JaLCDOI 10.18926/AMO/64363
FullText URL 77_1_65.pdf
Author Sato, Ken| Takigawa, Nagio| Kubo, Toshio| Katayama, Hideki| Kishino, Daizo| Okada, Toshiaki| Hisamoto, Akiko| Mimoto, Junko| Ochi, Nobuaki| Yoshino, Tadashi| Ueoka, Hiroshi| Tanimoto, Mitsune| Maeda, Yoshionobu| Kiura, Katsuyuki|
Abstract We investigated the effects of celecoxib combined with (−)-epigallocatechin-3-gallate (EGCG) or polyphenon E in a cisplatin-induced lung tumorigenesis model. Four-week-old female A/J mice were divided into seven groups: (i) Control, (ii) 150 mg/kg celecoxib (150Cel), (iii) 1,500 mg/kg celecoxib (1500Cel), (iv) EGCG+150 mg/kg celecoxib (EGCG+150Cel), (v) EGCG+1,500 mg/kg celecoxib (EGCG+1500Cel), (vi) polyphenon E+150 mg/kg celecoxib (PolyE+150Cel), and (vii) polyphenon E+1,500 mg/kg celecoxib (PolyE+1500Cel). All mice were administered cisplatin (1.62 mg/kg of body weight, i.p.) 1×/week for 10 weeks and sacrificed at week 30; the numbers of tumors on the lung surface were then determined. The tumor incidence and multiplicity (no. of tumors/mouse, mean±SD) were respectively 95% and 2.15±1.50 in Control, 95% and 2.10±1.29 in 150Cel, 86% and 1.67±1.20 in 1500Cel, 71% and 1.38±1.24 in EGCG+150Cel, 67% and 1.29±1.38 in EGCG+1500Cel, 80% and 1.95±1.36 in PolyE+150Cel, and 65% and 1.05±0.10 in PolyE+1500Cel. The combination of high-dose celecoxib with EGCG or polyphenon E significantly reduced multiplicity in cisplatin-induced lung tumors.
Keywords celecoxib cisplatin EGCG lung tumor polyphenon E
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2023-02
Volume volume77
Issue issue1
Publisher Okayama University Medical School
Start Page 65
End Page 70
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders Copyright Ⓒ 2023 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 36849147
Web of Science KeyUT 000952992100004
JaLCDOI 10.18926/AMO/55446
FullText URL 71_5_453.pdf
Author Taniguchi, Akihiko| Miyahara, Nobuaki| Oda, Naohiro| Morichika, Daisuke| Ichihara, Eiki| Oze, Isao| Tanimoto, Yasushi| Ichikawa, Hirohisa| Fujii, Utako| Tanimoto, Mitsune| Kanehiro, Arihiko| Kiura, Katsuyuki|
Abstract Although recent retrospective studies suggested that the use of β-blockers appears to help improve the mortality rate and decrease the rate of exacerbation in chronic obstructive pulmonary disease (COPD) patients with heart failure, the effects of β-blockers on COPD patients without heart failure have not been established. Based on previous reports, we have launched a multicenter, prospective, single-arm phase II study to evaluate the preventive effect of the cardioselective β-blocker bisoprolol in COPD exacerbation, in Japanese individuals with moderate-to-severe COPD who do not have heart failure but do have hypertension requiring the use of medication. The primary endpoint is the rate of mild-to-severe COPD exacerbation. The results of this study will clarify whether bisoprolol can prevent exacerbation in COPD patients without heart failure.
