Biomedical subjects

N Fukunishi

Publications and source records attributed to N Fukunishi.

11 recordsLinked to original sources

PubMed2005

Radiation protection system at the RIKEN RI beam factory.

The RIKEN RI (radioactive isotope) Beam Factory is scheduled to commence operations in 2006, and its maximum energy will be 400 MeV u(-1) for ions lighter than Ar and 350 MeV u(-1) for uranium. The beam intensity will be 1 pmicroA (6 x 10(12) particles s(-1)) for any element at the goal. For the hands-on-maintenance and the rational shield thickness of the building, the beam loss must be controlled with several kinds of monitors. Three types of radiation monitors will be installed. The first one consists of a neutron dose equivalent monitor and an ionisation chamber, which are commercially available area monitors. The second one is a conventional hand-held dose equivalent monitor wherein the logarithmic signal is read by a programmable logic controller based on the radiation safety interlock system (HIS). The third one is a simple plastic scintillator called a beam loss monitor. All the monitors have threshold levels for alarm and beam stop, and HIS reads all these signals.

Equipment Design↗

PubMed2002

Cellular responses to low dose heavy-ion exposure in human cells.

The human lymphoblastoid cell line TK6 was used to study the cellular responses after low-dose (100, 200, 500 mGy) or high-dose (3 Gy) of X rays, C (22 keV.micron-1) and Fe (1000 keV.micron-1) ion exposures. p53 protein induction in individual cells was determined by indirect immunofluorescence staining. Cell-cycle progression after heavy-ion exposure was determined by using a laser scanning cytometer. A characteristic pattern of cell-cycle progression was observed with 3 Gy exposure of Fe ions but not with 100 mGy. Similarly such a pattern with 100 mGy C ion exposure did not match that with 3 Gy. The proportion of p53-induced cells is proportional to the probability of cell being hit by a primary heavy ion. The observed low-dose effect can be reflected in the probability of a hit, although detailed nature about their energy deposition must be considered for more precise estimation of such an effect. New detection methodology must be developed for identification of heavy-ion specific cellular responses.

Cell Cycle↗

PubMed2001

Cellular responses by exposure to heavy-ions.

To better understand cellular responses in human lymphoblastoid cell TK6 after exposure to C-ion (22 keV/micrometer) and Fe-ion (1000 keV/micrometer), both protein induction and cell-cycle progression have been extensively analyzed by the recently developed techniques. While proceeding this line of analyses, we realized the importance of studying low-dose effect, in relation to the genetic alterations. Adaptive response by 5~20 cGy of such C- or Fe-ion irradiation to both lethal and mutagenic effects of the challenging X-ray exposure (1~3 Gy) was difficult to be seen in this TK6 cells, but surprisingly, a relatively high level of p53 and its related proteins induction was observed after low-dose irradiations of heavy-ions. Here, we focus to introduce the above results of genetic and biochemical studies to elucidate the adaptive response.

Carbon↗

PubMed1999

Complex hprt deletion events are recovered after exposure of human lymphoblastoid cells to high-LET carbon and neon ion beams.

Hypoxanthine phosphoribosyltransferase gene (hprt) mutations were induced in human TK-6 lymphoblastoid cells by irradiation at a linear energy transfer (LET) of 250 or 310 keV/micron for carbon and neon ions, respectively. At such a high level of LET, ions will lose most of their total energy and stop shortly after passing through the cell. The hprt mutations were analyzed by multiplex PCR, long-PCR and DNA sequencing of both genomic and cDNA. Over half of the C ion-induced hprt mutations (10 of 19) were point mutations, in contrast to 15% of the mutations induced by Ne ions (three of 20). The remaining 47 and 85% of the C and Ne ion-induced mutants, respectively, are deletion events. The latter events include three complex losses of multiple non-contiguous exon regions in both ion irradiation collections. We note that mutations involving the exon 6 region are frequent in the Ne ion collection: all three of the complex events retained the exon 6 region with flanking deletion of sequence and three other mutants involved deletion of this region. It may be concluded that these high-LET C and Ne ion irradiations produce different mutational spectra.

Carbon↗

PubMed1996