Factor H

DiScipio, Richard G.

doi:10.1016/b978-012733360-1/50029-4

Cited by 2 publications

(1 citation statement)

References 36 publications

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“…There are several methods for synthesis of well‐defined Au‐NPs in solution with narrow size distribution 6. One of the most common methods is the reduction of tetrachloroauric acid by various reducing agents such as sodium borohydride,7, 8 sodium cyanoborohydride,8 thiocyanate,9 white phosphorous,10 sodium citrate, ascorbic acid,11 aspartic acid,12 hydrazine hydrate, hydroxylamine,13, 14 aminodextran,15 citrate/tannic acid,6, 7 etc. During the reduction, trivalent gold utilized to zero‐valent gold and as a result colloidal solution with Au‐NPs was formed.…”

Section: Introductionmentioning

confidence: 99%

Assembly and Characterization of Polyurethane–Gold Nanoparticle Conjugates

Romaskevic¹,

Sedlevicius²,

Budrienė³

et al. 2011

Macro Chemistry & Physics

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The PU/Au-NPs conjugates based on poly(vinyl alcohol)-containing polyurethane microparticles coated with Au-NPs are prepared by a heat-treated method. The PU/Au-NPs conjugates are characterized by FT-IR , SEM, TEM analysis. The appearance of characteristic peaks in the FT-IR spectra at 1574 and 1624 cm − 1 , which are attributed to urethane groups, are presented for both PU and PU/Au-NPs conjugate. The absorption band at 1716-1718 cm − 1 , attributed to the hydrogen-bonded urethane carbonyl groups of PU/Au-NPs (13nm) -A is higher than that obtained for unmodifi ed PU. The Au-NPs (13nm) are found to be well dispersed in the PU. The Au-NPs (3.5nm) tend toward agglomeration when they are entrapped within PU. It is determined, that Au-NPs present in PU-Au conjugates quench the luminescence of PU.

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Section: Introductionmentioning

confidence: 99%

Assembly and Characterization of Polyurethane–Gold Nanoparticle Conjugates

Romaskevic¹,

Sedlevicius²,

Budrienė³

et al. 2011

Macro Chemistry & Physics

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The benefit of targeted and selective inhibition of the alternative complement pathway for modulating autoimmunity and renal disease in MRL/lpr mice

Sekine¹,

Kinser²,

Qiao³

et al. 2011

Arthritis & Rheumatism

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Objective. Complement has both protective and pathogenic functions in lupus due to a balance between its role in the clearance of immune complexes (ICs) and apoptotic cells and its role in inflammation. The classical pathway contributes to IC and apoptotic cell clearance, whereas the alternative pathway is a key mediator of renal inflammation. The aim of this study was to investigate the effect of a new targeted inhibitor of the alternative pathway, CR2-fH, on lupus-like renal disease in MRL/lpr mice.Methods. Mice were treated with either saline, CR2-fH, CR2-Crry (which inhibits all complement pathways), or soluble CR2 (sCR2; C3d-binding targeting vehicle). Sera were analyzed every 2 weeks for autoantibodies, circulating ICs, and C3. Urinary excretion of albumin was also determined, and kidneys were collected at 23 weeks for histologic evaluation.Results. Treatment with CR2-fH or CR2-Crry improved survival and significantly reduced proteinuria, glomerular C3 deposition, and the level of circulating ICs. CR2-fH, but not CR2-Crry, also significantly reduced glomerulonephritis, expression of serum antidouble-stranded DNA (anti-dsDNA) antibodies, and glomerular IgG and C1q deposition. Interestingly, sCR2 also significantly reduced the levels of anti-dsDNA antibodies and circulating ICs and reduced glomerular deposition of IgG, C1q, and C3, although there was no significant reduction in glomerulonephritis, proteinuria, or mortality.Conclusion. Targeted and selective inhibition of the alternative complement pathway is an effective treatment of murine lupus and is more effective than blockade of all pathways. The data demonstrate benefits to leaving the classical/lectin pathways intact and indicate distinct roles for the classical and alternative pathways of complement in disease progression. The sCR2-targeting vehicle contributes to therapeutic activity, possibly via modulation of autoimmunity.The complement system can be activated by 1 of 3 pathways (classical, lectin, and alternative) and provides important host defense, homeostasis, and immune regulatory functions. However, the complement system also plays a pathogenic role in many autoimmune and inflammatory diseases, including systemic lupus erythematosus (SLE) (1). SLE is the prototypic human autoimmune disease, and complement-mediated injury is initiated by immune complexes (ICs) formed by autoantibodies directed against a broad range of self antigens (2,3). The kidney is a major site of immune complex formation and/or deposition, and lupus nephritis is a major cause of morbidity and mortality, in both human SLE and murine models of lupus. There is, however, an apparent dual role for complement in the development and progression of lupus, as highlighted by the different roles of the classical and alternative complement pathways in the disease.Patients with homozygous deficiencies of early Supported by grants from the US Department of Defense (W81 XWH-07-1-0161) and the NIH (HL-082485).

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Factor H

Cited by 2 publications

References 36 publications

Assembly and Characterization of Polyurethane–Gold Nanoparticle Conjugates

Assembly and Characterization of Polyurethane–Gold Nanoparticle Conjugates

The benefit of targeted and selective inhibition of the alternative complement pathway for modulating autoimmunity and renal disease in MRL/lpr mice

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