Omoromachi Medical Center

Naha-shi, Japan

Omoromachi Medical Center

Naha-shi, Japan
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Sugaya K.,Kitakami Central Hospital | Sugaya K.,Southern Knights Laboratory LLP | Sekiguchi Y.,Yokohama Motomachi Womens Clinic LUNA | Satoh T.,Satoh Continence Clinic | And 5 more authors.
International Journal of Urology | Year: 2014

Objectives: To investigate whether the anticholinergic agent, propiverine hydrochloride, is clinically effective for stress urinary incontinence. Methods: The participants were adult female patients with the chief complaint of stress incontinence. Propiverine (20 mg once daily) was given for 8 weeks. If the response was inadequate after 4 weeks of treatment, the dose was increased to 40 mg/day. Before and after 4 and 8 weeks of treatment, lower urinary tract symptoms were assessed. The urethral pressure and blood catecholamine levels were also measured. Results: A total of 37 patients (mean age 69 ± 11 years) were enrolled, including 15 patients with stress incontinence and 22 with mixed incontinence. The number of episodes of stress incontinence decreased significantly from 2.6 ± 2.3 times per day to 1.3 ± 2.2 times per day after 4 weeks, and 0.4 ± 0.6 times per day after 8 weeks. The daytime and night-time frequency of urination, and quality of life score showed significant improvement. The maximum urethral closing pressure and the functional urethral length increased significantly after treatment, but blood catecholamine levels, blood pressure and pulse rate at 8 weeks were not significantly different from those at baseline. Conclusions: Propiverine could be an effective drug for stress urinary incontinence by increasing urethral closing pressure without increasing blood catecholamine levels. © 2014 The Japanese Urological Association.

Nakama S.,University of Ryukyus | Nakama S.,Musashino Research Institute for Immunity | Ishikawa C.,University of Ryukyus | Ishikawa C.,Transdisciplinary Research Organization for Subtopics and Island Studies | And 3 more authors.
International Journal of Oncology | Year: 2011

We evaluated the effects of Bidens pilosa, a plant found in tropical and subtropical regions, and investigated the molecular pathways responsible for the anti-adult T-cell leukemia (ATL) effect. Water extracts of B. pilosa had growth suppressive effects on human T-cell leukemia virus type 1 (HTLV-1)-infected T-cell lines and ATL cells. B. pilosa extracts arrested cells in G 1 cell cycle and induced apoptosis of HTLV-1-infected T-cell lines. B. pilosa extracts inhibited also the phosphorylation of IκB kinase β and IκBα, and NF-κB-DNA binding, in conjunction with reduction of expression of proteins involved in G 1/S cell cycle transition and suppression of apoptosis. Reactive oxygen species played a role in B. pilosa-mediated suppression of NF-κB activity. B. pilosa extracts also inhibited the expression of JunB and JunD, resulting in suppression of AP-1-DNA binding. In animals harboring tumors of HTLV-1-infected T-cell origin, treatment with B. pilosa extracts suppressed tumor growth. Our results suggest that B. pilosa is a potentially useful medicinal plant for treatment of ATL.

Ishikawa C.,University of Ryukyus | Nakachi S.,University of Ryukyus | Senba M.,Nagasaki University | Sugai M.,Kyoto University | And 2 more authors.
Carcinogenesis | Year: 2011

Adult T-cell leukemia (ATL) is a T-cell malignancy associated with human T-cell leukemia virus type 1 (HTLV-1). Mutations of tumor suppressor genes have been described in ATL. Although Tax, a product of HTLV-1, is associated with cellular genetic aberrations, the mechanisms of such association are not fully clear. Activation-induced cytidine deaminase (AID) is involved in somatic DNA alterations of the immunoglobulin gene for amplification of immune diversity. However, inappropriate expression of AID acts as a genomic mutator that contributes to tumorigenesis. To gain insight into the molecular mechanism underlying the emergence of somatic mutations in various genes during leukemogenesis, we examined the expression of AID. HTLV-1-infected T-cell lines and ATL cells expressed high levels of AID compared with uninfected T-cell lines and normal peripheral blood mononuclear cells (PBMCs). Immunohistochemistry showed AID-positive ATL cells in lymph nodes and skin lesions. Infection of a human T-cell line and normal PBMCs with HTLV-1 induced AID expression. Tax transcriptionally activated AID gene through both the nuclear factor-kappaB subunit p50 and cyclic adenosine 3′,5′-monophosphate response element-binding protein signaling pathways. p50, which lacks a transactivation domain, interacted with the transcriptional coactivator Bcl-3 in HTLV-1-infected T cells. Thus, activation of p50/Bcl-3 complexes in T cells in response to Tax might explain the constitutive expression of AID in HTLV-1-infected T cells. The constitutive expression of AID in ATL cells can be speculated to result from mutations induced by the Tax-activated AID and/or other Tax-associated mutagenic mechanisms during the pre-leukemic stage, which cause functional modification within the AID promoter or in any of its cellular regulatory activator proteins. © The Author 2010. Published by Oxford University Press. All rights reserved.

