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Tsutakawa, Susan E.; Morikawa, Kosuke
Lawrence Berkeley National Lab., CA (United States). Funding organisation: USDOE Director, Office of Science (United States)
Lawrence Berkeley National Lab., CA (United States). Funding organisation: USDOE Director, Office of Science (United States)
AbstractAbstract
No abstract available
Primary Subject
Source
23 May 2001; [vp.]; AC03-76SF00098; Available from Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720 (US)
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Daniels, D.S.
Ernest Orlando Lawrence Berkeley National Lab., Advanced Light Source, CA (United States). Funding organisation: US Department of Energy (United States)
Ernest Orlando Lawrence Berkeley National Lab., Advanced Light Source, CA (United States). Funding organisation: US Department of Energy (United States)
AbstractAbstract
No abstract available
Primary Subject
Source
1 Aug 2001; [vp.]; AC03-76SF00098; Available from www.als.lbl.gov; Submitted to the The Scripps Research Institute, La Jolla, CA (US); Thesis (Ph.D.)
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Report
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Gonzalez B, F.
Universidad Nacional Autonoma de Mexico, Facultad de Ciencias, Posgrado en Ciencias Biologicas, 04510 Mexico D.F. (Mexico)
Universidad Nacional Autonoma de Mexico, Facultad de Ciencias, Posgrado en Ciencias Biologicas, 04510 Mexico D.F. (Mexico)
AbstractAbstract
[en] In this work you determines the repair of the lesions inductoras of Sister chromatid exchange (ICHs) generated in the cells of the salivary gland of mouse, for the treatment with the N-Methyl-N-Nitrosourea (MNU), the N-Ethyl-N-Nitrosourea (ENU), the Methyl methanesulfonate (MMS) and the Ethyl methanesulfonate (EMS) in early and slow G1 of the first one and the second cellular division, that is to say before and after the cells incorporate 5-bromine-2 -Desoxyuridine (BrdU) in the DNA. Groups witness non treaties were included with mutagen. The cells of the salivary gland repaired the generated lesions partially by the MNU, the MMS and the EMS in the 1st division, and only the lesions induced by the ENU and MMS were repaired partially in the 2nd division. The ENU generates injure that they were not repaired in the 1st division and those taken place by the EMS were little repaired in the 2nd division. The methylating agents generated but ICHs that the ethylating. One observes that the BrdU makes to the molecule of the DNA but susceptible to the damage generated by the alkylating agents that induce the formation of the ICHs. This susceptibility was incremented around 150% for the treatment with the MNU, the ENU and the MMS, on the other hand for the EMS it was 3 times minor. It is proposed that the one electronegative atom of this analog of the timine would to work as a nucleophyllic center with which the electrophyllic compounds react. (Author)
Original Title
Reparabilidad durante G1 de las lesiones inductoras de intercambios en las cromatidas hermanas inducidos por agentes alquilantes en ADN sustituido y no sustituido con BrdU, en celulas de la glandula salival de raton In vivo
Primary Subject
Source
2004; 124 p; Available from the ININ, CIDN, A.P. 18-1027, 11801 Mexico D.F. (MX); Thesis (Ph.D. Biology)
Record Type
Miscellaneous
Literature Type
Thesis/Dissertation
Country of publication
ANIMALS, ANTIMETABOLITES, AZINES, BIOLOGICAL RECOVERY, BIOLOGICAL REPAIR, BODY, BROMOURACILS, CARBOXYLIC ACID SALTS, CHROMOSOMAL ABERRATIONS, DNA REPAIR, DRUGS, GLANDS, HETEROCYCLIC COMPOUNDS, HYDROXY COMPOUNDS, MAMMALS, MUTATIONS, NUCLEOSIDES, NUCLEOTIDES, ORGANIC BROMINE COMPOUNDS, ORGANIC COMPOUNDS, ORGANIC HALOGEN COMPOUNDS, ORGANIC NITROGEN COMPOUNDS, ORGANS, PYRIMIDINES, REPAIR, RIBOSIDES, RODENTS, SYNTHESIS, URACILS, VERTEBRATES
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SUTHERLAND, B.M.
