研究者詳細 - 川部　勤

論文 - 川部　勤

分割表示 124 件中 101 - 120 件目／全件表示 >>

総説：マウス喘息モデルを用いた疾患感受性遺伝子の検索招待有り査読有り

川部　勤

日本職業・環境アレルギー学会誌 13 巻 ( 2 ) 頁： 1-10 2006年5月

Pulmonary infectious complications associated with anti-TNF alpha therapy (infliximab) for rheumatoid arthritis 査読有り

Imaizumi Kazuyoshi, Sugishita Mihoko, Usui Miho, Kawabe Tsutomu, Hashimoto Naozumi, Hasegawa Yoshinori

INTERNAL MEDICINE 45 巻 ( 10 ) 頁： 685 - 688 2006年

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：Internal Medicine

Two patients with rheumatoid arthritis (RA) that developed serious infectious complications following anti-TNFα therapy (infliximab) are reported. Patient 1 developed tuberculosis with high fever, refractory diarrhea and mediastinal lymphadenopathy. Trans-bronchial needle biopsy was useful to confirm the diagnosis. Patient 2 showed sudden onset of dyspnea with diffuse bilateral lung infiltration caused by pneumocystis jiroveci pneumonia and the diagnosis was confirmed by broncho-alveolar lavage. Physicians should be alerted to infectious complications with atypical presentation and rapid progression in infliximab-treated patients. Invasive diagnostic procedures including fiber-optic bronchoscopy may be necessary early in the course for such cases. © 2006 The Japanese Society of Internal Medicine.

DOI： 10.2169/internalmedicine.45.1623

Web of Science

Scopus

PubMed

T-Helper Type 1/T-Helper Type 2 Balance in Malignant Pleural Effusions Compared to Tuberculous Pleural Effusions 査読有り

Chest 128 巻頁： p4030-4035 2005年12月

Interstitial lung disease associated with gefitinib. 査読有り

Kataoka K, Taniguchi H, Hasegawa Y, Kondoh Y, Kimura T, Nishiyama O, Imaizumi K, Kawabe T, Kume H, Shimokata K,

Respiratory Medicine 100 巻 ( 4 ) 頁： 698-704 2005年4月

Evaluation of interferon-gamma, interferon-gamma-inducing cytokines, and interferon-gamma-inducible chemokines in tuberculous pleural effusions 査読有り

Okamoto M, Kawabe T, Iwasaki Y, Hara T, Hashimoto N, Imaizumi K, Hasegawa Y, Shimokata K

J Lab Clin Med 145 巻 ( 2 ) 頁： 88-93 2005年2月

Krüppel-like factor 6 is frequently down-regulated and induces apoptosis in non-small cell lung cancer cells. 査読有り

Ito G, Uchiyama M, Kondo M, Mori S, Usami N, Maeda O, Kawabe T, Hasegawa Y, Shimokata K, Sekido Y

Cancer research 64 巻 ( 11 ) 頁： 3838 - 43 2004年6月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Cancer Research