Nakamura H.,University of Ryukyus | Tateyama M.,University of Ryukyus | Tasato D.,University of Ryukyus | Haranaga S.,University of Ryukyus | And 4 more authors.
Journal of Infection and Chemotherapy | Year: 2014

Background and objective: Previous studies have suggested that human immunodeficiency virus (HIV) infection and/or the airway colonization of Pneumocystis jirovecii (Pcj) impact on the progression of airway obstruction, such as chronic obstructive pulmonary disease (COPD). This study was aimed to evaluate the relationship between HIV infection, airway colonization of Pcj and airway obstruction in Japanese male patients. Methods: Case-control study of 49 HIV-positive and 257 HIV-negative men were enrolled in this study. Airway obstruction was determined by spirometry. Cigarette smoking was determined by a self report. Laboratory data were obtained from medical records. Among HIV positive patients, the airway colonization of Pcj was evaluated by induced sputum using the real time polymerase chain reaction method. Results: Forty-eight out of 49 (97.9%) HIV-positive patients received antiretroviral therapy, and their median CD4 cell counts were 491/μL (79-935). The prevalence of airway obstruction as determined by spirometry was 10.2% (5/49) in HIV-positive subjects and 2.4% (5/208) in HIV-negative subjects (p = 0.024). Compared with the control group, HIV-positive patients were significantly younger (median age 44 vs 40, p = 0.019). After adjusting for age, pack-years of smoking, HIV infectionwas an independent risk factor for airway obstruction (OR; 10.93, 95%CI 1.99-60.1, p = 0.006). None of patient was detected the airway colonization of Pcj. Conclusions: HIV infection was an independent risk factor for airway obstruction regardless of airway colonization of Pcj. Health-care providers should be aware of the increased likelihood of airway obstruction among HIV-positive patients. © 2014, Japanese Society of Chemotherapy and The Japanese Association for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.

Mori N.,University of Ryukyus | Mori N.,Omoromachi Medical Center | Ishikawa C.,University of Ryukyus | Senba M.,Nagasaki University | And 2 more authors.
Biochemical Pharmacology | Year: 2011

We studied the effects of AZD1152, an Aurora B kinase inhibitor, on Burkitt's lymphoma (BL) and Hodgkin's lymphoma (HL) in human tissues and cell cultures and in a murine xenograft model of lymphoma. Aurora kinase A and B levels were assessed by RT-PCR and immunohistochemistry. They were aberrantly expressed in BL and HL cell lines, and in lymph nodes from patients with BL and HL. Next, activation of the Aurora B promoter was detected by reporter gene assays. The promoter activity of Aurora B kinase was high in BL cell lines and the Aurora B promoter contained a positive regulatory region between -74 and -104 from the transcription initiation site. AZD1152-hQPA had antiproliferative effects in the BL and HL cell lines studied; inhibited the phosphorylation of histone H3 and retinoblastoma proteins, and resulted in cells with >4 N DNA content. AZD1152-hQPA induced caspase-dependent apoptosis of some cell lines, demonstrated by loss of mitochondrial membrane potential, activation of caspase-9, followed by activation of caspase-3. This effect was accompanied by the inhibition of survivin expression. In vivo efficacy was determined in NOD/SCID/γcnull mice implanted with the Ramos human BL cell line. AZD1152 had anti-tumour effects in this murine xenograft model. There preclinical data suggest that the inhibition of Aurora B kinase is a potentially useful therapeutic strategy in BL and HL. © 2011 Elsevier Inc. All rights reserved.

Mori N.,University of Ryukyus | Mori N.,Omoromachi Medical Center | Ishikawa C.,University of Ryukyus | Senba M.,Nagasaki University
World Journal of Gastroenterology | Year: 2011

AIM: To investigate and elucidate the molecular mechanism that regulates inducible expression of CD69 by Helicobacter pylori (H. pylori) infection. METHODS: The expression levels of CD69 in a T-cell line, Jurkat, primary human peripheral blood mononu-clear cells (PBMCs), and CD4 + T cells, were assessed by immunohistochemistry, reverse transcription polymerase chain reaction, and fow cytometry. Activation of CD69 promoter was detected by reporter gene. Nuclear factor (NF)-κB activation in Jurkat cells infected with H. pylori was evaluated by electrophoretic mobility shift assay. The role of NF-κB signaling in H. pylori-induced CD69 expression was analyzed using inhibitors of NF-κB and dominant-negative mutants. The isogenic mutants with disrupted cag pathogenicity island (cagPAI) and virD4 were used to elucidate the role of cagPAI-encoding type IV secretion system and CagA in CD69 expression. RESULTS: CD69 staining was detected in mucosal lymphocytes and macrophages in specimens of patients with H. pylori-positive gastritis. Although cagPAI-positive H. pylori and an isogenic mutant of virD4 induced CD69 expression, an isogenic mutant of cag-PAI failed to induce this in Jurkat cells. H. pylori also induced CD69 expression in PBMCs and CD4 + T cells. The activation of the CD69 promoter by H. pylori was mediated through NF-κB. Transfection of dominant-negative mutants of IκBs, IκB kinases, and NF-κB-inducing kinase inhibited H. pylori-induced CD69 activation. Inhibitors of NF-κB suppressed H. pylori-induced CD69 mRNA expression. CONCLUSION: The results suggest that H. pylori induces CD69 expression through the activation of NF-κB. cagPAI might be relevant in the induction of CD69 expression in T cells. CD69 in T cells may play a role in H. pylori-induced gastritis. © 2011 Baishideng. All rights reserved.

