Refine your search:     
Report No.
 - 
Search Results: Records 1-5 displayed on this page of 5
  • 1

Presentation/Publication Type

Initialising ...

Refine

Journal/Book Title

Initialising ...

Meeting title

Initialising ...

First Author

Initialising ...

Keyword

Initialising ...

Language

Initialising ...

Publication Year

Initialising ...

Held year of conference

Initialising ...

Save select records

Journal Articles

Nitric oxide-mediated bystander signal transduction induced by heavy-ion microbeam irradiation

Tomita, Masanori*; Matsumoto, Hideki*; Funayama, Tomoo; Yokota, Yuichiro; Otsuka, Kensuke*; Maeda, Munetoshi*; Kobayashi, Yasuhiko

Life Sciences in Space Research, 6, p.36 - 43, 2015/07

A radiation-induced bystander response is generally known as a cellular response induced in unirradiated cell by receiving bystander signaling factors released from directly irradiated cells of a cell population. Bystander responses induced by high-LET heavy ions at low fluence are an important problem concerning the health of astronauts in the space environment. Here we set out NO-mediated bystander signal transductions induced by high-LET heavy-ion microbeam irradiation in normal human fibroblasts. Our findings suggest that Akt- and NF-$$kappa$$B-dependent signaling pathway involving COX-2 plays an important role in the NO-mediated high-LET heavy-ion-induced bystander responses. Additionally, COX-2 may be used as a molecular marker of high-LET heavy-ion-induced bystander cells, which are distinguish form directly irradiated cells.

Journal Articles

Mechanisms for the induction of radioadaptive response by radiation-induced bystander response

Matsumoto, Hideki*; Tomita, Masanori*; Otsuka, Kensuke*; Hatashita, Masanori*; Maeda, Munetoshi*; Funayama, Tomoo; Yokota, Yuichiro; Suzuki, Michiyo; Sakashita, Tetsuya; Ikeda, Hiroko; et al.

JAEA-Review 2014-050, JAEA Takasaki Annual Report 2013, P. 76, 2015/03

The objective of this project is to elucidate molecular mechanisms for the induction of radioadaptive response through radiation-induced bystander responses induced by irradiation with heavy ion microbeams in JAEA. We found that the adaptive response was induced by Ar (520 MeV $$^{40}$$Ar$$^{14+}$$) microbeam-irradiation of a limited number of cells, followed by the broad beam-irradiation and that the adaptive response was almost completely suppressed by the addition of carboxy-PTIO, as a nitric oxide (NO) scavenger. In addition, we found several genes induced specifically and preferentially when radioadaptive response could be induced. We confirmed that ${it iNOS}$ expression was specifically induced only when radioadaptive response could be induced. Our findings strongly suggested that radioadaptive response can be induced by NO-mediated bystander responses evoked by irradiation with heavy ion microbeams.

Journal Articles

Microbeam irradiation facilities for radiobiology in Japan and China

Kobayashi, Yasuhiko; Funayama, Tomoo; Hamada, Nobuyuki*; Sakashita, Tetsuya; Konishi, Teruaki*; Imaseki, Hitoshi*; Yasuda, Keisuke*; Hatashita, Masanori*; Takagi, Keiichi*; Hatori, Satoshi*; et al.

Journal of Radiation Research, 50(Suppl.A), p.A29 - A47, 2009/03

 Times Cited Count:34 Percentile:72.55(Biology)

Oral presentation

Radiation-quality-dependence in bystander cellular effects on normal human cells induced by carbon-ion and X-ray microbeams

Suzuki, Masao*; Furusawa, Yoshiya*; Tsuruoka, Chizuru*; Kobayashi, Katsumi*; Usami, Noriko*; Maeda, Munetoshi*; Funayama, Tomoo; Sakashita, Tetsuya; Yokota, Yuichiro; Fukamoto, Kana; et al.

no journal, , 

no abstracts in English

Oral presentation

DNA base lesions induced by phorosphorus K-ionization and its Auger decay

Yokoya, Akinari; Usami, Noriko*; Maeda, Munetoshi*

no journal, , 

In previous studies, DNA double strand breaks (DSBs) induced by phosphorus K-shell ionization are studied in terms of its cell killing effect. Recently non-DSB type complex damage has been known to induce radiobiological effect such as mutation. The complex damage consists of several base lesions produced in a few nm of DNA molecule, and retard the enzymatic repair process. However there was very little knowledge about the base lesions induced by phosphorus K-shell ionization. In this study, experimental evidences of the production of the base lesions are reported using plasmid DNA as a model molecule. The yields of the base lesions were quantified using base excision repair proteins as enzymatic probes (glycosylases). Several irradiation conditions were tested and the obtained results are compared to discuss the process of the base lesions formation.

5 (Records 1-5 displayed on this page)
  • 1