Keywords chronic obstructive pulmonary disease β-blocker bisoprolol exacerbation heart failure
Amo Type Clinical Study Protocol
Publication Title Acta Medica Okayama
Published Date 2017-10
Volume volume71
Issue issue5
Publisher Okayama University Medical School
Start Page 453
End Page 457
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2017 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 29042706
Author Gotoda, Tatsuhiro| Kawano, Seiji| Kono, Yoshiyasu| Miura, Kou| Kanzaki, Hiromitsu| Iwamuro, Masaya| Kawahara, Yoshiro| Tanaka, Takehiro| Yoshino, Tadashi| Shirakawad, Yasuhiro| Tabata, Masahiro| Tanimoto, Mitsune| Okada, Hiroyuki|
Published Date 2016-12-01
Publication Title Journal of Okayama Medical Association
Volume volume128
Issue issue3
Content Type Journal Article
Author Tanimoto, Mitsune|
Published Date 2016-12-01
Publication Title Journal of Okayama Medical Association
Volume volume128
Issue issue3
Content Type Article
JaLCDOI 10.18926/AMO/54603
FullText URL 70_5_409.pdf
Author Maeda, Yoshinobu| Nishimori, Hisakazu| Inamoto, Yoshihiro| Nakamae, Hirohisa| Sawa, Masashi| Mori, Yasuo| Ohashi, Kazuteru| Fujiwara, Shin-ichiro| Tanimoto, Mitsune|
Abstract Chronic graft-versus-host disease (GVHD) is a major cause of late death and morbidity following allogeneic hematopoietic cell transplantation (HSCT). Retinoic acid (tamibarotene) exerts multiple effects on cell differentiation and is clinically used for the treatment of acute promyelocytic leukemia. Tamibarotene down-regulates both Th1 and Th17 differentiation in donor T cells after allogeneic HSCT, resulting in attenuation of experimental chronic GVHD. Based on preclinical data, we have launched a phase II study of tamibarotene in patients with steroid-refractory chronic GVHD. This study will clarify whether tamibarotene can exert beneficial effects in patients with steroid-refractory chronic GVHD.
Keywords Am80 tamibarotene retinoid chronic GVHD steroid-refractory GVHD
Amo Type Clinical Study Protocols
Publication Title Acta Medica Okayama
Published Date 2016-10
Volume volume70
Issue issue5
Publisher Okayama University Medical School
Start Page 409
End Page 412
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2016 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 27777437
Web of Science KeyUT 000388098700014
JaLCDOI 10.18926/AMO/54608
FullText URL 70_5_429.pdf
Author Asano, Takeru| Matsuoka, Ken-ichi| Iyama, Satoshi| Ohashi, Kazuteru| Inamoto, Yoshihiro| Ohwada, Chikako| Murata, Makoto| Satake, Atsushi| Yoshida, Chikamasa| Nakase, Koichi| Mori, Yasuo| Tanimoto, Mitsune|
Abstract Chronic graft versus host disease (cGVHD) remains a major problem for long survivors after allogeneic hematopoietic stem cell transplantation (HSCT). Currently, corticosteroid therapy is effective for cGVHD as the first line therapy. However, prolonged therapy with corticosteroids causes various severe adverse events. To develop the new therapeutic strategy of cGVHD, we have launched a multicenter phase I/IIa clinical trial of low dose subcutaneous interleukin-2 (IL-2) for treatment of steroid refractory cGVHD, which is constituted of 2 sequential phases (induction phase and maitanance phase). This study will provide the new therapeutic option for patients with refractory cGVHD after allogeneic HSCT.
Keywords chronic GVHD allogeneic HSCT steroid refractory IL-2
Amo Type Clinical Study Protocols
Publication Title Acta Medica Okayama
Published Date 2016-10
Volume volume70
Issue issue5
Publisher Okayama University Medical School
Start Page 429
End Page 433
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2016 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 27777442
Web of Science KeyUT 000388098700019
JaLCDOI 10.18926/AMO/54503
FullText URL 70_4_273.pdf
Author Makimoto, Go| Miyahara, Nobuaki| Yoshikawa, Mao| Taniguchi, Akihiko| Kanehiro, Arihiko| Tanimoto, Mitsune| Kiura, Katsuyuki|
Abstract Heerfordtʼs syndrome is a rare manifestation of sarcoidosis and is defined as a combination of facial palsy, parotid swelling, and uveitis, associated with a low-grade fever. We report a case of Heerfordtʼs syndrome presenting with a high fever and increased serum tumor necrosis factor alpha (TNF-α) levels. The patient had facial palsy, parotid swelling, uveitis, and swelling of the right supraclavicular and hilar lymph nodes. Corticosteroid therapy was initiated, and her symptoms soon resolved completely, in tandem with a decrease in TNF-α serum levels.