Hibiya K.,University of Ryukyus | Tateyama M.,University of Ryukyus | Teruya H.,University of Ryukyus | Nakamura H.,University of Ryukyus | And 8 more authors.
Pathology Research and Practice | Year: 2011

Immune reconstitution inflammatory syndrome (IRIS) caused by mycobacterium in patients with AIDS is often experienced in clinical practice. There is, however, a paucity of data documenting the histopathological findings and the pathogenesis. We determined the immunopathological characteristics of IRIS associated with Mycobacterium parascrofulaceum infection in an AIDS patient. A patient presented with pulmonary lymphadenitis and involvement of the pulmonary lingular segment. Portions of the involved lymph nodes and lung were excised, and the immunological properties were analyzed by immunohistochemical assays. The histological characteristics of lymph nodes showed a caseous necrosis. Histopathologically, the pulmonary lesion was composed of exudative and proliferative lesions. CD4 +, CD8 +, CD57 +, and CD25 +/FoxP3 + cells were observed in both types of lesions. Clusters of CD20 + cells and GATA3 + cells were predominantly observed in exudative lesions, while T-bet + cells were dominant in proliferative lesions. ROR-γ + cells were also observed in exudative lesions. These results indicate that the cellular immunity to mycobacteria was recovering in the lung tissue. In M. parascrofulaceum pulmonary infection, the exudative lesion had characteristics of Th2 and Th17-type immunities. In contrast, the proliferative lesion had characteristics of Th-1 type immunity. Our data provide the first evidence to reveal the status of the axis of distinctive immunity in the process of granuloma formation caused by a mycobacterium-related infection. © 2011 Elsevier GmbH.

Senba M.,Nagasaki University | Buziba N.,Moi University | Mori N.,Omoromachi Medical Center | Fujita S.,Nagasaki University | And 3 more authors.
Oncology Letters | Year: 2011

This study aimed to determine the relationship between human papillomavirus (HPV) and nuclear factor-κB (NF-κB) in cervical cancer using 62 tissues of cervical cancer, and to compare the findings to penile cancer. HPV-DNA integration is a crucial factor for malignant transformation in cervical cancer and can be identified using in situ hybridization. Of the 62 cases, HPV infection was detected in 28 (45.2%). This frequency was lower than in penile cancer (68.2%) as shown by our previous study. The earliest age of onset of cervical and penile cancer was 18 and 35, respectively, whereas the mean age of the initial diagnosis of cervical and penile cancer was 50.1 and 59.6, respectively. The discrepancies of HPV prevalence, earliest ages of onset and mean ages between cervical and penile cancer patients may result from the gender-based synergistic action of HPV associated with multiple epidemiological co-factors. Of the 28 HPV-infected cases, NF-κB expression was observed in the nucleus in 18 (64.3%), in the cytoplasm in 19 (67.9%) and in the nucleus and/or cytoplasm in 27 cases (96.4%). The overexpression of NF-κB in cervical cancer cases suggests that NF-κB activation is a key modulator in driving chronic inflammation to cancer.

Senba M.,Nagasaki University | Buziba N.,Moi University | Mori N.,Omoromachi Medical Center | Morimoto K.,Nagasaki University | Nakamura T.,Nagasaki University
Acta Virologica | Year: 2011

Kaposi's sarcoma (KS) had been endemic in Africa before the appearance of human immunodeficiency viruses (HIV) in 1985. Incidence of African KS has increased over the time and the risk of contracting KS become greater in HIV-positive as opposed to HIV-negative individuals. KS specimens were collected in 1981-2000 from 228 surgical cases originating from a KS-endemic area of Western Kenya and examined for Kaposi?s sarcoma-associated herpesvirus (KSHV) by an immunoperoxidase assay. The results showed that the specimens from 1981-1985 (before the HIV epidemic) were KSHV-positive in 10.3% in contrast to the KSHV positivity of 50.1-63.5% in 1986-2000. The linear increase of KSHV positivity in 1981-2000 was statistically significant. The most plausible explanation for the increased prevalence of KSHV in KS cases is that the endemic KS has changed to the epidemic one.

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