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Träfflista för sökning "WFRF:(Nash J.) srt2:(2005-2009)"

Search: WFRF:(Nash J.) > (2005-2009)

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1.
  • Schael, S, et al. (author)
  • Precision electroweak measurements on the Z resonance
  • 2006
  • In: Physics Reports. - : Elsevier BV. - 0370-1573 .- 1873-6270. ; 427:5-6, s. 257-454
  • Research review (peer-reviewed)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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2.
  • Greenhalgh, Christopher J, et al. (author)
  • SOCS2 negatively regulates growth hormone action in vitro and in vivo.
  • 2005
  • In: The Journal of clinical investigation. - 0021-9738. ; 115:2, s. 397-406
  • Journal article (peer-reviewed)abstract
    • Mice deficient in SOCS2 display an excessive growth phenotype characterized by a 30-50% increase in mature body size. Here we show that the SOCS2-/- phenotype is dependent upon the presence of endogenous growth hormone (GH) and that treatment with exogenous GH induced excessive growth in mice lacking both endogenous GH and SOCS2. This was reflected in terms of overall body weight, body and bone lengths, and the weight of internal organs and tissues. A heightened response to GH was also measured by examining GH-responsive genes expressed in the liver after exogenous GH administration. To further understand the link between SOCS2 and the GH-signaling cascade, we investigated the nature of these interactions using structure/function and biochemical interaction studies. Analysis of the 3 structural motifs of the SOCS2 molecule revealed that each plays a crucial role in SOCS2 function, with the conserved SOCS-box motif being essential for all inhibitory function. SOCS2 was found to bind 2 phosphorylated tyrosines on the GH receptor, and mutational analysis of these amino acids showed that both were essential for SOCS2 function. Together, the data provide clear evidence that SOCS2 is a negative regulator of GH signaling.
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6.
  • Nash, Peppi, et al. (author)
  • Placental dysfunction in Suramin-treated rats : impact of maternal diabetes and effects of antioxidative treatment
  • 2005
  • In: Journal of the Society for Gynecologic Investigation. - : Springer Science and Business Media LLC. - 1071-5576 .- 1556-7117. ; 12:3, s. 174-184
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: The aim of the present study was to evaluate a rat model of placental dysfunction/preeclampsia in pregnancies complicated by maternal diabetes. A second objective was to evaluate the effects of vitamin E treatment in this model. METHODS: Normal and streptozotocin-induced diabetic rats of two different strains (U and H) were given intraperitoneal (IP) injections of the angiogenesis inhibitor Suramin (Sigma Chemical Co, St Louis, MO) or saline in early pregnancy, and fed standard or vitamin E-enriched food. The outcome of pregnancy was evaluated on gestational day 20. RESULTS: In both rat strains Suramin caused fetal growth retardation, decreased placental blood flow, and increased placental concentration of the isoprostane 8-iso-PGF(2alpha). In the U rats Suramin also caused increased fetal resorption rate, increased maternal blood pressure, decreased renal blood flow, and diminished maternal growth. Diabetes caused severe maternal and fetal growth retardation, increased resorption rate, and increased placental 8-iso-PGF(2alpha) concentration independent of Suramin administration. The maternal and fetal effects of Suramin and diabetes were more pronounced in the U strain than in the H strain. Vitamin E treatment improved the status of Suramin-injected diabetic rats: in U rats the blood pressure increase was normalized; and in both U and H rats the decreased placental blood flow was marginally enhanced, and the increase in placental 8-iso-PGF(2alpha) was partly normalized by vitamin E. CONCLUSION: Suramin injections to pregnant rats cause a state of placental insufficiency, which in U rats resembles human preeclampsia. The induction of this condition is at least partly mediated by oxidative stress, and antagonized by antioxidative treatment. Maternal diabetes involves increased oxidative stress, and causes both maternal and fetal morbidity, which are only marginally affected by additional Suramin treatment.
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7.
  • Nash, Peppi, et al. (author)
  • Placental dysfunction in Suramin-treated rats : a new model for pre-eclampsia
  • 2005
  • In: Placenta. - : Elsevier BV. - 0143-4004 .- 1532-3102. ; 26:5, s. 410-418
  • Journal article (peer-reviewed)abstract
    • Impaired placentation and oxidative stress are proposed to play major roles in the pathogenesis of placental dysfunction and pre-eclampsia. This study was carried out to evaluate if inhibited angiogenesis by Suramin injections in early pregnancy may cause a condition resembling pre-eclampsia in rats. Rats of two different Sprague-Dawley strains, U and H, were given intraperitoneal injections of Suramin or saline in early pregnancy. The outcome of pregnancy was evaluated on gestational day 20. Suramin injections caused increased blood pressure and decreased renal blood flow in the U rats. In both rat strains Suramin decreased the placental blood flow and caused fetal growth retardation. In both strains the placental concentration of the isoprostane 8-epi-PGF2alpha was increased, indicating oxidative stress. The serum concentration of Endothelin-1 was increased in the U rats. The U strain had a lower basal placental blood flow, and the effects of Suramin were more pronounced in this strain. We conclude, that Suramin injections to pregnant rats cause a state of placental insufficiency, which partly resembles human pre-eclampsia. The induction of this condition is at least partly mediated by oxidative stress, and is subject to varied genetic susceptibility.
