start-ver=1.4 cd-journal=joma no-vol=6 cd-vols= no-issue=4 article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=20040615 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Addition of granulocyte-colony stimulating factor (G-CSF) may further increase chemosensitive state in premenopausal node-positive breast cancer patients with induced angiogenesis after surgery en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=AltundagKadri en-aut-sei=Altundag en-aut-mei=Kadri kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=AltundagOzden en-aut-sei=Altundag en-aut-mei=Ozden kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=GunduzMehmet en-aut-sei=Gunduz en-aut-mei=Mehmet kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Department of Medical Oncology, Hacettepe University Faculty of Medicine affil-num=2 en-affil= kn-affil=Department of Medical Oncology, Hacettepe University Faculty of Medicine affil-num=3 en-affil= kn-affil=Department of Oral Pathology and Medicine, Graduate School of Medicine and Dentistry, Okayama University END start-ver=1.4 cd-journal=joma no-vol=3 cd-vols= no-issue=1 article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20050415 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Comparable response of ccn1 with ccn2 genes upon arthritis: An in vitro evaluation with a human chondrocytic cell line stimulated by a set of cytokines en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Background: The chondrosarcoma-derived HCS-2/8 has been known to be an excellent model of human articular chondrocytes. By mimicking the arthritic conditions through the treatment of HCS-2/8 cells with cytokines, we estimated the gene expression response of ccn1 and ccn2 during the course of joint inflammation in vitro.
Results: In order to mimic the initiation of inflammation, HCS-2/8 cells were treated with tumor necrosis factor (TNF)-ƒ¿. To induce pro-inflammatory or reparative responses, TGF-ƒÀ was employed. Effects of an anti-inflammatory glucocorticoid were also evaluated. After stimulation, expression levels of ccn1 and ccn2 were quantitatively analyzed. Surprisingly, not only ccn2, but also ccn1 expression was repressed upon TNF-ƒ¿ stimulation, whereas both mRNAs were uniformly induced by transforming growth factor (TGF)-ƒÀ and a glucocorticoid.
Conclusion: These results describing the same response during the course of inflammation suggest similar and co-operative roles of these 2 ccn family members in the course of arthritis.

en-copyright= kn-copyright= en-aut-name=MoritaniNorifumi H en-aut-sei=Moritani en-aut-mei=Norifumi H kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 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=2 ORCID= en-aut-name=SugaharaToshio en-aut-sei=Sugahara en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 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=4 ORCID= affil-num=1 en-affil= kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine and Dentistry affil-num=2 en-affil= kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine and Dentistry affil-num=3 en-affil= kn-affil=Department of Oral and Maxillofacial Reconstructive Surgery, Okayama University Graduate School of Medicine and Dentistry affil-num=4 en-affil= kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine and Dentistry END start-ver=1.4 cd-journal=joma no-vol=6 cd-vols= no-issue=4 article-no= start-page=R291 end-page=R299 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=20040426 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Conjugated docosahexaenoic acid suppresses KPL-1 human breast cancer cell growth in vitro and in vivo: potential mechanisms of action en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Introduction The present study was conducted to examine the effect of conjugated docosahexaenoic acid (CDHA) on cell growth, cell cycle progression, mode of cell death, and expression of cell cycle regulatory and/or apoptosis-related proteins in KPL-1 human breast cancer cell line. This effect of CDHA was compared with that of docosahexaenoic acid (DHA).
Methods KPL-1 cell growth was assessed by colorimetric 3- (4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay; cell cycle progression and mode of cell death were examined by flow cytometry; and levels of expression of p53, p21Cip1/Waf1, cyclin D1, Bax, and Bcl-2 proteins were examined by Western blotting analysis. In vivo tumor growth was examined by injecting KPL-1 cells subcutaneously into the area of the right thoracic mammary fat pad of female athymic mice fed a CDHA diet.
Results CDHA inhibited KPL-1 cells more effectively than did DHA (50% inhibitory concentration for 72 hours: 97 ƒÊmol/l and 270 ƒÊmol/l, respectively). With both CDHA and DHA growth inhibition was due to apoptosis, as indicated by the appearance of a sub-G1 fraction. The apoptosis cascade involved downregulation of Bcl-2 protein; Bax expression was unchanged. Cell cycle progression was due to G0/G1 arrest, which involved increased expression of p53 and p21Cip1/Waf1, and decreased expression of cyclin D1. CDHA modulated cell cycle regulatory proteins and apoptosis-related proteins in a manner similar to that of parent DHA. In the athymic mouse system 1.0% dietary CDHA, but not 0.2%, significantly suppressed growth of KPL-1 tumor cells; CDHA tended to decrease regional lymph node metastasis in a dose dependent manner.
