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Nagasaki-shi, Japan

Nagataki S.,Nagasaki University | Nagataki S.,Radiation Effects Research Foundation | Takamura N.,Atomic Bomb Disease Institute | Kamiya K.,Hiroshima University | And 2 more authors.
Radiation Research | Year: 2013

At the outset of the accident at Fukushima Daiichi Nuclear Power Plant in March 2011, the radiation doses experienced by residents were calculated from the readings at monitoring posts, with several assumptions being made from the point of view of protection and safety. However, health effects should also be estimated by obtaining measurements of the individual radiation doses. The individual external radiation doses, determined by a behavior survey in the "evacuation and deliberate evacuation area" in the first 4 months, were <5 mSv in 97.4% of residents (maximum: 15 mSv). Doses in Fukushima Prefecture were <3 mSv in 99.3% of 386,572 residents analyzed. External doses in Fukushima City determined by personal dosimeters were <1 mSv/3 months (September-November, 2011) in 99.7% of residents (maximum: 2.7 mSv). Thyroid radiation doses, determined in March using a NaI (TI) scintillation survey meter in children in the evacuation and deliberate evacuation area, were <10 mSv in 95.7% of children (maximum: 35 mSv). Therefore, all doses were less than the intervention level of 50 mSv proposed by international organizations. Internal radiation doses determined by cesium-134 (134C) and cesium-137 ( 137C) whole-body counters (WBCs) were <1 mSv in 99% of the residents, and the maximum thyroid equivalent dose by iodine-131 WBCs was 20 mSv. The exploratory committee of the Fukushima Health Management Survey mentions on its website that radiation from the accident is unlikely to be a cause of adverse health effects in the future. In any event, sincere scientific efforts must continue to obtain individual radiation doses that are as accurate as possible. However, observation of the health effects of the radiation doses described above will require reevaluation of the protocol used for determining adverse health effects. The dose-response relationship is crucial, and the aim of the survey should be to collect sufficient data to confirm the presence or absence of radiation health effects. In particular, the schedule of decontamination needs reconsideration. The decontamination map is determined based on the results of airborne monitoring and the radiation dose calculated from readings taken at the monitoring posts at the initial period of the accident. The decontamination protocol should be reevaluated based on the individual doses of the people who desire to live in those areas. Source


Ueki I.,Atomic Bomb Disease Institute | Abiru N.,Endocrinology and Metabolism | Kobayashi M.,Endocrinology and Metabolism | Nakahara M.,Atomic Bomb Disease Institute | And 4 more authors.
Clinical and Experimental Immunology | Year: 2011

Graves' disease is a B cell-mediated and T cell-dependent autoimmune disease of the thyroid which is characterized by overproduction of thyroid hormones and thyroid enlargement by agonistic anti-thyrotrophin receptor (TSHR) autoantibody. In addition to antibody secretion, B cells have recently been recognized to function as antigen-presenting/immune-modulatory cells. The present study was designed to evaluate the efficacy of B cell depletion by anti-mouse (m) CD20 monoclonal antibody (mAb) on Graves' hyperthyroidism in a mouse model involving repeated injection of adenovirus expressing TSHR A-subunit (Ad-TSHR289). We observe that a single injection of 250μg/mouse anti-mCD20 mAb eliminated B cells efficiently from the periphery and spleen and to a lesser extent from the peritoneum for more than 3 weeks. B cell depletion before immunization suppressed an increase in serum immunoglobulin (Ig)G levels, TSHR-specific splenocyte secretion of interferon (IFN)-γ, anti-TSHR antibody production and development of hyperthyroidism. B cell depletion 2 weeks after the first immunization, a time-point at which T cells were primed but antibody production was not observed, was still effective at inhibiting antibody production and disease development without inhibiting splenocyte secretion of IFN-γ. By contrast, B cell depletion in hyperthyroid mice was therapeutically ineffective. Together, these data demonstrate that B cells are critical not only as antibody-producing cells but also as antigen-presenting/immune-modulatory cells in the early phase of the induction of experimental Graves' hyperthyroidism and, although therapeutically less effective, B cell depletion is highly efficient for preventing disease development. © 2011 The Authors. Clinical and Experimental Immunology © 2011 British Society for Immunology. Source


Khan K.N.,Nagasaki University | Fujishita A.,Saiseikai Nagasaki Hospital | Kitajima M.,Nagasaki University | Hiraki K.,Nagasaki University | And 2 more authors.
Human Reproduction | Year: 2014

