Calibration Systems of the ATLAS Tile Calorimeter

TileCal is the hadronic calorimeter covering the most central region of the ATLAS experiment at the LHC. This sampling calorimeter uses iron plates as absorber and plastic scintillating tiles as the active material. A multi-faceted calibration system allows to monitor and equalize the calorimeter response at each stage of the signal production, from scintillation light to digitization. This calibration system is based on signal generation from different sources: a Cs radioactive source, laser light, charge injection and minimum bias events produced in proton-proton collisions. A brief description of the different TileCal calibration systems is given and the latest results on their performance in terms of calibration factors, linearity and stability are presented.Comment: 4 pages, 2 figures. For the 32nd Symposium on Physics in Collision, Strbske Pleso 12th - 15th September 201

Mobile satellite services: International co-ordination, co-operation and competition

In the context of a discussion of international cooperation, coordination and competition regarding mobile satellite services, it is asserted that: there will be more than one civil mobile satellite service in the 1990's; competition between these separate mobile satellite systems is inevitable; no system should enjoy monopoly protection or subsidies; and coordination and cooperation are desirable and necessary, since the available L-band spectrum is in short supply

The contribution of alcohol consumption and smoking to educational inequalities in life expectancy among Swedish men and women during 1991-2008

To assess the level and changes in contribution of smoking and alcohol-related mortality to educational differences in life expectancy in Sweden. We used register data on the Swedish population at ages 30-74 during 1991-2008. Cause of death was used to identify alcohol-related deaths, while smoking-related mortality was estimated using lung cancer mortality to indirectly assess the impact of smoking on all-cause mortality. Alcohol consumption and smoking contributed to educational differences in life expectancy. Alcohol-related mortality was higher among men and contributed substantially to inequalities among men and made a small (but increasing) contribution to inequalities among women. Smoking-related mortality decreased among men but increased among women, primarily among the low educated. At the end of the follow-up, smoking-related mortality were at similar levels among men and women. The widening gap in life expectancy among women could largely be attributed to smoking. Smoking and alcohol consumption contribute to educational differences in life expectancy among men and women. The majority of the widening in the educational gap in mortality among women can be attributed to alcohol and smoking-related mortality.Peer reviewe

Planning in Small vs. Large Businesses: Do Managers Prefer Different Tools?

 Evidence that large and small businesses approach problems differently has raised ques- tions concerning the validity of applying large business prescriptions to small businesses. This issue was addressed bypresenting both large and small business planners with planning prob- lems differing in environmental volatility, system adaptation and nature of planning re- quirements. Different combinations of these factors were used togenerate twelve distinct plan- ning situations. Eight information processing aids were identified that have been described in the literature as planning tools. Each aid has been prescribed to be more appropriate for use in some planning situations than in others. The research tested hypotheses that planners in specific situations would use planning aids prescr ibed for those situations and that large and small business planners would approach the problems differently. Results are interpreted as indicating that use of planning aids does not correspond closely to the theoretical prescrip- tions but that other implicittheories may be operating and the implicit theories used in small businesses may be different than those used inlarge organizations

Overregulation of Health Care: Musings on Disruptive Innovation Theory

Disruptive innovation theory provides one lens through which to describe how regulations may stifle innovation and increase costs. Basing their discussion on this theory, Curtis and Schulman consider some of the effects that regulatory controls may have on innovation in the health sector

Electron Attachment and Electron Ionization of Formic Acid Clusters Embedded in Helium Nanodroplets

We report the results of an experimental study of electron ionization of large helium nanodroplets doped with formic acid (FA). Several homologous series of cluster anions are observed, including [FAn-H]−, undissociated FAn−, and these ions complexed with one or more H2O. Some major features resemble those observed upon sputtering of frozen FA films but they differ significantly from results obtained by electron attachment to bare FA clusters in the gas phase. The FAn− and (H2O)[FAn-H]− series show abrupt onsets above n = 2 and 5, respectively. A prominent resonance in the anion yield occurs at 22.5 eV due to the formation of an intermediate He−*. Also observed are homologous series of [FA-H]− or [FA2-H]− complexed with helium. The cation chemistry is dominated by the production of protonated formic acid clusters, [FAnH]+, but various other homologous cluster ion series are observed as well

The G protein-coupled oestrogen receptor 1 agonist G-1 disrupts endothelial cell microtubule structure in a receptor-independent manner.

