Possible correlation between work-hardening and fatigue-failure

Conceptual theory proposes that cyclic hardening due to non-uniform strain and stress amplitudes during testing, especially during the initial application of stress to a specimen, may correlate positively with the ultimate strength of the specimen under test

Radioactive decays at limits of nuclear stability

The last decades brought an impressive progress in synthesizing and studying properties of nuclides located very far from the beta stability line. Among the most fundamental properties of such exotic nuclides, usually established first, is the half-life, possible radioactive decay modes, and their relative probabilities. When approaching limits of nuclear stability, new decay modes set in. First, beta decays become accompanied by emission of nucleons from highly excited states of daughter nuclei. Second, when the nucleon separation energy becomes negative, nucleons start to be emitted from the ground state. Here, we present a review of the decay modes occurring close to the limits of stability. The experimental methods used to produce, identify and detect new species and their radiation are discussed. The current theoretical understanding of these decay processes is overviewed. The theoretical description of the most recently discovered and most complex radioactive process - the two-proton radioactivity - is discussed in more detail.Comment: Review, 68 pages, 39 figure

Collectivity and Configuration Mixing in \u3csup\u3e186,188\u3c/sup\u3ePb and \u3csup\u3e194\u3c/sup\u3ePo

Lifetimes of prolate intruder states in 186Pb and oblate intruder states in 194Po have been determined by employing, for the first time, the recoil-decay tagging technique in recoil distance Doppler-shift lifetime measurements. In addition, lifetime measurements of prolate states in 188Pb up to the 8+state were carried out using the recoil-gating method. The B(E2) values have been deduced from which deformation parameters lβ2l = 0.29(5) and lβ2l = 0.17(3) for the prolate and the oblate bands, respectively, have been extracted. The results also shed new light on the mixing between different shapes

Collectivity and configuration mixing in 186,188Pb and 194Po

Lifetimes of prolate intruder states in 186Pb and oblate intruder states in 194Po have been determined by employing, for the first time, the recoil-decay tagging technique in recoil distance Doppler-shift lifetime measurements. In addition, lifetime measurements of prolate states in 188Pb up to the 8+ state were carried out using the recoil-gating method. The B(E2) values have been deduced from which deformation parameters |β2|=0.29(5) and |β2|=0.17(3) for the prolate and the oblate bands, respectively, have been extracted. The results also shed new light on the mixing between different shapes

Lifetimes of intruder states in 186 Pb, 188 Pb and 194 Po

Lifetimes of prolate intruder states in 186Pb and 188Pb and oblate intruder states in 194Po have been determined through recoil distance Doppler-shift lifetime measurements. Deformation parameters of | β2 | = 0.29 (5) and | β2 | = 0.17(3) have been ext

BCL11B Regulates Epithelial Proliferation and Asymmetric Development of the Mouse Mandibular Incisor

Mouse incisors grow continuously throughout life with enamel deposition uniquely on the outer, or labial, side of the tooth. Asymmetric enamel deposition is due to the presence of enamel-secreting ameloblasts exclusively within the labial epithelium of the incisor. We have previously shown that mice lacking the transcription factor BCL11B/CTIP2 (BCL11B hereafter) exhibit severely disrupted ameloblast formation in the developing incisor. We now report that BCL11B is a key factor controlling epithelial proliferation and overall developmental asymmetry of the mouse incisor: BCL11B is necessary for proliferation of the labial epithelium and development of the epithelial stem cell niche, which gives rise to ameloblasts; conversely, BCL11B suppresses epithelial proliferation, and development of stem cells and ameloblasts on the inner, or lingual, side of the incisor. This bidirectional action of BCL11B in the incisor epithelia appears responsible for the asymmetry of ameloblast localization in developing incisor. Underlying these spatio-specific functions of BCL11B in incisor development is the regulation of a large gene network comprised of genes encoding several members of the FGF and TGFβ superfamilies, Sprouty proteins, and Sonic hedgehog. Our data integrate BCL11B into these pathways during incisor development and reveal the molecular mechanisms that underlie phenotypes of both Bcl11b−/− and Sprouty mutant mice

Hostility in adolescents and adults : a genome-wide association study of the Young Finns

Peer reviewe

Estimation of metabolite networks with regard to a specific covariable: applications to plant and human data

In systems biology, where a main goal is acquiring knowledge of biological systems, one of the challenges is inferring biochemical interactions from different molecular entities such as metabolites. In this area, the metabolome possesses a unique place for reflecting “true exposure” by being sensitive to variation coming from genetics, time, and environmental stimuli. While influenced by many different reactions, often the research interest needs to be focused on variation coming from a certain source, i.e. a certain covariable Xm . Objective Here, we use network analysis methods to recover a set of metabolite relationships, by finding metabolites sharing a similar relation to Xm . Metabolite values are based on information coming from individuals’ Xm status which might interact with other covariables. Methods Alternative to using the original metabolite values, the total information is decomposed by utilizing a linear regression model and the part relevant to Xm is further used. For two datasets, two different network estimation methods are considered. The first is weighted gene co-expression network analysis based on correlation coefficients. The second method is graphical LASSO based on partial correlations. Results We observed that when using the parts related to the specific covariable of interest, resulting estimated networks display higher interconnectedness. Additionally, several groups of biologically associated metabolites (very large density lipoproteins, lipoproteins, etc.) were identified in the human data example. Conclusions This work demonstrates how information on the study design can be incorporated to estimate metabolite networks. As a result, sets of interconnected metabolites can be clustered together with respect to their relation to a covariable of interest

Genome-wide study for circulating metabolites identifies 62 loci and reveals novel systemic effects of LPA

Genome-wide association studies have identified numerous loci linked with complex diseases, for which the molecular mechanisms remain largely unclear. Comprehensive molecular profiling of circulating metabolites captures highly heritable traits, which can help to uncover metabolic pathophysiology underlying established disease variants. We conduct an extended genome-wide association study of genetic influences on 123 circulating metabolic traits quantified by nuclear magnetic resonance metabolomics from up to 24,925 individuals and identify eight novel loci for amino acids, pyruvate and fatty acids. The LPA locus link with cardiovascular risk exemplifies how detailed metabolic profiling may inform underlying aetiology via extensive associations with very-low-density lipoprotein and triglyceride metabolism. Genetic fine mapping and Mendelian randomization uncover wide-spread causal effects of lipoprotein(a) on overall lipoprotein metabolism and we assess potential pleiotropic consequences of genetically elevated lipoprotein(a) on diverse morbidities via electronic health-care records. Our findings strengthen the argument for safe LPA-targeted intervention to reduce cardiovascular risk

Discovery and validation of plasma proteomic biomarkers relating to brain amyloid burden by SOMAscan assay.

Plasma proteins have been widely studied as candidate biomarkers to predict brain amyloid deposition to increase recruitment efficiency in secondary prevention clinical trials for Alzheimer's disease. Most such biomarker studies are targeted to specific proteins or are biased toward high abundant proteins. 4001 plasma proteins were measured in two groups of participants (discovery group = 516, replication group = 365) selected from the European Medical Information Framework for Alzheimer's disease Multimodal Biomarker Discovery study, all of whom had measures of amyloid. A panel of proteins (n = 44), along with age and apolipoprotein E (APOE) ε4, predicted brain amyloid deposition with good performance in both the discovery group (area under the curve = 0.78) and the replication group (area under the curve = 0.68). Furthermore, a causal relationship between amyloid and tau was confirmed by Mendelian randomization. The results suggest that high-dimensional plasma protein testing could be a useful and reproducible approach for measuring brain amyloid deposition