Keywords Heerfordtʼs syndrome sarcoidosis TNF-α
Amo Type Case Report
Publication Title Acta Medica Okayama
Published Date 2016-08
Volume volume70
Issue issue4
Publisher Okayama University Medical School
Start Page 273
End Page 277
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2016 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 27549672
Web of Science KeyUT 000384748600007
JaLCDOI 10.18926/AMO/54499
FullText URL 70_4_243.pdf
Author Osawa, Masahiro| Ohashi, Kadoaki| Kubo, Toshio| Ichihara, Eiki| Takata, Saburo| Takigawa, Nagio| Takata , Minoru| Tanimoto, Mitsune| Kiura, Katsuyuki|
Abstract Vandetanib (ZactimaTM) is a novel, orally available inhibitor of both vascular endothelial growth factor receptor-2 (VEGFR-2) and epidermal growth factor receptor (EGFR) tyrosine kinase. In the present study, a line of transgenic mice with a mouse Egfr gene mutation (delE748-A752) corresponding to a human EGFR mutation (delE746-A750) was established. The transgenic mice developed atypical adenomatous hyperplasia to adenocarcinoma of the lung at around 5 weeks of age and died of lung tumors at approximately 17 weeks of age. In the mice treated with vandetanib (6mg/kg/day), these lung tumors disappeared and the phosphorylations of EGFR and VEGFR-2 were reduced in lung tissues to levels comparable to those of non-transgenic control mice. The median overall survival time of the transgenic mice was 28 weeks in the vandetanib-treated group and 17 weeks in the vehicle-treated group. Vandetanib significantly prolonged the survival of the transgenic mice (log-rank test, p<0.01); resistance to vandetanib occurred at 20 weeks of age and the animals died from their lung tumors at about 28 weeks of age. These data suggest that vandetanib could suppress the progression of tumors harboring an activating EGFR mutation.
Keywords vandetanib VEGFR EGFR nonsmall cell lung cancer transgenic mouse
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2016-08
Volume volume70
Issue issue4
Publisher Okayama University Medical School
Start Page 243
End Page 253
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2016 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 27549668
Web of Science KeyUT 000384748600003
Title Alternative The 55th Annual Meeting of the Japanese Society for Lymphoreticular Tissue Research
FullText URL 128_67.pdf
Author Tanimoto, Mitsune|
Publication Title 岡山医学会雑誌
Published Date 2016-04-01
Volume volume128
Issue issue1
Start Page 67
End Page 68
ISSN 0030-1558
Related Url isVersionOf https://doi.org/10.4044/joma.128.67
language Japanese
Copyright Holders Copyright (c) 2016 岡山医学会
File Version publisher
DOI 10.4044/joma.128.67
NAID 130005149608
JaLCDOI 10.18926/AMO/53671
FullText URL 69_5_261.pdf
Author Nojima, Daisuke| Fujimoto, Nobukazu| Kato, Katsuya| Fuchimoto, Yasuko| Kiura, Katsuyuki| Kishimoto, Takumi| Tanimoto, Mitsune|
Abstract We investigated the clinical features of asbestos-induced diffuse pleural thickening (DPT) with severe respiratory compromise. We conducted a retrospective study of consecutive subjects with asbestos-induced DPT. Medical data such as initial symptoms, radiological findings, respiratory function test results, and clinical course were collected and analyzed. There were 24 patients between 2003 and 2012. All were men, and the median age at the development of DPT was 74 years. The top occupational category associated with asbestos exposure was dockyard workers. The median duration of asbestos exposure was 35.0 years, and the median latency from first exposure to the onset of DPT was 49.0 years. There were no significant differences in respiratory function test results between the higher and lower Brinkman index groups or between unilateral and bilateral DPT. Thirteen patients had a history of benign asbestos pleural effusion (BAPE), and the median duration from pleural fluid accumulation to DPT with severe respiratory compromise was 28.4 months. DPT with severe respiratory compromise can develop after a long latency following occupational asbestos exposure and a history of BAPE.
