The Role of Stakeholders in the Decommissioning of Salaspils Research Reactor -9109

ABSTRACT The paper describes the role of different stakeholders in the decommissioning of the Salaspils Research Reactor. Decommissioning was a large challenge for the Latvia, since the country in this moment had no decommissioning experience and necessary technologies for the implementation of the defined goals by the Government. In this case for facilitation of the decommissioning of Salaspils Research Reactor (SRR), the significant role plays the local and international stakeholders. The paper deals with information on the basic stages of decommissioning of SRR and the role of the wide spectrum of stakeholders in preparation, upgrade and implementation of the decommissioning plan. The role of governmental institutions in the decommissioning of Salaspils research reactor is discussed. It was shown, that local municipalities are very important stakeholders, which significantly influence the decommissioning of SRR. The Salaspils municipalities positive impact on the decommissioning processes are discussed. Basic problems with the Baldone municipality in context of radioactive wastes management are indicated. The role of international stakeholders in decommissioning of Salaspils research reactor is discussed. It was shown, that the support from International Atomic Energy Agency significantly promotes the decommissioning of SRR. The main issues were expert support for solution of different technical problems in radioactive wastes management, area monitoring, and verification of decommissioning plans, training of staff and technical expertise during whole process of decommissioning. It was shown, that technical and economical support from DOE, USA provides the possibility to solve the fuel problem during decommissioning of SRR, as well as, to increase the physical safety of SRR and repository "Radons". It was shown, that a proper coordination of all activities and using the services from stakeholders can significantly reduce the total project expenses. The cooperation between stakeholders during decommissioning of SRR is discussed in the paper

Decommissioning of the Salaspils Research Reactor

In May 1995, the Latvian government decided to shut down the Salaspils Research Reactor and to dispense with nuclear energy in the future. The reactor has been out of operation since July 1998. A conceptual study on the decommissioning of the Salaspils Research Reactor was drawn up by Noell-KRC-Energie- und Umwelttechnik GmbH in 1998-1999. On October 26th, 1999, the Latvian government decided to start the direct dismantling to “green-field” in 2001. The upgrading of the decommissioning and dismantling plan was carried out from 2003-2004, resulting in a change of the primary goal of decommissioning. Collecting and conditioning of “historical” radioactive wastes from different storages outside and inside the reactor hall became the primary goal. All radioactive materials (more than 96 tons) were conditioned for disposal in concrete containers at the radioactive wastes depository “Radons” at the Baldone site. Protective and radiation measurement equipment of the personnel was upgraded significantly. All non-radioactive equipment and materials outside the reactor buildings were released for clearance and dismantled for reuse or conventional disposal. Contaminated materials from the reactor hall were collected and removed for clearance measurements on a weekly basis

Induction and repair of clustered DNA damage sites after exposure to ionizing radiation

The mechanisms that maintain genomic stability safeguard cells from constant DNA damage produced by endogenous and external stressors. Therefore, this thesis aimed to specifically address questions regarding the requirement and involvement of DNA repair proteins in the repair of various types of radiation-induced DNA damage. The first aim was to determine whether the phosphorylation of DNA-PKcs, a major kinase involved in non-homologous end joining pathway, can be utilized to score the DNA double-strand break (DSB) content in cells. DNA-PKcs phosphorylated (pDNA-PKcs) at T2609 was more sensitive to the cellular DSB content than ɣH2AX, as analyzed by flow cytometry. Further, pDNA-PKcs at T2609 could discriminate between DSB repair-compromised and normal cells, confirming that the pDNA-PKcs can be used as a DSB repair marker. In paper II, the DSB repair was assessed in cells with reduced levels of DNA-PKcs. The reduction in DNA-PKcs resulted in decreased cell survival and unaffected DSB repair. These results clearly indicate that DNA-PKcs plays an additional role in promoting cell survival in addition to its function in DSB repair. The second part of the thesis focused on the characterization of complex DNA damage. DNA damage was investigated after exposure to α-particles originating from Ra-223. The Ra-223 treatment induced a nonrandom DSB distribution consistent with damage induced by high-linear energy transfer radiation. The exposure to Ra-223 significantly reduced cell survival in monolayers and 3D cell structures. The last paper unraveled the fate of heat-sensitive clustered DNA damage site (HSCS) repair in cells. HSCS repair was independent of DSB repair, and these lesions did not contribute to the generation of additional DSBs during repair. Prolonged heating of DNA at relatively low temperatures induced structural changes in the DNA that contributed to the production of DNA artifacts. In conclusion, these results demonstrate that DNA-PKcs can be used to monitor DSB repair in cells after exposure to ionizing radiation. However, the functions of DNA-PKcs are not limited to DSB repair, as it can promote cell survival through other mechanisms. The complexity of the DNA damage produced by high-LET radiation is a major contributor to cell death. However, not all clusters produced in irradiated cells are converted into DSBs during repair

