| 著者 | Sing’ombe Ombiro Geofrey| Sawai, Taku| Noutoshi, Yoshiteru| Nishina, Yuta| Matsui, Hidenori| Yamamoto, Mikihiro| Toyoda, Kazuhiro| Ichinose, Yuki| |
|---|---|
| 抄録 | Plant pathogenic bacteria cause huge yield losses in crops globally. Therefore, finding effective bactericides to these pathogens is an immediate challenge. In this study, we sought compounds that specifically inhibit the growth of Ralstonia solanacearum. As a result, we identified one promising compound, 1-(4-bromophenyl)-6-methoxy-2,3,4,9-tetrahydro-1H-β-carboline, which inhibited the growth of R. solanacearum (Rs1002) from a pilot library of 376 chemicals provided from RIKEN. We further obtained its structural analogues and assessed their ability to inhibit Rs1002 growth. Then we identified five compounds, named ralhibitins A to E, that specifically inhibit growth of Rs1002 at >5 μg/ml final concentration. The most effective compounds, ralhibitins A, C, and E completely inhibited the growth of Rs1002 at 1.25 μg/ml. In addition, ralhibitins A to E inhibited growth of Xanthomonas oryzae pv. oryzae but not the other bacteria tested at a final concentration of 10 μg/ml. Whereas, ralhibitin E, besides inhibiting R. solanacearum and X. oryzae pv. oryzae, completely inhibited the growth of X. campestris pv. campestris and the Gram-positive bacterium Clavibacter michiganensis subsp. michiganensis at 10 μg/ml. Growth inhibition by these compounds was stable at pH 6–9 and after autoclaving. Because Rs1002 grew in the culture medium in which ralhibitins were incubated with the ralhibitin-insensitive bacteria, the unaffected bacteria may be able to inactivate the inhibitory effect of ralhibitins. These results suggest that ralhibitins might be potential lead compounds for the specific control of phytopathogenic bacteria. |
| キーワード | Bactericide Ralhibitins Ralstonia solanacearum Lead compounds |
| 備考 | This is an Accepted Manuscript of an article published by Elsevier This fulltext will be available in June 2019 |
| 発行日 | 2018-10 |
| 出版物タイトル | Microbiological Research |
| 巻 | 215巻 |
| 出版者 | Elsevier |
| 開始ページ | 29 |
| 終了ページ | 35 |
| ISSN | 0944-5013 |
| NCID | AA11017780 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | English |
| OAI-PMH Set | 岡山大学 |
| 著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja |
| 論文のバージョン | author |
| DOI | 10.1016/j.micres.2018.06.005 |
| 関連URL | isVersionOf https://doi.org/10.1016/j.micres.2018.06.005 |
| フルテキストURL | Biochem_Biophy_Res_Comm_201807.pdf |
|---|---|
| 著者 | Fujiwara, Toshifumi| Eguchi, Takanori| Sogawa, Chiharu| Ono, Kisho| Murakami, Jun| Ibaragi, Soichiro| Asaumi, Jun-ichi| Okamoto, Kuniaki| Calderwood, Stuart K.| Kozaki, Ken-ichi| |
| 抄録 | Genetic amplification, overexpression, and increased signaling from the epidermal growth factor receptor (EGFR) are often found in oral squamous cell carcinoma (OSCC) and thus EGFR is frequently targeted molecularly by the therapeutic antibody cetuximab. We assessed effects of cetuximab in control of EGF-driven malignant traits of OSCC cells. EGF stimulation promoted progression level of mesenchymal traits in OSCC cells, which were attenuated by cetuximab but incompletely. We pursued a potential mechanism underlying such incomplete attenuation of OSCC malignant traits. Cetuximab promoted secretion of EGFR-EVs by OSCC cells and failed to inhibit EGF-driven secretion of EGFR-EVs. Cetuximab was also found to be robustly secreted with the EGFR-EVs by the OSCC cells. Thus, EGF promotes the level of mesenchymal traits of OSCC cells and secretion of EGFR-EVs, which involve cetuximab resistance. |
| キーワード | Extracellular vesicles Anti-EGFR antibody therapy Cetuximab Epithelial-to-mesenchymal transition Head and neck squamous cell carcinoma |
| 発行日 | 2018-07-13 |