Keywords asbestos pleural thickening MRC dyspnea scale respiratory function test costophrenic angle
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2015-10
Volume volume69
Issue issue5
Publisher Okayama University Medical School
Start Page 261
End Page 266
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2015 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 26490022
Web of Science KeyUT 000365519600001
JaLCDOI 10.18926/AMO/53025
FullText URL 68_6_363.pdf
Author Ota, Seisuke| Hiramatsu, Yasushi| Kondo, Eisei| Kasahara, Akinori| Takada, Saimon| Umena, Sachio| Noguchi, Toshio| Tanimoto, Mitsune| Matsumura, Tadashi|
Abstract Leukocytosis is occasionally seen in patients with presumptive but undiagnosed myeloproliferative disorders (MPD). A 74-year-old woman was admitted to our hospital for tarry stools, anemia, and marked peripheral leukocytosis of 1.4×105/μL. Gastroenteroscopy revealed an acute gastric and duodenal mucosal lesion that was treated successfully via endoscopic hemoclipping. Bone marrow aspiration revealed marked megakaryocyte proliferation with atypia of naked nuclei and marrow hypercellularity (90% cellularity). A fluorescence in situ hybridization test could not detect the BCR-ABL fusion gene. Bone marrow aspiration later revealed further abnormalities of megakaryocytes. The patient died from cerebral bleeding. The present case fulfilled 2 of the 3 major criteria of primary myelofibrosis according to the World Health Organization 2008 classification:namely, megakaryocytic hyperplasia with hypercellular marrow and granulocytic hyperplasia. However, the megakaryocytic abnormality was not strictly compatible with the criteria. Instead, we considered prefibrotic primary myelofibrosis as a possibility, although myelodysplastic syndrome/myeloproliferative neoplasm, unclassifiable (MDS/MPN-U) was technically the correct diagnosis. The present case shows that MPN diagnosis remains difficult and suggests that other cases of peripheral leukocytosis with diagnosed MDS/MPN-U might include similar findings.
Keywords prefibrotic primary myelofibrosis leukocytosis anemia acute gastric mucosal lesion multiple cerebral hemorrhages
Amo Type Case Report
Publication Title Acta Medica Okayama
Published Date 2014-12
Volume volume68
Issue issue6
Publisher Okayama University Medical School
Start Page 363
End Page 368
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2014 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 25519030
Web of Science KeyUT 000346882200006
Author Yasugi, Masayuki| Takigawa, Nagio| Ochi, Nobuaki| Ohashi, Kadoaki| Harada, Daijiro| Ninomiya, Takashi| Murakami, Toshi| Honda, Yoshihiro| Ichihara, Eiki| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2014-08-15
Publication Title Experimental Cell Research
Volume volume326
Issue issue2
Content Type Journal Article
Title Alternative Treatment for a non-compliant patient with cancer and epilepsy
FullText URL 126_133.pdf
Author Minami, Daisuke| Ichihara, Eiki| Okabe, Nobuyuki| Yokomichi, Naosuke| Kouge, Noriko| Kajizono, Makoto| Akimoto, Yutaka| Hori, Keisuke| Matsubara, Minoru| Nasu, Junichiro| Tanimoto, Mitsune| Kiura, Katsuyuki| Matsuoka, Junzi|
Abstract  A 58-year-old man with cervical esophageal cancer and a history of epilepsy was treated with chemoradiotherapy from May of 2013. When tube feeding was initiated due to aspiration pneumonitis, the patient showed a degree of irritability that affected routine staff work and treatment compliance. We attempted to perform supportive care for maladjustment by the notice, the fast, and the tube feeding, but there was no improvement. After we added carbamazepine, primidone, and propericiazine (which had been canceled at the initiation of the tube feeding) to the patient's intravenous phenytoin, the symptoms and treatment compliance improved significantly. We concluded that the causes of the patient's irritability were maladjustment and his epilepsy.