Conclusion CDHA inhibited growth of KPL-1 human breast cancer cells in vitro more effectively than did DHA. The mechanisms of action involved modulation of apoptosis cascade and cell cycle progression. Dietary CDHA at 1.0% suppressed KPL-1 cell growth in the athymic mouse system.

en-copyright= kn-copyright= en-aut-name=Tsujita-KyutokuMiki en-aut-sei=Tsujita-Kyutoku en-aut-mei=Miki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=YuriTakashi en-aut-sei=Yuri en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=DanbaraNaoyuki en-aut-sei=Danbara en-aut-mei=Naoyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SenzakiHideto en-aut-sei=Senzaki en-aut-mei=Hideto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KiyozukaYasuhiko en-aut-sei=Kiyozuka en-aut-mei=Yasuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=UeharaNorihisa en-aut-sei=Uehara en-aut-mei=Norihisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TakadaHideho en-aut-sei=Takada en-aut-mei=Hideho kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=HadaTakahiko en-aut-sei=Hada en-aut-mei=Takahiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MiyazawaTeruo en-aut-sei=Miyazawa en-aut-mei=Teruo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=OgawaYutaka en-aut-sei=Ogawa en-aut-mei=Yutaka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=TsuburaAiro en-aut-sei=Tsubura en-aut-mei=Airo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Department of Pathology II, Kansai Medical University affil-num=2 en-affil= kn-affil=Department of Pathology II, Kansai Medical University affil-num=3 en-affil= kn-affil=Department of Pathology II, Kansai Medical University affil-num=4 en-affil= kn-affil=Department of Pathology II, Kansai Medical University affil-num=5 en-affil= kn-affil=Department of Pathology II, Kansai Medical University affil-num=6 en-affil= kn-affil=Department of Pathology II, Kansai Medical University affil-num=7 en-affil= kn-affil=Division of Surgery, Kansai Medical University Kori Hospital affil-num=8 en-affil= kn-affil=R&D Division, Bizen Chemical Co., Ltd affil-num=9 en-affil= kn-affil=Laboratory of Biodynamic Chemistry, Tohoku University Graduate School of Life Science and Agriculture affil-num=10 en-affil= kn-affil=Department of Plastic and Reconstructive Surgery, Kansai Medical University affil-num=11 en-affil= kn-affil=Department of Pathology II, Kansai Medical University en-keyword=apoptosis kn-keyword=apoptosis en-keyword=breast cancer kn-keyword=breast cancer en-keyword=conjugated docosahexaenoic acid kn-keyword=conjugated docosahexaenoic acid en-keyword=docosahexaenoic acid kn-keyword=docosahexaenoic acid en-keyword=human kn-keyword=human END start-ver=1.4 cd-journal=joma no-vol=8 cd-vols= no-issue= article-no= start-page=81 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130515 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=De novo CD5-positive diffuse large B-cell lymphomas show high specificity for cyclin D2 expression en-subtitle= kn-subtitle= en-abstract= kn-abstract=@D cyclins positively regulate the cell cycle and mediate the pathogenesis of some lymphomas. Cyclin D1 overexpression is the hallmark of mantle cell lymphoma, whereas cyclins D2 and D3 are reportedly not as specific to certain lymphomas as cyclin D1. In this study, cyclin D2 was found to be overexpressed in 98% of de novo CD5-positive diffuse large B-cell lymphomas (DLBCLs) (50/51) and in 28% of CD5-negative DLBCLs (14/51). A statistically significant difference was observed between these two groups (p<0.0001). In contrast, no statistical difference was found in the cyclin D3 expression between CD5-positive (18/51) and CD5-negative (24/51) DLBCLs (p=0.23). Based on these findings, cyclin D2 is therefore considered to be closely associated with de novo CD5-positive DLBCLs. This insight may be useful for overcoming the inferior survival of this aggressive lymphoma. en-copyright= kn-copyright= en-aut-name=IgawaTakuro en-aut-sei=Igawa en-aut-mei=Takuro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SatoYasuharu en-aut-sei=Sato en-aut-mei=Yasuharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakataKatsuyoshi en-aut-sei=Takata en-aut-mei=Katsuyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IwakiNoriko en-aut-sei=Iwaki en-aut-mei=Noriko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TanakaTakehiro en-aut-sei=Tanaka en-aut-mei=Takehiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=AsanoNaoko en-aut-sei=Asano en-aut-mei=Naoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=OritaYorihisa en-aut-sei=Orita en-aut-mei=Yorihisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=NakamuraNaoya en-aut-sei=Nakamura en-aut-mei=Naoya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=NakamuraShigeo en-aut-sei=Nakamura en-aut-mei=Shigeo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=7 en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=8 en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=9 en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=10 en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=11 en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=Cyclin D2 kn-keyword=Cyclin D2 en-keyword=CD5 kn-keyword=CD5 en-keyword=Diffuse large B-cell lymphoma kn-keyword=Diffuse large B-cell lymphoma END start-ver=1.4 cd-journal=joma no-vol=3 cd-vols= no-issue=1 article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20051005 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Effect of connective tissue growth factor (CCN2/CTGF) on proliferation and differentiation of mouse periodontal ligament-derived cells en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Background: CCN2/CTGF is known to be involved in tooth germ development and periodontal tissue remodeling, as well as in mesenchymal tissue development and regeneration. In this present study, we investigated the roles of CCN2/CTGF in the proliferation and differentiation of periodontal ligament cells (murine periodontal ligament-derived cell line: MPL) in vitro.
