Isomeric fluorescence sensors for wide range detection of ionizing radiations

In order to achieve a wider range of ionizing radiations detection,novel fluorescence sensing materials have been developed that utilize the fluorescence enhancement phenomenon caused by the intramolecular photoinduced electron transfer(PET)effect.Two perylene diimide isomers PDI-P and PDI-B were designed and synthesized,and their molecular structures were characterized by high-resolution Fourier transform mass spectrometry(HRMS),nuclear magnetic resonance hydrogen and carbon spectroscopy(~1H and~(13)C NMR).The interaction between ionizing radiation and fluorescent molecules was simulated by HCl titration.The results show that combining PDIs and HCl can improve fluorescence through the retro-PET process.Despite the similarities in chemical structures,the fluorescent enhancement multiple of PDI-B with aromatic amine as electron donor is much higher than that of PDI-P with alkyl amine.In the direct irradiation experiments of ionizing radiation,the emission enhancement multiples of PDI-P and PDI-B are 2.01 and 45.4,respectively.Furthermore,density functional theory(DFT)and time-dependent density functional theory(TDDFT)calculations indicate that the HOMO and HOMO-1 energy ranges of PDI-P and PDI-B are 0.54 e V and 1.13 e V,respectively.A wider energy range has a stronger driving force on electrons,which is conducive to fluorescence quenching.Both femtosecond transient absorption spectroscopy(fs-TAS)and transient fluorescence spectroscopy(TFS)tests show that PDI-B has shorter charge separation lifetime and higher electron transfer rate constant.Although both isomers can significantly reduce LOD during PET process,PDI-B with aromatic amine has a wider detection range of 0.118—240 Gy due to its larger emission enhancement,which is a leap of three orders of magnitude.It breaks through the detection range of gamma radiation reported in existing studies,and provides theoretical support for the further study of sensitive and effective new materials for ionizing radiation detection.

The role of crm-1 in ionizing radiation-induced nervous system dysfunction in Caenorhabditis elegans

Ionizing radiation can cause changes in nervous system function.However,the underlying mechanism remains unclear.In this study,Coenorhabditis elegans(C.elegans)was irradiated with 75 Gy of ^(60)Co whole-body γ radiation.Behavioral indicators(head thrashes,touch avoidance,and foraging),and the development of dopaminergic neurons related to behavioral function,were evaluated to assess the effects of ionizing radiation on nervous system function in C.elegans.Various behaviors were impaired after whole-body irradiation and degeneration of dopamine neurons was observed.This suggests that 75 Gy of γ radiation is sufficient to induce nervous system dysfunction.The genes nhr-76 and crm-1,which are reported to be related to nervous system function in human and mouse,were screened by transcriptome sequencing and bioinformatics analysis after irradiation or sham irradiation.The expression levels of these two genes were increased after radiation.Next,RNAi technology was used to inhibit the expression of crm-1,a gene whose homologs are associated with motor neuron development in other species.Downregulation of crm-1 expression effectively alleviated the deleterious effects of ionizing radiation on head thrashes and touch avoidance.It was also found that the expression level of crm-1 was regulated by the nuclear receptor gene nhr-76.The results of this study suggest that knocking down the expression level of nhr-76 can reduce the expression level of crm-1,while down-regulating the expression level of crm-1 can alleviate behavioral disorders induced by ionizing radiation.Therefore,inhibition of crm-1 may be of interest as a potential therapeutic target for ionizing radiation-induced neurological dysfunction.