Keywords てんかん(epilepsy) 易怒性(irritability) 適応障害(maladjustment)
Publication Title 岡山医学会雑誌
Published Date 2014-08-01
Volume volume126
Issue issue2
Start Page 133
End Page 135
ISSN 0030-1558
language Japanese
Copyright Holders Copyright (c) 2014 岡山医学会
File Version publisher
DOI 10.4044/joma.126.133
NAID 130004685264
Title Alternative Molecular targeted therapy in myeloma and lymphoma
FullText URL 126_143.pdf
Author Saeki, Kyosuke| Maeda, Yoshinobu| Tanimoto, Mitsune|
Keywords 骨髄腫 リンパ腫 分子標的治療薬
Publication Title 岡山医学会雑誌
Published Date 2014-08-01
Volume volume126
Issue issue2
Start Page 143
End Page 150
ISSN 0030-1558
language Japanese
Copyright Holders Copyright (c) 2014 岡山医学会
File Version publisher
DOI 10.4044/joma.126.143
NAID 130004685266
Author Iwatani, Kayoko| Takata, Katsuyoshi| Sato, Yasuharu| Miyata-Takata, Tomoko| Iwaki, Noriko| Cui, Wei| Sawada-Kitamura, Seiko| Sonobe, Hiroshi| Tamura, Maiko| Saito, Katsuhiko| Miyatani, Katsuya| Yamasaki, Rie| Yamadori, Ichiro| Fujii, Nobuharu| Terasaki, Yasushi| Maeda, Yoshinobu| Tanimoto, Mitsune| Nakamura, Naoya| Yoshino, Tadashi|
Published Date 2014-07
Publication Title Human Pathology
Volume volume45
Issue issue7
Content Type Journal Article
Author Ebinuma, Takayuki| Soga, Yoshihiko| Sato, Takamaro| Matsunaga, Kazuyuki| Kudo, Chieko| Maeda, Hiroshi| Maeda, Yoshinobu| Tanimoto, Mitsune| Takashiba, Shogo|
Published Date 2014-06
Publication Title Supportive Care in Cancer
Volume volume22
Issue issue6
Content Type Journal Article
Title Alternative Molecular targeted therapies in leukemia
FullText URL 126_49.pdf
Author Maeda, Yoshinobu| Tanimoto, Mitsune|
Keywords 白血病 分子標的薬 チロシンキナーゼ阻害薬
Publication Title 岡山医学会雑誌
Published Date 2014-04-01
Volume volume126
Issue issue1
Start Page 49
End Page 54
ISSN 0030-1558
Related Url http://www.okayama-u.ac.jp/user/oma/
language Japanese
Copyright Holders Copyright (c) 2014 岡山医学会
File Version publisher
DOI 10.4044/joma.126.49
Author Ochi, Nobuaki| Takigawa, Nagio| Harada, Daijiro| Yasugi, Masayuki| Ichihara, Eiki| Hotta, Katsuyuki| Tabata, Masahiro| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2014-03-10
Publication Title Experimental Cell Research
Volume volume322
Issue issue1
Content Type Journal Article
Author Sugiyama, Haruko| Maeda, Yoshinobu| Nishimori, Hisakazu| Yamasuji, Yoshiko| Matsuoka, Ken-ichi| Fujii, Nobuharu| Kondo, Eisei| Shinagawa, Katsuji| Tanaka, Takehiro| Takeuchi, Kengo| Teshima, Takanori| Tanimoto, Mitsune|
Published Date 2014-02
Publication Title Biology of Blood and Marrow Transplantation
Volume volume20
Issue issue2
Content Type Journal Article
Author Murakami, Toshi| Takigawa, Nagio| Ninomiya, Takashi| Ochi, Nobuaki| Yasugi, Masaaki| Honda, Yoshihiro| Kubo, Toshio| Ichihara, Eiki| Hotta, Katsuyuki| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2014-01
Publication Title Lung Cancer
Volume volume83
Issue issue1
Content Type Journal Article