Integration of VICbus, FDL, SCI and Ethernet in the CERN CASCADE data acquisition system

Cascade is a multi-processor real-time data-acquisition system for HEP experiments developed at CERN by the ECP-DS group. Configurations supported today include VMEbus processors running OS-9 and UNIX workstations. The CASCADE data acquisition processes, called stages communicate via links, at present VICbus between VME crates and Ethernet between VMEbus processors and workstations. Work is in progress to introduce new inter-stage links based on the Fast Data Link between VME crates and on SCI for data exchange between SUN stations. The paper gives a short description of the architecture of CASCADE with emphasis on the link aspects. The implementation and current status of the inter-stage links based on VICbus, Ethernet, FDI, and SCI will be described and results on the performances presented

Expression and regulation of type 2A protein phosphatases and alpha4 signalling in cardiac health and hypertrophy

Abstract Cardiac physiology and hypertrophy are regulated by the phosphorylation status of many proteins, which is partly controlled by a poorly defined type 2A protein phosphatase-alpha4 intracellular signalling axis. Quantitative PCR analysis revealed that mRNA levels of the type 2A catalytic subunits were differentially expressed in H9c2 cardiomyocytes (PP2ACb[PP2ACa[PP4C[PP6C), NRVM (PP2ACb[PP2ACa = PP4C = PP6C), and adult rat ventricular myocytes (PP2ACa[ PP2ACb[PP6C[PP4C). Western analysis confirmed that all type 2A catalytic subunits were expressed in H9c2 cardiomyocytes; however, PP4C protein was absent in adult myocytes and only detectable following 26S proteasome inhibition. Short-term knockdown of alpha4 protein expression attenuated expression of all type 2A catalytic subunits. Pressure overload-induced left ventricular (LV) hypertrophy was associated with an increase in both PP2AC and alpha4 protein expression. Although PP6C expression was unchanged, expression of PP6C regulatory subunits (1) Sit4-associated protein 1 (SAP1) and (2) ankyrin repeat domain (ANKRD) 28 and 44 proteins was elevated, whereas SAP2 expression was reduced in hypertrophied LV tissue. Co-immunoprecipitation studies demonstrated that the interaction between alpha4 and PP2AC or PP6C subunits was either unchanged or reduced in hypertrophied LV tissue, respectively. Phosphorylation status of phospholemman (Ser63 and Ser68) was significantly increased by knockdown of PP2ACa, PP2ACb, or PP4C protein expression. DNA damage assessed by histone H2A.X phosphorylation (cH2A.X) in hypertrophied tissue remained unchanged. However, exposure of cardiomyocytes to H2O2 increased levels of cH2A.X which was unaffected by knockdown of PP6C expression, but was abolished by the short-term knockdown of alpha4 expression. This study illustrates the significance and altered activity of the type 2A protein phosphatase-alpha4 complex in healthy and hypertrophied myocardium

LKB1 and AMPK and the cancer-metabolism link - ten years after

The identification of a complex containing the tumor suppressor LKB1 as the critical upstream kinase required for the activation of AMP-activated protein kinase (AMPK) by metabolic stress was reported in an article in Journal of Biology in 2003. This finding represented the first clear link between AMPK and cancer. Here we briefly discuss how this discovery came about, and describe some of the insights, especially into the role of AMPK in cancer, that have followed from it. In September 2003, our groups published a joint paper [1] in Journal of Biology (now BMC Biology) that identified the long-sought and elusive upstream kinase acting on AMP-activated protein kinase (AMPK) as a complex containing LKB1, a known tumor suppressor. Similar findings were reported at about the same time by David Carling and Marian Carlson [2] and by Reuben Shaw and Lew Cantley [3]; at the time of writing these three papers have received between them a total of over 2,000 citations. These findings provided a direct link between a protein kinase, AMPK, which at the time was mainly associated with regulation of metabolism, and another protein kinase, LKB1, which was known from genetic studies to be a tumor suppressor. While the idea that cancer is in part a metabolic disorder (first suggested by Warburg in the 1920s [4]) is well recognized today [5], this was not the case in 2003, and our paper perhaps contributed towards its renaissance. The aim of this short review is to recall how we made the original finding, and to discuss some of the directions that these findings have taken the field in the ensuing ten years

The (In)Visibility of Gender in Scandinavian Climate Policy-Making

© 2014 Taylor & Francis. This article explores the link between gender representation and climate policy-making in Scandinavia. We ask to what extent equal descriptive representation (critical mass) results in substantive representation (critical acts). Our study shows that women and men are equally represented in administrative and political units involved in climate policy-making, and in some units women are in the majority. However, a text analysis of the outcomes, that is, the Scandinavian climate strategies, reveals a silence regarding gender, further confirmed through interviews. Accordingly, a critical mass of women does not automatically result in gender-sensitive climate policy-making, recognizing established gender differences in material conditions and in attitudes toward climate issues. In interviews, we also note that policy-makers are largely unaware of gender differences on climate issues in the Scandinavian context. We discuss why a critical mass of women in climate policy-making has not led to critical acts and offer alternative explanations informed by feminist IR theory. For example, poststructural feminism claims that masculine norms are deeply institutionalized in climate institutions; hence, policy-makers adapt their actions to the masculinized institutional environment. Thus, substantive representation should be understood in relation to gendered institutional processes

Coastal subsidence and relative sea level rise

Subsurface fluid-pressure declines caused by pumping of groundwater or hydrocarbons can lead to aquifer-system compaction and consequent land subsidence. This subsidence can be rapid, as much as 30 cm per year in some instances, and large, totaling more than 13 m in extreme examples. Thus anthropogenic subsidence may be the dominant contributor to relative sea-level rise in coastal environments where subsurface fluids are heavily exploited. Maximum observed rates of human-induced subsidence greatly exceed the rates of natural subsidence of unconsolidated sediments (∼0.1–1 cm yr ^−1 ) and the estimated rates of ongoing global sea-level rise (∼0.3 cm yr ^−1 )

Numerical Simulations of the Hydrothermal System at Lassen Volcanic National Park

The hydrothermal system in the vicinity of Lassen Volcanic National Park contains a central region of fluid upflow in which steam and liquid phases separate, with steam rising through a parasitic vapor-dominated zone and liquid flowing laterally toward areas of hot spring discharge south of the Park. A simplified numerical model was used to simulate the 10,000-20,000 year evolution of this system and to show that under certain circumstances fluid withdrawal from hot-water reservoirs south of the Park could significantly alter the discharge of steam from thermal areas within the Park