Today's data centers face extreme challenges in providing low latency. However, fair sharing, a principle commonly adopted in current congestion control protocols, is far from optimal for satisfying latency requirements.We propose Preemptive Distributed Quick (PDQ) flow scheduling, a protocol designed to complete flows quickly and meet flow deadlines. PDQ enables flow preemption to approximate a range of scheduling disciplines. For example, PDQ can emulate a shortest job first algorithm to give priority to the short flows by pausing the contending flows. PDQ borrows ideas from centralized scheduling disciplines and implements them in a fully distributed manner, making it scalable to today's data centers. Further, we develop a multipath version of PDQ to exploit path diversity.Through extensive packet-level and flow-level simulation, we demonstrate that PDQ significantly outperforms TCP, RCP and D 3 in data center environments. We further show that PDQ is stable, resilient to packet loss, and preserves nearly all its performance gains even given inaccurate flow information.
It is suggested that LPS released from the infected root canal triggers the synthesis of IL-1 alpha and TNF-alpha from macrophages. These pro-inflammatory cytokines up-regulate the production of MMP-1 by macrophages to promote periapical bone resorption.
Today's data centers face extreme challenges in providing low latency. However, fair sharing, a principle commonly adopted in current congestion control protocols, is far from optimal for satisfying latency requirements.We propose Preemptive Distributed Quick (PDQ) flow scheduling, a protocol designed to complete flows quickly and meet flow deadlines. PDQ enables flow preemption to approximate a range of scheduling disciplines. For example, PDQ can emulate a shortest job first algorithm to give priority to the short flows by pausing the contending flows. PDQ borrows ideas from centralized scheduling disciplines and implements them in a fully distributed manner, making it scalable to today's data centers. Further, we develop a multipath version of PDQ to exploit path diversity.Through extensive packet-level and flow-level simulation, we demonstrate that PDQ significantly outperforms TCP, RCP and D 3 in data center environments. We further show that PDQ is stable, resilient to packet loss, and preserves nearly all its performance gains even given inaccurate flow information.
Abstract-Antioxidants that prevent LDL from oxidation may reduce atherosclerosis. Salvia miltiorrhiza Bunge is a Chinese herb widely used for the treatment of atherosclerosis-related disorders. Salvianolic acid B (Sal B), a water-soluble polyphenolic antioxidant isolated from the roots of this plant, was found to scavenge 1,1-diphenyl-2-picrylhydrazyl radicals and inhibit LDL oxidation more effectively than probucol. In order to evaluate the antiatherogenic potential, New Zealand White rabbits were fed for 12 weeks a normal diet, a high cholesterol diet, a high cholesterol diet containing 1% probucol, or a high cholesterol diet containing a 5% water-soluble extract of S miltiorrhiza (SM). Both SM and probucol feeding reduced plasma cholesterol. LDLs from the SM-treated group were more resistant to Cu 2ϩ -induced oxidation and contained more vitamin E (21.7Ϯ2.1 nmol/mol LDL cholesterol) than did LDLs from the high cholesterol diet group (9.6Ϯ1.8 nmol/mol LDL cholesterol) (PϽ.005). Endothelial damage, determined at week 6, was reduced by 53% in the SM group (PϽ.01). SM treatment reduced the atherosclerotic area in the abdominal aorta by 56% (PϽ.005) and cholesterol deposition in the thoracic aorta by 50% (PϽ.005). The severity of atherosclerosis in the SM group was significantly reduced after adjustment by using cholesterol exposure as an index of the cholesterol-lowering effect. This study concludes that the reduction of atherosclerosis by SM relies not only on its cholesterol-lowering effect but more heavily on its antioxidant potential to prevent endothelial damage and inhibit LDL oxidative modification in hypercholesterolemic animals. (Arterioscler Thromb Vasc Biol. 1998;18:481-486.)
Numerous in vitro models have demonstraed the capacity of wear particles to stimulate the release of soluble pro‐inflammatory products with the ability to induce local bone resorption. Recent observations have demonstrated that binding of lipopolysaccharide (LPS) to particulate wear deris can significantly modulate the pattern of cell response in the in vitro models. These findings raise concerns over the possible role of LPS in the athogenesis of aseptic looseing after total joint replacements, and also indicates the importance of controlling for possible confounding effects of LPS contamination in the in vitro models used to study the reactive nature of wear debris. Our studies were undertaken to rigorously analyze the effects of particle‐associated LPS on cell responses and to assess the efficacy ofdifferent treatment protocols to inactivate LPS associated with different particulate materials. Particles of cobalt‐chrome alloy, titanium‐6‐aluminum‐4‐vanadium, titanium nitride and silica were pretreated with LPS and exposed to multiple treatment protocols. When cells were treated with „as‐received”︁ particles prepared by washing in ethanol, small amounts of TNF‐α, IL‐1β, and IL‐1α were detected. In contrast, all particle species pretreated with LPS produced marked increases in TNF‐α, IL‐1α, and IL‐1β release, as well as upregulation of corresponding mRNa levels even after ethanol washing. Boiling the LPS‐pretreated particles in 1% acetic acid or autoclaving and baking the particles also markedly reduced and in some instances abolished the effect of the LPS‐pretreatment. This indicates that LPS binds to the surface of particles of diverse composition and that the bound LPS is biologically active. Treatment protocols to inactivate particle‐associated LPS demonstrated significant differences in effcacy. When the most rigorous treatments were utilized, essentially all LPS activity could be eliminated. Particles treated with these methods retained some capacity to stimulated cytokine release, but activities were markedly reduced. These results provide further evidnce indicating that LPS contamination of particulate materials can markedly enhance their biological activity. This potential confounding effect needs to be carefully monitored and controlled in the in vitro model systems systems used to evaluate wear particles. Furthermore, the presence of particle‐associated endotoxin at the bone‐implant interface in vivo could markedly enhance the adverse biological activity of particulate wear debris. © 2002 Published by Elsevier Science Ltd. On behalf of Orthopaedic Research Society.
The present study examined the response of antioxidant systems to NaCl stress and the relative importance of Na 1 and Clin NaCl-induced antioxidant systems in roots of rice seedlings. NaCl treatment caused an increase in the activities of ascorbate peroxidase (APX) and glutathione reductase (GR) in roots of rice seedlings, but had no effect on the activities of superoxide dismutase (SOD) and catalase (CAT). There were detectable differences in APX and GR isoenzymes between control and NaCl-treated roots. Levels of activity for SOD and CAT isoenzymes did not change in NaCl-stressed roots compared with the control roots. NaCl treatment produced an increase in H 2 O 2 , ascorbate (AsA), dehydro-ascorbate (DHA), reduced glutathione (GSH), and oxidized glutathione (GSSG) levels. Treatment with 50 mM Na-gluconate (whose anion is not permeable to membrane) led to a similar Na 1 level in roots to that with 100 mM NaCl. It was found that treatment with 50 mM Na-gluconate affected H 2 O 2 , AsA, and DHA levels, APX and GR activities, OsAPX and OsGR mRNA induction in the same way as 100 mM NaCl. These observed changes seem to be mediated by Na 1 toxicity and not by Cltoxicity. On the other hand, it was found that NaCl, but not Na-gluconate and NaNO 3 , caused an increase in GSH and GSSG levels, indicating that Cl -, rather than Na 1 , is responsible for the NaCl-increased GSH and GSSG levels in roots of rice seedlings.
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