Results: In cell cultures of MPL, the mRNA expression of the CCN2/CTGF gene was stronger in sparse cultures than in confluent ones and was significantly enhanced by TGF-ƒÀ. The addition of Recombinant CCN2/CTGF (rCCN2) to MPL cultures stimulated DNA synthesis and cell growth in a dose-dependent manner. Moreover, rCCN2 addition also enhanced the mRNA expression of alkaline phosphatase (ALPase), type I collagen, and periostin, the latter of which is considered to be a specific marker of the periosteum and periodontium; whereas it showed little effect on the mRNA expression of typical osteoblastic markers, e.g., osteopontin and osteocalcin. Finally, rCCN2/CTGF also stimulated ALPase activity and collagen synthesis.
Conclusion: These results taken together suggest important roles of CCN2/CTGF in the development and regeneration of periodontal tissue including the periodontal ligament.

en-copyright= kn-copyright= en-aut-name=AsanoMasahiro en-aut-sei=Asano en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 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=2 ORCID= en-aut-name=NakanishiTohru en-aut-sei=Nakanishi en-aut-mei=Tohru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NishidaTakashi en-aut-sei=Nishida en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YamaaiTomoichiro en-aut-sei=Yamaai en-aut-mei=Tomoichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YosimichiGen en-aut-sei=Yosimichi en-aut-mei=Gen kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OhyamaKazumi en-aut-sei=Ohyama en-aut-mei=Kazumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=SugimotoTomosada en-aut-sei=Sugimoto en-aut-mei=Tomosada kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MurayamaYoji en-aut-sei=Murayama en-aut-mei=Yoji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 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=10 ORCID= affil-num=1 en-affil= kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Biochemistry and Molecular Dentistry, 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 Oral Functional Anatomy, 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 affil-num=7 en-affil= kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Oral Functional Anatomy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences END start-ver=1.4 cd-journal=joma no-vol=17 cd-vols= no-issue=1 article-no= start-page=314 end-page=322 dt-received= dt-revised= dt-accepted= dt-pub-year=2017 dt-pub=20170505 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Efficacy and safety of rebamipide liquid for chemoradiotherapy-induced oral mucositis in patients with head and neck cancer: a multicenter, randomized, double-blind, placebo-controlled, parallel-group phase II study en-subtitle= kn-subtitle= en-abstract= kn-abstract=BACKGROUND: Recent preclinical and phase I studies have reported that rebamipide decreased the severity of chemoradiotherapy-induced oral mucositis in patients with oral cancer. This placebo-controlled randomized phase II study assessed the clinical benefit of rebamipide in reducing the incidence of severe chemoradiotherapy-induced oral mucositis in patients with head and neck cancer (HNC). METHODS: Patients aged 20-75 years with HNC who were scheduled to receive chemoradiotherapy were enrolled. Patients were randomized to receive rebamipide 2% liquid, rebamipide 4% liquid, or placebo. The primary endpoint was the incidence of grade ? 3 oral mucositis determined by clinical examination and assessed by central review according to the Common Terminology Criteria of Adverse Events version 3.0. Secondary endpoints were the time to onset of grade ? 3 oral mucositis and the incidence of functional impairment (grade ? 3) based on the evaluation by the Oral Mucositis Evaluation Committee. RESULTS: From April 2014 to August 2015, 97 patients with HNC were enrolled, of whom 94 received treatment. The incidence of grade ? 3 oral mucositis was 29% and 25% in the rebamipide 2% and 4% groups, respectively, compared with 39% in the placebo group. The proportion of patients who did not develop grade ? 3 oral mucositis by day 50 of treatment was 57.9% in the placebo group, whereas the proportion was 68.0% in the rebamipide 2% group and 71.3% in the rebamipide 4% group. The incidences of adverse events potentially related to the study drug were 16%, 26%, and 13% in the placebo, rebamipide 2%, and rebamipide 4% groups, respectively. There was no significant difference in treatment compliance among the groups. CONCLUSIONS: The present phase II study suggests that mouth washing with rebamipide may be effective and safe for patients with HNC receiving chemoradiotherapy, and 4% liquid is the optimal dose of rebamipide. TRIAL REGISTRATION: ClinicalTrials.gov under the identifier NCT02085460 (the date of trial registration: March 11, 2014). en-copyright= kn-copyright= en-aut-name=YokotaT. en-aut-sei=Yokota en-aut-mei=T. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OgawaT. en-aut-sei=Ogawa en-aut-mei=T. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakahashiS. en-aut-sei=Takahashi en-aut-mei=S. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OkamiK. en-aut-sei=Okami en-aut-mei=K. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=FujiiT. en-aut-sei=Fujii en-aut-mei=T. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TanakaK. en-aut-sei=Tanaka en-aut-mei=K. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=IwaeS. en-aut-sei=Iwae en-aut-mei=S. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=OtaI. en-aut-sei=Ota en-aut-mei=I. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=UedaT. en-aut-sei=Ueda en-aut-mei=T. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=MondenN. en-aut-sei=Monden en-aut-mei=N. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=MatsuuraK. en-aut-sei=Matsuura en-aut-mei=K. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=KojimaH. en-aut-sei=Kojima en-aut-mei=H. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=UedaS. en-aut-sei=Ueda en-aut-mei=S. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=SasakiK. en-aut-sei=Sasaki en-aut-mei=K. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=FujimotoY. en-aut-sei=Fujimoto en-aut-mei=Y. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=HasegawaY. en-aut-sei=Hasegawa en-aut-mei=Y. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=BeppuT. en-aut-sei=Beppu en-aut-mei=T. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=NishimoriHisakazu en-aut-sei=Nishimori en-aut-mei=Hisakazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=HiranoS. en-aut-sei=Hirano en-aut-mei=S. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= en-aut-name=NakaY. en-aut-sei=Naka en-aut-mei=Y. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=20 ORCID= en-aut-name=MatsushimaY. en-aut-sei=Matsushima en-aut-mei=Y. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=21 ORCID= en-aut-name=FujiiM. en-aut-sei=Fujii en-aut-mei=M. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=22 ORCID= en-aut-name=TaharaM. en-aut-sei=Tahara en-aut-mei=M. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=23 ORCID= affil-num=1 en-affil=Division of Gastrointestinal Oncology, Shizuoka Cancer Center kn-affil= affil-num=2 en-affil=Department of Otolaryngology-Head and Neck Surgery, Tohoku University Graduate School of Medicine kn-affil= affil-num=3 en-affil=Department of Medical Oncology, The Cancer Institute Hospital of JFCR kn-affil= affil-num=4 en-affil=Department of Otolaryngology, Center of Head and Neck Surgery, Tokai University kn-affil= affil-num=5 en-affil=Department of Otolaryngology, Head and Neck Surgery, Osaka Medical Center for Cancer and Cardiovascular Diseases kn-affil= affil-num=6 en-affil=Department of Medical Oncology, Kindai University Faculty of Medicine kn-affil= affil-num=7 en-affil=Department of Head and Neck Cancer, Hyogo Cancer Center kn-affil= affil-num=8 en-affil=Department of Otolaryngology-Head and Neck Surgery, Nara Medical University kn-affil= affil-num=9 en-affil=Department of Otorhinolaryngology-Head and Neck Surgery, Hiroshima University Hospital kn-affil= affil-num=10 en-affil=Department of Head and Neck Surgery, Shikoku Cancer Center kn-affil= affil-num=11 en-affil=Department of Head and Neck Surgery, Miyagi Cancer Center kn-affil= affil-num=12 en-affil=Department of Otorhinolaryngology, Jikei University School of Medicine kn-affil= affil-num=13 en-affil= Medical Oncology, Nara Hospital, Kindai University School of Medicine kn-affil= affil-num=14 en-affil=Head and Neck, Chiba Cancer Center kn-affil= affil-num=15 en-affil=Department of Otorhinolaryngology, Nagoya University, Graduate School of Medicine kn-affil= affil-num=16 en-affil=Department of Head and Neck Surgery, Aichi Cancer Center Hospital and Research Institute kn-affil= affil-num=17 en-affil=Division of Head and Neck Surgery, Saitama Cancer Center kn-affil= affil-num=18 en-affil=Department of Hematology and Oncology, Okayama University Hospital kn-affil= affil-num=19 en-affil=Department of Otolaryngology-Head and Neck Surgery, Kyoto University Hospital kn-affil= affil-num=20 en-affil= Headquarters of New Product Evaluation and Development, Otsuka Pharmaceutical Co., Ltd. kn-affil= affil-num=21 en-affil= Headquarters of New Product Evaluation and Development, Otsuka Pharmaceutical Co., Ltd. kn-affil= affil-num=22 en-affil=Department of Otolaryngology, Eiju General Hospital kn-affil= affil-num=23 en-affil=Department of Head and Neck Medical Oncology, National Cancer Center Hospital East kn-affil= en-keyword=Chemoradiotherapy kn-keyword=Chemoradiotherapy en-keyword=Head and neck cancer kn-keyword=Head and neck cancer en-keyword=Oral mucositis kn-keyword=Oral mucositis en-keyword=Placebo-controlled kn-keyword=Placebo-controlled en-keyword=Randomized kn-keyword=Randomized en-keyword=Rebamipide liquid kn-keyword=Rebamipide liquid END start-ver=1.4 cd-journal=joma no-vol=3 cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=20040114 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Elevated levels of tissue inhibitor of metalloproteinases (TIMPS) in human hepatocellular carcinomas en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=MatsumotoEiji en-aut-sei=Matsumoto en-aut-mei=Eiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=NakatsukaHarushige en-aut-sei=Nakatsuka en-aut-mei=Harushige kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NousoKazuhi‚’o en-aut-sei=Nouso en-aut-mei=Kazuhi‚’o kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NakamuraShin-ichiro en-aut-sei=Nakamura en-aut-mei=Shin-ichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SuzukiMayumi en-aut-sei=Suzuki