A search for neutral Higgs bosons has been performed using the full sample of Z 0 decays collected by the OPAL detector at LEP up to 1995. The data were taken at centre-of-mass energies between 88 GeV and 95 GeV and correspond to an integrated luminosity of approximately 160 pb 1. The present search addresses the processes Z 0 !H 0 Z and h 0 Z , where H 0 is the Higgs boson predicted by the Standard Model and h 0 the lightest neutral scalar Higgs boson predicted in the framework of the Minimal Supersymmetric Standard Model. For the virtual Z 0 boson, Z , the following decay c hannels are considered: Z ! , e + e and +. One candidate event
The spectral functions of the vector current and the axial-vector current have been measured in hadronic τ decays using the OPAL detector at LEP. Within the framework of the Operator Product Expansion a simultaneous determination of the strong coupling constant α s , the non-perturbative operators of dimension 6 and 8 and of the gluon condensate has been performed. Different perturbative descriptions have been compared to the data. The Contour Improved Fixed Order Perturbation Theory gives α s (m 2 τ ) = 0.348±0.009 exp ±0.019 theo at the τ -mass scale and α s (m 2 Z ) = 0.1219±0.0010 exp ±0.0017 theo at the Z 0 -mass scale. The values obtained for α s (m 2 Z ) using Fixed Order Perturbation Theory or Renormalon Chain Resummation are 2.3 % and 4.1 % smaller, respectively. The 'running' of the strong coupling between s 0 ≃ 1.3 GeV 2 and s 0 = m 2 τ has been tested from direct fits to the integrated differential hadronic decay rate R τ (s 0 ). A test of the saturation of QCD sum rules at the τ -mass scale has been performed.
Abstract-Angiotensin II (Ang II) is now believed to play a critical role in the pathogenesis of hypertrophy and/or hyperplasia of vascular smooth muscle cells (VSMCs). Several G i -and G q -coupled receptors, including the Ang II type 1 (AT 1 ) receptor, activate Rho and Rho-associated kinase in Swiss 3T3 cells and cardiac myocytes. However, little is known about the role of Rho-kinase in Ang II-induced vascular hypertrophy in VSMCs. In the present study, we explored the role of Rho and Rho-kinase in Ang II-induced protein synthesis in VSMCs. In unstimulated cells, RhoA was observed predominantly in the cytosolic fraction, but it was translocated in part to the particulate fraction in response to Ang II (100 nmol/L). This effect was completely blocked by the AT 1 receptor blocker candesartan but not by the Ang II type 2 (AT 2 ) receptor antagonist PD123319. Botulinum C 3 exoenzyme, which inactivated RhoA, attenuated Ang II-induced [ 3 H]leucine incorporation. The specific Rho-kinase inhibitor, Y-27632, dose-dependently abolished Ang II-induced protein synthesis and also suppressed Ang II-induced c-fos mRNA expression. On the other hand, Y-27632 had no effect on Ang II-stimulated phosphorylation of p70 S6 kinase and extracellular signal-regulated kinase 1/2, which are reported to be involved in Ang II-induced protein synthesis, nor had it any effect on the Ang II-induced phosphorylation of PHAS-I, a heat-and acid-stable eIF-4E-binding protein. The phosphorylation of PHAS-I is regulating for translation initiation. These observations suggest that the Rho, Rho-kinase, and c-fos pathways may play a role in Ang II-induced hypertrophic changes of VSMCs through a novel pathway. Key Words: angiotensin II Ⅲ hypertrophy Ⅲ G proteins P revious studies have reported that medial thickening, at least in large conduit vessels, is due in part to increased vascular smooth muscle cell (VSMC) mass, which occurs primarily by enlargement or hypertrophy of preexisting VSMCs, with little or no change in the number of VSMCs. 1,2 There is clear evidence implicating a role for angiotensin II (Ang II) in the mediation of VSMC hypertrophy during chronic hypertension. For instance, angiotensin-converting enzyme inhibitors and Ang II receptor blockers have been shown to be highly effective in inhibiting the development of VSMC medial hypertrophy in a variety of hypertensive animal models. 3,4 Importantly, the effects of angiotensinconverting enzyme inhibitors or Ang II antagonists do not appear to be due simply to blood pressure lowering, because other antihypertensive drugs were not as efficacious in blocking hypertrophy despite equipotent reductions in blood pressure. Consistent with in vivo studies, several laboratories have shown that Ang II stimulates increased protein synthesis and cellular hypertrophy in cultured VSMCs by stimulating Ang II type 1 (AT 1 ) receptors. The mechanism of this pathway is not clear and seems to be complex. 5,6 There has been considerable interest in identifying the mechanism and cellular signaling pathways w...
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