The long-term stability of self-esteem: Its time-dependent decay and nonzero asymptote

How stable are individual differences in self-esteem? We examined the time-dependent decay of rank-order stability of self-esteem and tested whether stability asymptotically approaches zero or a nonzero value across long test–retest intervals. Analyses were based on 6 assessments across a 29-year period of a sample of 3,180 individuals aged 14 to 102 years. The results indicated that, as test–retest intervals increased, stability exponentially decayed and asymptotically approached a nonzero value (estimated as .43). The exponential decay function explained a large proportion of variance in observed stability coefficients, provided a better fit than alternative functions, and held across gender and for all age groups from adolescence to old age. Moreover, structural equation modeling of the individual-level data suggested that a perfectly stable trait component underlies stability of self-esteem. The findings suggest that the stability of self-esteem is relatively large, even across very long periods, and that self-esteem is a trait-like characteristic.

Spectroscopy of element 115 decay chains

A high-resolution α, x-ray, and γ-ray coincidence spectroscopy experiment was conducted at the GSI Helmholtzzentrum für Schwerionenforschung. Thirty correlated α-decay chains were detected following the fusion-evaporation reaction Ca48+Am243. The observations are consistent with previous assignments of similar decay chains to originate from element Z=115. For the first time, precise spectroscopy allows the derivation of excitation schemes of isotopes along the decay chains starting with elements Z>112. Comprehensive Monte Carlo simulations accompany the data analysis. Nuclear structure models provide a first level interpretation.

Determination of the Weak Axial Vector Coupling λ=g_{A}/g_{V} from a Measurement of the β-Asymmetry Parameter A in Neutron Beta Decay

We report on a new measurement of the neutron beta-asymmetry parameter A with the instrument \perkeo. Main advancements are the high neutron polarization of P=99.7(1) from a novel arrangement of super mirror polarizers and reduced background from improvements in beam line and shielding. Leading corrections were thus reduced by a factor of 4, pushing them below the level of statistical error and resulting in a significant reduction of systematic uncertainty compared to our previous experiments. From the result A0=−0.11996(58), we derive the ratio of the axial-vector to the vector coupling constant λ=gA/gV=−1.2767(16)

Mechanistic aspects of mRNA targeting for nonsense-mediated mRNA decay in human cells

The nonsense-mediated mRNA decay (NMD) pathway is best known as a translation-coupled quality control system that recognizes and degrades aberrant mRNAs with ORF-truncating premature termination codons (PTCs), but a more general role of NMD in posttranscriptional regulation of gene expression is indicated by transcriptome-wide mRNA profilings that identified a plethora of physiological mRNAs as NMD substrates. We try to decipher the mechanism of mRNA targeting to the NMD pathway in human cells. Recruitment of the conserved RNA-binding helicase UPF1 to target mRNAs has been reported to occur through interaction with release factors at terminating ribosomes, but evidence for translation-independent interaction of UPF1 with the 3’ untranslated region (UTR) of mRNAs has also been reported. We have transcriptome-wide determined the UPF1 binding sites by individual-nucleotide resolution UV crosslinking and immunoprecipitation (iCLIP) in human cells, untreated or after inhibiting translation. We detected a strongly enriched association of UPF1 with 3’ UTRs in undisturbed, translationally active cells. After translation inhibition, a significant increase in UPF1 binding to coding sequence (CDS) was observed, indicating that UPF1 binds RNA before translation and gets displaced from the CDS by translating ribosomes. This suggests that the decision to trigger NMD occurs after association of UPF1 with mRNA, presumably through activation of RNA-bound UPF1 by aberrant translation termination. In a second recent study, we re-visited the reported restriction of NMD in mammals to the ‘pioneer round of translation’, i.e. to cap-binding complex (CBC)-bound mRNAs. The limitation of mammalian NMD to early rounds of translation would indicate a – from an evolutionary perspective – unexpected mechanistic difference to NMD in yeast and plants, where PTC-containing mRNAs seem to be available to NMD at each round of translation. In contrast to previous reports, our comparison of decay kinetics of two NMD reporter genes in mRNA fractions bound to either CBC or the eukaryotic initiation factor 4E (eIF4E) in human cells revealed that NMD destabilizes eIF4E-bound transcripts as efficiently as those associated with CBC. These results corroborate an emerging unified model for NMD substrate recognition, according to which NMD can ensue at every aberrant translation termination event.

