start-ver=1.4 cd-journal=joma no-vol=114 cd-vols= no-issue=8 article-no= start-page=940 end-page=946 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=201612 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Relationship of the number and size of superficial groin lymph nodes with the stage of secondary lymphatic edema en-subtitle= kn-subtitle= en-abstract= kn-abstract=PURPOSE: This study evaluated the relationships of the size and number of superficial groin lymph nodes with the lower limb lymphedema stage and thus examined the role of superficial lymphatic lymph nodes in secondary lymphedema development. METHODS: We determined the number and size of superficial groin lymph nodes using horizontal plane computed tomography (CT) and the lymphedema stage in the lower limbs of 25 patients with gynecologic cancer. RESULTS: The patients had an average of 2.92 (range, 1-7) superficial groin lymph nodes; the mean size of the 146 evaluated lymph nodes was 7.55?mm (range, 5-15?mm). In 19 of 25 patients (76%), the side with major edema contained fewer superficial groin lymph nodes. In total, 22 patients (88%) had fewer superficial groin lymph nodes or a smaller total lymph node size on the edematous dominant side. CONCLUSIONS: In this evaluation of the link between superficial groin lymph node laterality and secondary lymphedema staging, we found that patients with large lymph node numbers and sizes tended to present with a relatively earlier stage of lymphedema. Our results therefore suggest that the size and number of superficial groin lymph nodes affect the lymphedema stage. en-copyright= kn-copyright= en-aut-name=OnodaSatoshi en-aut-sei=Onoda en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KimataYoshihiro en-aut-sei=Kimata en-aut-mei=Yoshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YamadaKiyoshi en-aut-sei=Yamada en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SekiNoriko en-aut-sei=Seki en-aut-mei=Noriko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HiramatsuYuji en-aut-sei=Hiramatsu en-aut-mei=Yuji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil=Department of Plastic and Reconstructive Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Science, University of Okayama kn-affil= affil-num=2 en-affil=Department of Plastic and Reconstructive Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Science, University of Okayama kn-affil= affil-num=3 en-affil=Department of Plastic and Reconstructive Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Science, University of Okayama kn-affil= affil-num=4 en-affil=Department of Obstetrics and Gynecology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, University of Okayama kn-affil= affil-num=5 en-affil=Department of Obstetrics and Gynecology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, University of Okayama kn-affil= en-keyword=gynecologic cancer kn-keyword=gynecologic cancer en-keyword=lower limb lymphedema kn-keyword=lower limb lymphedema en-keyword=risk factor kn-keyword=risk factor en-keyword=secondary lymphedema kn-keyword=secondary lymphedema en-keyword=superficial groin lymph nodes kn-keyword=superficial groin lymph nodes END start-ver=1.4 cd-journal=joma no-vol=203 cd-vols= no-issue=2 article-no= start-page=447 end-page=456 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=200412 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Connective Tissue Growth Factor Causes Persistent Proƒ¿2(I) Collagen Gene Expression Induced by Transforming Growth Factor-ƒÀ in a Mouse Fibrosis Model en-subtitle= kn-subtitle= en-abstract= kn-abstract=Skin fibrotic disorders such as systemic sclerosis (SSc) are characterized by an excessive production of extracellular matrix (ECM) and understood to develop under the influence of certain growth factors. Connective tissue growth factor (CTGF) is a cysteine-rich mitogenic peptide that is implicated in various fibrotic disorders and induced in fibroblasts after activation with transforming growth factor-beta (TGF-beta). To better understand the mechanisms of persistent fibrosis seen in SSc, we previously established an animal model of skin fibrosis induced by exogenous application of growth factors. In this model, TGF-beta transiently induced subcutaneous fibrosis and serial injections of CTGF after TGF-beta caused persistent fibrosis. To further define the mechanisms of skin fibrosis induced by TGF-beta and CTGF in vivo, we investigated in this study, the effects of growth factors on the promoter activity of the pro alpha 2 (1) collagen (COL1A2) gene in skin fibrosis. For this purpose, we utilized transgenic reporter mice harboring the -17 kb promoter sequence of the mouse COL1A2 linked to either a firefly luciferase gene or a bacterial P-galactosidase gene. Serial injections of CTGF after TGF-beta resulted in a sustained elevation of COL1A2 mRNA expression and promoter activity compared with consecutive injection of TGF-beta alone on day 8. We also demonstrated that the number of fibroblasts with activated COL1A2 transcription was increased by serial injections of CTGF after TGF-beta in comparison with the injection of TGF-beta alone. Furthermore, the serial injections recruited mast cells and macrophages. The number of mast cells reached a maximum on day 4 and remained relatively high up to day 8. In contrast to the kinetics of mast cells, the number of macrophages was increased on day 4 and continued to rise during the subsequent consecutive CTGF injections until day 8. These results suggested that CTGF maintains TGF-beta-induced skin fibrosis by sustaining COL1A2 promoter activation and increasing the number of activated fibroblasts. The infiltrated mast cells and macrophages may also contribute to the maintenance of fibrosis. en-copyright= kn-copyright= en-aut-name=ChujoSonoko en-aut-sei=Chujo en-aut-mei=Sonoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ShirasakiFumiaki en-aut-sei=Shirasaki en-aut-mei=Fumiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KawaraShigeru en-aut-sei=Kawara en-aut-mei=Shigeru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=InagakiYutaka en-aut-sei=Inagaki en-aut-mei=Yutaka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KinbaraTakuro en-aut-sei=Kinbara en-aut-mei=Takuro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=InaokiMakoto en-aut-sei=Inaoki en-aut-mei=Makoto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 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=7 ORCID= en-aut-name=TakeharaKazuhiko en-aut-sei=Takehara en-aut-mei=Kazuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Department of Dermatology, Kanazawa University Graduate School of Medical Science affil-num=2 en-affil= kn-affil=Department of Dermatology, Kanazawa University Graduate School of Medical Science affil-num=3 en-affil= kn-affil=Department of Dermatology, National Kanazawa Hospital affil-num=4 en-affil= kn-affil=Department of Community Health, Tokai University School of Medicine affil-num=5 en-affil= kn-affil=Department of Dermatology, Kanazawa University Graduate School of Medical Science affil-num=6 en-affil= kn-affil=Department of Dermatology, Kawasaki Medical School affil-num=7 en-affil= kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine and Dentistry affil-num=8 en-affil= kn-affil=Department of Dermatology, Kanazawa University Graduate School of Medical Science en-keyword=systemic sclerosis kn-keyword=systemic sclerosis en-keyword=fibrosis kn-keyword=fibrosis en-keyword=transforming growth factor-? kn-keyword=transforming growth factor-? en-keyword=connective tissue growth factor kn-keyword=connective tissue growth factor END