Molding procedure for casting a variety of alloys

General procedure and molding sand composition for preparing molds usable for casting variety of alloys are developed. Molds are prepared from mixture of sand, sodium silicate binder, and organic liquid ester. Castings of radiographic quality are produced from various alloys

The APS Control System Network Upgrade

When it was installed,the Advanced Photon Source (APS) control system network was at the state-of-the-art. Different aspects of the system have been reported at previous meetings [1,2]. As loads on the controls network have increased due to newer and faster workstations and front-end computers, we have found performance of the system declining and have implemented an upgraded network. There have been dramatic advances in networking hardware in the last several years. The upgraded APS controls network replaces the original FDDI backbone and shared Ethernet hubs with redundant gigabit uplinks and fully switched 10/100 Ethernet switches with backplane fabrics in excess of 20 Gbits/s (Gbps). The central collapsed backbone FDDI concentrator has been replaced with a Gigabit Ethernet switch with greater than 30 Gbps backplane fabric. Full redundancy of the system has been maintained. This paper will discuss this upgrade and include performance data and performance comparisons with the original network

Changes in specific metabolic pathways are essential steps in the early apoptotic process in the liver

the immunosuppressant Cyclosporine A (CsA), we used multinuclear NMR spectroscopy and molecular studies to characterize metabolic pathways in mice liver during anti-Fas-induced apoptosis. An upregulation of specific metabolic pathways of glucose was the earliest indicator of the effect of Fas on the liver. CsA prevented apoptosis and energy failure at late stages, while the reversal of Fas-induced metabolic upregulation at early stages preceded the protective effect of EGF on programmed cell death. These phenomena provide useful hints for the understanding of early mechanisms controlling apoptotic cell death

Electron cooling of 8-GeV antiprotons at Fermilab's Recycler: Results and operational implications

Electron cooling of 8 GeV antiprotons at Fermilab's Recycler storage ring is now routinely used in the collider operation. It requires a 0.1-0.5 A, 4.3 MeV dc electron beam and is designed to increase the longitudinal phase-space density of the circulating antiproton beam. This paper briefly describes the characteristics of the electron beam that were achieved to successfully cool antiprotons. Then, results from various cooling force measurements along with comparison to a nonmagnetized model are presented. Finally, operational aspects of the implementation of electron cooling at the Recycler are discussed, such as adjustments to the cooling rate and the influence of the electron beam on the antiproton beam lifetime

Time-dependent effects of imatinib in human leukaemia cells: a kinetic NMR-profiling study

The goal of this study was to evaluate the time course of metabolic changes in leukaemia cells treated with the Bcr-Abl tyrosine kinase inhibitor imatinib. Human Bcr-Abl+ K562 cells were incubated with imatinib in a dose-escalating manner (starting at 0.1 μM with a weekly increase of 0.1 μM imatinib) for up to 5 weeks. Nuclear magnetic resonance spectroscopy and liquid-chromatography mass spectrometry were performed to assess a global metabolic profile, including glucose metabolism, energy state, lipid metabolism and drug uptake, after incubation with imatinib. Initially, imatinib treatment completely inhibited the activity of Bcr-Abl tyrosine kinase, followed by the inhibition of cell glycolytic activity and glucose uptake. This was accompanied by the increased mitochondrial activity and energy production. With escalating imatinib doses, the process of cell death rapidly progressed. Phosphocreatine and NAD+ concentrations began to decrease, and mitochondrial activity, as well as the glycolysis rate, was further reduced. Subsequently, the synthesis of lipids as necessary membrane precursors for apoptotic bodies was accelerated. The concentrations of the Kennedy pathway intermediates, phosphocholine and phosphatidylcholine, were reduced. After 4 weeks of exposure to imatinib, the secondary necrosis associated with decrease in the mitochondrial and glycolytic activity occurred and was followed by a shutdown of energy production and cell death. In conclusion, monitoring of metabolic changes in cells exposed to novel signal transduction modulators supplements molecular findings and provides further mechanistic insights into longitudinal changes of the mitochondrial and glycolytic pathways of oncogenesis