The G protein-coupled oestrogen receptor GPER1, also known as GPR30, has been implicated in oestrogen signalling, but the physiological importance of GPER1 is not fully understood. The GPER1 agonist G-1 has become an important tool to assess GPER1-mediated cellular effects. Here, we report that this substance, besides acting via GPER1, affects the microtubule network in endothelial cells. Treatment with G-1 (3 μM) for 24 h reduced DNA synthesis by about 60 % in mouse microvascular endothelial bEnd.3 cells. Treatment with 3 μM G-1 prevented outgrowth of primary endothelial cells from mouse aortic explants embedded in Matrigel. Treatment with G-1 (0.3-3 μM) for 24 h disrupted bEnd.3 cell and HUVEC microtubule structure in a concentration-dependent manner as assessed by laser-scanning confocal immunofluorescence microscopy. G-1-induced (3 μM) disruption of microtubule was observed also after acute (3 and 6 h) treatment and in the presence of the protein synthesis inhibitor cycloheximide. Disruption of microtubules by 3 μM G-1 was observed in aortic smooth muscle cells obtained from both GPER1 knockout and wild-type mice, suggesting that G-1 influences microtubules through a mechanism independent of GPER1. G-1 dose dependently (10-50 μM) stimulated microtubule assembly in vitro. On the other hand, microtubules appeared normal in the presence of 10-50 μM G-1 as determined by electron microscopy. We suggest that G-1-promoted endothelial cell anti-proliferation is due in part to alteration of microtubule organization through a mechanism independent of GPER1. This G-1-promoted mechanism may be used to block unwanted endothelial cell proliferation and angiogenesis such as that observed in, e.g. cancer

The G Protein-Coupled Estrogen Receptor 1 (GPER1/GPR30) Agonist G-1 Regulates Vascular Smooth Muscle Cell Ca Handling.

The G protein-coupled estrogen receptor GPER1/GPR30 is implicated in blood pressure regulation but the mechanisms are not identified. Here, we hypothesize that GPER1 controls blood pressure by regulating vascular smooth muscle cell Ca(2+) handling. Treatment with the GPER1 agonist G-1 (in the µM concentration range) acutely reduced spontaneous and synchronous Ca(2+) spike activity in A7r5 vascular smooth muscle cells expressing mRNA for GPER1. Furthermore, G-1 (1 µM) attenuated the thromboxane A2 analogue U46619-stimulated Ca(2+) spike activity but had no effect on the U46619-induced increase in the basal level of Ca(2+). The voltage-sensitive L-type Ca(2+) channel blocker nifedipine (100 nM) reduced Ca(2+) spike activity similar to G-1. Pharmacological, but not physiological, concentrations of the estrogen 17β-estradiol reduced Ca(2+) spike activity. The GPER1 antagonist G-15 blocked G-1-induced downregulation of Ca(2+) spike activity, supporting a GPER1-dependent mechanism. G-1 (1 µM) and nifedipine (100 nM) attenuated the 30-mM KCl-evoked rise in intracellular Ca(2+) concentration, suggesting that G-1 blocks inflow of Ca(2+) via voltage-sensitive Ca(2+) channels. In conclusion, we demonstrate that the GPER1 agonist G-1 regulates vascular smooth muscle cell Ca(2+) handling by lowering Ca(2+) spike activity, suggesting a role for this mechanism in GPER1-mediated control of blood pressure. © 2013 S. Karger AG, Basel