Evaluation of Gigabit Ethernet with Java/HORB

We have evaluated a high speed network, Gigabit Ethernet(GbE), with Java/HORB, which means Java and Java-based Distributed Object Technology(DOT). Next generation of data acquisition(DAQ) needs high speed network such as ATM and GbE for data transfer in Level 3 and/or Level 2 trigger of the DAQ at large scale DAQ system like Large Hadron Collider(LHC). When evaluating the basic parameters of GbE, we considered bottleneck of network performance such as TCP buffer size, memory access speed, Maximum Transmission Unit(MTU) and so on. We used network tools called TTCP and Netperf and some Java benchmark programs for evaluating DOTs, namely, HORB, RMI and Voyager. Linux and Windows/NT operating systems Client Computer SW Network Interface Card Gigabit Ethernet Server Computer FIGURE 1. Setup for performance evaluation on PC computers, and Solaris on UltraSPARC workstation were used. MTU had an important role of the data transfer. When 2 Ultra30/Solaris systems via GbE were...\ud \ud Note: as at 14 April 2010, the archival site for this conference proceedings (http://www.hep.net/chep98) redirects to http://www.hep.net/chep95, which contains the proceedings of CHEP'95. http://www.particle.cz/conferences/chep2009/previouscheps.aspx lists the publishers for this series of conferences

Iloprost suppresses connective tissue growth factor production in fibroblasts and in the skin of scleroderma patients

Patients with scleroderma receiving Iloprost as a treatment for severe Raynaud’s phenomenon report a reduction in skin tightness, suggesting that this drug inhibits skin fibrosis. Connective tissue growth factor (CTGF), a recently described profibrotic cytokine, acts downstream and in concert with TGF-β to stimulate the fibrotic process and is involved in the fibrosis seen in scleroderma. Here we show that Iloprost, acting by elevation of cAMP, blocks the induction of CTGF and the increase in collagen synthesis in fibroblasts exposed to TGF-β. The potency of Iloprost with respect to suppression of CTGF far exceeds that of other prostanoid receptor agonists, suggesting that its effect is mediated by the prostacyclin receptor IP. By sampling dermal interstitial fluid using a suction blister device, we show that CTGF levels are greatly elevated in the dermis of scleroderma patients compared with healthy controls and that Iloprost infusion causes a marked decrease in dermal CTGF levels. These studies suggest that Iloprost could be reducing the level of a key profibrotic cytokine in scleroderma patients and that endogenous production of eicosanoids may limit the fibrotic response to TGF-β