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OBJECTIVE In a previous study, the authors showed that the migration of Schwann cells (SCs) through end-to-side (ETS) neurorrhaphy promotes axonal regrowth within an acellular nerve graft. In the present study, the authors investigated whether a similar strategy using an artificial nerve (AN) would allow reconstruction of a long nerve gap (20 mm) in rats. METHODS Forty-eight 8- to 12-week-old Sprague Dawley rats were divided into control (AN) and experimental (SC migration-induced AN [SCiAN]) groups. Prior to the experiment, the ANs used in the SCiAN group were populated in vivo with SCs over a 4-week period by ETS neurorrhaphy onto the sciatic nerve. In both groups, a 20-mm sciatic nerve defect was reconstructed in an end-to-end fashion using 20-mm ANs. Sections from the nerve graft and distal sciatic nerve in both groups underwent assessments at 4 weeks for SC migration by immunohistochemical analysis and quantitative reverse transcription–polymerase chain reaction. At 16 weeks, axonal elongation was assessed by immunohistochemical analysis, histomorphometry, and electron microscopy. The number of myelinated fibers was counted, the g-ratio was calculated, and myelin sheath thickness and axon diameter were measured. Furthermore, functional recovery was evaluated at 16 weeks using the Von Frey filament test for sensory recovery and by calculating the muscle fiber area for motor recovery. RESULTS The area occupied by SCs at 4 weeks and by axons at 16 weeks was significantly larger in the SCiAN group than in the AN group. Histomorphometric evaluation of the distal sciatic nerve revealed a significantly greater number of axons. At 16 weeks, plantar perception in the SCiAN group was significantly better, demonstrating improvement in sensory function. However, no tibialis anterior muscle motor improvement was observed in either group. CONCLUSIONS The induction of SC migration into an AN by ETS neurorrhaphy is a useful technique for repairing 20-mm nerve defects in rats, with better nerve regeneration and sensory recovery. No motor recovery was observed in either group; however, motor recovery might require a longer period of time than the lifespan of the AN used in this study. Future studies should investigate whether structural and material reinforcement of the AN, to lower its decomposition rate, can improve functional recovery.

In this study, we aimed to investigate how homologous recombinant (HR)-related genomic instability is involved in ionizing radiation (IR)-induced thymic lymphoma in mice. We divided five-week-old Rosa26 Direct Repeat- GFP (RaDR-GFP) transgenic mice into non-IR control and IR groups and exposed the mice in the IR group to a 7.2 Gy dose of γ-rays, delivered in 1.8 Gy fractions, once a week for four weeks. We then estimated mouse survival and recorded their body, thymus, and spleen weights. The frequency of HR events in the chromosomes of the thymus, bone marrow, and spleen cells and the phenotype of thymic lymphoma cells were analyzed using fluorescence- activated cell sorting (FACS). We found that most mice in the IR group developed thymic lymphoma, their survival rate decreasing to 20% after 180 days of IR exposure, whereas no mice died in the non-IR control group until day 400. The thymus and spleen weighed significantly more in the IR-4-month group than that in the non-IR group; however, we observed no significant differences between the body weights of the control and IR mice. FACS analysis indicated that the frequency of HR events significantly increased at two and four months after the last IR dose in the bone marrow and thymus cells, but not in the spleen cells of RaDR-GFP transgenic mice, suggesting that recombi- nant cells accumulated in the thymus upon IR exposure. This suggests that IR induces genome instability, revealed as increased HR, that drives the development of thymic lymphoma. Additionally, phenotypic analysis of lymphoma cells showed an increase in the CD4-/CD8+ (CD8SP) cell population and a decrease in the CD4+/CD8- (CD4SP) cell population in the IR-4-month group compared to that in the non-IR group, indicating that IR induces an aberrant cell phenotype characteristic of lymphoma. In conclusion, we observed a significant increase in HR events and abnormal phenotype in thymic lymphoma cells at two and four months after IR exposure in both the thymus and bone marrow tissues, suggesting that genomic instability is involved in the early stages of thymic lymphomagenesis. Our study indicates that HR-visualizing RaDR-GFP transgenic mice can help explore the links between the molecular mecha- nisms of genome instability and IR-induced tumorigenesis.

The study investigated the molecular mechanisms that killed pancreatic cancer cells, including cancer stem cells (CSCs), by carbon ion beam irradiation alone or in combination with miRNA-200c under in vitro and in vivo conditions.

