chondrogenic property than MCL-derived cells. The chondrogenic marker genes, Sox9 and α1(II) collagen (Col2a1), were induced faster in ACL-derived pellets than in MCL-derived pellets. Sox9 expression preceded the increase of Col2a1 in both pellet-cultured cells. However, the expression level of Sox9 and a ligament/tendon transcription factor Scleraxis did not parallel the increase of Col2a1 expression along with chondrogenic induction. The present study demonstrates that the balance between Sox9 and Scleraxis have an important role in the chondrogenic differentiation of ligament-derived cells. en-copyright= kn-copyright= en-aut-name=FurumatsuTakayuki en-aut-sei=Furumatsu en-aut-mei=Takayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HachiojiMotomi en-aut-sei=Hachioji en-aut-mei=Motomi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=SaigaKenta en-aut-sei=Saiga en-aut-mei=Kenta kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TakataNaoki en-aut-sei=Takata en-aut-mei=Naoki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YokoyamaYusuke en-aut-sei=Yokoyama en-aut-mei=Yusuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OzakiToshifumi en-aut-sei=Ozaki en-aut-mei=Toshifumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences en-keyword=Anterior cruciate ligament kn-keyword=Anterior cruciate ligament en-keyword=Medial collateral ligament kn-keyword=Medial collateral ligament en-keyword=Chondrogenesis kn-keyword=Chondrogenesis en-keyword=Sox9 kn-keyword=Sox9 en-keyword=Scleraxis kn-keyword=Scleraxis en-keyword=Differentiation kn-keyword=Differentiation END start-ver=1.4 cd-journal=joma no-vol=411 cd-vols= no-issue=3 article-no= start-page=555 end-page=561 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20110805 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Ubiquitin chains in the Dsk2 UBL domain mediate Dsk2 stability and protein degradation in yeast en-subtitle= kn-subtitle= en-abstract= kn-abstract=Ubiquitin-like (UBL)-ubiquitin-associated (UBA) proteins, including Dsk2 and Rad23, act as delivery factors that target polyubiquitinated substrates to the proteasome. We report here that the Dsk2 UBL domain is ubiquitinated in yeast cells and that Dsk2 ubiquitination of the UBL domain is involved in Dsk2 stability, depending on the Dsk2 UBA domain. Also, Dsk2 lacking ubiquitin chains impaired ubiquitin-dependent protein degradation and decreased the interaction of Dsk2 with polyubiquitinated proteins in cells. Moreover, Dsk2 ubiquitination affected ability to restore the temperature-sensitive growth defect of dsk2 Delta. These results indicate that ubiquitination in the UBL domain of Dsk2 has in vivo functions in the ubiquitin-proteasome pathway in yeast. en-copyright= kn-copyright= en-aut-name=SekiguchiTakeshi en-aut-sei=Sekiguchi en-aut-mei=Takeshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SasakiToru en-aut-sei=Sasaki en-aut-mei=Toru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=FunakoshiMinoru en-aut-sei=Funakoshi en-aut-mei=Minoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IshiiTakashi en-aut-sei=Ishii en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SaitohYoh-hei en-aut-sei=Saitoh en-aut-mei=Yoh-hei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KanekoShu-ichi en-aut-sei=Kaneko en-aut-mei=Shu-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KobayashiHideki en-aut-sei=Kobayashi en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Department of Molecular Biology, Graduate School of Medical Sciences, Kyushu University affil-num=2 en-affil= kn-affil=Center for Faculty Development, Okayama University affil-num=3 en-affil= kn-affil=Center for Faculty Development, Okayama University affil-num=4 en-affil= kn-affil=Department of Molecular Biology, Graduate School of Medical Sciences, Kyushu University affil-num=5 en-affil= kn-affil=Department of Molecular Biology, Graduate School of Medical Sciences, Kyushu University affil-num=6 en-affil= kn-affil=Department of Molecular Biology, Graduate School of Medical Sciences, Kyushu University affil-num=7 en-affil= kn-affil=Center for Faculty Development, Okayama University en-keyword=UBL–UBA protein kn-keyword=UBL–UBA protein en-keyword=Dsk2 kn-keyword=Dsk2 en-keyword=UBL domain kn-keyword=UBL domain en-keyword=UBA domain kn-keyword=UBA domain en-keyword=Ubiquitin kn-keyword=Ubiquitin en-keyword=Proteasome kn-keyword=Proteasome END start-ver=1.4 cd-journal=joma no-vol=412 cd-vols= no-issue=2 article-no= start-page=391 end-page=395 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20110826 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Tumor suppressor REIC/Dkk-3 interacts with the dynein light chain, Tctex-1 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Persistent hepatitis C virus (HCV) infection causes chronic liver diseases and is a global health problem. HuH-7 hepatoma-derived cells are widely used as the only cell-based HCV replication system for HCV research, including drug assays. Recently, using different hepatoma Li23-derived cells, we developed an HCV drug assay system (ORL8), in which the genome-length HCV RNA (O strain of genotype 1b) encoding renilla luciferase replicates efficiently. In this study, using the HuH-7-derived OR6 assay system that we developed previously and the ORL8 assay system, we evaluated 26 anti-HCV reagents, which other groups had reported as anti-HCV candidates using HuH-7-derived assay systems other than ORB. The results revealed that more than half of the reagents showed different anti-HCV activities