Brookhaven National Lab., Upton, NY (United States). Funding organisation: USDOE Office of Energy Research (ER) (United States)
Brookhaven National Lab., Upton, NY (United States). Funding organisation: USDOE Office of Energy Research (ER) (United States)
AbstractAbstract
[en] Radiation can damage cellular components, including DNA. Organisms have developed a panoply of means of dealing with DNA damage. Some repair paths have rather narrow substrate specificity (e.g. photolyases), which act on specific pyrimidine photoproducts in a specific type (e.g., DNA) and conformation (double-stranded B conformation) of nucleic acid. Others, for example, nucleotide excision repair, deal with larger classes of damages, in this case bulky adducts in DNA. A detailed discussion of DNA repair mechanisms is beyond the scope of this article, but one can be found in the excellent book of Friedberg et al.[1] for further detail. However, some DNA damages and paths for repair of those damages important for photobiology will be outlined below as a basis for the specific examples of genetic and molecular analysis that will be presented below
Primary Subject
Source
26 Jul 2001; 12 p; Brookhaven National Laboratory; Upton, NY (United States); AC02-98CH10886; KP1102020; Available from Refer requests to OSTI; OSTI as DE00785050
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Miscellaneous
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Guyot, Christian.
CEA Centre d'Etudes Nucleaires de Saclay, 91 - Gif-sur-Yvette (France). Services d'Electronique
CEA Centre d'Etudes Nucleaires de Saclay, 91 - Gif-sur-Yvette (France). Services d'Electronique
AbstractAbstract
[en] The author gives the general lines of a method for the allocation and for the evaluation of maintainability of complex systems which is to be developed during the conference. The maintainability objective is supposed to be formulated under the form of a mean time to repair (M.T.T.R.)
[fr]
L'auteur indique dans ses grandes lignes une methode pour l'allocation et pour l'evaluation de la maintenabilite de systemes complexes qui sera developpee en conference. L'objectif de maintenabilite est suppose formule sous la forme d'une moyenne des temps techniques de reparation (MTTR)Original Title
Allocation de la maintenabilite
Source
Jun 1980; 12 p; French-Yugoslavian summer school; Dubrovnik, Yugoslavia; 23 - 28 Jun 1980
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Report
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Conference
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Charazac, Aurelie
Universite de Grenoble Alpes, 621 avenue Centrale 38400 Saint Martin d'Heres (France); CEA, DSM-INAC (France)
Universite de Grenoble Alpes, 621 avenue Centrale 38400 Saint Martin d'Heres (France); CEA, DSM-INAC (France)
AbstractAbstract
[en] The Gorlin syndrome is a rare genetic disorder characterized by several developmental abnormalities. Due to mutations in PTCH1, a key player of the sonic hedgehog signaling pathway, clinical manifestations also includes hyper-radiosensitivity and an increased predisposition to the development of basal cell carcinomas. Given the implication of DNA repair system defects in hyper-radiosensitivity pathologies, we decided to study the effect of PTCH1 mutations on the DNA damage response in order to better understand the cellular and molecular mechanisms leading to Gorlin's phenotype.This study demonstrate a global failure of the DNA damage repair systems in Gorlin fibroblasts with respect to controls. It highlights in particular the collapse of the base excision repair pathway (BER) responsible for the repair of oxidative DNA damage. (author)
[fr]
Le syndrome de Gorlin est une maladie rare caracterisee par de nombreuses anomalies du developpement. Ces manifestations cliniques, dues a des mutations d'un acteur essentiel de la voie de signalisation sonic hedgehog, incluent aussi une hyper-radiosensibilite et une forte predisposition a developper des carcinomes basocellulaires. Etant donne l'implication de defaut de la reparation de l'ADN au niveau des affections liees a l'hyper-radiosensibilite, nous avons decide d'etudier l'effet des mutations du gene PTCH1 sur la reponse aux dommages de l'ADN afin de mieux comprendre les mecanismes cellulaires et moleculaires conduisant au phenotype Gorlin. Cette etude permet de mettre en evidence une defaillance globale des systemes de reparation des dommages de l'ADN dans les fibroblastes issus de patients Gorlin par rapport a des fibroblastes normaux. Elle met notamment en exergue un ecroulement de la reparation par excision de bases (BER) responsable de la reparation des dommages oxydatifsOriginal Title
Effet de la deregulation de la voie Sonic Hedgehog sur les reponses aux dommages de I'ADN et la predisposition aux cancers
Primary Subject
Source
29 Oct 2015; 220 p; 239 refs.; Available from the INIS Liaison Officer for France, see the 'INIS contacts' section of the INIS-NKM website for current contact and E-mail addresses: http://www.iaea.org/inis/Contacts/; Also available from Bibliotheques Universitaires Grenoble Alpes, scd@ujf-grenoble.fr; Biologie Cellulaire
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Aksenov, S.V.
Division of Radiation and Radiobiological Research, Joint Institute for Nuclear Research, Dubna (Russian Federation)
Division of Radiation and Radiobiological Research, Joint Institute for Nuclear Research, Dubna (Russian Federation)
AbstractAbstract
[en] Regulation of the SOS response in Escherichia coli, which is a set of inducible cellular reactions introduced after DNA damage, is due to specific interaction of LexA and RecA proteins. LexA protein is a common repressor of the genes of the SOS system, and RecA protein, once transiently activated by the so-called SOS-inducing signal, promotes LexA protein destruction. We have described the SOS regulation by means of differential equations with regard to LexA and RecA concentrations elsewhere. The 'input' function for model equations is the level of the SOS-inducing signal against time. Here we present a means for calculating the concentration of single-stranded DNA (SOS-inducing signal) as a function of time in wild-type cells after ultraviolet irradiation. With model equations one can simulate kinetic curves of SOS regulatory proteins after DNA damage to survey the SOS response kinetics. Simulation of LexA protein kinetics agrees with experimental data. We compare simulated LexA kinetic curves in wild-type and uνr- mutant bacteria, which is useful in investigating the way uνrABC-dependent excision repair modulates the SOS response kinetics. Possible applications of the model to investigating various aspects of the SOS induction are discussed
Primary Subject
Source
1997; 15 p; 11 refs., 3 figs., 2 tabs. Submitted to the International Conference on Deterministic and Stochastic Modelling of Biointeraction, Sofia (BG), 28-31 Aug 1997.
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Garcia, Omar, E-mail: omar@cphr.edu.cu
Proceedings of III International Seminar. III National Workshop. Use and development of health- related industrial isotope products
Proceedings of III International Seminar. III National Workshop. Use and development of health- related industrial isotope products
AbstractAbstract
[en] This work discussed the following topics: Radiation damage and time. Short and Long term effects. Ionising radiation affect all cellular components. DNA main target for ionising radiation. Direct, Indirect and Bystander effect of radiation. Biological effect. Influence of different factors (Physical factors and Biological factors). Cellular repair of DNA damage. Cells with different repair capability. Cellular death detection. Chromosome aberration detection
Primary Subject
Secondary Subject
Source
[1 CD-ROM]; ISBN 959-7136-21-X;
; 2006; 855 KB; 3. International Seminar - 3. National Workshop. Use and development of health- related industrial isotope products; La Habana (Cuba); 22-24 Mar 2006; Available from Centro de Gestion de la Informacion y Desarrollo de la Energia (Cubaenergia) calle 20 No 4111 esquina 47, Playa, La Habana, Cuba. E-mail belkis@cubaenergia.cu; iraida@cubaenergia.cu; 22 figs.

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AbstractAbstract
No abstract available
Original Title
Deficiency report on helium circulators
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1972; 9 p
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Yuan, Fang; Chang, Shuang; Luo, Longlong; Li, Yaning; Wang, Liping; Song, Yaying; Qu, Meijie; Zhang, Zhijun; Yang, Guo-Yuan; Wang, Yongting, E-mail: gyyang@sjtu.edu.cn, E-mail: ytwang@sjtu.edu.cn
AbstractAbstract
[en] Highlights: • cxcl12 gene engineering of EPCs promoted VEGF and IGF expression by EPCs. • Conditioned media from CXCL12-EPCs further promoted the functions of OPCs. • CXCL12-EPCs conditioned media affected the expression of trophic factors by OPCs. • CXCR4 knockdown suppressed the proliferation and migration of OPCs and reduced PDGFR-α and bFGF expression. • CXCR7 knockdown inhibited the expression of MBP by OPCs and caused slower differentiation. Oligodendrocyte precursor cells (OPCs) are needed for white matter repair after various brain injury. Means that promote OPC functions could benefit white matter recovery after injury. Chemokine CXCL12 and endothelial progenitor cells (EPCs) both have been shown to promote remyelination. We hypothesize that the beneficial effects of EPCs and CXCL12 can be harnessed by genetically modifying EPCs with cxcl12 to synergistically improve the functions of OPCs. In this work, CXCL12-EPC was generated using virus-mediated gene transfer. OPCs were cultured with CXCL12-EPC conditioned media (CM) to analyze its impact on the proliferation, migration, differentiation and survival properties of OPCs. We blocked or knocked-down the receptors of CXCL12, namely CXCR4 and CXCR7, respectively to investigate their functions in regulating OPCs properties. Results revealed that CXCL12-EPC CM further promoted OPCs behavioral properties and upregulated the expression of PDGFR-α, bFGF, CXCR4 and CXCR7 in OPCs, albeit following different time course. Blocking CXCR4 diminished the beneficial effects of CXCL12 on OPCs proliferation and migration, while knocking down CXCR7 inhibited OPCs differentiation. Our results supported that cxcl12 gene modification of EPCs further promoted EPCs’ ability in augmenting the remyelination properties of OPCs, suggesting that CXCL12-EPC hold great potential in white matter repair.
Primary Subject
Source
S0014482718302015; Available from http://dx.doi.org/10.1016/j.yexcr.2018.03.040; Copyright (c) 2018 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
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