STUDY QUESTION: Is there any risk of intra-uterine bacterial colonization and concurrent occurrence of endometritis in women with endometriosis?SUMMARY ANSWER: An increase in intra-uterine microbial colonization and concurrent endometritis occurred in women with endometriosis that was further increased after GnRH agonist (GnRHa) treatment.WHAT IS KNOWN ALREADY: Higher bacterial contamination of menstrual blood and increased endotoxin level in menstrual and peritoneal fluids have been found in women with endometriosis than in control women. However, information on intra-uterine microbial colonization across the phases of the menstrual cycle and possible occurrence of endometritis in women with endometriosis is still lacking.STUDY DESIGN, SIZE AND DURATION: This is a case-controlled study with prospective collection of vaginal smears/endometrial samples from women with and without endometriosis and retrospective evaluation.PARTICIPANTS/MATERIALS, SETTING, METHODS: Vaginal smears and endometrial smears were collected from 73 women with endometriosis and 55 control women. Twenty of the women with endometriosis and 19 controls had received GnRHa therapy for a period of 4-6 months. Vaginal pH was measured by intra-vaginal insertion of a pH paper strip. The bacterial vaginosis (BV) score was analyzed by Gram-staining of vaginal smears and based on a modified Nugent-BV scoring system. A panel of bacteria was analyzed by culture of endometrial samples from women treated with GnRHa or not treated. Immunohistochemcial analysis was performed using antibody against Syndecan-1 (CD138) and myeloperoxidase in endometrial biopsy specimens from women with and without endometriosis.MAIN RESULTS AND THE ROLE OF CHANCE: A significant shifting of intra-vaginal pH to 4.5 was observed in women with endometriosis compared with control women (79.3 versus 58.4%, P < 0.03). Compared with untreated women, use of GnRHa therapy also shifted vaginal pH to 4.5 in both control women (P = 0.004) and in women with endometriosis (P = 0.03). A higher risk of increasing intermediate flora (total score, 4-6) (P = 0.05) was observed in women with endometriosis who had GnRHa treatment versus untreated women. The number of colony forming units (CFU/ml) of Gardnerella, α-Streptococcus, Enterococci and Escherichia coli was significantly higher in endometrial samples from women with endometriosis than control women (P < 0.05 for each bacteria). GnRHa-treated women also showed significantly higher colony formation for some of these bacteria in endometrial samples than in untreated women (Gardnerella and E. coli for controls; Gardnerella, Enterococci and E. coli for women with endometriosis, P < 0.05 for all). Although there was no significant difference in the occurrence of acute endometritis between women with and without endometriosis, both GnRHa-treated controls and women with endometriosis had a significantly higher occurrence of acute endometritis (P = 0.003 for controls, P = 0.001 for endometriosis versus untreated women). Multiple analysis of covariance analysis revealed that an intra-vaginal pH of 4.5 (P = 0.03) and use of GnRHa (P = 0.04) were potential factors that were significantly and independently associated with intra-uterine microbial colonization and occurrence of endometritis in women with endometriosis. These findings indicated the occurrence of sub-clinical uterine infection and endometritis in women with endometriosis after GnRHa treatment.LIMITATIONS, REASONS FOR CAUTION: We cannot exclude the introduction of bias from unknown previous treatment with immunosuppressing or anti-microbial agents. We have studied a limited range of bacterial species and used only culture-based methods. More sensitive molecular approaches would further delineate the similarities/differences between the vaginal cavity and uterine environment.WIDER IMPLICATIONS OF THE FINDINGS: Our current findings may have epidemiological and biological implications and help in understanding the pathogenesis of endometriosis and related disease burden. The worsening of intra-uterine microbial colonization and higher occurrence of endometritis in women with endometriosis who were treated with GnRHa identifies some future therapeutic avenues for the management, as well as prevention of recurrence, of endometriosis. Further studies are needed to examine intra-uterine colonization of a broad range of common bacteria as well as different viruses and their role in the occurrence of endometritis.STUDY FUNDING/COMPETING INTEREST(S): This work was supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Sports, Culture, Science and Technology of Japan. There is no conflict of interest related to this study. © 2014 The Author. Source


Khan K.N.,Nagasaki University | Kitajima M.,Nagasaki University | Inoue T.,Nagasaki University | Fujishita A.,Saiseikai Nagasaki Hospital | And 2 more authors.
Reproductive Sciences | Year: 2015

Endometriosis is a multifactorial disease mostly affecting women of reproductive age. An additive effect between inflammation and stress reaction on the growth of endometriosis has been demonstrated. Here we investigated the combined effect between 17β-estradiol (E2) and lipopolysaccharide (LPS) on pelvic inflammation and growth of endometriotic cells. Peritoneal fluid was collected from 46 women with endometriosis and 30 control women during laparoscopy. Peritoneal macrophages (M) and stromal cells from eutopic/ectopic endometrial stromal cells (ESCs) were isolated from 10 women each with and without endometriosis in primary culture. Changes in cytokine secretion (interleukin 6 [IL-6] and tumor necrosis factor α [TNF-α]) by M and proliferation of ESCs in response to single and combined treatment with E2 and LPS were measured by enzyme-linked immunosorbent assay and by bromodeoxyuridine incorporation assay, respectively. A significantly increased secretion of IL-6 and TNF-α in M culture media was found in response to E2 (10-8 mol/L) compared to nontreated M. This effect of E2 was abrogated after pretreatment of cells with ICI 182720 (10-6 mol/L; an estrogen receptor [ER] antagonist). Combined treatment with E2 and LPS (10 ng/mL) additively promoted IL-6 and TNF-α secretion by peritoneal M and growth of eutopic/ectopic ESCs. The additive effects of E2 + LPS on cytokine secretion and growth of ESCs were effectively suppressed after combined blocking of ER and Toll-like receptor 4. An additive effect was observed between E2 and LPS on promoting proinflammatory response in pelvis and growth of endometriosis. © The Author(s) 2014. © 2014 The Author(s). Source


Khan K.N.,Nagasaki University | Kitajima M.,Nagasaki University | Hiraki K.,Nagasaki University | Yamaguchi N.,Nagasaki University | And 6 more authors.
Fertility and Sterility | Year: 2010

To test the hypothesis that bacterial contamination of menstrual blood could be a local biologic event in the development of endometriosis, menstrual blood was cultured and bacterial endotoxin was measured in menstrual blood and peritoneal fluid. Our results suggest that compared with control women, higher colony formation of Escherichia coli in menstrual blood and endotoxin levels in menstrual fluid and peritoneal fluid in women with endometriosis may promote Toll-like receptor 4-mediated growth of endometriosis. Copyright © 2010 American Society for Reproductive Medicine, Published by Elsevier Inc. Source

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