| 出版物タイトル | Biochemical and Biophysical Research Communications A |
| 出版者 | Elsevier |
| ISSN | 0006291X |
| NCID | AA00564395 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | English |
| OAI-PMH Set | 岡山大学 |
| 著作権者 | http://creativecommons.org/licenses/by-nc-nd/4.0/ |
| 論文のバージョン | publisher |
| DOI | 10.1016/j.bbrc.2018.07.035 |
| 関連URL | isVersionOf https://doi.org/10.1016/j.bbrc.2018.07.035 |
| 著者 | Hashimoto, Mitsuyasu| |
|---|---|
| 抄録 | Using the description of the Frobenius limit of modules over the ring of invariants under an action of a finite group on a polynomial ring over a field of characteristic p>0 developed by Symonds and the author, we give a characterization of the ring of invariants with a positive dual F-signature. Combining this result and Kemper's result on depths of the ring of invariants under an action of a permutation group, we give an example of an F-rational, but non-F-regular ring of invariants under the action of a finite group. |
| キーワード | F-rational F-regular Dual F-signature Frobenius limit |
| 備考 | This is an Accepted Manuscript of an article published by Elsevier This fulltext available in Aug 2019 |
| 発行日 | 2017-08-15 |
| 出版物タイトル | Journal of Algebra |
| 巻 | 484巻 |
| 出版者 | Elsevier |
| 開始ページ | 207 |
| 終了ページ | 223 |
| ISSN | 0021-8693 |
| NCID | AA00692420 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | English |
| OAI-PMH Set | 岡山大学 |
| 著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja |
| 論文のバージョン | author |
| DOI | 10.1016/j.jalgebra.2017.04.017 |
| Web of Sience KeyUT | 000403626100010 |
| 関連URL | https://doi.org/10.1016/j.jalgebra.2017.04.017 |
| フルテキストURL | J_Orthop_Sci_22_4_731.pdf fig.pdf tbl.pdf |
|---|---|
| 著者 | Furumatsu, Takayuki| Fujii, Masataka| Kodama, Yuya| Ozaki, Toshifumi| |
| 抄録 | BACKGROUND: The posterior root ligament of the medial meniscus (MM) has a critical role in regulating the MM movement. An accurate diagnosis of the MM posterior root tear (MMPRT) using magnetic resonance imaging (MRI) is important for preventing sequential osteoarthritis following the MMPRT. However, diagnosis of the MMPRT is relatively difficult even after using several characteristic MRI findings. The aim of this study was to identify a useful meniscal body sign of the MMPRT for improving diagnostic MRI reading. METHODS: Eighty-five patients who underwent surgical treatments for the MMPRT (39 knees) and other types of MM tears (49 knees) were included. The presence of characteristic MRI findings such as cleft sign, ghost sign, radial tear sign, medial extrusion sign, and new meniscal body shape-oriented "giraffe neck sign" was evaluated in 120 MRI examinations. RESULTS: Giraffe neck signs were observed in 81.7% of the MMPRTs and in 3.3% of other MM tears. Cleft, ghost, and radial tear signs were highly positive in the MMPRTs compared with other MM tears. Medial extrusion signs were frequently observed in both groups. Coexistence rates of any 2 MRI signs, except for medial extrusion sign, were 91.7% in the MMPRT group and 5% in other MM tears. CONCLUSIONS: This study demonstrated that a new characteristic MRI finding "giraffe neck sign" was observed in 81.7% of the MMPRT. Our results suggest that the combination of giraffe neck, cleft, ghost, and radial tear signs may be important for an accurate diagnostic MRI reading of the MMPRT. |
| 備考 | This is an Accepted Manuscript of an article published by Elsevier |
| 発行日 | 2017-07 |
| 出版物タイトル | Journal of Orthopaedic Science |
| 巻 | 22巻 |
| 号 | 4号 |
| 出版者 | Elsevier |
| 開始ページ | 731 |
| 終了ページ | 736 |
| ISSN | 0949-2658 |
| NCID | AA11052566 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | English |
| OAI-PMH Set | 岡山大学 |
| 著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja |
| 論文のバージョン | author |
| PubMed ID | 28416188 |
| DOI | 10.1016/j.jos.2017.03.013 |