Aurora A Kinase Plays a Key Role in Mitosis Skip during Senescence Induced by Ionizing Radiation

Objective To investigate the fate and underlying mechanisms of G2 phase arrest in cancer cells elicited by ionizing radiation(IR).Methods Human melanoma A375 and 92-1 cells were treated with X-rays radiation or Aurora A inhibitor MLN8237(MLN)and/or p21 depletion by small interfering RNA(si RNA).Cell cycle distribution was determined using flow cytometry and a fluorescent ubiquitin-based cell cycle indicator(FUCCI)system combined with histone H3 phosphorylation at Ser10(p S10 H3)detection.Senescence was assessed using senescence-associated-β-galactosidase(SA-β-Gal),Ki67,andγH2AX staining.Protein expression levels were determined using western blotting.Results Tumor cells suffered severe DNA damage and underwent G2 arrest after IR treatment.The damaged cells did not successfully enter M phase nor were they stably blocked at G2 phase but underwent mitotic skipping and entered G1 phase as tetraploid cells,ultimately leading to senescence in G1.During this process,the p53/p21 pathway is hyperactivated.Accompanying p21 accumulation,Aurora A kinase levels declined sharply.MLN treatment confirmed that Aurora A kinase activity is essential for mitosis skipping and senescence induction.Conclusion Persistent p21 activation during IR-induced G2 phase blockade drives Aurora A kinase degradation,leading to senescence via mitotic skipping.

3D-printed engineered bacteria-laden gelatin/sodium alginate composite hydrogels for biological detection of ionizing radiation

Nuclear safety is a global growing concern,where ionizing radiation(IR)is a major injury factor resulting in serious damage to organisms.The detection of IR is usually conducted with physical dosimeters;however,biological IR detection methods are deficient.Here,a living composite hydrogel consisting of engineered bacteria and gelatin/sodium alginate was 3D-printed for the biological detection of IR.Three strains of PrecA::egfp gene circuit-containing engineered Escherichia coli were constructed with IR-dependent fluorescence,and the DH5αstrain was finally selected due to its highest radiation response and fluorescence.Engineered bacteria were loaded in a series of gelatin/sodium alginate matrix hydrogels with different rheology,3D printability and bacterial applicability.A high-gelatin-content hydrogel containing 10%gelatin/1.25%sodium alginatewas optimal.The optimal living composite hydrogelwas 3D-printedwith the special bioink,which reported significant green fluorescence underγ-ray radiation.The living composite hydrogel provides a biological strategy for the detection of environmental ionizing radiation.

Protective effects of ferulic acid against ionizing radiation-induced oxidative damage in rat lens through activating Nrf2 signal pathway

AIM: To examine the protection of ferulic acid(FA) against ionizing radiation(IR)-induced lens injury in rats, as well as the underlying mechanisms.METHODS: FA(50 mg/kg) was administered to rats for 4 consecutive days before they were given 10 Gy γ-radiation, as well as for 3 consecutive days afterward. Two weeks after radiation, the eye tissues were collected. Histological alterations were evaluated by hematoxylineosin staining. Enzyme linked immunosorbent assay(ELISA) was utilized to assess the activities of glutathione reductase(GR) and superoxide dismutase(SOD), as well as the levels of glutathione(GSH) and malondialdehyde(MDA) in the lenses. The protein and m RNA levels of Bcl-2, caspase-3, Bax, heme oxygenase-1(HO-1), and glutamatecysteine ligase catalytic subunit(GCLC) were quantified using Western blot and quantitative reverse transcription polymerase chain reaction, respectively. With nuclear extracts, the nuclear factor erythroid-2 related factor(Nrf2) protein expressions in the nuclei were also measured.RESULTS: Rats exposed to IR showed lens histological alterations which could be alleviated by FA. FA treatment reversed apoptosis-related markers in IR-induced lens, as evidenced by lower levels of Bax and caspase-3 and higher level of Bcl-2. Furthermore, IR induced oxidative damage manifested by decreased GSH level, increased MDA level, and decreased SOD and GR activities. FA boosted nuclear translocation of Nrf2 and increased the expressions of HO-1 and GCLC to inhibit oxidative stress, as evidenced by an increase in GSH, a decrease in MDA, and an increase in GR and SOD activities.CONCLUSION: FA may work well in preventing and treating IR-induced cataract through promoting the Nrf2 signal pathway to attenuate oxidative damage and cell apoptosis.