from those in the previous studies, and that anti-HCV activities evaluated by the ORB and ORL8 assays were also frequently different. In further evaluation using the HuH-7-derived AH1R assay system, which was developed using the AH1 strain of genotype 1b, several reagents showed different anti-HCV activities in comparison with those evaluated by the OR6 and ORL8 assays. These results suggest that the different activities of anti-HCV reagents are caused by the differences in cell lines or HCV strains used for the development of assay systems. Therefore, we conclude that plural HCV assay systems developed using different cell lines or HCV strains are required for the objective evaluation of anti-HCV reagents. en-copyright= kn-copyright= en-aut-name=OchiaiKazuhiko en-aut-sei=Ochiai en-aut-mei=Kazuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=WatanabeMasami en-aut-sei=Watanabe en-aut-mei=Masami kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=UekiHideo en-aut-sei=Ueki en-aut-mei=Hideo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HuangPeng en-aut-sei=Huang en-aut-mei=Peng kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=FujiiYasuyuki en-aut-sei=Fujii en-aut-mei=Yasuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=NasuYasutomo en-aut-sei=Nasu en-aut-mei=Yasutomo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=NoguchiHirofumi en-aut-sei=Noguchi en-aut-mei=Hirofumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=HirataTakeshi en-aut-sei=Hirata en-aut-mei=Takeshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=SakaguchiMasakiyo en-aut-sei=Sakaguchi en-aut-mei=Masakiyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=HuhNam-ho en-aut-sei=Huh en-aut-mei=Nam-ho kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=KashiwakuraYuji en-aut-sei=Kashiwakura en-aut-mei=Yuji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=KakuHaruki en-aut-sei=Kaku en-aut-mei=Haruki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=KumonHiromi en-aut-sei=Kumon en-aut-mei=Hiromi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= affil-num=1 en-affil= kn-affil=Innovation Center Okayama for Nanobio-Targeted Therapy, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=2 en-affil= kn-affil=Innovation Center Okayama for Nanobio-Targeted Therapy, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=3 en-affil= kn-affil=Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=4 en-affil= kn-affil=Innovation Center Okayama for Nanobio-Targeted Therapy, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=5 en-affil= kn-affil=Innovation Center Okayama for Nanobio-Targeted Therapy, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=6 en-affil= kn-affil=Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=7 en-affil= kn-affil=Department of Gastroenterological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=8 en-affil= kn-affil=Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=9 en-affil= kn-affil=Department of Cell Biology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=10 en-affil= kn-affil=Department of Cell Biology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=11 en-affil= kn-affil= affil-num=12 en-affil= kn-affil= affil-num=13 en-affil= kn-affil= en-keyword=REIC kn-keyword=REIC en-keyword=Dkk-3 kn-keyword=Dkk-3 en-keyword=Tctex-1 kn-keyword=Tctex-1 en-keyword=Dynein kn-keyword=Dynein en-keyword=Endoplasmic reticulum kn-keyword=Endoplasmic reticulum en-keyword=Two-hybrid screening kn-keyword=Two-hybrid screening END start-ver=1.4 cd-journal=joma no-vol=356 cd-vols= no-issue=2 article-no= start-page=598 end-page=607 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20110815 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Defective proventriculus specifies the ocellar region in the Drosophila head en-subtitle= kn-subtitle= en-abstract= kn-abstract=A pair of the Drosophila eye-antennal disc gives rise to four distinct organs (eyes, antennae, maxillary palps, and ocelli) and surrounding head cuticle. Developmental processes of this imaginal disc provide an excellent model system to study the mechanism of regional specification and subsequent organogenesis. The dorsal head capsule (vertex) of adult Drosophila is divided into three morphologically distinct subdomains: ocellar, frons, and orbital. The homeobox gene orthodenticle (otd) is required for head vertex development, and mutations that reduce or abolish ad expression in the vertex primordium lead to ocelliless flies. The homeodomain-containing transcriptional repressor Engrailed (En) is also involved in ocellar specification, and the En expression is completely lost in otd mutants. However, the molecular mechanism of ocellar specification remains elusive. Here, we provide evidence that the homeobox gene defective proventriculus (dye) is a downstream effector of Otd, and also that the repressor activity of Dye is required for en activation through a relief-of-repression mechanism. Furthermore, the Dye activity is involved in repression of the frons identity in an incoherent feedforward loop of Otd and Dye. en-copyright= kn-copyright= en-aut-name=YorimitsuTakeshi en-aut-sei=Yorimitsu en-aut-mei=Takeshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KiritooshiNaruto en-aut-sei=Kiritooshi en-aut-mei=Naruto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NakagoshiHideki en-aut-sei=Nakagoshi en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Graduate School of Natural Science and Technology, Okayama University affil-num=2 en-affil= kn-affil=Graduate