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ABSTRACT: Repeated Waon therapy, which uses a far infrared-ray dry sauna system, improved the vascular endothelial function and the cardiac function in patients with chronic heart failure. In patients with chronic obstructive pulmonary disease (COPD), pulmonary hypertension (PH) is associated with a poor prognosis. We investigated whether repeated Waon therapy improves PH, cardiac function, exercise tolerance, and the quality of life (QOL) in patients with COPD.
Consecutive 13 patients with COPD, who met the Global Initiative for Chronic Obstructive Lung Disease criteria and had breathlessness despite receiving conventional treatments, were recruited for this study. They underwent Waon therapy at 60 degrees C in sauna for 15 min following 30 min warmth with blankets outside of the sauna room. This therapy was performed once a day, for 4 weeks. Cardiac function, exercise tolerance, and St. George's Respiratory Questionnaire (SGRQ) were assessed before and 4 weeks after Waon therapy.
Right ventricular positive dP/dt at rest elevated significantly from 397 +/- 266 to 512 +/- 320 mmHg/s (p = 0.024) after the therapy. While the PH at rest did not significantly decrease, the PH during exercise decreased significantly from 64 +/- 18 to 51 +/- 13 mmHg (p = 0.028) after Waon therapy. Furthermore, the therapy prolonged the mean exercise time of the constant load of cycle ergometer exercise test from 360 +/- 107 to 392 +/- 97 s (p = 0.032). The total scores of SGRQ improved from 59.7 +/- 16.9 to 55.3 +/- 17.2 (p = 0.002). In addition, no adverse effects were observed related to Waon therapy.
Repeated Waon therapy improved right ventricular positive dP/dt, PH during exercise, exercise tolerance and the QOL in patients with severe COPD.
Journal of Cardiology 04/2008; 51(2):106-13. · 1.28 Impact Factor
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Mitsuhiro Suenaga,
Kakushi Matsushita,
Nakaaki Kawamata,
Toshimasa Kukita,
Yuji Hamakawa,
Kentaro Gejima,
Reiri Onodera,
Tetsuo Sato, Akihiko Yamaguchi,
Hirosaka Inoue,
Kosei Arimura,
Naomichi Arima,
Hiroki Yoshida,
Chuwa Tei
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ABSTRACT: A 24-year-old Japanese man was admitted due to bloody phlegm in May 2002. A diagnosis of mediastinal germ cell tumor, mixed type involving seminoma, immature teratoma and embryonal carcinoma, was made by transthoracic needle biopsy. Three months later, his complete blood counts revealed pancytopenia with high fever. Examination of bone marrow revealed increased atypical large histiocytes (5.6%) with hemophagocytosis, and thus, hemophagocytic syndrome related to germ cell tumor was diagnosed. In addition, chromosomal analysis of the bone marrow cells revealed a 47, XY, +9 genotype. Chemotherapies for germ cell tumor and hemophagocytic syndrome were performed without any improvement, and he died of diffuse alveolar damage. Autopsy revealed diffuse infiltration of immature histiocytes with hemophagocytosis in the liver, spleen and bone marrow. The atypical histiocytes were positive for CD68 and lysozyme and negative for lymphoid markers, and the diagnosis of true malignant histiocytosis associated with mediastinal germ cell tumor was made. The rare chromosomal abnormality of trisomy 9, a marker for benzene-related leukemia, was seen in the present case without apparent benzene exposure.
Acta Haematologica 02/2006; 116(1):62-6. · 1.35 Impact Factor
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Kosei Arimura,
Hirosaka Inoue,
Toshimasa Kukita,
Kakushi Matsushita,
Masaki Akimot,
Nakaaki Kawamata, Akihiko Yamaguchi,
Hideaki Kawada,
Atsuo Ozak,
Naomichi Arima,
Chuwa Te
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ABSTRACT: Granulocyte-colony stimulating factor (G-CSF), a hematopoietic growth factor, is widely used to accelerate recovery from neutropenia after severe chemotherapy, both decreasing the risk of infection and mobilizing peripheral blood stem cells. Adverse effects occur with G-CSF use in approximately 30% of cases, comprised predominantly of bone pain, headache, and general fatigue. Pulmonary toxicity is very rare. Here, we describe a healthy donor for allogeneic hematopoietic stem cell transplantation who developed acute lung injury (ALI) after 4 days of G-CSF administration. Among the serum cytokines examined, only Interleukin (IL)-1beta level was elevated in this case. As a high level of IL-1beta was detected at the onset of ALI, on day 4 after G-CSF administration, and decreased to below the level of detection on day 11, it is possible in a certain part that IL-1beta was involved in the onset of G-CSF-related ALI in the present case. Granulocyte-colony stimulating factor (G-CSF) is commonly administered to healthy donors to mobilize peripheral blood stem cells (PBSC) for allogeneic hematopoietic stem cell transplantation (allo-HSCT). Adverse events from G-CSF use in healthy donors have been described in approximately 30% of cases, and are comprised predominantly of bone pain, headache, and general fatigue. Pulmonary complications caused by G-CSF include cough, dyspnea, and interstitial or alveolar pulmonary edema with mild-to-severe deterioration of blood oxygen level. Few cases of acute respiratory distress syndrome (ARDS) following G-CSF administration have been reported. The present report describes a healthy donor for allo-HSCT with acute lung injury (ALI) after 4 days of G-CSF administration. The cytokine-related mechanisms of G-CSF administration that contribute to ALI are discussed.