en-aut-mei=Mayumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KobayashiYoshiyuki en-aut-sei=Kobayashi en-aut-mei=Yoshiyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=UemuraMasayuki en-aut-sei=Uemura en-aut-mei=Masayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=SatoSyuichiro en-aut-sei=Sato en-aut-mei=Syuichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=SatoEi-ichiro en-aut-sei=Sato en-aut-mei=Ei-ichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=YokoyamaJunko en-aut-sei=Yokoyama en-aut-mei=Junko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=TsuboiSou en-aut-sei=Tsuboi en-aut-mei=Sou kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=TanakaHironori en-aut-sei=Tanaka en-aut-mei=Hironori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=TakumaYoshitake en-aut-sei=Takuma en-aut-mei=Yoshitake kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=FujikawaTatsuya en-aut-sei=Fujikawa en-aut-mei=Tatsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=ShiratoriYasushi en-aut-sei=Shiratori en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= affil-num=1 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=2 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=3 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=4 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=5 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=6 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=7 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=8 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=9 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=10 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=11 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=12 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=13 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=14 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry affil-num=15 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry END start-ver=1.4 cd-journal=joma no-vol=5 cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=2005823 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Evaluation of the Total Design Method in a survey of Japanese dentists en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Background: This study assessed the application of the Total Design Method (TDM) in a mail survey of Japanese dentists. The TDM was chosen because survey response rates in Japan are unacceptably low and the TDM had previously been used in a general population survey.
Methods: Four hundred and seventy eight dentist members of the Okayama Medical and Dental Practitioner's Association were surveyed. The nine-page, 27-item questionnaire covered dentist job satisfaction, physical practice, and dentist and patient characteristics. Respondents to the first mailing or the one-week follow-up postcard were defined as early responders; others who responded were late responders. Responder bias was assessed by examining age, gender and training.
Results: The overall response rate was 46.7% (223/478). The response rates by follow-up mailing were, 18% after the first mailing, 35.4% after the follow-up postcard, 42.3% after the second mailing, and 46.7% after the third mailing. Respondents did not differ from non-respondents in age or gender, nor were there differences between early and late responders.
Conclusion: The application of TDM in this survey of Japanese dentists produced lower rates of response than expected from previous Japanese and US studies.

en-copyright= kn-copyright= en-aut-name=NakaiYukie en-aut-sei=Nakai en-aut-mei=Yukie kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MilgromPeter en-aut-sei=Milgrom en-aut-mei=Peter kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YoshidaToshiko en-aut-sei=Yoshida en-aut-mei=Toshiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IshiharaChikako en-aut-sei=Ishihara en-aut-mei=Chikako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=ShimonoTsutomu en-aut-sei=Shimono en-aut-mei=Tsutomu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Department of Behavioral Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Dental Public Heath Sciences, University of Washington affil-num=3 en-affil= kn-affil=Department of Behavioral Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Behavioral Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Behavioral Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences END start-ver=1.4 cd-journal=joma no-vol=5 cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20050120 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Functional promoter upstream p53 regulatory sequence of IGFBP3 that is silenced by tumor specific methylation en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Background: Insulin-like growth factor binding protein (IGFBP)-3 functions as a carrier of insulinlike growth factors (IGFs) in circulation and a mediator of the growth suppression signal in cells. There are two reported p53 regulatory regions in the IGFBP3 gene; one upstream of the promoter and one intronic. We previously reported a hot spot of promoter hypermethylation of IGFBP-3 in human hepatocellular carcinomas and derivative cell lines. As the hot spot locates at the putative upstream p53 consensus sequences, these p53 consensus sequences are really functional is a question to be answered.