eIF4E-bound mRNPs are substrates for nonsense-mediated mRNA decay in mammalian cells

Eukaryotic mRNAs with premature translation-termination codons (PTCs) are recognized and degraded by a process referred to as nonsense-mediated mRNA decay (NMD). The evolutionary conservation of the core NMD factors UPF1, UPF2 and UPF3 would imply a similar basic mechanism of PTC recognition in all eukaryotes. However, unlike NMD in yeast, which targets PTC-containing mRNAs irrespectively of whether their 5' cap is bound by the cap-binding complex (CBC) or by the eukaryotic initiation factor 4E (eIF4E), mammalian NMD has been claimed to be restricted to CBC-bound mRNAs during the pioneer round of translation. In our recent study we compared decay kinetics of two NMD reporter systems in mRNA fractions bound to either CBC or eIF4E in human cells. Our findings reveal that NMD destabilizes eIF4E bound transcripts as efficiently as those associated with CBC. These results corroborate an emerging unified model for NMD substrate recognition, according to which NMD can ensue at every aberrant translation termination event. Additionally, our results indicate that the closed loop structure of mRNA forms only after the replacement of CBC with eIF4E at the 5' cap.

eIF4E‐bound mRNPs are substrates for nonsense‐mediated mRNA decay in mammalian cells

Eukaryotic mRNAs with premature translation-termination codons (PTCs) are recognized and degraded by a process referred to as nonsense-mediated mRNA decay (NMD). The evolutionary conservation of the core NMD factors UPF1, UPF2 and UPF3 would imply a similar basic mechanism of PTC recognition in all eukaryotes. However, unlike NMD in yeast, which targets PTC-containing mRNAs irrespectively of whether their 5' cap is bound by the cap-binding complex (CBC) or by the eukaryotic initiation factor 4E (eIF4E), mammalian NMD has been claimed to be restricted to CBC-bound mRNAs during the pioneer round of translation. In our recent study we compared decay kinetics of two NMD reporter systems in mRNA fractions bound to either CBC or eIF4E in human cells. Our findings reveal that NMD destabilizes eIF4E bound transcripts as efficiently as those associated with CBC. These results corroborate an emerging unified model for NMD substrate recognition, according to which NMD can ensue at every aberrant translation termination event. Additionally, our results indicate that the closed loop structure of mRNA forms only after the replacement of CBC with eIF4E at the 5' cap.

eIF4E-bound mRNPs are substrates for nonsense-mediated mRNA decay in mammalian cells

Eukaryotic mRNAs with premature translation-termination codons (PTCs) are recognized and degraded by a process referred to as nonsense-mediated mRNA decay (NMD). The evolutionary conservation of the core NMD factors UPF1, UPF2 and UPF3 would imply a similar basic mechanism of PTC recognition in all eukaryotes. However, unlike NMD in yeast, which targets PTC-containing mRNAs irrespectively of whether their 5' cap is bound by the cap-binding complex (CBC) or by the eukaryotic initiation factor 4E (eIF4E), mammalian NMD has been claimed to be restricted to CBC-bound mRNAs during the pioneer round of translation. In our recent study we compared decay kinetics of two NMD reporter systems in mRNA fractions bound to either CBC or eIF4E in human cells. Our findings reveal that NMD destabilizes eIF4E bound transcripts as efficiently as those associated with CBC. These results corroborate an emerging unified model for NMD substrate recognition, according to which NMD can ensue at every aberrant translation termination event. Additionally, our results indicate that the closed loop structure of mRNA forms only after the replacement of CBC with eIF4E at the 5' cap.

eIF4E‐bound mRNPs are substrates for nonsense‐mediated mRNA decay in mammalian cells

Eukaryotic mRNAs with premature translation-termination codons (PTCs) are recognized and degraded by a process referred to as nonsense-mediated mRNA decay (NMD). The evolutionary conservation of the core NMD factors UPF1, UPF2 and UPF3 would imply a similar basic mechanism of PTC recognition in all eukaryotes. However, unlike NMD in yeast, which targets PTC-containing mRNAs irrespectively of whether their 5' cap is bound by the cap-binding complex (CBC) or by the eukaryotic initiation factor 4E (eIF4E), mammalian NMD has been claimed to be restricted to CBC-bound mRNAs during the pioneer round of translation. In our recent study we compared decay kinetics of two NMD reporter systems in mRNA fractions bound to either CBC or eIF4E in human cells. Our findings reveal that NMD destabilizes eIF4E bound transcripts as efficiently as those associated with CBC. These results corroborate an emerging unified model for NMD substrate recognition, according to which NMD can ensue at every aberrant translation termination event. Additionally, our results indicate that the closed loop structure of mRNA forms only after the replacement of CBC with eIF4E at the 5' cap.