| Web of Sience KeyUT | 000407394700025 |
| 関連URL | isVersionOf https://doi.org/10.1016/j.jos.2017.03.013 |
| フルテキストURL | J_Orthop_Sci_22_4_715.pdf fig.pdf |
|---|---|
| 著者 | Lu, Zhichao| Furumatsu, Takayuki| Fujii, Masataka| Maehara, Ami| Ozaki, Toshifumi| |
| 抄録 | BACKGROUND: The meniscus plays an important role in controlling the complex biomechanics of the knee. Meniscus injury is common in the knee joint. The perimeniscal capillary plexus supplies the outer meniscus, whereas the inner meniscus is composed of avascular tissue. Angiogenesis factors, such as vascular endothelial growth factor (VEGF), have important roles in promoting vascularization of various tissues. VEGF-mediated neovascularization is beneficial to the healing of injured tissues. However, the distribution and angiogenic role of VEGF remains unclear in the meniscus and injured meniscus. We hypothesized that VEGF could affect meniscus cells and modulate the meniscus healing process. METHODS: Menisci were obtained from total knee arthroplasty patients. Meniscal injury was created ex vivo by a microsurgical blade. VEGF mRNA and protein expression were detected by the polymerase chain reaction and immunohistochemical analyses, respectively. RESULTS: In native meniscal tissue, the expression of VEGF and HIF-1α mRNAs could not be detected. However, VEGF and HIF-1α mRNAs were found in cultured meniscal cells (VEGF: outer > inner; HIF-1α: outer = inner). Injury increased mRNA levels of both VEGF and HIF-1α, with the increase being greatest in the outer area. Immunohistochemical analyses revealed that VEGF protein was detected mainly in the outer region and around injured areas of the meniscus. However, VEGF concentrations were similar between inner and outer menisci-derived media. CONCLUSIONS: This study demonstrated that both the inner and outer regions of the meniscus contained VEGF. HIF-1α expression and VEGF deposition were high in injured meniscal tissue. Our results suggest that injury stimulates the expression of HIF-1α and VEGF that may be preserved in the extracellular matrix as the healing stimulator of damaged meniscus, especially in the outer meniscus. |
| キーワード | vascular endothelial growth factor (VEGF) meniscus meniscal injury hypoxia-inducible factor-1α (HIF-1α) |
| 備考 | This is an Accepted Manuscript of an article published by Elsevier |
| 発行日 | 2017-07 |
| 出版物タイトル | Journal of Orthopaedic Science |
| 巻 | 22巻 |
| 号 | 4号 |
| 出版者 | Elsevier |
| 開始ページ | 715 |
| 終了ページ | 721 |
| ISSN | 0949-2658 |
| NCID | AA11052566 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | English |
| OAI-PMH Set | 岡山大学 |
| 著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja |
| 論文のバージョン | author |
| PubMed ID | 28318650 |
| DOI | 10.1016/j.jos.2017.02.006 |
| Web of Sience KeyUT | 000407394700022 |
| 関連URL | isVersionOf https://doi.org/10.1016/j.jos.2017.02.006 |
| フルテキストURL | BBRC_485_2_261.pdf |
|---|---|
| 著者 | Kawaguchi, Yuka| Nariki, Hiroaki| Kawamoto, Naoko| Kanehiro, Yuichi| Miyazaki, Satoshi| Suzuki, Mari| Magari, Masaki| Tokumitsu, Hiroshi| Kanayama, Naoki| |
| 抄録 | Activation-induced cytidine deaminase (AID) is essential for diversification of the Ig variable region (IgV). AID is excluded from the nucleus, where it normally functions. However, the molecular mechanisms responsible for regulating AID localization remain to be elucidated. The SR-protein splicing factor SRSF1 is a nucleocytoplasmic shuttling protein, a splicing isoform of which called SRSF1-3, has previously been shown to contribute to IgV diversification in chicken DT40 cells. In this study, we examined whether SRSF1-3 functions in IgV diversification by promoting nuclear localization of AID. AID expressed alone was localized predominantly in the cytoplasm. In contrast, co-expression of AID with