Methods: In this study, we examined the p53 consensus sequences upstream of the IGFBP-3 promoter for the p53 induced expression of IGFBP-3. Deletion, mutagenesis, and methylation constructs of IGFBP-3 promoter were assessed in the human hepatoblastoma cell line HepG2 for promoter activity.
Results: Deletions and mutations of these sequences completely abolished the expression of IGFBP-3 in the presence of p53 overexpression. In vitro methylation of these p53 consensus sequences also suppressed IGFBP-3 expression. In contrast, the expression of IGFBP-3 was not affected in the absence of p53 overexpression. Further, we observed by electrophoresis mobility shift assay that p53 binding to the promoter region was diminished when methylated.
Conclusion: From these observations, we conclude that four out of eleven p53 consensus sequences upstream of the IGFBP-3 promoter are essential for the p53 induced expression of IGFBP-3, and hypermethylation of these sequences selectively suppresses p53 induced IGFBP-3 expression in HepG2 cells.

en-copyright= kn-copyright= en-aut-name=HanafusaTadashi en-aut-sei=Hanafusa en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ShinjiToshiyuki en-aut-sei=Shinji en-aut-mei=Toshiyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=ShirahaHidenori en-aut-sei=Shiraha en-aut-mei=Hidenori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NousoKazuhiro en-aut-sei=Nouso en-aut-mei=Kazuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=IwasakiYoshiaki en-aut-sei=Iwasaki en-aut-mei=Yoshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YumotoEichiro en-aut-sei=Yumoto en-aut-mei=Eichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OnoToshiro en-aut-sei=Ono en-aut-mei=Toshiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KoideNorio en-aut-sei=Koide en-aut-mei=Norio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Okayama University Advanced Science Research Center, Department of Radiation Research, Shikata Laboratory affil-num=2 en-affil= kn-affil=Department of Laboratory Medicine, Okayama University Graduate School of Medicine and Dentistry affil-num=3 en-affil= kn-affil=First Department of Internal Medicine, Okayama University Graduate School of Medicine and Dentistry affil-num=4 en-affil= kn-affil=First Department of Internal Medicine, Okayama University Graduate School of Medicine and Dentistry affil-num=5 en-affil= kn-affil=First Department of Internal Medicine, Okayama University Graduate School of Medicine and Dentistry affil-num=6 en-affil= kn-affil=First Department of Internal Medicine, Okayama University Graduate School of Medicine and Dentistry affil-num=7 en-affil= kn-affil=Okayama University Advanced Science Research Center, Department of Radiation Research, Shikata Laboratory affil-num=8 en-affil= kn-affil=Department of Laboratory Medicine, Okayama University Graduate School of Medicine and Dentistry END start-ver=1.4 cd-journal=joma no-vol=2 cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2002 dt-pub=20020402 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=High-susceptibility of photosynthesis to photoinhibition in the tropical plant Ficus microcarpa L. f. cv. Golden Leaves en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Background: The tropical plant Ficus microcarpa L. f. cv. Golden Leaves (GL) is a high-light sensitive tropical fig tree in which sun-leaves are yellow and shade-leaves are green. We compared the response of photosynthetic activities to strong light between GL and its wild-type (WT, Ficus microcarpa L. f.).

Results: Field measurements of maximum photosystem II (PSII) efficiency (Fv/Fm) of intact sunleaves in GL showed that photo synthetic activity was severely photoinhibited during the daytime (Fv/Fm = 0.46) and subsequently recovered in the evening (Fv/Fm = 0.76). In contrast, WT did not show any substantial changes of Fv/Fm values throughout the day (between 0.82 and 0.78). Light dependency of the CO2 assimilation rate in detached shade-leaves of GL showed a response similar to that in WT, suggesting no substantial difference in photosynthetic performance between them.Several indicators of photoinhibition, including declines in PSII reaction center protein (D1)content, Fv/Fm value, and O2 evolution and CO2 assimilation rates, all indicated that GL is much more susceptible to photoinhibition than WT. Kinetics of PAM chlorophyll a fluorescence revealed that nonphotochemical quenching (NPQ) capacity of GL was lower than that of WT.

Conclusion: We conclude that the photosynthetic apparatus of GL is more highly susceptible to photoinhibition than that of WT.