Krüppel-like factor 6 (KLF6) is a ubiquitously expressed zinc finger transcriptional factor, which has been suggested to be a candidate tumor suppressor gene in prostate cancer and astrocytic glioma. Because KLF6 is located at chromosome 10p15, where non-small cell lung cancers (NSCLCs) also exhibit frequent allelic loss, we hypothesized that the inactivation of KLF6 is also involved in the development of NSCLC. To determine this, we performed mutational analysis for 105 NSCLCs, including 9 cell lines and 96 primary tumors, and Northern blot analysis for 74 NSCLCs, including the 9 cell lines and 65 primary tumors. Although somatic mutations were not detected in the coding sequence of KLF6, expression of KLF6 mRNA was down-regulated in the 9 cell lines and in 55 (85%) of the 65 primary tumors compared with normal lung tissue. Treatment of two cell lines expressing KLF6 at low levels with 5-azacytidine did not induce KLF6 expression, suggesting that KLF6 down-regulation is not due to promoter hypermethylation. We also performed loss of heterozygosity (LOH) analysis using the laser capture microdissection technique, and found that 21 of 62 (34%) informative samples had LOH in the KLF6 gene locus. Comparing the LOH status with mRNA expression of KLF6, we found that 14 of the 14 (100%) samples with LOH showed KLF6 down-regulation, and that even 23 of 31 (74%) samples without LOH also showed this down-regulation. We also studied the expression of the WAF1 gene, a possible downstream gene of KLF6, and detected simultaneous down-regulation of WAF1 and KLF6 mRNA in 6 of 9 (67%) cell lines and 48 of the 55 (87%) primary tumors, although there was not a significant association between loss of KLF6 and WAF1 expression. Furthermore, colony formation assay of two NSCLC cell lines (NCI-H1299 and NCI-H2009) induced a markedly reduced colony formation by KLF6 transfection, and Annexin V staining and terminal deoxynucleotidyl transferase-mediated nick end labeling assays revealed that KLF6 induced apoptosis. Our present studies demonstrated that KLF6 is frequently down-regulated in NSCLC and suppresses tumor growth via induction of apoptosis in NSCLC, which may suggest that KLF6 is a tumor suppressor for NSCLC.

DOI： 10.1158/0008-5472.CAN-04-0185

Scopus

PubMed

CD40 plays a crucial role in lipopolysaccharide-induced acute lung injury 査読有り

Hashimoto N, Kawabe T, Imaizumi K, Hara T, Okamoto M, Kojima K, Shimokata K, Hasegawa Y

AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY 30 巻 ( 6 ) 頁： 808 - 815 2004年6月

DR1-like element in human topoisomerase II alpha gene involved in enhancement of etoposide-induced apoptosis by PPAR gamma ligand 査読有り

Kanbe E, Abe A, Towatari M, Kawabe T, Saito H, Emi N

EXPERIMENTAL HEMATOLOGY 31 巻 ( 4 ) 頁： 300 - 308 2003年4月

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：Experimental Hematology

Objective. The nuclear peroxisome proliferator-activated receptor γ (PPARγ) ligands may enhance the etoposide-induced apoptosis by modulating the topoisomerase (Topo) IIα expression through binding to direct repeat 1 (DR1)-like element. Methods. To investigate the effect of etoposide-induced apoptosis by PPARγ ligands, leukemia cell lines were treated with troglitazone and 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) in the presence of etoposide and studied about various biological responses. Results. We found the enhancement of etoposide-induced apoptosis by PPARγ ligands in several leukemia cell lines, which was dependent on the expression of PPARγ and specific for TopoIIα inhibitor. We also observed the increased expression of TopoIIα protein by 15d-PGJ2 in Jurkat and HUVEC cells, which might lead to the increased sensitivity to etoposide. Furthermore, we demonstrated that 15d-PGJ2 enhanced the promoter activity of human TopoIIα promoter construct with a DR1-like site by sevenfold when expressed with PPARγ and RXRα. The mutation of DR1-like site decreased the promoter activity, although the direct binding between DR1-like site and PPARγ/RXRα heterodimer was not demonstrated. Conclusions. We conclude that the induction of TopoIIα expression by PPARγ ligands via DR1-like site is an important mechanism for the enhancement of etoposide-induced apoptosis and a DR1-like site in TopoIIα promoter is involved in transcriptional regulation dependent on PPARγ ligands and PPARγ/RXRα heterodimer. © 2003 International Society for Experimental Hematology. Published by Elsevier Science Inc.

DOI： 10.1016/S0301-472X(03)00003-1

Web of Science

Scopus

PubMed

Perfusion and ventilation isotope lung scans in constrictive bronchiolitis obliterans. A series of three cases 査読有り

Hasegawa Y, Imaizumi K, Sekido Y, Iinuma Y, Kawabe T, Hashimoto N, Shimokata K

Respiration 69 巻 ( 6 ) 頁： 550-555 2002年4月

Critical involvement of CD40 in protection against herpes simplex virus infection in a murine model of genital herpes 査読有り

Inagaki-Ohara K, Kawabe T, Hasegawa Y, Hashimoto N, Nishiyama Y.