Background The aim of this study was to investigate whether carbon-ion beam irradiation in combination with 5-fluorouracil (5-FU) is superior to carbon-ion beam irradiation alone in targeting colorectal cancer stem-like cells (CSCs). Materials and Methods Human colorectal cancer (CRC) cells, HCT116 and HT29, were treated with carbon-ion beam irradiation alone or in combination with 5-FU. Cell viability assay, colony and spheroid formation assay, apoptotic assay, and quantitative real-time PCR analysis of apoptosis- and autophagy-related gene expression were performed. Results Carbon-ion beam irradiation dose-dependently decreased CRC cell viability and showed significantly enhanced cell killing effect when combined with 5-FU. Carbon-ion beam irradiation in combination with 5-FU significantly increased the percentage of apoptotic cells. The expression of some apoptotic and autophagy-related genes such as Bax, Bcl2, Beclin1 and ATG7 was significantly induced by carbon-ion beam irradiation alone and was further enhanced when the beam was combined with 5-FU. The spheroid forming capacity of CD133+ cell subpopulations was significantly inhibited by carbon-ion beam in combination with 5-FU. Histopathologically, the combination of carbon-ion beam irradiation and 5-FU destroyed more xenograft tumor cells, and resulted in increased necrosis, cavitation, and fibrosis, compared to carbon-ion beam irradiation alone. Conclusion In conclusion, carbon-ion beam treatment combined with 5-FU has the potential to kill CRC cells including CSCs by inducing increased apoptosis and autophagy.

Background: The aim of this study was to investigate whether carbon-ion beam irradiation in combination with 5-fluorouracil (5-FU) is superior to carbon-ion beam irradiation alone in targeting colorectal cancer stem-like cells (CSCs). Materials and Methods: Human colorectal cancer (CRC) cells, HCT116 and HT29, were treated with carbon-ion beam irradiation alone or in combination with 5-FU. Cell viability assay, colony and spheroid formation assay, apoptotic assay, and quantitative real-time PCR analysis of apoptosis- and autophagy-related gene expression were performed. Results: Carbon-ion beam irradiation dose-dependently decreased CRC cell viability and showed significantly enhanced cell killing effect when combined with 5-FU. Carbon-ion beam irradiation in combination with 5-FU significantly increased the percentage of apoptotic cells. The expression of some apoptotic and autophagy-related genes such as Bax, Bcl2,Beclin1 and ATG7 was significantly induced by carbon-ion beam irradiation alone and was further enhanced when the beam was combined with 5-FU. The spheroid forming capacity of CD133+ cell subpopulations was significantly inhibited by carbon-ion beam in combination with 5-FU. Histopathologically, the combination of carbon-ion beam irradiation and 5-FU destroyed more xenograft tumor cells, and resulted in increased necrosis, cavitation, and fibrosis, compared to carbon-ion beam irradiation alone. Conclusion: In conclusion, carbon-ion beam treatment combined with 5-FU has the potential to kill CRC cells including CSCs by inducing increased apoptosis and autophagy.

The amount of potentially lethal damage repair (PLDR) is a significant factor in the process of modeling the survival curves of cells irradiated with fractionated carbon beams. Because the amount of PLDR generally depends on the features of the cells and the linear energy transfer (LET), the amount of PLDR of cells irradiated with fractionated carbon beams shows distinct differences from that of cells irradiated with X-rays. This study considered a new parameter dependent on the correlation between the PLDR trait (T) of the cells over a time interval (Δ) at the fractionated carbon beam irradiation. The survival curves of the cells irradiated with fractionated carbon beams n times were predicted using the ζ and the Ψ values from the delay assay. This study aims to overcome the barriers of traditional methods by developing a new survival curve model with new parameters based on an analysis of the PLDR traits of cells over time interval in fractionated carbon beam irradiation and to suggest a model that produces results significantly closer to the experimental data.