Eukaryotic Initiation Factor 4G Suppresses Nonsense-Mediated mRNA Decay by Two Genetically Separable Mechanisms

Nonsense-mediated mRNA decay (NMD), which is best known for degrading mRNAs with premature termination codons (PTCs), is thought to be triggered by aberrant translation termination at stop codons located in an environment of the mRNP that is devoid of signals necessary for proper termination. In mammals, the cytoplasmic poly(A)-binding protein 1 (PABPC1) has been reported to promote correct termination and therewith antagonize NMD by interacting with the eukaryotic release factors 1 (eRF1) and 3 (eRF3). Using tethering assays in which proteins of interest are recruited as MS2 fusions to a NMD reporter transcript, we show that the three N-terminal RNA recognition motifs (RRMs) of PABPC1 are sufficient to antagonize NMD, while the eRF3-interacting C-terminal domain is dispensable. The RRM1-3 portion of PABPC1 interacts with eukaryotic initiation factor 4G (eIF4G) and tethering of eIF4G to the NMD reporter also suppresses NMD. We identified the interactions of the eIF4G N-terminus with PABPC1 and the eIF4G core domain with eIF3 as two genetically separable features that independently enable tethered eIF4G to inhibit NMD. Collectively, our results reveal a function of PABPC1, eIF4G and eIF3 in translation termination and NMD suppression, and they provide additional evidence for a tight coupling between translation termination and initiation.

Search for displaced muonic lepton jets from light Higgs boson decay in proton-proton collisions at sqrts TeV with the ATLAS detector

A search is performed for collimated muon pairs displaced from the primary vertex produced in the decay of long-lived neutral particles in proton-proton collisions at root s = 7 TeV centre-of-mass energy, with the ATLAS detector at the LHC. In a 1.9 fb(-1) event sample collected during 2011, the observed data are consistent with the Standard Model background expectations. Limits on the product of the production cross section and the branching ratio of a Higgs boson decaying to hidden-sector neutral long-lived particles are derived as a function of the particles' mean lifetime.

Search for resonant diboson production in the lvjj decay channels with the ATLAS detector at 7 TeV

A search for resonant diboson production using a data sample corresponding to 4.7 fb(-1) of integrated luminosity collected by the ATLAS experiment at the Large Hadron Collider in pp collisions at root s = 7 TeV is presented. The search for a narrow resonance in the WW or WZ mass distribution is conducted in a final state with an electron or a muon, missing transverse momentum, and at least two jets. No significant excess is observed and limits are set using three benchmark models: WW resonance masses below 940 and 710 GeV are excluded at 95% confidence level for spin-2 Randall-Sundrum and bulk Randall-Sundrum gravitons, respectively; WZ resonance masses below 950 GeV are excluded at 95% confidence level for a spin-1 extended gauge model W' boson.

Search for a light charged Higgs boson in the decay channel H⁺ o c ars in t art events using collisions at sqrts = 7 TeV with the ATLAS detector

A search for a charged Higgs boson (H+) in t (t) over bar decays is presented, where one of the top quarks decays via t -> H(+)b, followed by H+ -> two jets (c (s) over bar). The other top quark decays to Wb, where the W boson then decays into a lepton (e/mu) and a neutrino. The data were recorded in pp collisions at root s = 7 TeV by the ATLAS detector at the LHC in 2011, and correspond to an integrated luminosity of 4.7 fb(-1). With no observation of a signal, 95 % confidence level (CL) upper limits are set on the decay branching ratio of top quarks to charged Higgs bosons varying between 5 % and 1 % for H+ masses between 90 GeV and 150 GeV, assuming B(H+ -> c (s) over bar) = 100 %.