Arch Virol 147 巻 ( 1 ) 頁： 187-194 2002年4月

Induction of antitumor immunity by transduction of CD40 ligand gene and interferon-γ gene into lung cancer 査読有り

Noguchi M., Imaizumi K., Kawabe T., Wakayama H., Horio Y., Sekido Y., Hara T., Hashimoto N., Takahashi M., Shimokata K., Hasegawa Y.

Cancer Gene Therapy 8 巻 ( 6 ) 頁： 421 - 429 2001年8月

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：Cancer Gene Therapy

CD40-CD40 ligand (CD40L) interaction is an important costimulatory signaling pathway in the crosstalk between T cells and antigen-presenting cells. This receptor-ligand system is known to be essential in eliciting strong cellular immunity. Here we demonstrate that murine lung cancer cells (3LLSA) transduced with the CD40L gene (3LLSA-CD40L) were rejected in syngeneic C57BL/6 mice, but grew in CD40-deficient mice to the same extent as control tumor cells. Immunohistochemical study showed that inflammatory cells, including CD4+, CD8+ T cells and NK cells, infiltrated into the inoculated 3LLSA-CD40L tumor tissue. Inoculation of 3LLSA-CD40L cells into mice resulted in the induction of 3LLSA-specific cytotoxic T-cell immunity, and the growth of parental 3LLSA tumors was inhibited when 3LLSA cells were inoculated into C57BL/6 mice mixed with 3LLSA-CD40L cells or when they were rechallenged 4 weeks after 3LLSA-CD40L cells were rejected. Furthermore, co-inoculation of interferon (IFN)-γ-transduced cells (3LLSA-IFNγ) with 3LLSA-CD40L cells enhanced the antitumor immunity efficiently in vivo. These results indicate that the in vivo priming with CD40L- and IFN-γ gene-transduced lung cancer cells is a promising strategy for inducing antitumor immunity in the treatment of lung cancer.

DOI： 10.1038/sj.cgt.7700320

Scopus

Effect of erythromycin on matrix metalloproteinase-9 and cell migration 査読有り

Hashimoto N, Kawabe T, Hara T, Imaizumi K, Wakayama H, Saito H, Shimokata K, Hasegawa Y.

J Lab Clin Med 137 巻 ( 3 ) 頁： 176-183 2001年4月

Abolition of anti-glomerular basement membrane antibody-mediated glomerulonephritis in FcRγ-deficient mice 査読有り

Wakayama H., Hasegawa Y., Kawabe T., Hara T., Matsuo S., Mizuno M., Takai T., Kikutani H., Shimokata K.

European Journal of Immunology 30 巻 ( 4 ) 頁： 1182 - 1190 2000年5月

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：European Journal of Immunology

Several recent studies have demonstrated the central role of Fc receptors (FcR) rather than the complement system in triggering hypersensitivity reactions. We investigated the role of FcR for IgG (FcγR) using a murine model of accelerated anti-glomerular basement membrane (GBM) antibody-mediated glomerulonephritis as a representative of type II hypersensitivity diseases. Intravenous injection of rabbit anti-GBM antibody after preimmunization with normal rabbit IgG induced proteinuria and azotemia in wild-type C57BL/6 and CD40(+/-) mice but not in FcR γ chain (FcRγ)(-/-) mice or CD40(-/-) mice. Light microscopic findings revealed marked tissue damage in the glomeruli of wild-type C57BL/6 and CD40(+/-) mice. However, no tissue damage except polymorphonuclear cell infiltration was observed in the glomeruli of FcRγ(-/-) mice. The glomeruli of CD40(-/-) mice were almost normal. Immunohistochemistry revealed the binding of rabbit IgG to the GBM in all mice injected with anti-GBM antibody. However, depositions of mouse IgG and complement to the glomeruli were not observed in CD40(-/-) mice, and deposition of fibrin was not observed in FcRγ(-/-) or CD40(-/-) mice. These findings suggest that FcγR may initiate anti-GBM antibody-mediated renal disease. We conclude that FcγR rather than the complement system is critically involved in the development of type II hypersensitivity diseases.