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8.
  • Persson, S., et al. (author)
  • Fabrication and characterisation of strained Si heterojunction bipolar transistors on virtual substrates
  • 2008
  • In: IEEE INTERNATIONAL ELECTRON DEVICES MEETING 2008, TECHNICAL DIGEST. - NEW YORK : IEEE. ; , s. 735-738
  • Conference paper (peer-reviewed)abstract
    • Strained Si HBTs have been demonstrated for the first time with a maximum current gain (P) of 3700 using a relaxed Si(0.85)Ge(0.15) virtual substrate, Si(0.7)Ge(0.3) base and strained Si emitter. This represents 10x and 27x larger gain compared with pseudomorphic SiGe HBTs and Si control BJTs which were manufactured in parallel and had current gains of 334 and 135, respectively. The strained Si HBTs exhibited satisfactory breakdown voltage (2.5 V) compared with SiGe HBTs (2.7 V) and Si BJTs (4.5 V) and excellent control of collector off-state leakage (< 20 fA).
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9.
  • Wikström, Anna-Karin, et al. (author)
  • Early postpartum changes in circulating pro- and anti-angiogenic factors in early-onset and late-onset pre-eclampsia
  • 2008
  • In: Acta Obstetricia et Gynecologica Scandinavica. - : Wiley. - 0001-6349 .- 1600-0412. ; 87:2, s. 146-153
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Pre-eclampsia is associated with altered plasma concentrations of the pro- and anti-angiogenic factors placental growth factor (PlGF), vascular endothelial growth factor-A (VEGF-A) and soluble fms-like tyrosine kinase 1 (sFlt1). However, there is insufficient knowledge about how these concentrations change after delivery, and whether the changes differ between early-onset and late-onset pre-eclampsia. METHODS: Plasma concentrations of sFlt1, PlGF and VEGF-A were measured before delivery and on days 1, 3 and 7 postpartum in women with early-onset (24-32 weeks' gestation) (n=18) and late-onset pre-eclampsia (35-42 weeks' gestation) (n=20) and in control groups delivered in corresponding weeks of gestation. RESULTS: All groups showed a rapid decrease in median sFlt1 concentration postpartum. Women with late-onset pre-eclampsia did not differ in sFlt1 concentration from controls on day 1 postpartum, whereas women with early-onset pre-eclampsia displayed a persistently elevated sFlt1 concentration on day 7 postpartum compared with controls. PlGF concentrations did not change from before delivery to any time point postpartum in the pre-eclampsia groups. VEGF-A concentrations were slightly increased on day 7 postpartum in both pre-eclampsia and control groups compared to concentrations prior to delivery. CONCLUSION: Median sFlt1 concentrations decreased rapidly postpartum in all groups, but remained higher in early-onset pre-eclampsia than controls on day 7. Postpartum, the median PlGF concentrations were similar to the concentrations measured before delivery in women with pre-eclampsia.
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10.
  • Wikström, Anna-Karin, et al. (author)
  • Evidence of increased oxidative stress and a change in the plasminogen activator inhibitor (PAI)-1 to PAI-2 ratio in early-onset but not late-onset preeclampsia
  • 2009
  • In: American Journal of Obstetrics and Gynecology. - : Elsevier BV. - 0002-9378 .- 1097-6868. ; 201:6, s. 597.e1-
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: The aims of this study were to measure the degree of oxidative stress and alterations in plasminogen activator inhibitor (PAI) type 1 and PAI-2 ratio in women with early-onset and late-onset preeclampsia. STUDY DESIGN: A case-control study was conducted in women with early-onset (24-32 weeks' gestation; n=18) and late-onset (35-42 weeks' gestation; n=20) preeclampsia and in control pregnant women at corresponding gestational weeks. Placenta, urine, and serum samples were collected. RESULTS: In early-onset preeclampsia, the median placental concentration of 8-iso-prostaglandin (PG)-F2alpha was higher and the PAI-1 to PAI-2 ratio higher than in early controls. These values did not differ between women with late-onset preeclampsia and their corresponding controls. Serum concentrations of 8-iso-PGF2alpha and vitamins C and E did not differ between cases and controls. CONCLUSION: Early-onset but not late-onset preeclampsia is associated with increased placental oxidative stress and increased PAI-1 to PAI-2 ratio.
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