Measurement of dynamic beam-beam effects Ieiri, T.; Funakoshi, Y.; Kawamoto, T. ...
Physical review special topics. Accelerators and beams,
12/2005, Letnik:
8, Številka:
12
Journal Article
Recenzirano
Odprti dostop
A series of measurements were carried out to investigate the dynamic beam-beam effects at KEKB. The beam-beam kick and the coherent beam-beam tune shift were measured by comparing the beam parameters ...between a colliding bunch and a noncolliding one. We found that collisions occur with a horizontal orbit offset to obtain the maximum luminosity, and that this reproducible offset appears to be attributed to an electron cloud effect, which might play an important role in the beam-beam interaction. The horizontal beam size estimated from the beam-beam kick slightly decreased as the beam-beam parameter increased. The horizontal emittance estimated from the beam-beam tune shift was higher than an unperturbed emittance, and agreed with the calculated emittance using a higher-mode tune. The ratio of the square-root betatron function between two locations in the ring was measured as a function of the beam-beam parameter. These experimental results would provide useful information on dynamic beam-beam effects.
Messenger RNA decay, which is a regulated process intimately linked to translation, begins with the deadenylation of the poly(A) tail at the 3′ end. However, the precise mechanism triggering the ...first step of mRNA decay and its relationship to translation have not been elucidated. Here, we show that the translation termination factor eRF3 mediates mRNA deadenylation and decay in the yeast Saccharomyces cerevisiae. The N-domain of eRF3, which is not necessarily required for translation termination, interacts with the poly(A)-binding protein PABP. When this interaction is blocked by means of deletion or overexpression of the N-domain of eRF3, half-lives of all mRNAs are prolonged. The eRF3 mutant lacking the N-domain is deficient in the poly(A) shortening. Furthermore, the eRF3-mediated mRNA decay requires translation to proceed, especially ribosomal transition through the termination codon. These results indicate that the N-domain of eRF3 mediates mRNA decay by regulating deadenylation in a manner coupled to translation.
The mammalian GTP-binding protein GSPT, whose carboxy-terminal sequence is homologous to the eukaryotic elongation factor EF1alpha, binds to the polypeptide chain releasing factor eRF1 to function as ...eRF3 in translation termination. However, the amino-terminal domain of GSPT, which contains a prion-like sequence, is not required for the binding. Instead, the amino-terminal domain is capable of binding to the carboxy-terminal domain of polyadenylate-binding protein (PABP), whose amino terminus is associating with the poly(A) tail of mRNAs, presumably for their stabilization. Interestingly, multimerization of PABP with poly(A), which is ascribed to the action of its carboxy-terminal domain, was completely inhibited by the interaction with the amino-terminal domain of GSPT. This may facilitate shortening of the poly(A) tail of mRNAs by an RNase. Thus, GSPT/eRF3 appears to function not only as a stimulator of eRF1 in the translation termination but also as an initiator of the mRNA degradation machinery. Further physiological and cell biological approaches will be necessary to show whether our current in vitro findings on GSPT/eRF3 indeed reflect its bifunctional properties in living cells.
This paper demonstrates a practical application of coupling a hydrodynamic model with a wave model for the calculation of storm tide elevations in the St. Johns River (Northeastern Florida). ...Hurricane Floyd (1999) is chosen as the storm of interest due to its track which paralleled the northeast coast of Florida without making a direct landfall on the St. Johns River. The advanced circulation (ADCIRC) numerical code is applied as the hydrodynamic model for the computation of two-dimensional circulation resulting from astronomic tides and meteorologically induced storm surge. The simulating waves nearshore (SWAN) numerical code is applied as the wave model for the computation of wind-induced waves. Two model implementations are considered in order to investigate the effect of short wave contributions on the overall storm tide water level: (1) a one-way coupling procedure that transfers gradient of wave radiation stresses from SWAN to ADCIRC; and (2) a two-way coupling procedure that builds on the former to include feedback of water levels and currents from ADCIRC to SWAN. Simulated storm tide elevations are compared to historical National Ocean Service data to result in two major conclusions: (1) wind-induced waves play a significant role in the storm tide (contributing 10–15% of the peak water level), namely with respect to the transfer of momentum from the dissipation of short waves to the long-wave motion of the storm surge; and (2) a local-scale hydrodynamic model requires the application of a hydrograph boundary condition in order to account for the remote effects of the storm surge response.
Recently, it was shown that Rho-kinase plays an important role in blood pressure regulation. However, it is not known whether Rho-kinase is involved in atherogenesis. Monocyte chemoattractant ...protein-1 (MCP-1) is an important chemokine that regulates monocyte recruitment and atherogenesis. Therefore, we examined the role of Rho and Rho-kinase in the angiotensin (Ang) II-induced expression of MCP-1. Ang II dose- and time-dependently enhanced the expression of MCP-1 mRNA and the protein production in vascular smooth muscle cells. CV11974, an Ang II type 1 receptor (AT(1)-R) specific antagonist inhibited the enhancement of MCP-1 expression by Ang II, suggesting that the effect of Ang II is mediated by the AT(1)-R. Botulinum C3 exotoxin, a specific inhibitor of Rho, suppressed Ang II-induced MCP-1 production. To examine the role of Rho-kinase in Ang II-induced MCP-1 expression, we used adenovirus-mediated overexpression of the dominant negative mutant of Rho-kinase (AdDNRhoK) or Y-27632, a specific inhibitor of Rho-kinase. Both AdDNRhoK and Y-27632 strongly inhibited Ang II-induced MCP-1 expression. Although inhibition of extracellular signal-regulated protein kinase (ERK) by PD 098,059 also inhibited Ang II-induced MCP-1 expression, Y-27632 did not affect Ang II-induced activation of ERK. These results indicate that Rho-kinase plays a critical role in Ang II-induced MCP-1 production independent of ERK. The Rho-Rho-kinase pathway may be a novel target for the inhibition of Ang II signaling and the treatment of atherosclerosis.
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