SRSF1-3 led to the nuclear accumulation of both AID and SRSF1-3 and the formation of a protein complex that contained them both, although SRSF1-3 was dispensable for nuclear import of AID. Expression of either SRSF1-3 or a C-terminally-truncated AID mutant increased IgV diversification in DT40 cells. However, overexpression of exogenous SRSF1-3 was unable to further enhance IgV diversification in DT40 cells expressing the truncated AID mutant, although SRSF1-3 was able to form a protein complex with the AID mutant. These results suggest that SRSF1-3 promotes nuclear localization of AID probably by forming a nuclear protein complex, which might stabilize nuclear AID and induce IgV diversification in an AID C-terminus-dependent manner. |
| キーワード | AID DT40 Gene conversion Ig SRSF1 Somatic hypermutation |
| 発行日 | 2017-04 |
| 出版物タイトル | Biochemical and Biophysical Research Communications |
| 巻 | 485巻 |
| 号 | 2号 |
| 出版者 | Elsevier |
| 開始ページ | 261 |
| 終了ページ | 266 |
| ISSN | 0006-291X |
| NCID | AA00564395 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | English |
| OAI-PMH Set | 岡山大学 |
| 著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja |
| 論文のバージョン | author |
| PubMed ID | 28235482 |
| DOI | 10.1016/j.bbrc.2017.02.097 |
| Web of Sience KeyUT | 000396798300007 |
| 関連URL | isVersionOf https://doi.org/10.1016/j.bbrc.2017.02.097 |
| フルテキストURL | Adv_Math_305_144.pdf |
|---|---|
| 著者 | Hashimoto, Mitsuyasu| Symondsb, Peter| |
| 抄録 | We define the Frobenius limit of a module over a ring of prime characteristic to be the limit of the normalized Frobenius direct images in a certain Grothendieck group. When a finite group acts on a polynomial ring, we calculate this limit for all the modules over the twisted group algebra that are free over the polynomial ring; we also calculate the Frobenius limit for the restriction of these to the ring of invariants. As an application, we generalize the description of the generalized F-signature of a ring of invariants by the second author and Nakajima to the modular case. |
| キーワード | Frobenius direct image Hilbert–Kunz multiplicity F-signature Frobenius limit |
| 備考 | This is an Accepted Manuscript of an article published by Elsevier |
| 発行日 | 2017-01-10 |
| 出版物タイトル | Advances in Mathematics |
| 巻 | 305巻 |
| 出版者 | Elsevier |
| 開始ページ | 144 |
| 終了ページ | 164 |
| ISSN | 0001-8708 |
| NCID | AA00513055 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | English |
| OAI-PMH Set | 岡山大学 |
| 著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja |
| 論文のバージョン | author |
| DOI | 10.1016/j.aim.2016.09.020 |
| Web of Sience KeyUT | 000406169200003 |
| 関連URL | isVersionOf https://doi.org/10.1016/j.aim.2016.09.020 |
| フルテキストURL | BBRC_480_4_564.pdf BBRC_480_4_564_highlights.pdf BBRC_480_4_564_fig.pdf BBRC_480_4_564_suppl_fig.pdf |
|---|---|
| 著者 | Ujihara, Yoshihiro| Mohria, Satoshi| Katanosaka, Yuki| |
| 抄録 | The Na+/Ca2+ exchanger 1 (NCX1) is an essential Ca2+ efflux system in cardiomyocytes. Although NCX1 is distributed throughout the sarcolemma, a subpopulation of NCX1 is localized to transverse (T)-tubules. There is growing evidence that T-tubule disorganization is a causal event that shifts the transition from hypertrophy to heart failure (HF). However, the detailed molecular mechanisms have not been clarified. Previously, we showed that induced NCX1 expression in pressure-overloaded hearts attenuates defective excitation-contraction coupling and HF progression. Here, we examined the effects of induced NCX1 overexpression on the spatial distribution of L-type Ca2+ channels (LTCCs) and junctophilin-2 (JP2), a structural protein that connects the T-tubule and sarcoplasmic reticulum membrane, in pressure-overloaded hearts. Quantitative analysis showed that the regularity of NCX1 localization was significantly