en-copyright= kn-copyright= en-aut-name=TakahashiShunichi en-aut-sei=Takahashi en-aut-mei=Shunichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TamashiroAyumu en-aut-sei=Tamashiro en-aut-mei=Ayumu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=SakihamaYasuko en-aut-sei=Sakihama en-aut-mei=Yasuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YamamotoYasusi en-aut-sei=Yamamoto en-aut-mei=Yasusi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KawamitsuYoshinobu en-aut-sei=Kawamitsu en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YamasakiHideo en-aut-sei=Yamasaki en-aut-mei=Hideo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Laboratory of Cell and Functional Biology, Faculty of Science, University of the Ryukyus affil-num=2 en-affil= kn-affil=Laboratory of Cell and Functional Biology, Faculty of Science, University of the Ryukyus affil-num=3 en-affil= kn-affil=Laboratory of Cell and Functional Biology, Faculty of Science, University of the Ryukyus affil-num=4 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=5 en-affil= kn-affil=Laboratory of Crop Science, Faculty of Agriculture, University of the Ryukyus affil-num=6 en-affil= kn-affil=Laboratory of Cell and Functional Biology, Faculty of Science, University of the Ryukyus en-keyword=Carbon dioxide kn-keyword=Carbon dioxide en-keyword=Chlorophyll kn-keyword=Chlorophyll en-keyword=Ficus kn-keyword=Ficus en-keyword=Genotype kn-keyword=Genotype en-keyword=Oxygen kn-keyword=Oxygen en-keyword=Photosynthesis kn-keyword=Photosynthesis en-keyword=Photosystem II protein complex kn-keyword=Photosystem II protein complex en-keyword=Plant leaves kn-keyword=Plant leaves END start-ver=1.4 cd-journal=joma no-vol=5 cd-vols= no-issue=1 article-no= start-page=36 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20131203 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Inflammatory diarrhea due to enteroaggregative Escherichia coli: evidence from clinical and mice model studies en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background@ This study was conducted to determine the role of enteroaggregative Escherichia coli (EAEC) in inflammatory diarrhea among hospitalized patients in Kolkata. The inflammatory pathogenesis of EAEC was established in mice model and histopathological studies. Presence of fecal leucocytes (FLCs) can be suspected for EAEC infection solely or as a mixed with other enteric pathogens.@ Methods@ Active surveillance was conducted for 2 years on 2 random days per week with every 5th patient admitted to the Infectious Diseases Hospital (IDH). Diarrheal samples were processed by conventional culture, microscopy, ELISA and molecular methods. Two EAEC isolated as sole pathogens were examined in mice after induced intestinal infection. The intestinal tissue samples were processed to analyze the histological changes.@ Results@ Of the 2519 samples screened, fecal leucocytes, erythrocytes and occult blood were detected in 1629 samples. Most of the patients had acute watery diarrhea (75%) and vomiting (78%). Vibrio cholerae O1 was the main pathogen in patients of 5?10 years age group (33%). Shigellosis was more in children from 2?5 years of age (19%), whereas children <2 years appeared to be susceptible for infection caused by EAEC (16%). When tested for the pathogenicity, the EAEC strains colonized well and caused inflammatory infection in the gut mucosa of BALB/C mice.@ Conclusion@ This hospital-based surveillance revealed prevalence of large number of inflammatory diarrhea. EAEC was the suspected pathogen and <2 years children appeared to be the most susceptible age group. BALB/C mice may be a suitable animal model to study the EAEC-mediated pathogenesis. en-copyright= kn-copyright= en-aut-name=Dhira Rani Saha en-aut-sei=Dhira Rani Saha en-aut-mei= kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=GuinSucharita en-aut-sei=Guin en-aut-mei=Sucharita kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KrishnanRajendran en-aut-sei=Krishnan en-aut-mei=Rajendran kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NagDhrubajyoti en-aut-sei=Nag en-aut-mei=Dhrubajyoti kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KoleyHemanta en-aut-sei=Koley en-aut-mei=Hemanta kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ShinodaSumio en-aut-sei=Shinoda en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=RamamurthyThandavarayan en-aut-sei=Ramamurthy en-aut-mei=Thandavarayan kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil=Division of Histology & Electron microscopy, National Institute of Cholera and Enteric Diseases kn-affil= affil-num=2 en-affil=Natl Inst Cholera & Enter Dis, Div Bacteriol kn-affil= affil-num=3 en-affil=Natl Inst Cholera & Enter Dis, Div Data Management kn-affil= affil-num=4 en-affil=Natl Inst Cholera & Enter Dis, Div Bacteriol kn-affil= affil-num=5 en-affil=Natl Inst Cholera & Enter Dis, Div Bacteriol kn-affil= affil-num=6 en-affil=Okayama Univ Infect Dis India, Collaborat Res Ctr kn-affil= affil-num=7 en-affil=Natl Inst Cholera & Enter Dis, Div Bacteriol kn-affil= END start-ver=1.4 cd-journal=joma no-vol=3 cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2003 dt-pub=20031021 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=No association between the sigma receptor type 1 gene and schizophrenia: results of analysis and meta-analysis of case-control studies en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Background: Several lines of evidence have supported possible roles of the sigma receptors in the etiology of schizophrenia and mechanisms of antipsychotic efficacy. An association study provided genetic evidence that the sigma receptor type 1 gene (SIGMAR1) was a possible susceptibility factor for schizophrenia, however, it was not replicated by a subsequent study. It is necessary to evaluate further the possibility that the SIGMAR1 gene is associated with susceptibility to schizophrenia. Methods: A case-control association study between two polymorphisms of the SIGMAR1 gene, G-241T/C-240T and Gln2Pro, and schizophrenia in Japanese population, and meta-analysis including present and previous studies.