Radiation-Associated Cardiotoxicity during Breast Cancer Treatment with Ionizing Radiation

Introduction: Breast cancer is the most common cancer in women. The treatment of breast carcinoma has advanced in the last decade and nowadays there are treatment protocols for all stages of the disease. Depending on the histopathology and stage breast cancer is treated with surgery, chemotherapy and radiotherapy. Regarding radiation, the field of irradiation includes the chest wall in patients with mastectomy, or the breast glandular tissue in patients with conserving surgical approaches. It is often treated with radiation therapy with two opposing tangential fields, and when indicated supraclavicular lymph nodes have to be irradiated. In this case an additional anterior field is applied. The tangential as well as the other radiation beams have a potential damaging effect on the healthy surrounding tissues, particularly over the heart in the left breast irradiation and in the lungs as well. Material and Methods: The study included 25 patients with left breast carcinoma, all post surgery, treated with radiation therapy, with the Elekta accelerator at our department. For academic purpose the treatment plans were generated following two methods. The first one with two tangential opposite beams plus a supraclavicular beam. In this method the angles of the tangential internal and external create an angle that is equal to 180˚{310˚& 130˚};no further changes were made to the beam geometry. Even though this is not the best option from the dose distribution point of view, it is still the most applied method, probably because of the semplicity of it. For each patient, a second plan was generated using two opposite tangential beams plus the supraclavicular beam. The angles of the internal and external beam were changed from 1˚to 3˚, depending on the surface of the body, so that the resulting angle was 180˚± 3˚{310˚± 3˚& 130˚± 3˚} with the aim to adapt the beam geometry as much as possible to the shape of the thoracic wall and to spare the OAR-s. Results and Discussion: The data show that the dose in the organs at risk, in terms of dose percentage, is lower when the angles of the beams are changed with 1˚- 3˚, compared to the classic method where the internal and external angles equal 180˚. This dose is not only non-negligible but significant;for every angle change from 1˚to 3˚, there is a significant reduction in the integral dose in the radiated volume, expressed in percentage, up to 5%. Conclusion: In most centers, the radiation treatment of breast is realized with two tangential opposite beams, which usually are mirror beams, or in other words, the internal and external beam angles create an angle of 180˚{α + β = 180˚}. This is a simple method, which provides a good dose distribution, but leaves a relatively high dose in the organs at risk. This study shows the difference in the dose percentage in the heart and lung when the beam angles are changed adapting to the anatomy of the patient. Reducing these doses allows for better overall treatment and less longtime toxicity, particularly for the heart tissues.

Total Ionizing Dose Radiation Effects in the P-Type Polycrystalline Silicon Thin Film Transistors

The total ionizing dose radiation effects in the polycrystalline silicon thin film transistors are studied. Transfer characteristics, high-frequency capacitance-voltage curves and low-frequency noises (LFN) are measured before and after radiation. The experimental results show that threshold voltage and hole-field-effect mobility decrease, while sub-threshold swing and low-frequency noise increase with the increase of the total dose. The contributions of radiation induced interface states and oxide trapped charges to the shift of threshold voltage are also estimated. Furthermore, spatial distributions of oxide trapped charges before and after radiation are extracted based on the LFN measurements.

Computer-assisted formulas predicting cancer mortality risk after exposure to acute low dose ionizing radiation in humans

A clear relationship between dose of radiation and mortality in humans is still not known because of lack of human data that would enable to determine human tolerance in total body irradiation. Human data for analysis have been primarily from radiation accidents, radiotherapy and the atomic bomb victims. A general formula that predicts mortality probability as a function of dose rate and duration of exposure to acute high dose ionizing radiation in humans was published by the author, applying the “probacent” model to the reported data on animal-model-predicted dose versus mortality. In this study, the “probacent” model is applied to the data on dose versus cancer mortality risk, published by the United Nations (UNSCEAR, 2010) and other investigators to construct general formulas expressing a relationship between dose and solid cancer or leukemia mortality probability after exposure to acute low dose ionizing radiation in humans. There is a remarkable agreement between formula-derived and published values of dose and solid cancer or leukemia mortality probability (p > 0.99). The general formula might be helpful in preventing radiation hazard and injury in acute low dose ionizing radiation, and for safety in radiotherapy.