School of Natural Science and Technology, Okayama University affil-num=3 en-affil= kn-affil=Graduate School of Natural Science and Technology, Okayama University en-keyword=Drosophila kn-keyword=Drosophila en-keyword=Eye kn-keyword=Eye en-keyword=Orthodenticle kn-keyword=Orthodenticle en-keyword=Hedgehog kn-keyword=Hedgehog en-keyword=Engrailed kn-keyword=Engrailed en-keyword=Iroquois kn-keyword=Iroquois END start-ver=1.4 cd-journal=joma no-vol=40 cd-vols= no-issue=4 article-no= start-page=514 end-page=535 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=200805 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Mixed expansion formula for the rectangular Schur functions and the affine Lie algebra A(1)((1)) en-subtitle= kn-subtitle= en-abstract= kn-abstract=Formulas are obtained that express the Schur S-functions indexed by Young diagrams of rectangular shape as linear combinations of "mixed" products of Schur's S- and Q-functions. The proof is achieved by using representations of the affine Lie algebra of type A(1)((1)). A realization of the basic representation that is of "D-2((2))"-type plays the central role. en-copyright= kn-copyright= en-aut-name=IkedaTakeshi en-aut-sei=Ikeda en-aut-mei=Takeshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MizukawaHiroshi en-aut-sei=Mizukawa en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NakajimaTatsuhiro en-aut-sei=Nakajima en-aut-mei=Tatsuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YamadaHiro-Fumi en-aut-sei=Yamada en-aut-mei=Hiro-Fumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Department of Applied Mathematics, Okayama University of Science affil-num=2 en-affil= kn-affil=Department of Mathematics, National Defense Academy affil-num=3 en-affil= kn-affil=Faculty of Economics, Meikai University, affil-num=4 en-affil= kn-affil=Department of Mathematics, Okayama University en-keyword=Schur function kn-keyword=Schur function en-keyword=Schur's Q-function kn-keyword=Schur's Q-function en-keyword=Boson-fermion correspondence kn-keyword=Boson-fermion correspondence END start-ver=1.4 cd-journal=joma no-vol=423 cd-vols= no-issue=4 article-no= start-page=744 end-page=749 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=20120713 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Oral administration of FAK inhibitor TAE226 inhibits the progression of peritoneal dissemination of colorectal cancer en-subtitle= kn-subtitle= en-abstract= kn-abstract=Peritoneal dissemination is one of the most terrible types of colorectal cancer progression. Focal adhesion kinase (FAK) plays a crucial role in the biological processes of cancer, such as cell attachment, migration, proliferation and survival, all of which are essential for the progression of peritoneal dissemination. Since we and other groups have reported that the inhibition of FAK activity exhibited a potent anticancer effect in several cancer models, we hypothesized that TAE226, a novel ATP-competitive tyrosine kinase inhibitor designed to target FAK, can prevent the occurrence and progression of peritoneal dissemination. In vitro, TAE226 greatly inhibited the proliferation and migration of HCT116 colon cancer cells, while their adhesion on the matrix surface was minimally inhibited when FAK activity and expression was suppressed by TAE226 and siRNA. In vivo, when HCT116 cells were intraperitoneally inoculated in mice, the cells could attach to the peritoneum and begin to grow within 24 h regardless of the pretreatment of cells with TAE226 or FAK-siRNA, suggesting that FAK is not essential, at least for the initial integrin-matrix contact. Interestingly, the treatment of mice before and after inoculation significantly suppressed cell attachment to the peritoneum. Furthermore, oral administration of TAE226 greatly reduced the size of disseminated tumors and prolonged survival in tumor-bearing mice. Taken together, a possible strategy for inhibiting peritoneal dissemination by targeting FAK with TAE226 appears to be applicable through anti-proliferative and anti-invasion/anti-migration mechanisms. en-copyright= kn-copyright= en-aut-name=HaoHui-fang en-aut-sei=Hao en-aut-mei=Hui-fang kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakaokaMunenori en-aut-sei=Takaoka en-aut-mei=Munenori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=BaoXiao-hong en-aut-sei=Bao en-aut-mei=Xiao-hong kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=WangZhi-gang en-aut-sei=Wang en-aut-mei=Zhi-gang kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TomonoYasuko en-aut-sei=Tomono en-aut-mei=Yasuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SakuramaKazufumi en-aut-sei=Sakurama en-aut-mei=Kazufumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OharaToshiaki en-aut-sei=Ohara en-aut-mei=Toshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=FukazawaTakuya en-aut-sei=Fukazawa en-aut-mei=Takuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=YamatsujiTomoki en-aut-sei=Yamatsuji en-aut-mei=Tomoki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=FujiwaraToshiyoshi en-aut-sei=Fujiwara en-aut-mei=Toshiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=NaomotoYoshio en-aut-sei=Naomoto en-aut-mei=Yoshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Surg Gastroenterol affil-num=2 en-affil= kn-affil=Kawasaki Med Univ, Dept Gen Surg affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Surg Gastroenterol affil-num=4 en-affil= kn-affil=Inner Mongolia Univ, Coll Life Sci, Key Lab Mammal Reprod Biol & Biotechnol, Minist Educ affil-num=5 en-affil= kn-affil=Shigei Med Res Inst, Div Mol & Cell Biol affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Surg Gastroenterol affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Surg Gastroenterol affil-num=8 en-affil= kn-affil=Kawasaki Med Univ, Dept Gen Surg affil-num=9 en-affil= kn-affil=Kawasaki Med Univ, Dept Gen Surg affil-num=10 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Surg Gastroenterol affil-num=11 en-affil= kn-affil=Kawasaki Med Univ, Dept Gen Surg en-keyword=Focal adhesion kinase kn-keyword=Focal adhesion kinase en-keyword=TAE226 kn-keyword=TAE226 en-keyword=Peritoneal dissemination kn-keyword=Peritoneal dissemination en-keyword=Prolonged survival kn-keyword=Prolonged survival en-keyword=Anti-proliferation kn-keyword=Anti-proliferation en-keyword=Colon cancer kn-keyword=Colon cancer END start-ver=1.4 cd-journal=joma no-vol=430 cd-vols= no-issue=2 article-no= start-page=592 end-page=597 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130111 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=PML tumor suppressor protein is required for HCV production en-subtitle= kn-subtitle= en-abstract= kn-abstract=PML tumor suppressor protein, which forms discrete nuclear structures termed PML-nuclear bodies, has been associated with several cellular functions, including cell proliferation, apoptosis and antiviral defense. Recently, it was reported that the HCV core protein colocalizes with PML in PML-NBs and abrogates the PML function through interaction with PML. However, role(s) of PML in HCV life cycle is unknown. To test whether or not PML affects HCV life cycle, we examined the level of secreted HCV core and the infectivity of HCV in the culture supernatants as well as the level of HCV RNA in HuH-7-derived RSc cells, in which HCV-JFH1 can infect and efficiently replicate, stably expressing short hairpin RNA targeted to PML. In this context, the level of secreted HCV core and the infectivity in the supernatants from PML knockdown cells was remarkably reduced, whereas the level of HCV RNA in the PML knockdown cells was not significantly affected in spite of very effective knockdown of PML. In fact, we showed that PML is unrelated to HCV RNA replication using the subgenomic HCV-JFH1 replicon RNA, JRN/3-5B. Furthermore, the infectivity of HCV-like particle in the culture supernatants was significantly reduced in PML knockdown JRN/3-5B cells expressing core to NS2 coding region of HCV-JFH1 genome using the trans-packaging system. Finally, we also demonstrated that INI1 and DDX5, the PML-related proteins, are involved in HCV production. Taken together, these findings suggest that PML is required for HCV production. en-copyright= kn-copyright= en-aut-name=KurokiMisao en-aut-sei=Kuroki en-aut-mei=Misao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=AriumiYasuo en-aut-sei=Ariumi en-aut-mei=Yasuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HijikataMakoto en-aut-sei=Hijikata en-aut-mei=Makoto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=DansakoHiromichi en-aut-sei=Dansako en-aut-mei=Hiromichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=WakitaTakaji en-aut-sei=Wakita en-aut-mei=Takaji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ShimotohnoKunitada en-aut-sei=Shimotohno en-aut-mei=Kunitada kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci affil-num=2 en-affil= kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci affil-num=3 en-affil= kn-affil=Kyoto Univ, Dept Viral Oncol, Inst Virus Res affil-num=4 en-affil= kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci affil-num=5 en-affil= kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci affil-num=6 en-affil= kn-affil=Natl Inst Infect Dis, Dept Virol 2 affil-num=7 en-affil= kn-affil=Natl Ctr Global Hlth & Med, Res Ctr Hepatitis & Immunol affil-num=8 en-affil= kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci en-keyword=Hepatitis C virus kn-keyword=Hepatitis C virus en-keyword=PML kn-keyword=PML en-keyword=INI1 kn-keyword=INI1 en-keyword=DDX5 kn-keyword=DDX5 en-keyword=Tumor suppressor kn-keyword=Tumor suppressor en-keyword=Lipid droplet kn-keyword=Lipid droplet END start-ver=1.4 cd-journal=joma no-vol=231 cd-vols= no-issue= article-no= start-page=117754 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=202105 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Different activation signatures in the primary sensorimotor and higher-level regions for haptic three-dimensional curved surface exploration en-subtitle= kn-subtitle= en-abstract= kn-abstract=Haptic object perception begins with continuous exploratory contact, and the human brain needs to accumulate sensory information continuously over time. However, it is still unclear how the primary sensorimotor cortex (PSC) interacts with these higher-level regions during haptic exploration over time. This functional magnetic resonance imaging (fMRI) study investigates time-dependent haptic object processing by examining brain activity during haptic 3D curve and roughness estimations. For this experiment, we designed sixteen haptic stimuli (4 kinds of curves x 4 varieties of roughness) for the haptic curve and roughness estimation tasks. Twenty participants were asked to move their right index and middle fingers along the surface twice and to estimate one of the two features -roughness or curvature -depending on the task instruction. We found that the brain activity in several higher-level regions (e.g., the bilateral posterior parietal cortex) linearly increased as the number of