Results:There was no significant association of any allele or genotype of the polymorphisms with schizophrenia. Neither significant association was observed with hebephrenic or paranoid subtype of schizophrenia. Furthermore, a meta-analysis including the present and previous studies comprising 779 controls and 636 schizophrenics also revealed no significant association between the SIGMAR1 gene and schizophrenia.
Conclusion: In view of this evidence, it is likely that the SIGMAR1 gene does not confersusceptibility to schizophrenia.

en-copyright= kn-copyright= en-aut-name=UchidaNaohiko en-aut-sei=Uchida en-aut-mei=Naohiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=UjikeHiroshi en-aut-sei=Ujike en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NakataKenji en-aut-sei=Nakata en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TakakiManabu en-aut-sei=Takaki en-aut-mei=Manabu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NomuraAkira en-aut-sei=Nomura en-aut-mei=Akira kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KatsuTakeshi en-aut-sei=Katsu en-aut-mei=Takeshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TanakaYuji en-aut-sei=Tanaka en-aut-mei=Yuji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=ImamuraTakaki en-aut-sei=Imamura en-aut-mei=Takaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=SakaiAyumu en-aut-sei=Sakai en-aut-mei=Ayumu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KurodaShigetoshi en-aut-sei=Kuroda en-aut-mei=Shigetoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry affil-num=2 en-affil= kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry affil-num=3 en-affil= kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry affil-num=4 en-affil= kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry affil-num=5 en-affil= kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry affil-num=6 en-affil= kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry affil-num=7 en-affil= kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry affil-num=8 en-affil= kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry affil-num=9 en-affil= kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry affil-num=10 en-affil= kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry END start-ver=1.4 cd-journal=joma no-vol=7 cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2006 dt-pub=20060803 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Simultaneous gene transfer of bone morphogenetic protein (BMP)-2 and BMP-7 by in vivo electroporation induces rapid bone formation and BMP-4 expression en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Background: Transcutaneous in vivo electroporation is expected to be an effective gene-transfer method for promoting bone regeneration using the BMP-2 plasmid vector. To promote enhanced osteoinduction using this method, we simultaneously transferred cDNAs for BMP-2 and BMP-7, as inserts in the non-viral vector pCAGGS.
Methods: First, an in vitro study was carried out to confirm the expression of BMP-2 and BMP-7 following the double-gene transfer. Next, the individual BMP-2 and BMP-7 plasmids or both together were injected into rat calf muscles, and transcutaneous electroporation was applied 8 times at 100 V, 50 msec.
Results: In the culture system, the simultaneous transfer of the BMP-2 and BMP-7 genes led to a much higher ALP activity in C2C12 cells than did the transfer of either gene alone. In vivo, ten days after the treatment, soft X-ray analysis showed that muscles that received both pCAGGS-BMP-2 and pCAGGS-BMP-7 had better-defined opacities than those receiving a single gene. Histological examination showed advanced ossification in calf muscles that received the double-gene transfer. BMP-4 mRNA was also expressed, and RT-PCR showed that its level increased for 3 days in a timedependent manner in the double-gene transfer group. Immunohistochemistry confirmed that BMP- 4-expressing cells resided in the matrix between muscle fibers.
Conclusion: The simultaneous transfer of BMP-2 and BMP-7 genes using in vivo electroporation induces more rapid bone formation than the transfer of either gene alone, and the increased expression of endogenous BMP-4 suggests that the rapid ossification is related to the induction of BMP-4.

en-copyright= kn-copyright= en-aut-name=KawaiMariko en-aut-sei=Kawai en-aut-mei=Mariko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=BesshoKazuhisa en-aut-sei=Bessho en-aut-mei=Kazuhisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MaruyamaHiroki en-aut-sei=Maruyama en-aut-mei=Hiroki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MiyazakiJun-ichi en-aut-sei=Miyazaki en-aut-mei=Jun-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YamamotoToshio en-aut-sei=Yamamoto en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Oral and Maxillofacial Surgery, Graduate School of Medicine, Kyoto University affil-num=3 en-affil= kn-affil=Division of Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences affil-num=4 en-affil= kn-affil=Division of Stem Cell Regulation Research, Osaka University Medical School affil-num=5 en-affil= kn-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences END