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        Saw-tooth softening/stiffening - a stable computational procedure for RC

        Jan G. Rots,Stefano Invernizzi,Beatrice Belletti 한국계산역학회 2006 Computers and Concrete, An International Journal Vol.3 No.4

        Over the past years techniques for non-linear analysis have been enhanced significantly via improved solution procedures, extended finite element techniques and increased robustness of constitutive models. Nevertheless, problems remain, especially for real world structures of softening materials like concrete. The softening gives negative stiffness and risk of bifurcations due to multiple cracks that compete to survive. Incremental-iterative techniques have difficulties in selecting and handling the local peaks and snap-backs. In this contribution, an alternative method is proposed. The softening diagram of negative slope is replaced by a saw-tooth diagram of positive slopes. The incremental-iterative Newton method is replaced by a series of linear analyses using a special scaling technique with subsequent stiffness/strength reduction per critical element. It is shown that this event-by-event strategy is robust and reliable. First, the model is shown to be objective with respect to mesh refinement. Next, the example of a large-scale dog-bone specimen in direct tension is analyzed using an isotropic version of the saw-tooth model. The model is capable of automatically providing the snap-back response. Subsequently, the saw-tooth model is extended to include anisotropy for fixed crack directions to accommodate both tensile cracking and compression strut action for reinforced concrete. Three different reinforced concrete structures are analyzed, a tension-pull specimen, a slender beam and a slab. In all cases, the model naturally provides the local peaks and snap-backs associated with the subsequent development of primary cracks starting from the rebar. The secant saw-tooth stiffness is always positive and the analysis always 멵onverges? Bifurcations are prevented due to the scaling technique.

      • Lack of Association between Polymorphisms in Genes MTHFR and MDR1 with Risk of Childhood Acute Lymphoblastic Leukemia

        Kreile, Madara,Rots, Dmitrijs,Piekuse, Linda,Cebura, Elizabete,Grutupa, Marika,Kovalova, Zhanna,Lace, Baiba Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.22

        Background: Acute lymphoblastic leukemia (ALL) is a complex disease caused by interactions between hazardous exogenous or/and endogenous agents and many mild effect inherited susceptibility mutations. Some of them are known, but their functional roles still requireinvestigation. Age is a recognized risk factor; children with disease onset after the age of ten have worse prognosis, presumably also triggered by inherited factors. Materials and Methods: The MDR1 gene polymorphisms rs1045642, rs2032582 and MTHFR gene polymorphisms rs1801131 and rs1801133 were genotyped in 68 ALL patients in remission and 102 age and gender matched controls; parental DNA samples were also available for 42 probands. Results: No case control association was found between analyzed polymorphisms and a risk of childhood ALL development. Linkage disequilibrium was not observed in a family-based association study either. Only marginal association was observed between genetic marker rs2032582A and later disease onset (p=0.04). Conclusions: Our data suggest that late age of ALL onset could be triggered by mild effect common alleles.

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        Photofragmentation in selected tautomers of protonated adenine

        Cheong, Nu Ri,Nam, Sang Hwan,Park, Hye Sun,Ryu, Seol,Song, Jae Kyu,Park, Seung Min,,rot, Marie,Lucas, Bruno,Barat, Michel,Fayeton, Jacqueline A.,Jouvet, Christophe Royal Society of Chemistry 2011 Physical chemistry chemical physics Vol.13 No.1

        <P>The photofragmentation by UV excitation of selectively prepared 1<SUP>+</SUP> and 3<SUP>+</SUP> tautomers of protonated adenine is studied after excitation at a 266 and 263 nm wavelengths with two different experimental set-ups located in Seoul and Orsay. While the production of 1<SUP>+</SUP> tautomers with an electrospray ion source is now well accepted, calculations were used to ascribe the preparation of 3<SUP>+</SUP> tautomers from cold adenine dimers. The fragmentation patterns are rather similar for both tautomers, suggesting similar mechanisms as a statistical fragmentation in the ground electronic state after internal conversion.</P> <P>Graphic Abstract</P><P>The UV fragmentation pathway of protonated adenine is independent of the tautomer. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c000961j'> </P>

      • High-resolution metabolomics of occupational exposure to trichloroethylene

        Walker, Douglas I,Uppal, Karan,Zhang, Luoping,Vermeulen, Roel,Smith, Martyn,Hu, Wei,Purdue, Mark P,Tang, Xiaojiang,Reiss, Boris,Kim, Sungkyoon,Li, Laiyu,Huang, Hanlin,Pennell, Kurt D,Jones, Dean P,Rot Oxford University Press 2016 International journal of epidemiology Vol.45 No.5

        <P><B>Background:</B> Occupational exposure to trichloroethylene (TCE) has been linked to adverse health outcomes including non-Hodgkin’s lymphoma and kidney and liver cancer; however, TCE’s mode of action for development of these diseases in humans is not well understood.</P><P><B>Methods:</B> Non-targeted metabolomics analysis of plasma obtained from 80 TCE-exposed workers [full shift exposure range of 0.4 to 230 parts-per-million of air (ppm<SUB>a</SUB>)] and 95 matched controls were completed by ultra-high resolution mass spectrometry. Biological response to TCE exposure was determined using a metabolome-wide association study (MWAS) framework, with metabolic changes and plasma TCE metabolites evaluated by dose-response and pathway enrichment. Biological perturbations were then linked to immunological, renal and exposure molecular markers measured in the same population.</P><P><B>Results:</B> Metabolic features associated with TCE exposure included known TCE metabolites, unidentifiable chlorinated compounds and endogenous metabolites. Exposure resulted in a systemic response in endogenous metabolism, including disruption in purine catabolism and decreases in sulphur amino acid and bile acid biosynthesis pathways. Metabolite associations with TCE exposure included uric acid (<I>β</I> = 0.13, <I>P</I>-value = 3.6 × 10<SUP>−5</SUP>), glutamine (<I>β</I> = 0.08, <I>P</I>-value = 0.0013), cystine (<I>β</I> = 0.75, <I>P</I>-value = 0.0022), methylthioadenosine (<I>β</I> = −1.6, <I>P</I>-value = 0.0043), taurine (<I>β</I> = −2.4, <I>P</I>-value = 0.0011) and chenodeoxycholic acid (<I>β</I> = −1.3, <I>P</I>-value = 0.0039), which are consistent with known toxic effects of TCE, including immunosuppression, hepatotoxicity and nephrotoxicity. Correlation with additional exposure markers and physiological endpoints supported known disease associations.</P><P><B>Conclusions:</B> High-resolution metabolomics correlates measured occupational exposure to internal dose and metabolic response, providing insight into molecular mechanisms of exposure-related disease aetiology.</P>

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