Abetimus sodium (riquent) for the prevention of nephritic flares in patients with systemic lupus erythematosus.
ABSTRACT Abetimus sodium has been under development for the treatment of systemic lupus erythematosus since the early 1990s. Because its administration results in the selective reduction of circulating double-stranded DNA antibodies, La Jolla Pharmaceutical Company has focused on the agent's ability to prolong time to nephritic flare. Fourteen trials have been initiated since 1994, but the two pivotal registration trials failed to meet primary end points. The US Food and Drug Administration issued a letter in October 2004 that stated abetimus sodium was "approvable" pending the successful completion of a trial demonstrating clinical benefit. The fate of this agent lies in the ability of the company to successfully complete a phase III study.
Conference Paper: Implementation of the performance evaluation system for the NTP server[Show abstract] [Hide abstract]
ABSTRACT: Most routers working in the Internet support NTP and register the current accurate time on the NTP control message. But how precisely the time is maintained depends on the topology and/or load of mutual references of NTP. We implemented the application to send continuously NTP control messages with variable time intervals. We experimented to watch the behavior of the NTP daemon and then we can get the following results of the clock offset. First, we extracted effects of the dock offset maintained by different types of stratum servers. We have 0.133 msec/sec drift on the host with no support of NTP. Second, we extracted two cyclic jitters of clock offset on the stratum 1 server. One long cyclic interval is 50 second and the other is 2 second. Finally, we compared between the clock offset on the local stratum 2 server and the remote(long network distance) stratum 2 server and extracted the element of precision of the clock offset.Communications, Computers and signal Processing, 2003. PACRIM. 2003 IEEE Pacific Rim Conference on; 09/2003
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ABSTRACT: The glomerulonephritides are a collection of separate diseases with differing pathogeneses that collectively are common and important causes of renal disease. Effective, non-toxic immunomodulatory treatments for glomerulonephritis are lacking. This review will focus on our understanding of the role of leukocytes in immune glomerular disease, specifically in severe and rapidly progressive forms of glomerulonephritis, and provide examples of potential therapeutic targets. The glomerulus is a high flow, high pressure capillary plexus bounded by arterioles that is vulnerable to a variety of immune or inflammatory insults. The variety in the pathogenesis of different forms of glomerulonephritis, together with the capacity of both humoral and cellular effector arms to induce injury, means that understanding the pathogenesis of glomerulonephritis is necessary to effectively apply new treatments. Leukocytes are involved in the pathogenesis of glomerulonephritis at several levels, including the loss of tolerance, adaptive immune responses directed by T cells, cellular effectors inducing injury in delayed type hypersensitivity-like reactions, and by macrophage/neutrophil recruitment via the deposition of circulating immune complexes or in situ immune complexes. Evidence is emerging that anti-neutrophil cytoplasmic antibodies activate neutrophils, leading to glomerular capillaritis. Some therapeutic options limit local inflammation, while others modify the underlying pathogenetic immune response. Areas of current interest include the relationship between infiltrating and local cells, limiting effector cell activation, particularly macrophages; as well as understanding and targeting leukocyte recruitment to this unique vasculature. Modifying pathogenetic T or B cells also is a promising strategy in both systemic autoimmunity affecting the kidney and organ specific autoimmunity.Current Medicinal Chemistry 02/2008; 15(5):448-58. DOI:10.2174/092986708783503230 · 3.72 Impact Factor
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ABSTRACT: Current treatment options for systemic lupus erythaematosus (SLE) are diverse and poorly defined, and aggressive therapy can be associated with serious toxicity and tolerability issues. There is, therefore, a need for new and improved treatments to be studied thoroughly in well-designed controlled trials. B Cell dysfunction has emerged as a key pathophysiological component of SLE and is a prime target for the development of new agents for a wide range of lupus severity, including advanced disease. Although many current drugs appear to modify B cell function, the advent of new, targeted therapies offers the hope of improved efficacy and a better long-term tolerability profile.Annals of the rheumatic diseases 09/2007; 67(10):1374-81. DOI:10.1136/ard.2007.076745 · 9.27 Impact Factor