To investigate whether carbon-ion beam alone, or in combination with lapatinib, has a beneficial effect in targeting HER2-positive breast cancer stem-like cells (CSCs) compared to that of X-rays, human breast CSCs derived from BT474 and SKBR3 cell lines were treated with a carbon-ion beam or X-rays irradiation alone or in combination with lapatinib, and then cell viability, spheroid formation assays, apoptotic analyses, gene expression analysis of related genes, and immunofluorescent gamma-H2AX foci assays were performed. Spheroid formation assays confirmed that ESA+/CD24- cells have CSC properties compared to ESA-/CD24+ cells. CSCs were more highly enriched after X-ray irradiation combined with lapatinib, whereas carbon-ion beam combined with lapatinib significantly decreased the proportion of CSCs. Carbon-ion beam combined with lapatinib significantly suppressed spheroid formation compared to X-rays combined with lapatinib or carbon ion beam alone. Cell cycle analysis showed that carbon ion beam combined with lapatinib predominantly enhanced sub-G1 and G2/M arrested population compared to that of carbon-ion beam, X-ray treatments alone. Carbon-ion beam combined with lapatinib significantly enhanced apoptosis and carbon-ion beam alone dose-dependently increased autophagy-related expression of Beclin1 and in combination with lapatinib greatly enhanced ATG7 expression at protein levels. In addition, a large sized gamma H2AX foci in CSCs were induced by carbon ion beam combined with lapatinib treatment in CSCs compared to cells receiving X-rays or carbon-ion beam alone. Altogether, combination of carbon-ion beam irradiation and lapatinib has a high potential to kill HER2-positive breast CSCs, causing severe irreparable DNA damage, enhanced autophagy, and apoptosis.

The amount of potentially lethal damage repair (PLDR) is a significant factor in the process of modeling the survival curves of cells irradiated with fractionated carbon beams. Because the amount of PLDR generally depends on the features of the cells and the linear energy transfer (LET), the amount of PLDR of cells irradiated with fractionated carbon beams shows distinct differences from that of cells irradiated with X-rays. This study considered a new parameter dependent on the correlation between the PLDR trait (T) of the cells over a time interval (Δ) at the fractionated carbon beam irradiation. The survival curves of the cells irradiated with fractionated carbon beams n times were predicted using the ζ and the Ψ values from the delay assay. This study aims to overcome the barriers of traditional methods by developing a new survival curve model with new parameters based on an analysis of the PLDR traits of cells over time interval in fractionated carbon beam irradiation and to suggest a model that produces results significantly closer to the experimental data.

Purpose The purpose is to verify experimentally whether application of magnetic fields longitudinal and perpendicular to a proton beam alters the biological effectiveness of the radiation. Methods and Materials Proton beams with linear energy transfer of 1.1 and 3.3 keV/μm irradiated human cancer and normal cells under a longitudinal (perpendicular) magnetic field of BL (BP) = 0, 0.3, or 0.6 T. Cell survival curves were constructed to evaluate the effects of the magnetic fields on the biological effectiveness. The ratio of dose that would result in a survival fraction of 10% without the magnetic field Dwo to the dose with the magnetic field Dw, R10 = Dwo/Dw, was determined for each cell line and magnetic field. Results For cancer cells exposed to the 1.1- (3.3-) keV/μm proton beams, R10s were increased to 1.10 ± 0.07 (1.11 ± 0.07) and 1.11 ± 0.07 (1.12 ± 0.07) by the longitudinal magnetic fields of BL = 0.3 and 0.6 T, respectively. For normal cells, R10s were increased to 1.13 ± 0.06 (1.17 ± 0.06) and 1.17 ± 0.06 (1.30 ± 0.06) by the BLs. In contrast, R10s were not changed significantly from 1 by the perpendicular magnetic fields of BP = 0.3 and 0.6 T for both cancer and normal cells exposed to 1.1- and 3.3-keV/μm proton beams. Conclusions The biological effectiveness of proton beams was significantly enhanced by longitudinal magnetic fields of BL = 0.3 and 0.6 T, whereas the biological effectiveness was not altered by perpendicular magnetic fields of the same strengths. This enhancement effect should be taken into account in magnetic resonance imaging guided proton therapy with a longitudinal magnetic field.

Background and Purpose The purpose is to verify experimentally whether application of magnetic fields longitudinal and perpendicular to a proton beam alters the biological effectiveness of the radiation. Methods and Materials Proton beams with linear energy transfer (LET) of 1.1 and 3.3 keV/μm were irradiated onto human cancer and normal cells under the longitudinal (perpendicular) magnetic field of BL (BP) = 0, 0.3, or 0.6 T. Cell survival curves were constructed to evaluate the effects of the magnetic fields on the biological effectiveness. The ratio of dose that would result in a survival fraction of 10% without the magnetic field Dwo to the dose with the magnetic field Dw, R10 = Dwo / Dw, was determined for each cell line and magnetic field. Results For cancer cells exposed to the 1.1- (3.3-) keV/μm proton beams, R10s were increased to 1.10±0.07 (1.11±0.07) and 1.11±0.07 (1.12±0.07) by the longitudinal magnetic fields of BL = 0.3 and 0.6 T, respectively. For normal cells, R10s were increased to 1.13±0.06 (1.17±0.06) and 1.17±0.06 (1.30±0.06) by the BLs. In contrast, R10s were not changed significantly from 1 by the perpendicular magnetic fields of BP = 0.3 and 0.6 T for both cancer and normal cells exposed to 1.1- and 3.3-keV/μm proton beams. Conclusions The biological effectiveness of proton beams was significantly enhanced by the longitudinal magnetic fields of BL = 0.3 and 0.6 T, while the biological effectiveness was not altered by the perpendicular magnetic fields of the same strengths. This enhancement effect should be taken into account in MRI guided proton therapy with a longitudinal magnetic field.

高エネルギー加速器研究機構放射光科学研究施設での放射光共同研究課題『細胞質へのX線照射がトリガーとなる放射線適応応答へのバイスタンダー効果の関与』（課題番号：2021G539、課題代表者：鈴木雅雄）において、放射光X線マイクロビーム細胞照射装置を駆使して、ヒト培養細胞の細胞核または細胞質のみに限定的にX線を照射したときの細胞応答（バイスタンダー効果）の現象論と誘導メカニズム解明を目的とし計画した。

Past two years, we reported the cell-killing effect irradiated with carbon-ion beams accelerated with the HIMAC was enhanced by combining with the longitudinal magnetic fields. We, so far, have been studying fundamental radiology for heavy-ion radiotherapy using the microbeam-irrardiation systems and set up the hypothesis from the data as follows; “When cytoplasm of targeted cells are irradiated with low-LET radiations, unknown cellular response(s) is induced in the cell and in consequence the cell becomes protective to radiation damage.” We focus on the hypothesis as a possible mechanism of magnetic-field mediated enhanced cell-killing effect. Targeted cytoplasmic to cells were carried out using X-ray microbeams generated with the synchrotron radiations at Photon Factory, KEK. Cell killing was detected with targeted nuclear irradiation alone or targeted cytoplasmic irradiation  targeted nuclear irradiation. The surviving fraction for nuclear irradiation alone (0.092Gy) was 0.79, however it was going up 0.97 when cytoplasmic irradiation (0.092Gy) beforehand. The obtained data showed that the surviving fraction was drastically recovered by the pre-irradiated cytoplasm of the low-dose of X rays. There is clear evidence that the radio-adaptive response should occur in the cells pre-irradiated to cytoplasm with the low-dose irradiation of the X-ray microbeams. We would like to discuss the relationship between magnetic-field mediated cell killing and radio-adaptive response by targeted cytoplasmic irradiations with X-ray microbeams via bystander effects., 第80回日本癌学会学術総会

Study using a microbeam can provide us very important scientific evidence to understand radio-biological responses induced by low-fluence irradiations. Especially, the study of such biological responses for low LET radiation can surely provide the critical information for evaluating risk such low-dose exposure as the accident of Fukushima Daiichi Nuclear Power Plants caused by the Great East Japan Earthquake. We have been studying biological effects using the microbeams and set up a hypothesis from the data as follows; “When cytoplasm of targeted cells are irradiated with low-LET radiations, unknown cellular response(s) is induced in the cell and in consequence the cell becomes protective to radiation damage (radio-adaptive response).” Targeted cytoplasmic irradiations with X-ray microbeams to normal human fibroblasts were carried out using the cell-irradiation system at Photon Factory, KEK. Briefly, we used the microbeam covering the areas of 30µm x 30µm in which the center was masked by the gold-made post of 22 micrometer in diameter. When cell nucleus was irradiated, we used the microbeams collimating the beam size of 10µm x 10µm. Cell death (0.092Gy) was examined with nuclear irradiation alone or cytoplasmic irradiation  nuclear irradiation. Surviving fraction irradiated with all cell nuclei alone was 0.79, however it was rising to 0.97 when cytoplasm of all cells was irradiated beforehand. The result showed the same even if cytoplasmic irradiations were done randomly selected at 10%. There is evidence that radio-adaptive response is induced in the cells preirradiated to cytoplasm with the low-dose X rays via intracellular or intercellular responses., 日本放射線影響学会第64回大会

In this study, we aimed to investigate how homologous recombinant (HR)-related genomic instability is involved in ionizing radiation (IR)-induced thymic lymphoma in mice. We divided five-week-old Rosa26 Direct Repeat-GFP (RaDR-GFP) transgenic mice into non-IR control and IR groups and exposed the mice in the IR group to a 7.2 Gy dose of γ-rays, delivered in 1.8 Gy fractions, once a week for four weeks. We then estimated mouse survival and recorded their body, thymus, and spleen weights. The frequency of HR events in the chromosomes of the thymus, bone marrow, and spleen cells and the phenotype of thymic lymphoma cells were analyzed using fluorescence-activated cell sorting (FACS). We found that most mice in the IR group developed thymic lymphoma, their survival rate decreasing to 20% after 180 days of IR exposure, whereas no mice died in the non-IR control group until day 400. The thymus and spleen weighed significantly more in the IR-4-month group than that in the non-IR group; however, we observed no significant differences between the body weights of the control and IR mice. FACS analysis indicated that the frequency of HR events significantly increased at two and four months after the last IR dose in the bone marrow and thymus cells, but not in the spleen cells of RaDR-GFP transgenic mice, suggesting that recombinant cells accumulated in the thymus upon IR exposure. This suggests that IR induces genome instability, revealed as increased HR, that drives the development of thymic lymphoma. Additionally, phenotypic analysis of lymphoma cells showed an increase in the CD4(-)/CD8(+) (CD8SP) cell population and a decrease in the CD4(+)/CD8(-) (CD4SP) cell population in the IR-4-month group compared to that in the non-IR group, indicating that IR induces an aberrant cell phenotype characteristic of lymphoma. In conclusion, we observed a significant increase in HR events and abnormal phenotype in thymic lymphoma cells at two and four months after IR exposure in both the thymus and bone marrow tissues, suggesting that genomic instability is involved in the early stages of thymic lymphomagenesis. Our study indicates that HR-visualizing RaDR-GFP transgenic mice can help explore the links between the molecular mechanisms of genome instability and IR-induced tumorigenesis.

Background: External fixator is an effective treatment option in the comminuted or unstable metacarpal fractures. The new linked-wire type of external fixator (the Ichi-Fixator System) developed for hand and wrist fractures enables fine adjustment of the fixation under fluoroscopic inspection through small screws inside the fixator fitted externally. This technique is designed to reinforce the stability and rigidity of conventional percutaneous Kirchner wire fixation. The aim of this study is to assess the effectiveness of the fixator for comminuted or unstable metacarpal fractures through the evaluation of short-term results in ten cases. Methods: Patients were fixated with fixator pins and metal clamps using the Ichi-Fixator System. All patients were then examined for post-operative complications, functional recovery, visual analogue scale (VAS) score, and the Quick Disabilities of the Arm, Shoulder, and Hand (Q-DASH) score at the end of the final follow-up consultation. Results: Operative treatment using the Ichi-Fixator System facilitates anatomical reduction and allows immediate full mobilization, producing good outcomes. No infections were observed in all cases, including those at pin insertion sites. There were no implant failure and nonunion. Patients could perform all routine activities with normal grip strength and retained a full range of hand motion without pain. This treatment method with improved postoperative comfort would allow immediate return to work, which would clearly boost patient satisfaction. Conclusions: Ichi-Fixator System is considered to be useful for the treatment of metacarpal fractures, and this will provide a new surgical option for all hand fractures.

The cells responsible for cancer start their journey much like any other in the body. However, they grow uncontrollably through the body as a result of the accumulation of certain mutations. If left unchecked, cancer will impact on a number of the human body's key processes, leading, ultimately, to death. There are many challenges associated with treating this disease, but they generally stem from the difficulty in differentiating the disease from the host and the ability of even a few cells to survive, recover and return. The most common treatments generally combine surgery with some type of chemotherapy or radiotherapy. Chemotherapy utilises chemicals that kill fast-growing cells and thereby disproportionally affect the rapidly multiplying cancer cells. Radiotherapy targets the tumour with radiation to cause damage and cell death. Both have their advantages and disadvantages, and both are often not 100 per cent effective. To improve these treatments, it is necessary to understand more about their precise effects on cells and, particularly, what defences cells have against their effects. Senior Principal Researcher Dr Masao Suzuki of the National Institutes for Quantum and Radiological Science and Technology (QST) is utilising the considerable radiological resources of QST to investigate the effects of different types of radiation on cells under different conditions.

Previous studies have revealed application of a magnetic field longitudinal to a carbon-ion beam enhances its biological effectiveness. This communication investigated how timing of the magnetic field application with respect to beam irradiation influenced this effect. Human cancer cells were exposed to carbon-ion beams with linear energy transfer (LET) of 12 and 50 keV/μm. The longitudinal magnetic field of 0.3 T was applied to the cells just before, during, or right after the beam irradiation. The effects of the timing on the biological effectiveness were evaluated by cell survival. The biological effectiveness increased only if the magnetic field was applied during beam irradiation for both LET beams.

Purpose: We studied lethal and mutagenic bystander effects in normal human fibroblasts irradiated with low-energy-carbon ions.Materials and methods: After cells reached confluence, cells were irrad...

We studied lethal and mutagenic bystander effects in normal human fibroblasts irradiated with low-energy-carbon ions. After cells reached confluence, cells were irradiated with initial energies of 6 MeV/n carbon ions. The residual energy and LET value were 4.6 MeV/n and 309 keV/µm. The doses used for survival and mutational studies were 0.082 and 0.16 Gy. Irradiation was carried out using 4 different irradiation conditions and plating conditions: (1) The entire cell area on the Mylar film was irradiated (We abbreviate as 'all irradiation'); (2) Irradiated and unirradiated cells were pooled in a 1:1 ratio and plated as a single culture until the plating for lethal and mutagenic experiments (We abbreviate as 'mixed population'); (3) Only half of the area on the Mylar film were irradiated using an ion-beam stopper (We abbreviate as 'half irradiation'); and (4) Only half of the area of the cells were irradiated, and a specific inhibitor of gap junctions was added to the culture (We abbreviate as 'half irradiation with inhibitor'). Cell samples were analyzed for lethal and mutagenic bystander effects, including a PCR evaluation of the mutation spectrum. The surviving fraction of all irradiation was the same as the half irradiation case. The surviving fractions of both mixed population and the half irradiation with inhibitor were the same level and higher than those of all irradiation and half irradiation. The mutation frequencies at the (the hypoxanthine-guanine phosphoribosyl transferase) locus of all irradiation and half irradiation were at the same level and were higher than those of mixed population and half irradiation with inhibitor, respectively. There is evidence that the bystander effects for both lethality and mutagenicity occurred in the unirradiated half of the cells, in which only half of the cells were irradiated with the carbon ions. These results suggest that the bystander cellular effects via gap-junction-mediated cell-cell communication are induced by high-LET-carbon ions.

Purpose: Our previous study revealed that the application of a magnetic field longitudinal to a carbon-ion beam of 0.1 ≤ B//≤ 0.6 T enhances the biological effectiveness of the radiation. T...

The effects of the charged ion species 4He, 12C and 20Ne on glioblastoma multiforme (GBM) T98G, U87 and LN18 cell lines were compared with the effects of 200 kVp X-rays (1.7 keV/μm). These cell lines have different genetic profiles. Individual GBM relative biological effectiveness (RBE) was estimated in two ways: the RBE10 at 10% survival fraction and the RBE2Gy after 2 Gy doses. The linear quadratic model radiosensitivity parameters α and β and the α/β ratio of each ion type were determined as a function of LET. Mono-energetic 4He, 12C and 20Ne ions were generated by the Heavy Ion Medical Accelerator at the National Institute of Radiological Sciences in Chiba, Japan. Colony-formation assays were used to evaluate the survival fractions. The LET of the various ions used ranged from 2.3 to 100 keV/μm (covering the depth–dose plateau region to clinically relevant LET at the Bragg peak). For U87 and LN18, the RBE10 increased with LET and peaked at 85 keV/μm, whereas T98G peaked at 100 keV/μm. All three GBM α parameters peaked at 100 keV/μm. There is a statistically significant difference between the three GBM RBE10 values, except at 100 keV/μm (P < 0.01), and a statistically significant difference between the α values of the GBM cell lines, except at 85 and 100 keV/μm. The biological response varied depending on the GBM cell lines and on the ions used.

Purpose: A magnetic field longitudinal to an ion beam will potentially affect the biological effectiveness of the radiation. The purpose of this study is to experimentally verify the significance o...

An investigation of 53 saturated absorption lines of titanium at wavelengths ranging from 695 to 1005 nm is performed. In addition, transitions 3d34s a5FJ → 3d34p y5FJ (J = 3, 4, 5) in the ultraviolet range are measured. The isotope lines of 46Ti, 48Ti, and 50Ti are clearly observed for 53 transitions. A facing target sputtering system containing a magnetic field is used as a sample cell of titanium in this experiment. The Zeeman effect in a hyperfine structure is calculated for the condition of an intermediate field approximation to determine the unperturbed line positions in the odd mass isotopes 47Ti and 49Ti. For all observed transitions, the King plot analysis is performed to determine the electronic factors of the field shift and specific mass shift.