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Progressive Evolution (progressive + evolution)
Selected AbstractsSeismicity in a model governed by competing frictional weakening and healing mechanismsGEOPHYSICAL JOURNAL INTERNATIONAL, Issue 3 2009G. Hillers SUMMARY Observations from laboratory, field and numerical work spanning a wide range of space and time scales suggest a strain dependent progressive evolution of material properties that control the stability of earthquake faults. The associated weakening mechanisms are counterbalanced by a variety of restrengthening mechanisms. The efficiency of the healing processes depends on local material properties and on rheologic, temperature, and hydraulic conditions. We investigate the relative effects of these competing non-linear feedbacks on seismogenesis in the context of evolving frictional properties, using a mechanical earthquake model that is governed by slip weakening friction. Weakening and strengthening mechanisms are parametrized by the evolution of the frictional control variable,the slip weakening rate R,using empirical relationships obtained from laboratory experiments. In our model, weakening depends on the slip of an earthquake and tends to increase R, following the behaviour of real and simulated frictional interfaces. Healing causes R to decrease and depends on the time passed since the last slip. Results from models with these competing feedbacks are compared with simulations using non-evolving friction. Compared to fixed R conditions, evolving properties result in a significantly increased variability in the system dynamics. We find that for a given set of weakening parameters the resulting seismicity patterns are sensitive to details of the restrengthening process, such as the healing rate b and a lower cutoff time, tc, up to which no significant change in the friction parameter is observed. For relatively large and small cutoff times, the statistics are typical of fixed large and small R values, respectively. However, a wide range of intermediate values leads to significant fluctuations in the internal energy levels. The frequency-size statistics of earthquake occurrence show corresponding non-stationary characteristics on time scales over which negligible fluctuations are observed in the fixed- R case. The progressive evolution implies that,except for extreme weakening and healing rates,faults and fault networks possibly are not well characterized by steady states on typical catalogue time scales, thus highlighting the essential role of memory and history dependence in seismogenesis. The results suggest that an extrapolation to future seismicity occurrence based on temporally limited data may be misleading due to variability in seismicity patterns associated with competing mechanisms that affect fault stability. [source] Evolution of multi-drug resistant hepatitis B virus during sequential therapy,HEPATOLOGY, Issue 3 2006Hyung Joon Yim Multi-drug resistant hepatitis B virus (HBV) has been reported in hepatitis B patients who received sequential antiviral therapy. In vitro studies showed that HBV constructs with mutations resistant to lamivudine and adefovir have marked reduction in sensitivity to combination of lamivudine and adefovir, whereas constructs with mutations resistant to either drug remain sensitive to the other drug. We conducted this study to determine whether mutations conferring resistance to multiple antiviral agents co-locate on the same HBV genome in vivo and to describe the evolution of these mutations. Sera from six patients who had been found to have multi-drug resistant HBV mutations to lamivudine + adefovir, lamivudine + hepatitis B immunoglobulin (HBIG), or lamivudine + entecavir on direct sequencing were cloned after nested polymerase chain reaction (PCR). Analysis of 215 clones from 11 samples with multi-drug resistant mutations on direct sequencing showed that 183 (85%) clones had mutations to both therapies on the same genome; 31 clones had lamivudine-resistant mutants only. Clonal analysis of serial samples from three patients showed progressive evolution from all clones with lamivudine-resistant HBV mutations only to mixtures of clones that have multi-drug resistant mutations and clones that have lamivudine-resistant HBV mutations only, and ultimately all clones having multi-drug resistant HBV mutations. In conclusion, mutations conferring resistance to multiple antiviral agents co-locate on the same viral genome, suggesting that combination therapy directed against mutants resistant to each treatment may not be adequate in suppressing multi-drug resistant HBV. De novo combination therapy may prevent the emergence of multi-drug resistant mutants. (HEPATOLOGY 2006;44:703,712.) [source] The lissamphibian humerus and elbow joint, and the origins of modern amphibiansJOURNAL OF MORPHOLOGY, Issue 12 2009Trond Sigurdsen Abstract The origins and evolution of the three major clades of modern amphibians are still a source of controversy, and no general consensus exists as to their relationship to the various known Paleozoic taxa. This may indicate that additional character complexes should be studied to resolve their phylogenetic relationship. The salamander elbow joint has been fundamentally misinterpreted in previous morphological descriptions. In caudates and anurans, both the radius and ulna (fused in anurans) articulate with the characteristically large capitulum (radial condyle), although part of the ulnar articulating surface fits into to the smooth trochlear region. The salamander "ulnar condyle" of previous descriptions is in fact the entepicondyle. The condition seen in batrachians (i.e., salamanders and frogs) may be a lissamphibian synapomorphy because the elbow region of the primitive fossil caecilian Eocaecilia resembles those of frogs and salamanders. In addition to the large and bulbous capitulum, all lissamphibian humeri lack an entepicondylar foramen, and possess a distally pointing entepicondyle, a low and rounded ectepicondyle, and an elongated shaft. These characters are identified in key fossil forms to assess the support for the different hypotheses proposed for the evolutionary origins of lissamphibians. Temnospondyli is the only group of early tetrapods that shows a progressive evolution of lissamphibian traits in the humerus and elbow joint. Furthermore, among Paleozoic taxa, the dissorophoid temnospondyl Doleserpeton annectens is the only taxon that has the full set of humeral features shared by all lissamphibians. These results add support for the theory of a monophyletic origin of lissamphibians from dissorophoidtemnospondyls. J. Morphol., 2009. © 2009 Wiley-Liss, Inc. [source] Chronic Actinic Dermatitis to Sesquiterpene Lactones: [2+2] Photoreaction Toward Thymidine of (+) and (,) ,-Methylene-Hexahydrobenzofuranone with a cis Ring JunctionPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2010Sébastien Fuchs (+) and (,) ,-methylene-hexahydrobenzofuranone derivatives with a stereochemically pure cis ring junction were used as models of sesquiterpene lactones to study their photoreactivity toward thymidine. After 313 nm irradiation of a deoxygenated acetone solution of lactone models and thymidine, six [2+2] photoadducts were isolated for each enantiomer and fully characterized by a combination of NMR experiments. A common syn regioselectivity and exo stereoselectivity were observed for photoadducts. This high photoreactivity of ,-methylene-,-butyrolactone ring toward thymidine could be an explanation of the progressive evolution of allergic contact dermatitis toward chronic actinic dermatitis. [source] 2464: Phenotype/genotype evolution in corneal dystrophiesACTA OPHTHALMOLOGICA, Issue 2010F CHIAMBARETTA Purpose The corneal dystrophies are a group of genetically determined diseases usually characterized by loss of corneal transparency, which may be caused by a progressive accumulation of abnormal material within the cornea. The genetic characterization of corneal dystrophies revealed both genetic heterogeneity, that is, different genes (KRT3 and KRT12) causing a single dystrophy phenotype (Meesmann dystrophy), and phenotypic heterogeneity with a single gene (TGFBI) causing different allelic dystrophy phenotypes (RBCD, TBCD, granular type 1, granular type 2, and lattice type 1). But less is known about the evolution of the phenotype during life. Methods We were interesting in following the corneal phénotype progressive evolution during childhood. During several years we analyzed corneal phénotype of families of Lattice type 1 and granular type 1, using Scheimpflug camera. Results We were able to follow the accumulation of abnormal material, his corneal localisation and evolution during years. Conclusion The phenotype of both Lattice type 1 and granular type 1 is totally different in childhood, with subepithelial localization. [source] | |||||||||||||