Haematologica 04/2005; 90(3):ECR10. · 6.42 Impact Factor
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Yoshimune Sakaki,
Kenji Terashi, Akihiko Yamaguchi,
Nakaaki Kawamata,
Yuichi Tokito,
Hiroyasu Mori,
Megumi Umehara,
Takeshi Yoshiyama,
Hideo Ohtsubo,
Kosei Arimura,
Naomichi Arima,
Chuwa Tei
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ABSTRACT: We examined the significance of human T-cell lymphotropic virus type I (HTLV-I) Tax protein-induced resistance to anticancer drugs and the relationship between Tax and multidrug resistance proteins.
S1T cell, a leukemic non-Tax-producing T-cell clone established from an adult T-cell leukemia (ATL) patient, S1TcTax05 and S1TcTax10 clones, transfected with Tax stably expressing cDNA, and S1Tneo, transfected with a neomycin-resistant gene, were examined for Tax-related anticancer drug resistance. Resistance of those cells to the anticancer drugs doxorubicin, etoposide, cisplatin, and vindesine was tested with the MTT method. Expression of multidrug resistance protein mRNAs (MDR1, MRP1, cMOAT/MRP2, and LRP) was analyzed with reverse transcriptase polymerase chain reaction (RT-PCR). Doxorubicin subcellular distribution in those cells was examined by fluorescence microscopy.
S1TcTax05 and S1TcTax10 showed resistance to doxorubicin, etoposide, and vindesine, but not to cisplatin as compared with S1T or S1Tneo. RT-PCR demonstrated that MRP1 mRNA was expressed, but MDR1, cMOAT, and LRP mRNAs were not in S1T or S1Tneo. Marked expression of LRP mRNA was detected, but no change of MDR1, MRP1, or cMOAT mRNA expression in Tax-expressing S1TcTax05 and S1TcTax10. Fluorescence microscopy demonstrated that doxorubicin was distributed mainly in the cytoplasm of S1TcTax05 and S1TcTax10, and in the nucleus of S1T and S1Tneo.
These findings suggest that Tax-related drug resistance of ATL cells is due to LRP and not MDR1, as reported previously. These findings in cells derived from an ATL patient suggest a novel mechanism for drug resistance in Tax-expressing ATL cells.
Experimental Hematology 05/2002; 30(4):340-5. · 2.90 Impact Factor
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Mitsuhiro Suenaga,
Hiroshi Soda,
Mikio Oka, Akihiko Yamaguchi,
Katsumi Nakatomi,
Ken Shiozawa,
Shigeru Kawabata,
Takashi Kasai,
Yasuaki Yamada,
Shimeru Kamihira,
Chuwa Tei,
Shigeru Kohno
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ABSTRACT: Telomerase activity is involved in cellular immortality. We have recently demonstrated that telomerase activity is closely associated with cell proliferation in prostate cancers. Telomerase is composed primarily of the catalytic subunit (hTERT) and the RNA template (hTERC), and hTERT expression is regulated by several factors such as c-MYC and p21(Waf1). Histone deacetylase (HDAC) inhibitors are known to modulate transcription and exhibit antiproliferative effects on cancer cells. The present study was designed to evaluate the effects of HDAC inhibitors on hTERT mRNA expression in prostate cancer cells. LNCaP and PC-3 cells were treated with HDAC inhibitors, trichostatin A (TSA) and sodium butyrate (NaB); mRNA expression and telomerase activity were evaluated by RT-PCR and the TRAP assay, respectively. In LNCaP cells, hTERT mRNA expression was suppressed at 1 and 3 hr after treatment with 1 microM TSA and 4 mM NaB, respectively, followed by inhibition of telomerase activity. The inhibition of hTERT mRNA expression preceded suppression of cell proliferation. In PC-3 cells, TSA and NaB also inhibited cell proliferation, hTERT mRNA expression and telomerase activity. In both cell lines, TSA and NaB had no effect on hTERC expression, or on expression of c-myc and p21(Waf1) mRNA. These effects of TSA and NaB were unlikely to be consequences of cell cycle arrest, apoptosis, or cell differentiation. Thus, HDAC inhibitors down-regulated telomerase activity via suppression of hTERT mRNA expression. Our study identified a novel mechanism for the antiproliferative effects of HDAC inhibitors on prostate cancer cells.
International Journal of Cancer 03/2002; 97(5):621-5. · 5.44 Impact Factor
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Mitsuhiro Suenaga, Akihiko Yamaguchi,
Hiroshi Soda,
Koji Orihara,
Yuichi Tokito,
Yoshimune Sakaki,
Megumi Umehara,
Kenji Terashi,
Nakaaki Kawamata,
Mikio Oka,
Shigeru Kohno,
Chuwa Tei
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ABSTRACT: Gefitinib (Iressa, ZD1839) is a selective epidermal growth factor receptor tyrosine kinase inhibitor. E2F-1 is a critical determinant in cell cycle. Growth signals up-regulate telomerase activity. The effects of gefitinib on E2F-1 and telomerase in A549, H23 and A431 cells were examined.
Cell proliferation and cell cycle progression were measured by the WST-1 assay and flow cytometry. The expression of E2F-1 and cyclin-dependent kinase inhibitors was evaluated, and hTERT mRNA expression and telomerase activity were analyzed.
In the A431 and A549 cells, treatment with gefitinib inhibited cell proliferation and was associated with an increase in G1-phase. In both cell types, gefitinib decreased the expression of E2F-1 mRNA and protein, followed by the suppression of hTERT mRNA and telomerase activity. In the H23 cells, gefitinib did not affect cell proliferation.
The antiproliferative effects of gefitinib may be, at least in part, due to the inhibition of E2F-1 expression and telomerase activity.
Anticancer research 26(5A):3387-91. · 1.73 Impact Factor