curves increased during the haptic exploration phase. Surprisingly, we found that the contralateral PSC was parametrically modulated by the number of curves only during the late exploration phase but not during the early exploration phase. In contrast, we found no similar parametric modulation activity patterns during the haptic roughness estimation task in either the contralateral PSC or in higher-level regions. Thus, our findings suggest that haptic 3D object perception is processed across the cortical hierarchy, whereas the contralateral PSC interacts with other higher-level regions across time in a manner that is dependent upon the features of the object. en-copyright= kn-copyright= en-aut-name=YangJiajia en-aut-sei=Yang en-aut-mei=Jiajia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MolfesePeter J. en-aut-sei=Molfese en-aut-mei=Peter J. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YuYinghua en-aut-sei=Yu en-aut-mei=Yinghua kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HandwerkerDaniel A. en-aut-sei=Handwerker en-aut-mei=Daniel A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=ChenGang en-aut-sei=Chen en-aut-mei=Gang kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TaylorPaul A. en-aut-sei=Taylor en-aut-mei=Paul A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=EjimaYoshimichi en-aut-sei=Ejima en-aut-mei=Yoshimichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=WuJinglong en-aut-sei=Wu en-aut-mei=Jinglong kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=BandettiniPeter A. en-aut-sei=Bandettini en-aut-mei=Peter A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University kn-affil= affil-num=2 en-affil=Section on Functional Imaging Methods, National Institute of Mental Health kn-affil= affil-num=3 en-affil=Section on Functional Imaging Methods, National Institute of Mental Health kn-affil= affil-num=4 en-affil=Section on Functional Imaging Methods, National Institute of Mental Health kn-affil= affil-num=5 en-affil=Scientific and Statistical Computational Core, National Institute of Mental Health kn-affil= affil-num=6 en-affil=Scientific and Statistical Computational Core, National Institute of Mental Health kn-affil= affil-num=7 en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University kn-affil= affil-num=8 en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University kn-affil= affil-num=9 en-affil=Section on Functional Imaging Methods, National Institute of Mental Health kn-affil= en-keyword=Haptic object perception kn-keyword=Haptic object perception en-keyword=Primary somatosensory cortex kn-keyword=Primary somatosensory cortex en-keyword=Primary motor cortex kn-keyword=Primary motor cortex en-keyword=fMRI kn-keyword=fMRI en-keyword=Parametric modulation kn-keyword=Parametric modulation en-keyword=Cortical hierarchy kn-keyword=Cortical hierarchy END start-ver=1.4 cd-journal=joma no-vol=144 cd-vols= no-issue=3 article-no= start-page=272 end-page=282 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201209 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Spred-2 deficiency exacerbates acetaminophen-induced hepatotoxicity in mice en-subtitle= kn-subtitle= en-abstract= kn-abstract=MAPKs are involved in acetaminophen (APAP)-hepatotoxicity, but the regulatory mechanism remains unknown. Here, we explored the role of Spred-2 that negatively regulates Ras/ERK pathway in APAP-hepatotoxicity. Spred-2 knockout (KO) mice demonstrated exacerbated liver injury, an event that was associated with increased numbers of CD4(+) T, CD8(+) T and NK cells in the liver compared to the control. Levels of CXCL9/CXCL10 that attract and activate these cells were increased in Spred-2 KO-liver. Kupffer cells isolated from Spred-2 KO mice after APAP challenge expressed higher levels of CXCL9/CXCL10 than those from the control. Upon stimulation with APAP or IFN gamma, naive Kupffer cells from Spred-2 KO mice expressed higher levels of CXCL9/CXCL10. NK cell-depletion attenuated APAP-hepatotoxicity with lowered hepatic IFN gamma and decreased numbers of not only NK cells but also CD4(+) T and CD8(+) T cells in the liver. These results suggest that Spred-2 negatively regulates APAP-hepatotoxicity under the control of Kupffer cells and NK cells. en-copyright= kn-copyright= en-aut-name=WakabayashiHiroshi en-aut-sei=Wakabayashi en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ItoToshihiro en-aut-sei=Ito en-aut-mei=Toshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=FushimiSoichiro en-aut-sei=Fushimi en-aut-mei=Soichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NakashimaYuki en-aut-sei=Nakashima en-aut-mei=Yuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=ItakuraJyunya en-aut-sei=Itakura en-aut-mei=Jyunya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=LiuQiuying en-aut-sei=Liu en-aut-mei=Qiuying kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=WinMin Min en-aut-sei=Win en-aut-mei=Min Min kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=SunCuiming en-aut-sei=Sun en-aut-mei=Cuiming kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=ChenCao en-aut-sei=Chen en-aut-mei=Cao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=SatoMiwa en-aut-sei=Sato en-aut-mei=Miwa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=MinoMegumi en-aut-sei=Mino en-aut-mei=Megumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=OginoTetsuya en-aut-sei=Ogino en-aut-mei=Tetsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=MakinoHirofumi en-aut-sei=Makino