Induction and repair of clustered DNA damage sites after exposure to ionizing radiation

The mechanisms that maintain genomic stability safeguard cells from constant DNA damage produced by endogenous and external stressors. Therefore, this thesis aimed to specifically address questions regarding the requirement and involvement of DNA repair proteins in the repair of various types of radiation-induced DNA damage. The first aim was to determine whether the phosphorylation of DNA-PKcs, a major kinase involved in non-homologous end joining pathway, can be utilized to score the DNA double-strand break (DSB) content in cells. DNA-PKcs phosphorylated (pDNA-PKcs) at T2609 was more sensitive to the cellular DSB content than ɣH2AX, as analyzed by flow cytometry. Further, pDNA-PKcs at T2609 could discriminate between DSB repair-compromised and normal cells, confirming that the pDNA-PKcs can be used as a DSB repair marker. In paper II, the DSB repair was assessed in cells with reduced levels of DNA-PKcs. The reduction in DNA-PKcs resulted in decreased cell survival and unaffected DSB repair. These results clearly indicate that DNA-PKcs plays an additional role in promoting cell survival in addition to its function in DSB repair. The second part of the thesis focused on the characterization of complex DNA damage. DNA damage was investigated after exposure to α-particles originating from Ra-223. The Ra-223 treatment induced a nonrandom DSB distribution consistent with damage induced by high-linear energy transfer radiation. The exposure to Ra-223 significantly reduced cell survival in monolayers and 3D cell structures. The last paper unraveled the fate of heat-sensitive clustered DNA damage site (HSCS) repair in cells. HSCS repair was independent of DSB repair, and these lesions did not contribute to the generation of additional DSBs during repair. Prolonged heating of DNA at relatively low temperatures induced structural changes in the DNA that contributed to the production of DNA artifacts. In conclusion, these results demonstrate that DNA-PKcs can be used to monitor DSB repair in cells after exposure to ionizing radiation. However, the functions of DNA-PKcs are not limited to DSB repair, as it can promote cell survival through other mechanisms. The complexity of the DNA damage produced by high-LET radiation is a major contributor to cell death. However, not all clusters produced in irradiated cells are converted into DSBs during repair

Removal of heat-sensitive clustered damaged DNA sites is independent of double-strand break repair

DNA double-strand breaks (DSBs) are the most deleterious lesions that can arise in cells after ionizing radiation or radiometric drug treatment. In addition to prompt DSBs, DSBs may also be produced during repair, evolving from a clustered DNA damaged site, which is composed of two or more distinct lesions that are located within two helical turns. A specific type of cluster damage is the heat-sensitive clustered site (HSCS), which transforms into DSBs upon treatment at elevated temperatures. The actual lesions or mechanisms that mediate the HSCS transformation into DSBs are unknown. However, there are two possibilities; either these lesions are transformed into DSBs due to DNA lesion instability, e.g., transfer of HSCS into single-strand breaks (SSBs), or they are formed due to local DNA structure instability, e.g., DNA melting, where two SSBs on opposite strands meet and transform into a DSB. The importance of these processes in living cells is not understood, but they significantly affect estimates of DSB repair capacity. In this study, we show that HSCS removal in human cells is not affected by defects in DSB repair or inhibition of DSB repair. Under conditions where rejoining of prompt DSBs was almost completely inhibited, heat-sensitive DSBs were successfully rejoined, without resulting in increased DSB levels, indicating that HSCS do not transfer into DSB in cells under physiological conditions. Furthermore, analysis by atomic force microscopy suggests that prolonged heating of chromosomal DNA can induce structural changes that facilitate transformation of HSCS into DSB. In conclusion, the HSCS do not generate additional DSBs at physiological temperatures in human cells, and the repair of HSCS is independent of DSB repair

The syntax of the ti construction in Tunxi Hui

This thesis is a study of the syntax of the ti construction in Tunxi Hui, an understudied Hui dialect in the Sinitic family of languages. The aims of this these are three-fold: (i) to provide a sketch of the syntax of Tunxi Hui, and (ii) to explore the polyfunctionality of the ti morpheme and the syntax of the ti construction in Tunxi Hui, and (iii) to examine the north-south division of passive markers particularly with respect to languages in Anhui Province, and the type of passive marker the Tunxi Hui ti belongs to, as well as some properties of the ti passive construction. This thesis explores the polyfunctionality of the ti morpheme in Tunxi Hui, as a lexical verb ‘give’ and as a coverb. When ti is a lexical verb, the construction it appears in is a double object construction (DOC), and the linear order of the two objects has to be the recipient NP before the Theme NP. When ti is a coverb, it is often found in a serial verb construction (SVC) or a pivotal construction. As far as an SVC is concerned, the coverb ti can serve as a recipient marker, a benefactive marker or a locative marker. Otherwise, if the coveb ti occurs in a pivotal construction where the two or more verbs in the sentence do not share the same structural subject, it can serve as a permissive marker, a causative marker or a passive marker. With respect to passive markers, we first give an overview of the types of passives markers in Sinitic languages. Aside from the bei passives, we also have the zhuo ‘attach’ passives, the causative passives and the ‘give’-passives. We propose a revision of Hashimoto’s (1988) north-south division of passive markers, i.e. the causative passives versus the ‘give’-passives, particularly with respect to languages of Anhui Province. We find that the passive marker ti in Tunxi Hui belongs to the give type of passives. The ti passive construction in Tunxi Hui is characterized by the obligatory occurrence of an agent phrase and the semantic implication of adversity. It is hoped that this study can contribute to the understanding of the syntax of the ti construction in Tunxi Hui, and can provide useful authentic data of an understudied language for further linguistic analyses.published_or_final_versionLinguisticsMasterMaster of Philosoph

Ra-223 induces clustered DNA damage and inhibits cell survival in several prostate cancer cell lines

The bone-seeking radiopharmaceutical Xofigo (Radium-223 dichloride) has demonstrated both extended sur-vival and palliative effects in treatment of bone metastases in prostate cancer. The alpha-particle emitter Ra-223, targets regions undergoing active bone remodeling and strongly binds to bone hydroxyapatite (HAp). However, the toxicity mechanism and properties of Ra-223 binding to hydroxyapatite are not fully understood. By exposing 2D and 3D (spheroid) prostate cancer cell models to free and HAp-bound Ra-223 we here studied cell toxicity, apoptosis and formation and repair of DNA double-strand breaks (DSBs). The rapid binding with a high affinity of Ra-223 to bone-like HAp structures was evident (KD= 19.2 x 10-18 M) and almost no dissociation was detected within 24 h. Importantly, there was no significant uptake of Ra-223 in cells. The Ra-223 alpha-particle decay produced track-like distributions of the DNA damage response proteins 53BP1 and gamma H2AX induced high amounts of clustered DSBs in prostate cancer cells and activated DSB repair through non-homologous end-joining (NHEJ). Ra-223 inhibited growth of prostate cancer cells, independent of cell type, and induced high levels of apoptosis. In summary, we suggest the high cell killing efficacy of the Ra-223 was attributed to the clustered DNA damaged sites induced by alpha-particles