decreased at 8 weeks after transverse aortic constriction (TAC)-surgery; however, T-tubule organization and the regularities of LTCC and JP2 immunofluorescent signals were maintained at this time point. These observations demonstrated that release of NCX1 from the T-tubule area occurred before the onset of T-tubule disorganization and LTCC and JP2 mislocalization. Moreover, induced NCX1 overexpression at 8 weeks post-TAC not only recovered NCX1 regularity but also prevented the decrease in LTCC and JP2 regularities at 16 weeks post-TAC. These results suggested that NCX1 may play an important role in the proper spatial distribution of LTCC and JP2 in T-tubules in the context of pressure-overloading. |
| キーワード | Heart failure Junctophilin-2 L-type Ca(2+) channel Na(+)/Ca(2+) exchanger 1 Pressure-overloading Transverse-tubule |
| 備考 | 2017年11月公開予定 |
| 発行日 | 2016-11 |
| 出版物タイトル | Biochemical and Biophysical Research Communications |
| 巻 | 480巻 |
| 号 | 4号 |
| 出版者 | Elsevier |
| 開始ページ | 564 |
| 終了ページ | 569 |
| ISSN | 0006-291X |
| NCID | AA00564395 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | English |
| OAI-PMH Set | 岡山大学 |
| 著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja |
| 論文のバージョン | author |
| PubMed ID | 27789286 |
| DOI | 10.1016/j.bbrc.2016.10.090 |
| Web of Sience KeyUT | 000389015400011 |
| 関連URL | https://doi.org/10.1016/j.bbrc.2016.10.090 |
| フルテキストURL | IFAC_49_8_7.pdf |
|---|---|
| 著者 | Imai, Jun| Noso, Katsuyuki| Takahashi, Akiko| Funabiki, Shigeyuki| |
| 抄録 | For linear distributed parameter systems with a finite number of boundary inputs, we propose a framework to implement the method of weighted residuals using candidate trial functions without boundary homogenization. Proposed scheme utilizes inner product matrix, or Grammian, of the trial functions to separate appropriate homogenized basis functions and the other trial functions matching inhomogeneous boundary conditions. The finite-dimensional approximate model by using the proposed scheme is represented in descriptor form and it is proved to be straightforwardly transformed into state space form. Feasibility of the method is illustrated by a brief controller design example using the approximate model of a heat conduction rod with Dirichlet boundary input. |
| キーワード | Distributed parameter systems Method of weighted residuals Boundary conditions Reduced-order models |
| 備考 | This is an Accepted Manuscript of an article published by Elsevier |
| 発行日 | 2016-08-09 |
| 出版物タイトル | IFAC-Papers OnLine |
| 巻 | 49巻 |
| 号 | 8号 |
| 出版者 | Elsevier |
| 開始ページ | 7 |
| 終了ページ | 12 |
| ISSN | 2405-8963 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | Japanese |
| OAI-PMH Set | 岡山大学 |
| 著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja |
| 論文のバージョン | author |
| DOI | 10.1016/j.ifacol.2016.07.410 |
| Web of Sience KeyUT | 000381505200003 |
| 関連URL | https://doi.org/10.1016/j.ifacol.2016.07.410 |
| フルテキストURL | J_Orthop_Sci_21_4_524.pdf fig.pdf |
|---|---|
| 著者 | Furumatsu, Takayuki| Maehara, Ami| Ozaki, Toshifumi| |
| 抄録 | BACKGROUND: Proper functioning of the meniscus depends on the composition and organization of its fibrocartilaginous extracellular matrix. We previously demonstrated that the avascular inner meniscus has a more chondrocytic phenotype compared with the outer meniscus. Inhibition of the Rho family GTPase ROCK, the major regulator of the actin cytoskeleton, stimulates the chondrogenic transcription factor Sry-type HMG box (SOX) 9-dependent α1(II) collagen (COL2A1) expression in inner meniscus cells. However, the crosstalk between ROCK inhibition, SOX9, and other transcription modulators on COL2A1 upregulation remains unclear in meniscus cells. The aim of this study was to investigate the role of SOX9-related transcriptional complex on COL2A1 expression under the inhibition of ROCK in human meniscus cells. METHODS: Human inner and outer meniscus cells were prepared from macroscopically intact lateral menisci. Cells were cultured in the presence or absence of ROCK inhibitor (ROCKi, Y27632). Gene expression, collagen synthesis, and nuclear translocation of SOX9 and Smad2/3 were analyzed. RESULTS: Treatment of ROCKi increased the ratio of type I/II collagen double positive cells derived from the inner meniscus. In real-time PCR analyses, expression of SOX9 and COL2A1 genes was stimulated by ROCKi treatment in inner meniscus cells. ROCKi treatment also induced nuclear translocation of SOX9 and phosphorylated Smad2/3 in immunohistological analyses. Complex formation between SOX9 and Smad3 was increased by ROCKi treatment in inner meniscus cells. Chromatin immunoprecipitation analyses revealed that association between SOX9/Smad3 transcriptional complex with the COL2A1 enhancer region was increased by ROCKi treatment. CONCLUSIONS: This study demonstrated that ROCK inhibition stimulated SOX9/Smad3-dependent COL2A1 expression through the immediate nuclear translocation of Smad3 in inner meniscus cells. Our results suggest that ROCK inhibition can stimulates type II collagen synthesis through the cooperative activation of Smad3 in inner meniscus cells. ROCKi treatment may be useful to promote the fibrochondrocytic healing of the injured inner meniscus. |
| 備考 | This is an Accepted Manuscript of an article published by Elsevier |
| 発行日 | 2016-07 |
| 出版物タイトル | Journal of Orthopaedic Science |
| 巻 | 21巻 |
| 号 | 4号 |
| 出版者 | Elsevier |
| 開始ページ | 524 |
| 終了ページ | 529 |
| ISSN | 0949-2658 |
| NCID | AA11052566 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | English |
| OAI-PMH Set | 岡山大学 |
| 著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja |
| 論文のバージョン | author |
| PubMed ID | 27113646 |
| DOI | 10.1016/j.jos.2016.02.013 |
| Web of Sience KeyUT | 000381142800020 |
| 関連URL | isVersionOf https://doi.org/10.1016/j.jos.2016.02.013 |
| フルテキストURL | K0005427_other1.pdf |
|---|---|
| 著者 | Okano, Mitsuhiro| Fujiwara, Tazuko| Kariya, Shin| Higaki, Takaya| Makihara, Sei-ichiro| Haruna, Takenori| Noyama, Yasuyuki| Koyama, Takahisa| Omichi, Ryotaro| Orita, Yorihisa| Miki, Kentaro| Kanai, Kengo| Nishizaki, Kazunori| |
| 抄録 | BACKGROUND: Toll-like receptor 3 (TLR3) is expressed in upper airways, however, little is known regarding whether Toll-like receptor 3 (TLR3) signals exert a regulatory effect on the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP), especially on eosinophilic inflammation. We sought to investigate the effect of Poly(IC), the ligand for TLR3, on cytokine production by dispersed nasal polyp cells (DNPCs). METHODS: DNPCs were pretreated with or without Poly(IC), and were then cultured in the presence or absence of staphylococcal enterotoxin B (SEB), following which the levels of IL-5, IL-10, IL-13, IL-17A and interferon (IFN)-γ in the supernatant were measured. To determine the involvement of IL-10 and cyclooxygenase in Poly(IC)-mediated signaling, DNPCs were treated with anti-IL-10 monoclonal antibody and diclofenac, the cyclooxygenase inhibitor, respectively. Poly(IC)-induced prostaglandin E2 (PGE2) production was also determined. RESULTS: Exposure to Poly(IC) induced a significant production of IL-10, but not of IL-5, IL-13, IL-17A or IFN-γ by DNPCs. Pretreatment with Poly(IC) dose-dependently inhibited SEB-induced IL-5, IL-13 and IL-17A, but not IFN-γ production. Neutralization of IL-10 significantly abrogated the inhibitory effect of Poly(IC). Treatment with diclofenac also abrogated the inhibitory effect of Poly(IC) on SEB-induced IL-5 and IL-13 production. However, unlike exposure of diclofenac-treated DNPCs to lipopolysaccharide, the ligand for TLR4, exposure of these cells to Poly(IC) did not enhance IL-5 or IL-13 production. Poly(IC) did not significantly increase PGE2 production by DNPCs. CONCLUSIONS: These results suggest that TLR3 signaling regulates eosinophilia-associated cytokine production in CRSwNP, at least in part, via IL-10 production. |