en-aut-mei=Hirofumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=YoshimuraAkihiko en-aut-sei=Yoshimura en-aut-mei=Akihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=MatsukawaAkihiro en-aut-sei=Matsukawa en-aut-mei=Akihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=2 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=3 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=4 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=5 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=6 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=7 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=8 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=9 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=10 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=11 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=12 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=13 en-affil= kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci affil-num=14 en-affil= kn-affil=Keio Univ, Sch Med, Dept Microbiol & Immunol affil-num=15 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci en-keyword=Acetaminophen kn-keyword=Acetaminophen en-keyword=Hepatotoxicity kn-keyword=Hepatotoxicity en-keyword=Liver immunology kn-keyword=Liver immunology en-keyword=Signaling pathway kn-keyword=Signaling pathway en-keyword=Toxicology kn-keyword=Toxicology END start-ver=1.4 cd-journal=joma no-vol=249 cd-vols= no-issue= article-no= start-page=118904 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=20220401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=On co-activation pattern analysis and non-stationarity of resting brain activity en-subtitle= kn-subtitle= en-abstract= kn-abstract=The non-stationarity of resting-state brain activity has received increasing attention in recent years. Functional connectivity (FC) analysis with short sliding windows and coactivation pattern (CAP) analysis are two widely used methods for assessing the dynamic characteristics of brain activity observed with functional magnetic resonance imaging (fMRI). However, the statistical nature of the dynamics captured by these techniques needs to be verified. In this study, we found that the results of CAP analysis were similar for real fMRI data and simulated stationary data with matching covariance structures and spectral contents. We also found that, for both the real and simulated data, CAPs were clustered into spatially heterogeneous modules. Moreover, for each of the modules in the real data, a spatially similar module was found in the simulated data. The present results suggest that care needs to be taken when interpreting observations drawn from CAP analysis as it does not necessarily reflect non-stationarity or a mixture of states in resting brain activity. en-copyright= kn-copyright= en-aut-name=MatsuiTeppei en-aut-sei=Matsui en-aut-mei=Teppei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=Trung QuangPham en-aut-sei=Trung Quang en-aut-mei=Pham kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=JimuraKoji en-aut-sei=Jimura en-aut-mei=Koji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=ChikazoeJunichi en-aut-sei=Chikazoe en-aut-mei=Junichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil=Department of Biology, Okayama University kn-affil= affil-num=2 en-affil=Section of Brain Function Information, Supportive Center for Brain Research, National Institute for Physiological Sciences kn-affil= affil-num=3 en-affil=Keio University kn-affil= affil-num=4 en-affil=Section of Brain Function Information, Supportive Center for Brain Research, National Institute for Physiological Sciences kn-affil= en-keyword=Resting-state fMRI kn-keyword=Resting-state fMRI en-keyword=Co-activation pattern analysis kn-keyword=Co-activation pattern analysis en-keyword=Non-stationarity kn-keyword=Non-stationarity END start-ver=1.4 cd-journal=joma no-vol=248 cd-vols= no-issue= article-no= start-page=118867 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=202203 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Layer-specific activation in human primary somatosensory cortex during tactile temporal prediction error processing en-subtitle= kn-subtitle= en-abstract= kn-abstract=The human brain continuously generates predictions of incoming sensory input and calculates corresponding prediction errors from the perceived inputs to update internal predictions. In human primary somatosensory cortex (area 3b), different cortical layers are involved in receiving the sensory input and generation of error signals. It remains unknown, however, how the layers in the human area 3b contribute to the temporal prediction error processing. To investigate prediction error representation in the area 3b across layers, we acquired layer specific functional magnetic resonance imaging (fMRI) data at 7T from human area 3b during a task of index finger poking with no-delay, short-delay and long-delay touching sequences. We demonstrate that all three tasks increased activity in both superficial and deep layers of area 3b compared to the random sensory input. The fMRI signal was differentially modulated solely in the deep layers rather than the superficial layers of area 3b by the delay time. Compared with the no-delay stimuli, activity was greater in the deep layers of area 3b during the short delay stimuli but lower during the long-delay stimuli. This difference activity features in the superficial and deep layers suggest distinct functional contributions of area 3b layers to tactile temporal prediction error processing. The functional segregation in area 3b across layers may reflect that the excitatory and inhibitory interplay in the sensory cortex contributions to flexible communication between cortical layers or between cortical areas. en-copyright= kn-copyright= en-aut-name=YuYinghua en-aut-sei=Yu en-aut-mei=Yinghua kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HuberLaurentius en-aut-sei=Huber en-aut-mei=Laurentius kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YangJiajia en-aut-sei=Yang en-aut-mei=Jiajia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=FukunagaMasaki en-aut-sei=Fukunaga en-aut-mei=Masaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=ChaiYuhui en-aut-sei=Chai en-aut-mei=Yuhui kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=JangrawDavid C. en-aut-sei=Jangraw en-aut-mei=David C. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ChenGang en-aut-sei=Chen en-aut-mei=Gang kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=HandwerkerDaniel A. en-aut-sei=Handwerker en-aut-mei=Daniel A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MolfesePeter J. en-aut-sei=Molfese en-aut-mei=Peter J. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=EjimaYoshimichi en-aut-sei=Ejima en-aut-mei=Yoshimichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=SadatoNorihiro en-aut-sei=Sadato en-aut-mei=Norihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=WuJinglong en-aut-sei=Wu en-aut-mei=Jinglong kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=BandettiniPeter A. en-aut-sei=Bandettini en-aut-mei=Peter A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= affil-num=1 en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University kn-affil= affil-num=2 en-affil=MR-Methods Group, MBIC, Cognitive Neuroscience Department, Faculty of Psychology and Neuroscience, University of Maastricht, Cognitive Neuroscience kn-affil= affil-num=3 en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University kn-affil= affil-num=4 en-affil=Division of Cerebral Research, National Institute for Physiological Sciences kn-affil= affil-num=5 en-affil=Section on Functional Imaging Methods, National Institute of Mental Health kn-affil= affil-num=6 en-affil=Section on Functional Imaging Methods, National Institute of Mental Health kn-affil= affil-num=7 en-affil=Scientific and Statistical Computational Core, National Institute of Mental Health kn-affil= affil-num=8 en-affil=Section on Functional Imaging Methods, National Institute of Mental Health kn-affil= affil-num=9 en-affil=Section on Functional Imaging Methods, National Institute of Mental Health kn-affil= affil-num=10 en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University kn-affil= affil-num=11 en-affil=Division of Cerebral Research, National Institute for Physiological Sciences kn-affil= affil-num=12 en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University kn-affil= affil-num=13 en-affil=Section on Functional Imaging Methods, National Institute of Mental Health kn-affil= en-keyword=Layer-specific fMRI kn-keyword=Layer-specific fMRI en-keyword=Tactile prediction kn-keyword=Tactile prediction en-keyword=Primary somatosensory cortex kn-keyword=Primary somatosensory cortex en-keyword=Temporal prediction error kn-keyword=Temporal prediction error en-keyword=High-resolution CBV-fMRI kn-keyword=High-resolution CBV-fMRI END start-ver=1.4 cd-journal=joma no-vol=178 cd-vols= no-issue=2 article-no= start-page=700 end-page=707 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201212 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Jejunal interposition reconstruction with a stomach preserving esophagectomy improves postoperative weight loss and reflux symptoms for esophageal cancer patients en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background: Conventional reconstruction after an esophagectomy uses a gastric tube, which commonly causes several postoperative complaints such as gastric acid reflux in long-term survival cases. Intestinal interposition between the remnant esophagus and the stomach is an option to reduce complaints, and in this study, the advantages of jejunal interposition reconstruction with a stomach preserving esophagectomy (SPE) were assessed. Materials and methods: Eleven cases of jejunal interposition with an SPE and 16 cases with gastric tube reconstruction as a control were subject to a comparison of operation time, amount of bleeding, postoperative quality of life, and endoscopic findings. Results: The SPE group had a longer operation time (SPE: 560 +/- 121 min, control 414 +/- 83 min, P = 0.038), whereas there was no significant difference in blood loss. Postoperative weight loss was significantly recovered in the SPE group (SPE versus control = 94.0 +/- 5.4% versus 87.5 +/- 4.7% at 3 mo, P = 0.017; 97.2 +/- 7.5% versus 85.0 +/- 5.2% at 6 mo, P = 0.010), and there was a significant decrease in the occurrence of reflux symptoms such as heartburn, odynophagia, and cough when jejunal interposition with an SPE was done. Furthermore, reflux esophagitis and Barrett's epithelium were found in six out of 12 cases (50%) of the control group by postoperative endoscopy, while no cases in the SPE group had either condition (P < 0.01). Conclusions: This reconstruction method is a promising option to improve postoperative quality of life, mainly due to the long-term elimination of reflux esophagitis, which assists in the recovery of postoperative weight loss. en-copyright= kn-copyright= en-aut-name=YamadaEiji en-aut-sei=Yamada en-aut-mei=Eiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ShirakawaYasuhiro en-aut-sei=Shirakawa en-aut-mei=Yasuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YamatsujiTomoki en-aut-sei=Yamatsuji en-aut-mei=Tomoki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SakumaLeon en-aut-sei=Sakuma en-aut-mei=Leon kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakaokaMunenori en-aut-sei=Takaoka en-aut-mei=Munenori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YamadaTakako en-aut-sei=Yamada en-aut-mei=Takako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=NomaKazuhiro en-aut-sei=Noma en-aut-mei=Kazuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=SakuramaKazufumi en-aut-sei=Sakurama en-aut-mei=Kazufumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=FujiwaraYasuhiro en-aut-sei=Fujiwara en-aut-mei=Yasuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanabeShunsuke en-aut-sei=Tanabe en-aut-mei=Shunsuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=NagasakaTakeshi en-aut-sei=Nagasaka en-aut-mei=Takeshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=FujiwaraToshiyoshi en-aut-sei=Fujiwara en-aut-mei=Toshiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=NaomotoYoshio en-aut-sei=Naomoto en-aut-mei=Yoshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol Surg Transplant & Surg Oncol, Grad Sch Med Dent & Pharmaceut Sci affil-num=2 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol Surg Transplant & Surg Oncol, Grad Sch Med Dent & Pharmaceut Sci affil-num=3 en-affil= kn-affil=Kawasaki Hosp, Kawasaki Med Sch, Dept Gen Surg affil-num=4 en-affil= kn-affil=Kawasaki Univ Med Welf, Dept Universal Design affil-num=5 en-affil= kn-affil=Kawasaki Hosp, Kawasaki Med Sch, Dept Gen Surg affil-num=6 en-affil= kn-affil=Kawasaki Hosp, Kawasaki Med Sch, Dept Gen Surg affil-num=7 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol Surg Transplant & Surg Oncol, Grad Sch Med Dent & Pharmaceut Sci affil-num=8 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol Surg Transplant & Surg Oncol, Grad Sch Med Dent & Pharmaceut Sci affil-num=9 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol Surg Transplant & Surg Oncol, Grad Sch Med Dent & Pharmaceut Sci affil-num=10 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol Surg Transplant & Surg Oncol, Grad Sch Med Dent & Pharmaceut Sci affil-num=11 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol Surg Transplant & Surg Oncol, Grad Sch Med Dent & Pharmaceut Sci affil-num=12 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol Surg Transplant & Surg Oncol, Grad Sch Med Dent & Pharmaceut Sci affil-num=13 en-affil= kn-affil=Kawasaki Hosp, Kawasaki Med Sch, Dept Gen Surg en-keyword=Esophageal cancer kn-keyword=Esophageal cancer en-keyword=Jejunal interposition reconstruction kn-keyword=Jejunal interposition reconstruction en-keyword=Stomach preserving esophagectomy kn-keyword=Stomach preserving esophagectomy en-keyword=Postoperative QOL kn-keyword=Postoperative QOL en-keyword=Reflux esophagitis kn-keyword=Reflux esophagitis END start-ver=1.4 cd-journal=joma no-vol=447 cd-vols= no-issue=1 article-no= start-page=108 end-page=114 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20140425 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Hypoxia-inducible factor 1 alpha regulates branching morphogenesis during kidney development en-subtitle= kn-subtitle= en-abstract= kn-abstract=The kidneys are exposed to hypoxic conditions during development. Hypoxia-inducible factor (HIF), an important mediator of the response to hypoxia, is believed to have an important role in development. However, the relationship between HIF and branching morphogenesis has not been elucidated clearly. In this study, we examined whether HIF regulates kidney development. We harvested kidneys from day 13 rat embryos (E13K5) and cultured the organs under normoxic (20% 02/5% CO2) or hypoxic (5% 02/5% CO2) conditions. We evaluated the kidneys based on morphology and gene expression. El3K5 cultured under hypoxic conditions had significantly more ureteric bud (UB) branching than the E13Ks cultured under normoxic conditions. In addition, the mRNA levels of GDNF and GDNF receptor (GFR-alpha l), increased under hypoxic conditions in E13K5. When we cultured E13Ks( with the HIF-1 alpha inhibitor digoxin or with siRNA targeting HIF-l alpha under hypoxic conditions, we did not observe increased UB branching. In addition, the expression of GDNF and GFR-alpha 1 was inhibited under hypoxic conditions when the kidneys were treated with siRNA targeting HIF-1 alpha. We also elucidated that hypoxia inhibited UB cell apoptosis and promoted the expression of FGF7 mRNA levels in metanephric mesenchymal (MM) cells in vitro. These findings suggest that hypoxic condition has important roles in inducing branching morphogenesis during kidney development. Hypoxia might mediate branching morphogenesis via not only GDNF/Ret but also FGF signaling pathway. en-copyright= kn-copyright= en-aut-name=TsujiKenji en-aut-sei=Tsuji en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KitamuraShinji en-aut-sei=Kitamura en-aut-mei=Shinji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MakinoHirofumi en-aut-sei=Makino en-aut-mei=Hirofumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci affil-num=2 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci en-keyword=HIF-I alpha kn-keyword=HIF-I alpha en-keyword=Kidney development kn-keyword=Kidney development en-keyword=Hypoxia kn-keyword=Hypoxia en-keyword=Ureteric bud branching kn-keyword=Ureteric bud branching END