Bioflavonoids as Important Component of Biological Protection from Ionizing Radiation

New advances in the area of deciphering the mechanism for a possible modification of the biological effects of radiation exposure at the genetic level make it possible to distinguish the group of radiation protective agents having their own specific features in the implementation of their beneficial effects. The mechanism of the radioprotective action of bioflavonoids is worthy of a detailed analysis in view of their great biological importance. Radiobiological studies show that antioxidants can reduce the radiation damage to membranes and favor more adequate energy dependent adaptive and reparative processes after the exposure to radiation. Bioflavonoids are significant component of “biological protection” for a enhance of resistance of the body to environmental factors that are adverse for human health, including ionizing radiation, with reducing the risk of carcinogenic effects and decreasing the biological age. The best practical value of bioflavonoids, can be considered as the agents for prophylaxis against the development of oxidative stress. These are the reasons why the administration of natural antioxidants have a pathogenetic justification for exposures to chronic (months, years) low-rate-dose ionizing radiation. These agents were previously and are currently being developed for use during long-term, low-ratedose exposures to radiation, under conditions of long space missions. Acting as low-dose stressors through a hormetic mechanism and a “substrate” support of adaptive shifts radiomodulators results in an increase in the antioxidant defense of the body and the rearrangement of its functioning in the new environment with the modulation of gene expression of antioxidant response elements by activation of Nrd2/KeapI and Sirtuin/FoxO pathways and a decrease in the transcription factor NF-κB.

Influence of Total Ionizing Dose Irradiation on Low-Frequency Noise Responses in Partially Depleted SOI nMOSFETs

Total ionizing dose effect induced low frequency degradations in 130nm partially depleted silicon-on-insulator （SOI） technology are studied by ^60Co γ -ray irradiation. The experimental results show that the flicker noise at the front gate is not affected by the radiation since the radiation induced trapped charge in the thin gate oxide can be ignored. However, both the Lorenz spectrum noise, which is related to the linear kink effect （LKE） at the front gate, and the flicker noise at the back gate are sensitive to radiation. The radiation induced trapped charge in shallow trench isolation and the buried oxide can deplete the nearby body region and can activate the traps which reside in the depletion region. These traps act as a GR center and accelerate the consumption of the accumulated holes in the floating body. It results in the attenuation of the LKE and the increase of the Lorenz spectrum noise. Simultaneously, the radiation induced trapped charge in the buried oxide can directly lead to an enhanced flicker noise at the back gate. The trapped charge density in the buried oxide is extracted to increase from 2.21×10^18 eV^-1 cm^-3 to 3.59×10^18？eV^-1 cm^-3 after irradiation.

Effect of Ionizing Radiation on the Expression of p16, CyclinDI and CDK4 in Mouse Thymocytes and Splenocytes

Objective To investigate the effect of ionizing radiation on the expression of p16, CyclinDl, and CDK4 in mouse thymocytes and splenocytes. Methods Fluorescent staining and flow cytometry analysis were employed for the measurement of protein expression. Results In time course experiments, it was found that the expression of p16 protein was significantly increased at 8, 24, and 48 h for thymocytes (P<0.05, P<0.01, and P<0.05, respectively) and at 24 h for splenocytes (P<0.05) after whole body irradiation (WBI) with 2.0 Gy X-rays. However, the expression of CDK4 protein was significantly decreased from 8 h to 24 h for thymocytes (P<0.05,P<0.01) and from 8 h to 72 h for splenocytes (P<0.05-P<0.01). In dose effect experiments, it was found that the expression of p16 protein in thymocytes and splenocytes was significantly increased at 24 h after WBI with 1.0, 2.0, and 4.0 Gy (P<0.05-P<0.01), whereas the expression of CDK4 protein was significantly decreased with 2.0Gy for thymocytes (P<0.05) and 0.5-6.0 Gy for splenocytes (P<0.05-P<0.01). Results also showed that the expression of CyclinDl protein decreased markedly in both thymocytes and splenocytes after exposure. Conclusion The results indicate that the expression of p 16 protein in thymocytes and splenocytes can be induced by ionizing radiation, and the p16-CyclinD1/CDK4 pathway may play an important role for G1 arrest of thymocytes induced by X-rays.

Combination of genistein with ionizing radiation on andro-gen-independent prostate cancer cells

Aim: To study the effect of the combined use of genistein and ionizing radiation (IR) on prostate DU145 cancer cells. Methods: DU145, an androgen-independent human prostate cancer cell line, was used in the experiment. Clonogenic assay was used to compare the survival of DU145 cells after treatments with genistein alone and in combination with graded IR. Apoptosis was assayed by DNA ladder and TUNEL stain. Cell cycle alterations were observed by flow cytometry and related protein expressions by immunoblotting. Results: Clonogenic assay demonstrated that genistein, even at low to medium concentrations, enhanced the radiosensitivity of DU145 cells. Twenty-four hours after treatment with IR and/or genistein, apoptosis was mainly seen with genistein at high concentrations and was minimally related to IR. At 72 h, apoptosis also occurred in treatment with lower concentration of genistein, especially when combined with IR. While both IR and genistein led to G2/M cell cycle arrest, combination of them further increased the DU145 cells at G2/M phase. This Gz/M arrest was largely maintained at 72 h, accompanied by increasing apoptosis and hyperdiploid cell population. Cell-cycle related protein analysis disclosed biphasic changes in cyclin B1 and less dramatically cdc-2, but stably elevated p21cipl levels with increasing genistein concentrations. Conclusion: Genistein enhanced the radiosensitivity of DU145 prostate cancer cells. The mechanisms might be involved in the increased apoptosis, prolonged cell cycle arrest and impaired damage repair.

Effect of ionizing radiation on transcription of colorectal cancer MDR1 gene of HCT-8 cells

Objective:To discuss effect of ionizing radiation on transcription of colorectal cancer multidrug resistance(MDR) 1 gene of HCT-8 cells.Methods:Total RNA was extracted by guanidine thiocyanate one-step method.Northern blot was applied to detect transcription level of MDR1 gene.The expression of P-gp protein was detected by flow cytometry.Results:The expression of MDRl of normal colorectal cancer HCT-8 cells was low.It was increased by 8.35 times under stimulus with 2 Gy.When treated with low doses in advance,high expressed MDR was decreased significantly under 0.05,0.1 Gy,which was 69.00%,62.89%in 2 Cy group and 5.77 times,5.25 times in sham irradiation group.No obvious difference was detected between(0.2+2) Gy group and 2 Gy group.Compared with sham irradiation group,the percentage of P-gp positive cells after radiation of a high 2 Gy dose was increased significantly(P【0.01).When treated with high radiation dose following low radiation dose(0.05 Gy,0.1 Gy) in advance,the percentage of P-gp positive cells were also increased significantly.The percentage of P-gp positive cells were increased obviously in 0.2 Gy and 2 Gy groups.Compared with simple high radiation 2 Gy group,the percentage of P-gp positive cells was decreased significantly(P【0.05).Conclusions: Low radiation dose can reverse multidrug resistance of colorectal cancer cells caused by high radiation dose.

Surveying ionizing radiations in real time using a smartphone

Surveying ionizing radiations of the surrounding with a smartphone provides a low-cost and convenient utility for the general public. We developed a smartphone application(App) that uses the built-in camera with a CMOS sensor and a radiation signal extraction algorithm.After a calibration through a series of radiation exposures,the App could display radiation dose rate and cumulative dose in real time without requiring covering the camera lens. A smartphone with this App can be used as a fast survey tool for ionizing radiations.

Typical Cell Signaling Response to Ionizing Radiation: DNA Damage and Extranuclear Damage

To treat many types of cancer, ionizing radiation （IR） is primarily used as external-beam radiotherapy, brachytherapy, and targeted radionuclide therapy. Exposure of tumor cells to JR can induce DNA damage as well as generation of reactive oxygen species （ROS） and reactive nitrogen species （RNS） which can cause non-DNA lesions or extracellular damage like lipid perioxidation. The initial radiation-induced cell responses to DNA damage and ROS like the proteolytic processing, as well as synthesis and releasing ligands （such as growth factors, cytokines, and hormone） can cause the delayed secondary responses in irradiated and unirradiated bystander cells through paracrine and autocrine pathways.

Identification of Two Novel Mitochondrial DNA Deletions Induced by Ionizing Radiation

Abstract Objective We identify ionizing radiation-induced mitochondrial DNA （mtDNA） deletions in human lymphocytes and their distribution in normal populations. Methods Long-range polymerase chain reactions （PCR） using two pairs of primers specific for the human mitochondrial genome were used to analyze the lymphoblastoid cell line following exposure to 10 Gy 6~Co y-rays. Limited-condition PCR, cloning and sequencing techniques were applied to verify the mtDNA deletions detected with long-range PCR. Human peripheral blood samples were irradiated with 0, 2 and 6 Gy ^60Co y-rays, and real-time PCR analysis was performed to validate the mtDNA deletions. In order to know the distribution of mtDNA deletions in normal population, 222 healthy Chinese adults were also investigated. Results Two mtDNA deletions, a 7455-bp deletion （nt475-nt7929 in heavy strand） and a 9225-bp deletion （nt7714 -nt369 in heavy strand）, occurring between two 8-bp direct repeats, were identified in lymphoblastoid cells using long-range PCR, limited-condition PCR and sequencing. These results were also observed for ^60Co y-rays irradiated human peripheral blood cells. Conclusion Two novel mtDNA deletions, a 7455-bp deletion and a 9225-bp deletion, were induced by ionizing radiation. The rate of the mtDNA deletions within a normal population was related to the donors＇ age, but was independent of gender.

p21 is Responsible for Ionizing Radiation-induced Bypass of Mitosis

Objective To explore the role of p21 in ionizing radiation-induced changes in protein levels during the G2/M transition and long-term G2 arrest.Methods Protein expression levels were assessed by western blot in the human uveal melanoma 92-1 cells after treatment with ionizing radiation.Depletion of p21 was carried out by employing the siR NA technique.Cell cycle distribution was determined by flow cytometry combined with histone H3 phosphorylation at Ser28,an M-phase marker.Senescence was assessed by senescenceassociated-β-galactosidase（SA-β-gal） staining combined with Ki67 staining,a cell proliferation marker.Results Accompanying increased p21,the protein levels of G2/M transition genes declined significantly in 92-1 cells irradiated with 5 Gy of X-rays.Furthermore,these irradiated cells were blocked at the G2 phase followed by cellular senescence.Depletion of p21 rescued radiation-induced G2 arrest as demonstrated by the upregulation of G2/M transition kinases,as well as the high expression of histone H3 phosphorylated at Ser28.Knockdown of p21 resulted in entry into mitosis of irradiated 92-1 cells.However,cells with serious DNA damage failed to undergo cytokinesis,leading to the accumulation of multinucleated cells.Conclusion Our results indicated that p21 was responsible for the downregulation of G2/M transition regulatory proteins and the bypass of mitosis induced by irradiation.Downregulation of p21 by siR NA resulted in G2-arrested cells entering into mitosis with serious DNA damage.This is the first report on elucidating the role of p21 in the bypass of mitosis.

An investigation of ionizing radiation damage in different SiGe processes

Different SiGe processes and device designs are the critical influences of ionizing radiation damage. Based on the different ionizing radiation damage in SiGe HBTs fabricated by Huajie and an IBM SiGe process, quantitatively numerical simulation of ionizing radiation damage was carried out to explicate the distribution of radiation-induced charges buildup in KT9041 and IBM SiGe HBTs. The sensitive areas of the EB-spacer and isolation oxide of KT9041 are much larger than those of the IBM SiGe HBT, and the distribution of charge buildup in KT9041 is several orders of magnitude greater than that of the IBM SiGe HBT. The result suggests that the simulations are consistent with the experiment, and indicates that the geometry of the EB-spacer, the area of the Si/SiO2 interface and the isolation structure could be contributing to the different ionizing radiation damage.

Increased Levels of p53 and PARP-1 in EL-4 Cells Probably Related with the Immune Adaptive Response Induced by Low Dose Ionizing Radiation in vitro

Objective This paper is to explore the DNA repair mechanism of immune adaptive response （AR） induced by low dose radiation （LDR）, the changes of mRNA levels and protein expressions of p53, ATM, DNA-PK catalytic subunit （DNA-PKcs） and PARP-1 genes in the LDR-induced AR in EL-4 cells. Methods The apoptosis and cell cycle progression of EL-4 cells were detected by flow cytometry in 12 h after the cells received the pre-exposure of 0.075 Gy X-rays （inductive dose, D 1） and the succeeding high dose irradiation （challenge dose, D2; 1.0, 1.5, and 2.0 Gy X-rays, respectively） with or without wortmannin （inhibitor of ATM and DNA-PK） and 3-aminobenzamid （inhibitor of PARP-1）. And the protein expressions and mRNA levels related to these genes were detected with flow cytometry and reverse transcription-polymerase chain reaction in 12 h after irradiation with D2. Results The mRNA and protein expressions of p53 and PARP-1 in EL-4 cells in the D1 ＋ D2 groups were much lower than those in the D2 groups, and those of PARP-1 in the 3-AB ＋ D2 and the 3-AB ＋ D1 ＋ D2 groups were much lower than those in the D2 and the D1 ＋ D2 groups. The percentage of apoptotic EL-4 cells in the 3-AB ＋ D1 ＋ D2 groups was much higher than that in the D1 ＋ D2 groups, that in the G0/G1 and the G2 ＋ M phases was much higher, and that in the S phase were much lower. Although the ATM and DNA-PKcs mRNA and protein expressions in wortmannin ＋ D1 ＋ D2 groups were much lower than those in the D1 ＋ D2 groups, there were no significant changes in the apoptosis and cell cycle progression between the wortmannin ＋ D1 ＋ D2 and the D1 ＋ D2 groups. Conclusion PARP-1 and p53 might play important roles in AR induced by LDR.

Total ionizing radiation-induced read bit-errors in toggle magnetoresistive random-access memory devices

The 1-Mb and 4-Mb commercial toggle magnetoresistive random-access memories（MRAMs） with 0.13 μm and 0.18-μm complementary metal–oxide–semiconductor（CMOS） process respectively and different magnetic tunneling junctions（MTJs） are irradiated with a Cobalt-60 gamma source. The electrical functions of devices during the irradiation and the room temperature annealing behavior are measured. Electrical failures are observed until the dose accumulates to 120-krad（Si） in 4-Mb MRAM while the 1-Mb MRAM keeps normal. Thus, the 0.13-μm process circuit exhibits better radiation tolerance than the 0.18-μm process circuit. However, a small quantity of read bit-errors randomly occurs only in 1-Mb MRAM during the irradiation while their electrical function is normal. It indicates that the store states of MTJ may be influenced by gamma radiation, although the electrical transport and magnetic properties are inherently immune to the radiation. We propose that the magnetic Compton scattering in the interaction of gamma ray with magnetic free layer may be the origin of the read bit-errors. Our results are useful for MRAM toward space application.