| 1. |
- Niemi, MEK, et al.
(författare)
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- 2021
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swepub:Mat__t
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| 2. |
- Kanai, M, et al.
(författare)
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- 2023
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swepub:Mat__t
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| 9. |
- Schael, S, et al.
(författare)
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Precision electroweak measurements on the Z resonance
- 2006
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Ingår i: Physics Reports. - : Elsevier BV. - 0370-1573 .- 1873-6270. ; 427:5-6, s. 257-454
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Forskningsöversikt (refereegranskat)abstract
- We report on the final electroweak measurements performed with data taken at the Z resonance by the experiments operating at the electron-positron colliders SLC and LEP. The data consist of 17 million Z decays accumulated by the ALEPH, DELPHI, L3 and OPAL experiments at LEP, and 600 thousand Z decays by the SLID experiment using a polarised beam at SLC. The measurements include cross-sections, forward-backward asymmetries and polarised asymmetries. The mass and width of the Z boson, m(Z) and Gamma(Z), and its couplings to fermions, for example the p parameter and the effective electroweak mixing angle for leptons, are precisely measured: m(Z) = 91.1875 +/- 0.0021 GeV, Gamma(Z) = 2.4952 +/- 0.0023 GeV, rho(l) = 1.0050 +/- 0.0010, sin(2)theta(eff)(lept) = 0.23153 +/- 0.00016. The number of light neutrino species is determined to be 2.9840 +/- 0.0082, in agreement with the three observed generations of fundamental fermions. The results are compared to the predictions of the Standard Model (SM). At the Z-pole, electroweak radiative corrections beyond the running of the QED and QCD coupling constants are observed with a significance of five standard deviations, and in agreement with the Standard Model. Of the many Z-pole measurements, the forward-backward asymmetry in b-quark production shows the largest difference with respect to its SM expectation, at the level of 2.8 standard deviations. Through radiative corrections evaluated in the framework of the Standard Model, the Z-pole data are also used to predict the mass of the top quark, m(t) = 173(+10)(+13) GeV, and the mass of the W boson, m(W) = 80.363 +/- 0.032 GeV. These indirect constraints are compared to the direct measurements, providing a stringent test of the SM. Using in addition the direct measurements of m(t) and m(W), the mass of the as yet unobserved SM Higgs boson is predicted with a relative uncertainty of about 50% and found to be less than 285 GeV at 95% confidence level. (c) 2006 Elsevier B.V. All rights reserved.
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| 12. |
- Glasbey, JC, et al.
(författare)
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- 2021
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swepub:Mat__t
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| 14. |
- Abdallah, J, et al.
(författare)
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Production of Xi(0)(c) and Xi(b) in Z decays and lifetime measurement of Xi(b)
- 2005
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Ingår i: European Physical Journal C. Particles and Fields. - : Springer Science and Business Media LLC. - 1434-6044 .- 1434-6052. ; C:44, s. 299-309
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Tidskriftsartikel (refereegranskat)abstract
- The charmed strange baryon Xi(c)(0) was searched for in the decay channel Xi(c)(0) -> Xi(-)pi(+), and the beauty strange baryon Xi(b) in the inclusive channel Xi(b) -> Xi(-)l(-)(nu) over barX, using the 3.5 million hadronic Z events collected by the DELPHI experiment in the years 1992-1995. The Xi(-) was reconstructed through the decay AT, using a constrained fit method for cascade decays. An iterative discriminant analysis was used for the Xi(c)(0) and Xi(b) selection. The production rates were measured to be f(Xi c)(0) x BR(Xi(c)(0) -> Xi(-)pi(+) = (4.7 +/- 1.4(stat.) +/- 1.1(syst.)) x 10(-4) per hadronic Z decay, and BR(b -> Xi(b))xBR(Xi(b) -> Xi(-)l(-)X) = (3.0 +/- 1.0(stat.) +/- 0.3(syst.)) x 10(-4) for each lepton species (electron or muon). The lifetime of the Xi(b) baryon was measured to be tau(Xi b) = 1.45(-0.43)(+0.55)(stat.)+/- 0.13(syst.) ps. A combination with the previous DELPHI lifetime measurement gives tau(Xi b) = 1.48(-0.31)(+0.40)(stat.)+/- 0.12(syst.) ps.
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| 26. |
- Goldman, RD, et al.
(författare)
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Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome
- 2004
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 101:24, s. 8963-8968
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Tidskriftsartikel (refereegranskat)abstract
- Hutchinson–Gilford progeria syndrome (HGPS) is a premature aging disorder, commonly caused by a point mutation in the lamin A gene that results in a protein lacking 50 aa near the C terminus, denoted LAΔ50. Here we show by light and electron microscopy that HGPS is associated with significant changes in nuclear shape, including lobulation of the nuclear envelope, thickening of the nuclear lamina, loss of peripheral heterochromatin, and clustering of nuclear pores. These structural defects worsen as HGPS cells age in culture, and their severity correlates with an apparent increase in LAΔ50. Introduction of LAΔ50 into normal cells by transfection or protein injection induces the same changes. We hypothesize that these alterations in nuclear structure are due to a concentration-dependent dominant-negative effect of LAΔ50, leading to the disruption of lamin-related functions ranging from the maintenance of nuclear shape to regulation of gene expression and DNA replication.
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| 41. |
- Shumaker, DK, et al.
(författare)
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Mutant nuclear lamin A leads to progressive alterations of epigenetic control in premature aging
- 2006
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 103:23, s. 8703-8708
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Tidskriftsartikel (refereegranskat)abstract
- The premature aging disease Hutchinson–Gilford Progeria Syndrome (HGPS) is caused by a mutant lamin A (LAΔ50). Nuclei in cells expressing LAΔ50 are abnormally shaped and display a loss of heterochromatin. To determine the mechanisms responsible for the loss of heterochromatin, epigenetic marks regulating either facultative or constitutive heterochromatin were examined. In cells from a female HGPS patient, histone H3 trimethylated on lysine 27 (H3K27me3), a mark for facultative heterochromatin, is lost on the inactive X chromosome (Xi). The methyltransferase responsible for this mark, EZH2, is also down-regulated. These alterations are detectable before the changes in nuclear shape that are considered to be the pathological hallmarks of HGPS cells. The results also show a down-regulation of the pericentric constitutive heterochromatin mark, histone H3 trimethylated on lysine 9, and an altered association of this mark with heterochromatin protein 1α (Hp1α) and the CREST antigen. This loss of constitutive heterochromatin is accompanied by an up-regulation of pericentric satellite III repeat transcripts. In contrast to these decreases in histone H3 methylation states, there is an increase in the trimethylation of histone H4K20, an epigenetic mark for constitutive heterochromatin. Expression of LAΔ50 in normal cells induces changes in histone methylation patterns similar to those seen in HGPS cells. The epigenetic changes described most likely represent molecular mechanisms responsible for the rapid progression of premature aging in HGPS patients.
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| 48. |
- Bravo, L, et al.
(författare)
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- 2021
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swepub:Mat__t
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| 49. |
- Tabiri, S, et al.
(författare)
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- 2021
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swepub:Mat__t
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