DOI： https://doi.org/10.1002/(SICI)1521-4141(200004)30:4<1182::AID-IMMU1182>3.0.CO;2-H

Scopus

Enhancement of tumoricidal activity of alveolar macrophages via CD40- CD40 ligand interaction 査読有り

Imaizumi K., Kawabe T., Ichiyama S., Kikutani H., Yagita H., Shimokata K., Hasegawa Y.

American Journal of Physiology - Lung Cellular and Molecular Physiology 277 巻 ( 1 21-1 ) 1999年7月

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：American Journal of Physiology - Lung Cellular and Molecular Physiology

CD40-CD40 ligand (CD40L) interaction was originally defined as important molecules for the development of humoral immunity. Thereafter, some investigations have focused on its essential roles for the induction of cell- mediated immunity in host defenses. Here we investigated the antitumor activity of murine alveolar macrophages through CD40-CD40L interaction. The CD40L gene was transfected into murine lung cancer cells (3LLSA), and CD40L- expressing clones (3LLSA-CD40L) were established. Stimulation of CD40 molecules on the surface of alveolar macrophages with 3LLSA-CD40L cells induced the production of nitric oxide, tumor necrosis factor-α, and interleukin-12 and the tumoricidal activity of alveolar macrophages in the presence of interferon-γ, which increased the surface expression of CD40 molecules on alveolar macrophages. These findings were not observed when alveolar macrophages were obtained from CD40-deficient mice. On the other hand, interleukin-6 production by alveolar macrophages did not depend on CD40-CD40L interaction. We also established a murine melanoma cell line expressing CD40L (B16 4A5-CD40L) that could induce tumoricidal activity of alveolar macrophages. Furthermore, when spleen cells were cocultivated with 3LLSA-CD40L cells, specific cytotoxic T lymphocytes for wild-type 3LLSA cells could be induced. These results suggest that CD40L gene transfer into tumor cells may induce antitumor immunity in a tumor-bearing host and may offer a new strategy for cancer gene therapy.

DOI： 10.1152/ajplung.1999.277.1.l49

Scopus

気管内挿管後高度の気管狭窄をきたした1例査読有り

佐藤光夫，川部勤，堀尾芳嗣，長谷川好規，下方薫

気管支学 21 巻 ( 6 ) 頁： 427-428 1999年6月

Effect of Gene Transfer of Tumor Necrosis Factor Receptors into Human Lung Carcinoma Cell Line 査読有り

OHARA Hisao, HASEGAWA Yoshinori, KAWABE Tsutomu, ICHIYAMA Satoshi, HARA Toru, SHIMONO Yohei, SAITO Hidehiko, SHIMOKATA Kaoru

Japanese journal of cancer research : gann 89 巻 ( 5 ) 頁： 589 - 595 1998年5月

Bystander tumoricidal effect and gap junctional communication in lung cancer cell lines 査読有り

Imaizumi K, Hasegawa Y, Kawabe T, Emi N, Saito H, Naruse K, Shimokata K

Am J Respir Cell Mol Biol 18 巻 ( 2 ) 頁： 205-212 1998年4月

IgG-mediated anaphylaxis via Fcγ receptor in CD40-deficient mice 査読有り

Wakayana H, Hasegawa Y, Kawabe T, Saito H, Kikutani H, Shimokata K

Clin Exp Immunol 114 巻 ( 2 ) 頁： 154-160 1998年4月

Effect of gene transfer of tumor necrosis factor receptors into human lung carcinoma cell line 査読有り

Ohara H, Hasegawa Y, Kawabe T, Ichiyama S, Hara T, Shimono Y, Saito H, Shimokata K

Jpn J Cancer Res 89 巻 ( 5 ) 頁： 589-595 1998年4月

Assignment of MARK3 alias KP78 to human chromosome band 14q32.3 by in situ hybridization 査読有り

Ono T.

Cytogenetic and Genome Research 79 巻 ( 1-2 ) 頁： 101 - 102 1997年1月

　前のページ - 次のページ　

<川部 勤>

論文 - 川部 勤

<川部　勤>

論文 - 川部　勤