| キーワード | Chronic rhinosinusitis with nasal polyps IL-10 IL-5 Poly(IC) Toll-like receptor |
| 備考 | 学位審査副論文 |
| 発行日 | 2016-01 |
| 出版物タイトル | Allergology international : official journal of the Japanese Society of Allergology |
| 巻 | 65巻 |
| 号 | 1号 |
| 出版者 | Elsevier |
| 開始ページ | 96 |
| 終了ページ | 102 |
| ISSN | 1323-8930 |
| NCID | AA11091750 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | English |
| OAI-PMH Set | 岡山大学 |
| 著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja |
| 論文のバージョン | publisher |
| PubMed ID | 26666485 |
| Web of Sience KeyUT | 000367238600015 |
| 関連URL | https://doi.org/10.1016/j.alit.2015.08.005 http://ousar.lib.okayama-u.ac.jp/54846 |
| フルテキストURL | K0005273 other2.pdf |
|---|---|
| 著者 | Sakamoto, Shinji| Takaki, Manabu| Okahisa, Yuko| Mizuki, Yutaka| Kodama, Masafumi| Ujike, Hiroshi| Uchitomi, Yosuke| |
| 備考 | 学位審査副論文 |
| 発行日 | 2014-05 |
| 出版物タイトル | Psychiatry Research |
| 巻 | 216巻 |
| 号 | 2号 |
| 出版者 | Elsevier |
| 開始ページ | 288 |
| 終了ページ | 289 |
| ISSN | 0165-1781 |
| NCID | AA0036432X |
| 資料タイプ | 学術雑誌論文 |
| 言語 | English |
| OAI-PMH Set | 岡山大学 |
| 著作権者 | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja |
| 論文のバージョン | author |
| PubMed ID | 24576429 |
| DOI | 10.1016/j.psychres.2014.02.006 |
| Web of Sience KeyUT | 000335099900020 |
| 関連URL | https://doi.org/10.1016/j.psychres.2014.02.006 |
| 著者 | Yoshioka-Nishimura, Miho| Yamamoto, Yasusi| |
|---|---|
| 発行日 | 2014 |
| 出版物タイトル | Journal of Photochemistry and Photobiology B: Biology |
| 巻 | 137巻 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | Nohara, Minoru| Kakiya, Satomi| Kudo, Kazutaka| Oshiro, Yoshihiro| Araki, Shingo| Kobayashi, Tatsuo C.| Oku, Kenta| Nishibori, Eiji| Sawa, Hiroshi| |
|---|---|
| 発行日 | 2012-04 |
| 出版物タイトル | Solid State Communications |
| 巻 | 152巻 |
| 号 | 8号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | Matsuura, Koji| Takenami, Mami| Kuroda, Yuka| Hyakutake, Toru| Yanase, Shinichiro| Naruse, Keiji| |
|---|---|
| 発行日 | 2012-01 |
| 出版物タイトル | Reproductive BioMedicine Online |
| 巻 | 24巻 |
| 号 | 1号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | Wajima, Takeaki| Sabui, Subrata| Fukumoto, Megumi| Kano, Shigeyuki| Ramamurthy, Thandavarayan| Chatterjee, Nabendu Sekhar| Hamabata, Takashi| |
|---|---|
| 発行日 | 2011-10 |
| 出版物タイトル | Microbial Pathogenesis |
| 巻 | 51巻 |
| 号 | 4号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | Khan, Shahbaz Manzoor| Debnath, Chanchal| Pramanik, Amiya Kumar| Xiao, Lihua| Nozaki, Tomoyoshi| Ganguly, Sandipan| |
|---|---|
| 発行日 | 2011-06-10 |
| 出版物タイトル | Veterinary Parasitology |
| 巻 | 178巻 |
| 号 | 3-4号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | Miyoshi, Shin-ichi| Abe, Yuki| Senoh, Mitsutoshi| Mizuno, Tamaki| Maehara, Yoko| Nakao, Hiroshi| |
|---|---|
| 発行日 | 2011-05 |
| 出版物タイトル | Toxicon |
| 巻 | 57巻 |
| 号 | 6号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | Ghosh, Souvik| Gatheru, Zipporah| Nyangao, James| Adachi, Noriaki| Urushibara, Noriko| Kobayashi, Nobumichi| |
|---|---|
| 発行日 | 2011-01 |
| 出版物タイトル | Infection, Genetics and Evolution |
| 巻 | 11巻 |
| 号 | 1号 |
| 資料タイプ | 学術雑誌論文 |
| 著者 | Okazaki, Hiroyuki| Yoshida, Rikiya| Iwai, Keisuke| Noami, Kengo| Muro, Takayuki| Nakamura, Tetsuya| Wakita, Takanori| Muraoka, Yuji| Hirai, Masaaki| Tomioka, Fumiaki| Takano, Yoshihiko| Takenaka, Asami| Toyoda, Masahiro| Oguch, Tamio| Yokoya, Takayoshi| |
|---|---|
| 発行日 | 2010-12 |
| 出版物タイトル | Physica C-Superconductivity and its Applications |
| 巻 | 470巻 |
| 号 | S1号 |
| 資料タイプ | 学術雑誌論文 |